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World Blood Cancer Day 2020: Bring down your risk of this condition with easy diet tips – TheHealthSite

By daniellenierenberg

Bloodcanceris one of the most common types of cancer that generally affects people of all age groups. According to a report published by WHOs International Agency for Research on Cancer, India has the third-highest number of haematologicalcancers,popularly known as blood cancer. There was a time when cancer was considered an incurable disease, but over the recent years, the situations have changed drastically with the evolution in medical technology. This has made cancer treatments possible with up to 90 per cent survival chances. The World Blood Cancer Day is observed every year on May 28th around the world to show support for blood cancer patients. According to experts, early diagnosis in cancer, especially blood cancer, increases the chance of survival, thanks to evolved treatment modalities of the modern times. Also Read - World Blood Cancer Day 2020: Understanding the types and symptoms

Mostly, heamatological cancers originate in bone marrow, where blood is produced. This condition occurs when faulty blood cells affect the function of the normal ones that fend off infections and generate new cells. There are three types of blood cancers leukaemia, lymphoma and myeloma. In leukaemia, your body develops too many abnormal white blood cells (leukocytes) and makes it tough for your bone marrow to produce red blood cells. Lymphoma occurs when in the lymphocites while myeloma has its origin in the plasma cells of the blood. These are white blood cells produced in your bone marrow. Also Read - Researchers discover role of mutation in blood cancers

The prominent symptoms of blood cancer include chills, fatigue and weakness, night sweats, pain in the bones and joints, and swollen lymph nodes. It takes a toll on your immunity, making you susceptible to various infections and other conditions. Cancer also affects the rate at which your blood clots. So, small cuts or injuries may tend to bleed for a longer period of time. You may also experience unusual bruising, bleeding of the gums, and blood in stool. Women may go through heavy bleeding during their periods. Also Read - Today health tips: 6 lifestyle modifications to bring down your breast cancer risk

Experts are of the opinion that lymphoma in adults is 80-90 per cent curable and acute leukaemia in adults can be 40-50 per cent curable. However, many of the myeloma cases are incurable. The treatment for blood cancer mostly depends on the type of cancer, age of the patient and the severity of the cancer. On the basis of these factors, doctors may suggest chemotherapy, supportive care, stem cell transplantation, etc.

According to the guidelines of the American Oncology Institute, one can decrease the risk of blood can by following certain lifestyle measures. They include exercising regularly, eating healthy, avoiding exposure to herbicides, insecticides and radiations. Here are some simple dietary tips to bring down your chance of falling prey to this condition.

Eat generous amounts of vegetables and fruits, salads, beans and cereals in your diet. This will try increase your immunity.

These acids have anti-cancer properties. The best food sources could be fish, walnuts, soya bean, so on and so forth. You can also opt for fish oil supplements.

An antioxidant known as lycopene is present in tomatoes. It comes with cancer fighting properties. The best way to get lycopene from tomatoes is to heat them well. So, tomato soup can be a good option. You can also have it with other anti-oxidant rich veggies in the form of a salad.

Several studies have associated high intake of olive oil with cancer risk reduction. You can have this oil in your salads or sprinkle it on cooked veggies too. Also, try using olive oil while marinating your meat, fish or poultry.

Published : May 28, 2020 12:30 pm | Updated:May 28, 2020 1:17 pm

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World Blood Cancer Day 2020: Bring down your risk of this condition with easy diet tips - TheHealthSite

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Leonhardts Launchpads Announces Issuance of New U.S. Patent for Bioelectric Plus Biologics Platform for Organ Regeneration and Healing – Life Pulse…

By daniellenierenberg

United States, California, Irvine 05-27-2020 (PRDistribution.com) Latest Patent Further Strengthens Intellectual Property Portfolio Covering Novel Platform for Precisely ControllingRegenerative Protein Expressions Including Stem Cell Homing and Differentiation Control

Technology Has Key Potential Applications in Regeneration of Failing Heart, Brain, Kidney, Liver, Pancreas, Lungs, Aorta, Vision and Hearing as well as Transcutaneous Uses for Accelerated Wound Healing, Skin, Hair and Penile Function Regeneration (ED)Irvine, California, May 27th, 2020 Leonhardts Launchpads, an innovation and startup launch accelerator focused on developing novel therapeutics that harness the bodys innate mechanisms to regenerate failing organs and to heal tissues, today announced the issuance of a new U.S. patent providing broad protection for the companys first-of-its-kind combination bioelectrics and biologics technology platform, which has multiple potential therapeutic applications in organ regeneration and recovery. Previous stem cell therapies that delivered stem cells alone in a single application failed to regenerate organs fully. Electrical stimulation technologies to date have failed to zero in on and deliver the precise right bioelectric signaling sequences for controlling specific regenerative protein expressions when and where needed. This pioneering technology platform is the first to combine the powerful ability of bioelectric stimulation with repeat deliveries of not just stem cells but a whole host of support factors similar to an egg yolk designed to help cells survive, proliferate, engraft and differentiate with the intention of fully regenerating failing organs. stated primary inventor, Executive Chairman and CEO Howard J. Leonhardt. U.S. Patent 10,646,644 Issued May 12th, 2020 https://patents.justia.com/patent/10646644covers bioelectric stimulation controlled release of SDF1 and PDGF known stem cell homing and proliferation factors as well as use of a re-fillable micro infusion pump for slow infusion of a mixed composition of stem cells, exosomes, micro RNAs, nutrient hydrogel, growth factor cocktail, selected alkaloids and anti-inflammatory agents with the intention of regenerating organs and healing tissues. SDF1 and PDGF highlighted in these new patent claims also have strong capabilities in promoting arteriogenesis (mature blood vessel growth).The Leonhardt team has separately filed or acquired patent claims for bioelectric controlled expression of follistatin, klotho, tropoelastin, VEGF, IGF1, CXCL5, HIF1a, EGF, HGF, OPG, RANKL and COL17A1 all known to have a role in organ healing https://patents.justia.com/patent/20180064935. Separately the Leonhardts Launchpads startup CancerCell has 9 issued U.S. patents https://cancercellinc.com/list-of-the-issued-cancer-patents/ for bioelectric treatment of cancer and dozens of additional cancer treatment related claims pending https://patents.justia.com/patent/20190030330. The team has filed patent clams on the combination of bioelectric stimulation and PRF https://patents.justia.com/patent/20200000709. Other important patent filings have been submitted on bioelectric inflammation management https://patents.justia.com/patent/20190022389 and blood pressure management https://patents.justia.com/patent/20190022396The Leonhardts Launchpads technology platform is based on foundational scientific research that began in the late 1980s working with Dr. Race Kao and Dr. George Magovern Sr. in Pittsburgh when they injected satellite cells (myoblasts or muscle stem cells) to repair damaged heart tissue in dogs and published the results in The Physiologist in 1989. In 1995 Howard Leonhardt filed his first patent for a stem cell and biologics delivery system for organ repair ProCell https://patents.google.com/patent/US5693029A/en based on work that began in 1988. In 1998 the Leonhardt team began collaboration with Dr. Doris Taylor whom that year published a landmark paper in Nature Medicine https://www.nature.com/articles/nm0898-929 on repair of infarcted hearts with myoblast cells. Dr. Taylor currently still serves as co-chair of our Scientific Advisory Board today. In 1999 the Leonhardt team worked with Dr. Shinichi Kanno to publish in Circulation, the Journal of the American Heart Association, pioneering results with bioelectric stimulation driven VEGF protein expression for limb salvage via angiogenesis in animals https://www.ahajournals.org/doi/abs/10.1161/01.cir.99.20.2682 and filed a patent application for the same within a year. Since then the Leonhardt team and LeonhardtsLaunchpads and itsportfolio of startupshas had issued, pending,optioned orlicensed over 600patentclaims for organregeneration andrecovery. In 2001 Howard Leonhardt and Dr. Juan Chachques filed patents on bioelectric stimulation controlled myogenesis and dynamic cardiac support with an early less potent stem cell homing signal. That same year a Leonhardt led team working with Dr. Patrick Serruys completed the landmark first ever case of non-surgical cell based regeneration of a damaged human heart in The Netherlands. Howard Leonhardt began a collaboration at that time with Dr. Jorge Genovese co-inventor of this patent, and BioLeonhardts VP of Bioelectric Regeneration Research, that continues to this day. Over 200 dedicated talented people help Leonhardts Launchpads and its startups advance their developments almost every day see Team https://leonhardtventures.com/team/ and Scientific Advisory Board https://calxstars.com/scientific-advisory-board/.About Leonhardts Launchpads:Leonhardts Launchpads by Cal-X Stars Business Accelerator, Inc. in California, Leonhardts Launchpads Utah, Inc., Leonhardts Launchpads Australia PTY and Leonhardts Launchpads branches in Minneapolis, Pittsburgh and Brazil are the innovation and startup launch accelerator arms of Leonhardt Ventures (Leonhardt Vineyards LLC DBA Leonhardt Ventures). Leonhardt Ventures has been developing breakthrough medtech and biotech innovations since the 1980s. In the 1980s the team patented, developed and commercialized the PolyCath line of cardiovascular balloon catheters. In the 1990s they developed and completed the first non-surgical repair of an aortic aneurysm (Melbourne, Australia 1995) and patented what is still today the leading endovascular stent graft for aortic aneurysm repair. In that time period they also patented one of the first percutaneous heart valve systems. Since 2000 the team has been focused almost exclusively on stem cell, biologics and bioelectric based organ regeneration and healing. In May of 2001 the team completed the landmark first ever non-surgical case of cell therapy for heart damage recovery. In 2008 the team began exploring if what they had learned from research in regenerating hearts could be translated to other organs. The organization now has 30 related startups and organ specific innovations in its 2020 portfolio class https://leonhardtventures.com/development-pipeline/ in these groups (1) Heart & Cardiovascular, (2) Brain, (3) Cosmetic & Reproductive Health, (4) Major Organ Regeneration and (5) Cancer. The accelerator business model is to accelerate each organ specific innovation through first in human studies and then secure a strategic partner to advance the product through commercialization. Click on Leonhardt Ventures and Leonhardts Launchpads 2020 Annual Report for more information https://leonhardtventures.com/wp-content/uploads/2020/04/4_23_2020.pdfand our web site at http://www.leonhardtventures.comSee previous PDGF related press release https://www.biospace.com/article/releases/-b-leonhardt-b-and-b-genovese-b-file-patent-for-bioelectric-controlled-expression-of-pdgf-a-powerful-organ-regeneration-cytokine-/See previous KLOTHO anti-aging related press release https://www.biospace.com/article/leonhardt-s-launchpads-announces-filing-of-patent-for-bioelectric-stimulation-controlled-klotho-expression-powerful-anti-aging-and-regeneration-promoting-protein-/Contact See contact page on web site for contact information for all locations and phone numbers https://leonhardtventures.com/contact/Leonhardts Launchpads[emailprotected]Warning and Disclaimers: Product(s) are not yet proven safe or effective. Patents pending may not be issued. Patents licensed or optioned may not be maintained. Patents issued may be invalidated. Products are in early stage development. Forward looking statements may change without notice. As an investment these startups mentioned are in the highest risk category for total loss and only suitable for sophisticated experienced accredited investors. The company does not have on hand sufficient resources to bring these products through clinical studies and may not obtain these resources. The company is under staffed and under funded compared to most other participants in this space. Due to a small staff at the accelerator to maintain all web sites and other published materials they may not be fully up to date and there may be out date inaccurate information. If you have any questions on our products or our company please write us to ask.Leonhardts Launchpads by Cal-X Stars,18575 Jamboree Rd #6, Irvine, CA 92612Leonhardts Launchpads Utah, Inc.Research Lab @ 2500 S State St. #D249, Salt Lake City, UT 84115

Media Contacts:

Company Name: Leonhardts Launchpads by Cal-X Stars Business Accelerator, Inc.Full Name: Howard J. LeonhardtPhone: (424) 291-2133Email Address: Send EmailWebsite: http://www.leonhardtventures.com

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Merck’s KEYTRUDA (pembrolizumab) Superior to Standard of Care Chemotherapy in Patients with MSI-H Colorectal Cancer – Maryville Daily Times

By daniellenierenberg

KENILWORTH, N.J.--(BUSINESS WIRE)--May 28, 2020--

Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced the first presentation of results from KEYNOTE-177, a Phase 3 trial evaluating KEYTRUDA, Mercks anti-PD-1 therapy, for the first-line treatment of patients with microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR) unresectable or metastatic colorectal cancer. In this pivotal study, KEYTRUDA monotherapy significantly reduced the risk of disease progression or death by 40% (HR=0.60 [95% CI, 0.45-0.80; p=0.0002]) and showed a median progression-free survival (PFS) of 16.5 months compared with 8.2 months for patients treated with chemotherapy (investigators choice of mFOLFOX6 or FOLFIRI, with or without bevacizumab or cetuximab), a current standard of care in this patient population. As previously announced, the study will continue without changes to evaluate overall survival (OS), the other dual primary endpoint. These results were selected for presentation on Sunday, May 31, 2020 in the plenary session of the virtual scientific program of the 2020 American Society of Clinical Oncology (ASCO) Annual Meeting (Abstract #LBA4).

For many years, the standard of care for the first-line treatment of patients with MSI-H colorectal cancer has been the combination of mFOLFOX6 plus bevacizumab. This is the first time a single-agent, anti-PD-1 therapy demonstrated a superior, statistically significant and clinically meaningful improvement in progression-free survival compared to chemotherapy for these patients, said Dr. Roy Baynes, senior vice president and head of global clinical development, chief medical officer, Merck Research Laboratories. There is an unmet need for new treatment options in the first-line setting that may provide sustained, long-term improvements in outcomes for patients with MSI-H colorectal cancer. We are grateful to have the opportunity to present these practice-changing findings at the plenary session of this years ASCO.

KEYTRUDA monotherapy significantly reduced the risk of disease progression or death by 40% versus standard of care chemotherapy, with fewer treatment-related adverse events observed, in patients with MSI-H metastatic colorectal cancer. KEYTRUDA also demonstrated a long-term, durable response that lasted over two years for those who responded to treatment, said Thierry Andre, MD, professor of medical oncology, Sorbonne University, and Head of the Medical Oncology Department in St. Antoine Hospital, Assistance Publique Hpitaux de Paris. Data from KEYNOTE-177 show that KEYTRUDA monotherapy has the potential to become the new standard of care for first-line treatment of patients with MSI-H metastatic colorectal cancer.

In May 2017, KEYTRUDA became the first cancer therapy approved by the U.S. Food and Drug Administration for use based on a biomarker, regardless of tumor type, in previously treated patients with MSI-H or dMMR solid tumors.

As announced, more than 80 abstracts in nearly 20 types of solid tumors and blood cancers will be presented from Mercks broad oncology portfolio and investigational pipeline at ASCO. A compendium of presentations and posters of Merck-led studies will be posted by Merck on Friday, May 29 at 8 a.m. ET. Follow Merck on Twitter via @Merck and keep up to date with ASCO news and updates by using the hashtag #ASCO20.

KEYNOTE-177 Study Design and Additional Data (Abstract #LBA4)

KEYNOTE-177 is a randomized, open-label, Phase 3 trial evaluating KEYTRUDA monotherapy versus standard of care chemotherapy for the first-line treatment of patients with MSI-H or dMMR metastatic colorectal cancer (ClinicalTrials.gov, NCT02563002 ). The dual primary endpoints are PFS and OS. The study enrolled 307 patients, who were randomized to receive either KEYTRUDA (200 mg intravenously on Day 1 of each three-week cycle for up to 35 cycles) or investigators choice of one of the following chemotherapy-based regimens: mFOLFOX6; mFOLFOX6 plus bevacizumab (5 mg/kg IV on Day 1 of each two-week cycle); mFOLFOX6 plus cetuximab (400 mg/m2 IV, then 250 mg/m2 weekly in each two-week cycle); FOLFIRI; FOLFIRI plus bevacizumab (5 mg/kg IV on Day 1 of each two-week cycle); or FOLFIRI plus cetuximab (400 mg/m2 IV, then 250 mg/m2 weekly in each two-week cycle).

In this study, KEYTRUDA demonstrated a statistically significant and clinically meaningful improvement in PFS (HR=0.60 [95% CI, 0.45-0.80; p=0.0002]) and showed a median PFS of 16.5 months compared with 8.2 months for patients treated with chemotherapy. The two-year PFS rate was 48% with KEYTRUDA versus 19% with chemotherapy. The ORR was 43.8% with KEYTRUDA versus 33.1% with chemotherapy, with a complete response observed in 11.1% and 3.9% of patients, respectively; partial responses were observed in 32.7% and 29.2% of patients, respectively. Median duration of response was not reached with KEYTRUDA (range, 2.3+ to 41.4+) versus 10.6 months with chemotherapy (range, 2.8 to 37.5+). Additionally, 83% of patients had durable responses lasting at least two years with KEYTRUDA versus 35% with chemotherapy. In the study, 59% of patients in the intent-to-treat population received subsequent anti-PD-1/PD-L1 therapy after discontinuing study treatment in the chemotherapy arm.

The safety profile of KEYTRUDA demonstrated a lower incidence of Grade 3 treatment-related adverse events (AEs) versus chemotherapy (22% versus 66%, respectively), and no new toxicities were observed. Immune-mediated AEs and infusion reactions occurred in 31% of patients receiving KEYTRUDA and 13% of patients receiving chemotherapy. The most commonly reported immune-mediated AEswere hypothyroidism (12%) and colitis (7%) with KEYTRUDA, and infusion reactions (8%) with chemotherapy.

Merck will hold a virtual investor event in conjunction with the ASCO Annual Meeting on Tuesday, June 2 at 2 p.m. ET. Details will be provided at a date closer to the event at http://investors.merck.com/home/default.aspx.

About Microsatellite Instability High (MSI-H)

Microsatellite instability (or MSI) is defined by the National Cancer Institute as a change that occurs in the DNA of certain cells (such as tumor cells) in which the number of repeats of microsatellites (short, repeated sequences of DNA) is different from the number of repeats that was in the DNA when it was inherited. The cause of MSI may be a defect in the ability to repair mistakes made when DNA is copied in the cell. This defect is also referred to as mismatch repair deficiency (dMMR). It is estimated that approximately 5-15% of colorectal cancer patients have tumors that score as either MSI-H or dMMR when testing is performed.

Colorectal cancer starts in the colon or the rectum, and these cancers are referred to as colon cancer and rectal cancer depending on where the cancer starts. Colorectal cancer often begins with growths on the inner lining of the colon or rectum called polyps, which can change into cancer over time. Colorectal cancer is the third most commonly diagnosed cancer and the second most common cause of cancer-related death worldwide. It is estimated there were nearly 850,000 new cases of colorectal cancer and more than 880,000 deaths from the disease globally in 2018. In the United States, it is estimated there will be nearly 105,000 new cases of colon cancer and more than 43,000 new cases of rectal cancer, resulting in more than 53,000 deaths from colorectal cancer in 2020. The five-year survival rates for advanced/metastatic colon cancer and rectal cancer (stage IV) are estimated to be 14% and 15%, respectively.

About KEYTRUDA (pembrolizumab) Injection, 100 mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,200 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patient's likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least 1 other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for treatment of patients with PMBCL who require urgent cytoreductive therapy.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [combined positive score (CPS) 10], as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

KEYTRUDA is indicated for the treatment of patients with Bacillus Calmette-Guerin (BCG)-unresponsive, high-risk, non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Microsatellite Instability-High (MSI-H) Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR)

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

KEYTRUDA, in combination with axitinib, is indicated for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grades 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

Immune-Mediated Hepatitis

KEYTRUDA can cause immune-mediated hepatitis. Hepatitis occurred in 0.7% (19/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.4%), and 4 (<0.1%). Monitor patients for changes in liver function. Administer corticosteroids for Grade 2 or greater hepatitis and, based on severity of liver enzyme elevations, withhold or discontinue KEYTRUDA.

Hepatotoxicity in Combination With Axitinib

KEYTRUDA in combination with axitinib can cause hepatic toxicity with higher than expected frequencies of Grades 3 and 4 ALT and AST elevations compared to KEYTRUDA alone. With the combination of KEYTRUDA and axitinib, Grades 3 and 4 increased ALT (20%) and increased AST (13%) were seen. Monitor liver enzymes before initiation of and periodically throughout treatment. Consider more frequent monitoring of liver enzymes as compared to when the drugs are administered as single agents. For elevated liver enzymes, interrupt KEYTRUDA and axitinib, and consider administering corticosteroids as needed.

Immune-Mediated Endocrinopathies

KEYTRUDA can cause adrenal insufficiency (primary and secondary), hypophysitis, thyroid disorders, and type 1 diabetes mellitus. Adrenal insufficiency occurred in 0.8% (22/2799) of patients, including Grade 2 (0.3%), 3 (0.3%), and 4 (<0.1%). Hypophysitis occurred in 0.6% (17/2799) of patients, including Grade 2 (0.2%), 3 (0.3%), and 4 (<0.1%). Hypothyroidism occurred in 8.5% (237/2799) of patients, including Grade 2 (6.2%) and 3 (0.1%). The incidence of new or worsening hypothyroidism was higher in 1185 patients with HNSCC (16%) receiving KEYTRUDA, as a single agent or in combination with platinum and FU, including Grade 3 (0.3%) hypothyroidism. Hyperthyroidism occurred in 3.4% (96/2799) of patients, including Grade 2 (0.8%) and 3 (0.1%), and thyroiditis occurred in 0.6% (16/2799) of patients, including Grade 2 (0.3%). Type 1 diabetes mellitus, including diabetic ketoacidosis, occurred in 0.2% (6/2799) of patients.

Monitor patients for signs and symptoms of adrenal insufficiency, hypophysitis (including hypopituitarism), thyroid function (prior to and periodically during treatment), and hyperglycemia. For adrenal insufficiency or hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 adrenal insufficiency or hypophysitis and withhold or discontinue KEYTRUDA for Grade 3 or Grade 4 adrenal insufficiency or hypophysitis. Administer hormone replacement for hypothyroidism and manage hyperthyroidism with thionamides and beta-blockers as appropriate. Withhold or discontinue KEYTRUDA for Grade 3 or 4 hyperthyroidism. Administer insulin for type 1 diabetes, and withhold KEYTRUDA and administer antihyperglycemics in patients with severe hyperglycemia.

Immune-Mediated Nephritis and Renal Dysfunction

KEYTRUDA can cause immune-mediated nephritis. Nephritis occurred in 0.3% (9/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.1%), and 4 (<0.1%) nephritis. Nephritis occurred in 1.7% (7/405) of patients receiving KEYTRUDA in combination with pemetrexed and platinum chemotherapy. Monitor patients for changes in renal function. Administer corticosteroids for Grade 2 or greater nephritis. Withhold KEYTRUDA for Grade 2; permanently discontinue for Grade 3 or 4 nephritis.

Immune-Mediated Skin Reactions

Immune-mediated rashes, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) (some cases with fatal outcome), exfoliative dermatitis, and bullous pemphigoid, can occur. Monitor patients for suspected severe skin reactions and based on the severity of the adverse reaction, withhold or permanently discontinue KEYTRUDA and administer corticosteroids. For signs or symptoms of SJS or TEN, withhold KEYTRUDA and refer the patient for specialized care for assessment and treatment. If SJS or TEN is confirmed, permanently discontinue KEYTRUDA.

Other Immune-Mediated Adverse Reactions

Immune-mediated adverse reactions, which may be severe or fatal, can occur in any organ system or tissue in patients receiving KEYTRUDA and may also occur after discontinuation of treatment. For suspected immune-mediated adverse reactions, ensure adequate evaluation to confirm etiology or exclude other causes. Based on the severity of the adverse reaction, withhold KEYTRUDA and administer corticosteroids. Upon improvement to Grade 1 or less, initiate corticosteroid taper and continue to taper over at least 1 month. Based on limited data from clinical studies in patients whose immune-related adverse reactions could not be controlled with corticosteroid use, administration of other systemic immunosuppressants can be considered. Resume KEYTRUDA when the adverse reaction remains at Grade 1 or less following corticosteroid taper. Permanently discontinue KEYTRUDA for any Grade 3 immune-mediated adverse reaction that recurs and for any life-threatening immune-mediated adverse reaction.

The following clinically significant immune-mediated adverse reactions occurred in less than 1% (unless otherwise indicated) of 2799 patients: arthritis (1.5%), uveitis, myositis, Guillain-Barr syndrome, myasthenia gravis, vasculitis, pancreatitis, hemolytic anemia, sarcoidosis, and encephalitis. In addition, myelitis and myocarditis were reported in other clinical trials, including classical Hodgkin lymphoma, and postmarketing use.

Treatment with KEYTRUDA may increase the risk of rejection in solid organ transplant recipients. Consider the benefit of treatment vs the risk of possible organ rejection in these patients.

Infusion-Related Reactions

KEYTRUDA can cause severe or life-threatening infusion-related reactions, including hypersensitivity and anaphylaxis, which have been reported in 0.2% (6/2799) of patients. Monitor patients for signs and symptoms of infusion-related reactions. For Grade 3 or 4 reactions, stop infusion and permanently discontinue KEYTRUDA.

Complications of Allogeneic Hematopoietic Stem Cell Transplantation (HSCT)

Immune-mediated complications, including fatal events, occurred in patients who underwent allogeneic HSCT after treatment with KEYTRUDA. Of 23 patients with cHL who proceeded to allogeneic HSCT after KEYTRUDA, 6 (26%) developed graft-versus-host disease (GVHD) (1 fatal case) and 2 (9%) developed severe hepatic veno-occlusive disease (VOD) after reduced-intensity conditioning (1 fatal case). Cases of fatal hyperacute GVHD after allogeneic HSCT have also been reported in patients with lymphoma who received a PD-1 receptorblocking antibody before transplantation. Follow patients closely for early evidence of transplant-related complications such as hyperacute graft-versus-host disease (GVHD), Grade 3 to 4 acute GVHD, steroid-requiring febrile syndrome, hepatic veno-occlusive disease (VOD), and other immune-mediated adverse reactions.

In patients with a history of allogeneic HSCT, acute GVHD (including fatal GVHD) has been reported after treatment with KEYTRUDA. Patients who experienced GVHD after their transplant procedure may be at increased risk for GVHD after KEYTRUDA. Consider the benefit of KEYTRUDA vs the risk of GVHD in these patients.

Increased Mortality in Patients With Multiple Myeloma

In trials in patients with multiple myeloma, the addition of KEYTRUDA to a thalidomide analogue plus dexamethasone resulted in increased mortality. Treatment of these patients with a PD-1 or PD-L1 blocking antibody in this combination is not recommended outside of controlled trials.

Based on its mechanism of action, KEYTRUDA can cause fetal harm when administered to a pregnant woman. Advise women of this potential risk. In females of reproductive potential, verify pregnancy status prior to initiating KEYTRUDA and advise them to use effective contraception during treatment and for 4 months after the last dose.

In KEYNOTE-006, KEYTRUDA was discontinued due to adverse reactions in 9% of 555 patients with advanced melanoma; adverse reactions leading to permanent discontinuation in more than one patient were colitis (1.4%), autoimmune hepatitis (0.7%), allergic reaction (0.4%), polyneuropathy (0.4%), and cardiac failure (0.4%). The most common adverse reactions (20%) with KEYTRUDA were fatigue (28%), diarrhea (26%), rash (24%), and nausea (21%).

In KEYNOTE-002, KEYTRUDA was permanently discontinued due to adverse reactions in 12% of 357 patients with advanced melanoma; the most common (1%) were general physical health deterioration (1%), asthenia (1%), dyspnea (1%), pneumonitis (1%), and generalized edema (1%). The most common adverse reactions were fatigue (43%), pruritus (28%), rash (24%), constipation (22%), nausea (22%), diarrhea (20%), and decreased appetite (20%).

In KEYNOTE-054, KEYTRUDA was permanently discontinued due to adverse reactions in 14% of 509 patients; the most common (1%) were pneumonitis (1.4%), colitis (1.2%), and diarrhea (1%). Serious adverse reactions occurred in 25% of patients receiving KEYTRUDA. The most common adverse reaction (20%) with KEYTRUDA was diarrhea (28%).

In KEYNOTE-189, when KEYTRUDA was administered with pemetrexed and platinum chemotherapy in metastatic nonsquamous NSCLC, KEYTRUDA was discontinued due to adverse reactions in 20% of 405 patients. The most common adverse reactions resulting in permanent discontinuation of KEYTRUDA were pneumonitis (3%) and acute kidney injury (2%). The most common adverse reactions (20%) with KEYTRUDA were nausea (56%), fatigue (56%), constipation (35%), diarrhea (31%), decreased appetite (28%), rash (25%), vomiting (24%), cough (21%), dyspnea (21%), and pyrexia (20%).

In KEYNOTE-407, when KEYTRUDA was administered with carboplatin and either paclitaxel or paclitaxel protein-bound in metastatic squamous NSCLC, KEYTRUDA was discontinued due to adverse reactions in 15% of 101 patients. The most frequent serious adverse reactions reported in at least 2% of patients were febrile neutropenia, pneumonia, and urinary tract infection. Adverse reactions observed in KEYNOTE-407 were similar to those observed in KEYNOTE-189 with the exception that increased incidences of alopecia (47% vs 36%) and peripheral neuropathy (31% vs 25%) were observed in the KEYTRUDA and chemotherapy arm compared to the placebo and chemotherapy arm in KEYNOTE-407.

In KEYNOTE-042, KEYTRUDA was discontinued due to adverse reactions in 19% of 636 patients with advanced NSCLC; the most common were pneumonitis (3%), death due to unknown cause (1.6%), and pneumonia (1.4%). The most frequent serious adverse reactions reported in at least 2% of patients were pneumonia (7%), pneumonitis (3.9%), pulmonary embolism (2.4%), and pleural effusion (2.2%). The most common adverse reaction (20%) was fatigue (25%).

In KEYNOTE-010, KEYTRUDA monotherapy was discontinued due to adverse reactions in 8% of 682 patients with metastatic NSCLC; the most common was pneumonitis (1.8%). The most common adverse reactions (20%) were decreased appetite (25%), fatigue (25%), dyspnea (23%), and nausea (20%).

Adverse reactions occurring in patients with SCLC were similar to those occurring in patients with other solid tumors who received KEYTRUDA as a single agent.

In KEYNOTE-048, KEYTRUDA monotherapy was discontinued due to adverse events in 12% of 300 patients with HNSCC; the most common adverse reactions leading to permanent discontinuation were sepsis (1.7%) and pneumonia (1.3%). The most common adverse reactions (20%) were fatigue (33%), constipation (20%), and rash (20%).

In KEYNOTE-048, when KEYTRUDA was administered in combination with platinum (cisplatin or carboplatin) and FU chemotherapy, KEYTRUDA was discontinued due to adverse reactions in 16% of 276 patients with HNSCC. The most common adverse reactions resulting in permanent discontinuation of KEYTRUDA were pneumonia (2.5%), pneumonitis (1.8%), and septic shock (1.4%). The most common adverse reactions (20%) were nausea (51%), fatigue (49%), constipation (37%), vomiting (32%), mucosal inflammation (31%), diarrhea (29%), decreased appetite (29%), stomatitis (26%), and cough (22%).

In KEYNOTE-012, KEYTRUDA was discontinued due to adverse reactions in 17% of 192 patients with HNSCC. Serious adverse reactions occurred in 45% of patients. The most frequent serious adverse reactions reported in at least 2% of patients were pneumonia, dyspnea, confusional state, vomiting, pleural effusion, and respiratory failure. The most common adverse reactions (20%) were fatigue, decreased appetite, and dyspnea. Adverse reactions occurring in patients with HNSCC were generally similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy, with the exception of increased incidences of facial edema and new or worsening hypothyroidism.

In KEYNOTE-087, KEYTRUDA was discontinued due to adverse reactions in 5% of 210 patients with cHL. Serious adverse reactions occurred in 16% of patients; those 1% included pneumonia, pneumonitis, pyrexia, dyspnea, GVHD, and herpes zoster. Two patients died from causes other than disease progression; 1 from GVHD after subsequent allogeneic HSCT and 1 from septic shock. The most common adverse reactions (20%) were fatigue (26%), pyrexia (24%), cough (24%), musculoskeletal pain (21%), diarrhea (20%), and rash (20%).

In KEYNOTE-170, KEYTRUDA was discontinued due to adverse reactions in 8% of 53 patients with PMBCL. Serious adverse reactions occurred in 26% of patients and included arrhythmia (4%), cardiac tamponade (2%), myocardial infarction (2%), pericardial effusion (2%), and pericarditis (2%). Six (11%) patients died within 30 days of start of treatment. The most common adverse reactions (20%) were musculoskeletal pain (30%), upper respiratory tract infection and pyrexia (28% each), cough (26%), fatigue (23%), and dyspnea (21%).

In KEYNOTE-052, KEYTRUDA was discontinued due to adverse reactions in 11% of 370 patients with locally advanced or metastatic urothelial carcinoma. Serious adverse reactions occurred in 42% of patients; those 2% were urinary tract infection, hematuria, acute kidney injury, pneumonia, and urosepsis. The most common adverse reactions (20%) were fatigue (38%), musculoskeletal pain (24%), decreased appetite (22%), constipation (21%), rash (21%), and diarrhea (20%).

In KEYNOTE-045, KEYTRUDA was discontinued due to adverse reactions in 8% of 266 patients with locally advanced or metastatic urothelial carcinoma. The most common adverse reaction resulting in permanent discontinuation of KEYTRUDA was pneumonitis (1.9%). Serious adverse reactions occurred in 39% of KEYTRUDA-treated patients; those 2% were urinary tract infection, pneumonia, anemia, and pneumonitis. The most common adverse reactions (20%) in patients who received KEYTRUDA were fatigue (38%), musculoskeletal pain (32%), pruritus (23%), decreased appetite (21%), nausea (21%), and rash (20%).

In KEYNOTE-057, KEYTRUDA was discontinued due to adverse reactions in 11% of 148 patients with high-risk NMIBC. The most common adverse reaction resulting in permanent discontinuation of KEYTRUDA was pneumonitis (1.4%). Serious adverse reactions occurred in 28% of patients; those 2% were pneumonia (3%), cardiac ischemia (2%), colitis (2%), pulmonary embolism (2%), sepsis (2%), and urinary tract infection (2%). The most common adverse reactions (20%) were fatigue (29%), diarrhea (24%), and rash (24%).

Adverse reactions occurring in patients with gastric cancer were similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy.

Adverse reactions occurring in patients with esophageal cancer were similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy.

In KEYNOTE-158, KEYTRUDA was discontinued due to adverse reactions in 8% of 98 patients with recurrent or metastatic cervical cancer. Serious adverse reactions occurred in 39% of patients receiving KEYTRUDA; the most frequent included anemia (7%), fistula, hemorrhage, and infections [except urinary tract infections] (4.1% each). The most common adverse reactions (20%) were fatigue (43%), musculoskeletal pain (27%), diarrhea (23%), pain and abdominal pain (22% each), and decreased appetite (21%).

Adverse reactions occurring in patients with hepatocellular carcinoma (HCC) were generally similar to those in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy, with the exception of increased incidences of ascites (8% Grades 3-4) and immune-mediated hepatitis (2.9%). Laboratory abnormalities (Grades 3-4) that occurred at a higher incidence were elevated AST (20%), ALT (9%), and hyperbilirubinemia (10%).

Among the 50 patients with MCC enrolled in study KEYNOTE-017, adverse reactions occurring in patients with MCC were generally similar to those occurring in patients with melanoma or NSCLC who received KEYTRUDA as a monotherapy. Laboratory abnormalities (Grades 3-4) that occurred at a higher incidence were elevated AST (11%) and hyperglycemia (19%).

In KEYNOTE-426, when KEYTRUDA was administered in combination with axitinib, fatal adverse reactions occurred in 3.3% of 429 patients. Serious adverse reactions occurred in 40% of patients, the most frequent (1%) were hepatotoxicity (7%), diarrhea (4.2%), acute kidney injury (2.3%), dehydration (1%), and pneumonitis (1%). Permanent discontinuation due to an adverse reaction occurred in 31% of patients; KEYTRUDA only (13%), axitinib only (13%), and the combination (8%); the most common were hepatotoxicity (13%), diarrhea/colitis (1.9%), acute kidney injury (1.6%), and cerebrovascular accident (1.2%). The most common adverse reactions (20%) were diarrhea (56%), fatigue/asthenia (52%), hypertension (48%), hepatotoxicity (39%), hypothyroidism (35%), decreased appetite (30%), palmar-plantar erythrodysesthesia (28%), nausea (28%), stomatitis/mucosal inflammation (27%), dysphonia (25%), rash (25%), cough (21%), and constipation (21%).

Because of the potential for serious adverse reactions in breastfed children, advise women not to breastfeed during treatment and for 4 months after the final dose.

There is limited experience in pediatric patients. In a trial, 40 pediatric patients (16 children aged 2 years to younger than 12 years and 24 adolescents aged 12 years to 18 years) with various cancers, including unapproved usages, were administered KEYTRUDA 2 mg/kg every 3 weeks. Patients received KEYTRUDA for a median of 3 doses (range 117 doses), with 34 patients (85%) receiving 2 doses or more. The safety profile in these pediatric patients was similar to that seen in adults; adverse reactions that occurred at a higher rate (15% difference) in these patients when compared to adults under 65 years of age were fatigue (45%), vomiting (38%), abdominal pain (28%), increased transaminases (28%), and hyponatremia (18%).

Mercks Focus on Cancer

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Merck's KEYTRUDA (pembrolizumab) Superior to Standard of Care Chemotherapy in Patients with MSI-H Colorectal Cancer - Maryville Daily Times

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Regenerative Medicine Market to Exhibit a CAGR of 26.1% by 2026; Rising Prevalence of Genetic Disorders to Fuel Demand, states Fortune Business…

By daniellenierenberg

Pune, May 27, 2020 (GLOBE NEWSWIRE) -- The global regenerative medicine market size is expected to reach USD 151,949.5 billion by 2026, exhibiting a CAGR of 26.1% during the forecast period. The growing R&D investment by key players for the development of innovative regenerative therapies can be a vital factor enabling the growth of the market during the forecast period, states Fortune Business Insights in a report, titled Regenerative Medicine Market Size, Share and Industry Analysis By Product (Cell Therapy, Gene Therapy, Tissue Engineering, Platelet Rich Plasma), By Application (Orthopaedics, Wound Care, Oncology), By Distribution Channel (Hospitals, Clinics) & Regional Forecast, 2019 2026 the market size stood at USD 23,841.5 Million in 2018. The growing organ transplantation surgeries will spur opportunities for the market during the forecast period.

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Market Driver:

Escalating Cases of Genetic Disorders to Augment Growth

The increasing prevalence of chronic disorders can be an essential factor enabling the growth of the market. Similarly, the growing incidence of genetic disorders will fuel demand for the market. The growing investment in R&D activities by major market players will have a positive impact on the regenerative medicine market growth during the forecast period. For instance, in March 2018, SanBio Group, a leader in regenerative medicine and therapies for neurological disorders announced that it has made a deal with Hitachi Chemical Advanced Therapeutics Solutions, LLC, a cell manufacturing company for the development and manufacturing of innovative regenerative medicines.

Furthermore, the rising cases of neurological disorders will influence the healthy growth of the market. The growing healthcare expenditure in developed and developing countries will boost the market in the forthcoming years. The ongoing clinical trials and robust pipeline products in stem cell andgene therapy will contribute tremendously to the growth of the market. The rising utilization of skin substitutes, grafts, bone matrix, and other tissue-engineered regenerative medicine in orthopedic and neurosurgical applications will augment the growth of the market.

An Overview of the Impact of COVID-19 on this Market:

The emergence of COVID-19 has brought the world to a standstill. We understand that this health crisis has brought an unprecedented impact on businesses across industries. However, this too shall pass. Rising support from governments and several companies can help in the fight against this highly contagious disease. There are some industries that are struggling and some are thriving. Overall, almost every sector is anticipated to be impacted by the pandemic.

We are taking continuous efforts to help your business sustain and grow during COVID-19 pandemics. Based on our experience and expertise, we will offer you an impact analysis of coronavirus outbreak across industries to help you prepare for the future.

To get the short-term and long-term impact of COVID-19 on this Market.

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Regional Analysis:

Development of Novel Therapies to Favor Growth in North America

The market in North America generated a revenue of USD 9,128.2 million in 2018 and is predicted to grow rapidly during the forecast period owing to the presence of major pharmaceutical companies. The growing launch of novel therapeutics and the availability of advanced technologies along with clinical trials will support growth in North America. Asia Pacific is expected to witness a high growth rate during the forecast period owing to the

developing healthcare infrastructure and facilities. The increasing stem cell research in developing countries such as India, Japan China will contribute positively to the growth of the market. For instance, In April 2013, the Japan Ministry of Health, Labor, and Welfare approved Regenerative Medicine law. The growing number of clinical developments of regenerative and cell-based therapies will drive the market in the region. The increasing government initiatives for human embryonic stem cell research and development will further encourage growth in the region. The surge in geriatric patients, the evolving lifestyle of people, and the growing need for novel therapies are factors likely to aid the expansion of the market in Asia Pacific.

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Key Development:

2018: Novartis announced that it has received EUs approval for one-time gene therapy Luxturna, to restore vision in people with rare and genetically-associated retinal disease.

List of the Key Companies Operating in the Regenerative Medicine Market are:

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Have a Look at Related Reports:

Gene Therapy Market Size, Share and Global Trend By Disease Indication(Cancer, Genetic disorders, Cardiovascular diseases, Ophthalmology, Neurological conditions) By Type of Vectors (Viral vectors, Non-viral vectors), By Type of Cells(Somatic cells, Germline cells) and Geography Forecast till 2026

Induced Pluripotent Stem Cells Market Size, Share and Global Trend By Derived Cell Type (Amniotic cells, Fibroblasts, Keratinocytes, Hepatocytes, Others), By Application (Regenerative medicines, Drug development, Toxicity testing, Reprogramming technology, Academic research, Others), By End-user (Hospitals, Education & research institutes, Biotechnological companies) and Geography Forecast till 2026

Platelet Rich Plasma Market Size, Share And Global Trend By Origin (Allogeneic, Autologous, Homologous), By Type (Pure PRP, Leukocyte rich PRP, Leukocyte rich fibrin), By Application (Orthopaedic surgery, Cosmetic surgery, General surgery, Neurosurgery, Others), And Geography Forecast Till 2026

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Regenerative Medicine Market to Exhibit a CAGR of 26.1% by 2026; Rising Prevalence of Genetic Disorders to Fuel Demand, states Fortune Business...

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BREAKTHROUGH! Scientists Discover Particular Protein that Could Block Cancer Growth – Science Times

By daniellenierenberg

The Faculty of Health and Medical Sciences at the University of Copenhagen recently discovered how a particular protein, Phosphoprotein phosphatase 2A (PP2A), inhibits tumor development in mice.

Proteins are complex molecules in cells that are necessary for the function, structure, and regulation of the body's organs and tissues. Proteins have five primary functions: antibodies, enzymes, messengers, structural components, and transport or storage of atoms or small molecules.

Professor Jakob Nilsson, from the Novo Nordisk Foundation Center for Protein Research, explained that PP2A is called a household protein as it can be commonly found in most places. Everything that lives with simple cells or complex cells contain PP2A.

The PP2A Protein is also being studied by pharmaceutical companies as it is known to show unique patterns of kinase opposition, or simply, it is a tumor suppressor. Protein kinases are enzymes that induce change, switching active proteins into an inactive form.

While there is still insufficient research on which specific types of proteins PP2A regulates to prevent cancer, results from the new data do gain more insight.

Other tumor suppressor proteins include the retinoblastoma protein (pRb) and the p53 gene. Both regulate the cycling behavior of cells in a process called cell proliferation and growth are known as cell cycle progression.

Rb has a vital part in regulation G1/S transition, which is the 'start' checkpoint which controls the production of starter kinase proteins. What follows is Rb's 'role in the functioning of normal andcancer stem cells,' as well as its effect on the 'energy metabolism of cancer cells.'

According to a study called Nanostructures for Cancer Therapy, P53 is a protein that can 'respond to hypoxia, DNA damage, and loss of normal cell contacts when activated,' as it mediates the growth and death of cells.

The same study notes, 'targeting p53-MDM2 interaction would be attractive in cancer therapy.'

Read Also: Metformin, a Drug for Diabetes, is Investigated for Cancer-Causing Contaminant

Associate Professor Marie Kveiborg from the Biotech Research and Innovation Centre notes that what is new about their study is that they can show how the specific PP2AB56 'selects the phosphate groups that shall be removed from other proteins,' while it turns off the enzyme ADAM17. ADAM17 being switched off resulted in 'inhibition of tumor growth in mice.'

A disintegrin and metalloprotease domain 17 (ADAM17) is a protein-coding gene associated with diseases including inflammatory skin (psoriasis), inflammatory bowel disease (Crohn's disease), and breast cancer. The test mice were all injected with three variations of ADAM17 cells.

On the day of injection, '4T1 A17wt, I762A, and LEE cells,' all ADAM17 variants, were given and the scientists monitored tumor growth through time.

When they began observing how PP2A-B56 interacted with ADAM17, 'none of the mice injected with ADAM17 LEE cells reached tumor endpoint criteria, as opposed to ADAM17 wt or I762A injected mice, which exhibited only 50% survival by the end of the experiment.'

The newly discovered data on cancer research will hopefully develop into studies with human tumors, expressed by the researchers. The scientists concluded, 'the B56 inhibitor displays excellent specificity toward the PP2AB56 holoenzyme family.' As a result, scientists also want to make additional research to determine if PP2A also can regulate other proteins with its tumor suppressor function.

Read Also:Will COVID-19 End Scientific Breakthroughs?

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A caveolin binding motif in Na/K-ATPase is required for stem cell differentiation and organogenesis in mammals and C. elegans – Science Advances

By daniellenierenberg

INTRODUCTION

Embryonic development is characterized by the temporal and spatial regulation of cell proliferation, migration, differentiation, and tissue formation. Although these processes are genetically determined, several signaling mechanisms including Wnt have been recognized as essential in regulating cell lineage specification and organogenesis (13).

The Na/Kadenosine triphosphatase (ATPase) (NKA), discovered in crab nerve fibers by Skou (4), belongs to the P-type ATPase superfamily. It has an enzymatic function that couples adenosine 5-triphosphate (ATP) hydrolysis to the transmembrane movement of Na+ and K+ in a cell lineagedependent manner. For example, while the NKA is involved in the formation of action potentials in excitable cells, its polarized distribution is key to the functionality of the epithelium.

In addition to its canonical enzymatic function, we and others have shown that the NKA has an enzymatic activityindependent signaling function through its interactions with membrane cholesterol and proteins such as Src, epidermal growth factor (EGF) receptor, and caveolin-1 (58). We use the term signaling with liberty here, referring to the ability of NKA to work as a receptor, a scaffold, and a signal integrator by regulating the functions of its interacting proteins. This newly appreciated signaling function of the NKA has been implicated in several cellular processes (912). However, direct genetic evidence supporting a role for NKA signaling in animal physiology and disease progression is still lacking. This is due, in part, to the technical difficulties in studying its signaling separately from its ATPase-mediated pumping function because the latter is required for the survival of animal cells (13). Fundamentally, it is unknown whether the signaling function is an intrinsic property of the protein NKA, as its Na+- and K+-driven enzymatic activity has been recognized as. Therefore, we were prompted to address two important questions: (i) Were the signaling and Na+/K+ transport functions of the NKA coevolved? (ii) If so, does the signaling function of NKA represent a primordial yet common mechanism for the regulation of a fundamental process in animal biology?

Structurally, the NKA is composed of both and subunits. The subunit contains the binding sites for Na+/K+ as well as ouabain, which are distinct from that of other P-type ATPases (14). It also has an N-terminal caveolin binding motif (CBM) proximal to the first transmembrane helix (fig. S1A). To assess the functionality of this motif, we made F97A and F100A mutations that map to the rat 1 NKA sequence. This strategy has been used by others to study the function of CBM in proteins other than the NKA (15). We used a knockdown and rescue protocol to generate a stable cell line (LW-mCBM) that essentially expresses just the CBM mutant 1, which was confirmed using [3H]ouabain binding assays (fig. S1B). Western blot and confocal imaging analyses showed that the expression of mutant 1 NKA in LW-mCBM was comparable to that in the control cell line, named AAC-19 cells (fig. S1, B and C). The expression of CBM mutant 1 was sufficient to restore the expression of the 1 subunit of the NKA, allowing normal plasma membrane targeting of the CBM mutant NKA in LW-mCBM cells (fig. S1, C and D). The successful generation of a stable CBM mutant 1 cell line suggests that the CBM is not essential for the enzymatic activity of the NKA because the ion-transporting function is necessary for animal cell survival (13). In further support, we conducted kinetic studies of the CBM mutant NKA. As shown in Fig. 1A, the overall enzymatic activity per unit of 1 NKA expression was identical between the control AAC-19 and LW-mCBM cells. The Km values of Na+, K+, and ouabain were comparable between the CBM mutant NKA and control (Fig. 1, B to D) (16). Together, these data indicate that the N-terminal CBM is not directly involved in the regulation of the enzymatic properties of the NKA.

(A) Crude membrane preparations were made from AAC-19 and LW-mCBM cells and measured for ouabain-sensitive ATPase activity as described in Material and Methods. (B) Ouabain concentration curve. Crude membrane from LW-mCBM cells was prepared and measured for ATPase activity in the presence of different concentrations of ouabain. Data are shown as percentage of control, and each point represents three independent experiments. Curve fit analysis and IC50 (median inhibitory concentration) were calculated by GraphPad. (C and D) Measurements of Na+ and K+ Km. Assays were done as in (B). The combined data were collected from at least three repeats, and Km value (means SEM) was calculated using GraphPad.

On the basis of the above, we next turned our attention to determining the effects of the CBM mutation on signaling capabilities of the 1 NKA. Specifically, we first conducted immunoprecipitation experiments. As we reported previously in many types of cells (8), immunoprecipitation of caveolin-1 coprecipitated 1 in AAC-19 cells. In contrast, mutation of the CBM resulted in an over 80% decrease in coprecipitated 1 in LW-mCBM cells (Fig. 2A).

(A) Cell lysates from AAC-19 and LW-mCBM were immunoprecipitated (IP) with polyclonal anticaveolin-1 antibody. Immunoprecipitated complex was analyzed by Western blot for 1 and caveolin-1 (n = 4). **P < 0.01 compared to AAC-19. (B) Cell lysates from AAC-19 and LW-mCBM cells were subjected to sucrose gradient fractionation as described in Materials and Methods. A representative Western blot of three independent experiments was shown. **P < 0.01 in comparison to AAC-19. (C) AAC-19 and LW-mCBM cells were treated with different concentrations of ouabain for 10 min and analyzed by Western blot. A representative Western blot was shown (n = 4). *P < 0.05 versus 0 mM ouabain. (D) Cell growth curves of AAC-19 and LW-mCBM. *P < 0.05 versus AAC-19 cells. (E) BrdU assay of AAC-19 and LW-mCBM. The values are means SEM from at least three independent experiments. Photo credit: Xiaoliang Wang, Marshall Institute for Interdisciplinary Research at Marshall University.

To substantiate these observations, we next conducted a detergent-free and carbonate-based density gradient fractionation procedure and found that 1 NKA and its main signaling partners (Src and caveolin-1) were co-enriched in the low-density caveolar fractions, as previously reported in epithelial cells (8, 17). In sharp contrast, the expression of the CBM mutant 1 caused the redistribution of these proteins from low-density to high-density fractions (Fig. 2B). Quantitatively, when the ratios of fraction 4/5 of each protein versus total were calculated, we found that the low-density fraction 4/5 prepared from the control AAC-19 cells contained ~60, ~70, and 80% of caveolin-1, Src, and 1 NKA, respectively. However, in LW-mCBM cells, only ~20% of caveolin-1, Src, and 1 NKA were detected in fraction 4/5 (Fig. 2B).

To address the functional consequences of the dissociation of the 1 NKA from its signaling partners in LW-mCBM cells, we exposed these cells to ouabain, a specific agonist of the receptor NKA/Src complex. As shown in Fig. 2C, while ouabain stimulated phosphorylation of extracellular signalregulated kinase (ERK), a downstream effector of the NKA/Src signaling pathway in AAC-19 cells (5, 8), it failed to do so in LW-mCBM cells.

We have previously shown that 1 NKA signaling is key to the dynamic regulation of cell growth (16, 18). As shown in Fig. 2D, LW-mCBM cells grew much slower than AAC-19 cells. 5-Bromo-2-deoxyuridine (BrdU) incorporation assays further verified that the expression of CBM mutant 1 resulted in an inhibition of cellular proliferation (Fig. 2E). In short, the above in vitro experiments indicate that the gain of CBM enables the NKA to perform the enzymatic activityindependent signaling functions.

With the preceding in vitro data suggesting that the CBM is critically important to the signaling function of the NKA, we next set forth to test the physiological significance of this finding. Thus, we generated a knock-in mouse line expressing the aforementioned CBM mutant 1. The CBM mutant (mCBM) mouse was generated using the Cre/LoxP gene targeting strategy (19), as depicted in fig. S2A. The chimeric offspring were crossed to C57BL6 females to yield mCBM heterozygous mice, and the desired F97A and F100A substitutions were verified (fig. S2B). mCBM heterozygous mice were born fertile and survived to adulthood. Our attempts to generate mCBM homozygous mice yielded no viable homozygous pups (Fig. 3A) in nearly 400 young mice genotyped by polymerase chain reaction (PCR). These results document for the first time that the CBM in the 1 subunit of the NKA represents a fundamental signaling mechanism essential for mouse embryonic development and survival.

(A) Early embryonic lethality of mCBM homozygous embryos. (B) Morphological comparison and body size of wild-type (WT) (top), heterozygous (middle), and homozygous (bottom) mCBM embryos at E9.5. Black bars, 0.3 mm. The arrows show the abnormal head morphology. Body size was measured from at least 12 embryos in different genotypes by ImageJ. Data are presented as means SEM. ***P < 0.01 versus the average of WT. (C) Sagittal sections of WT and homozygous (Homo) and heterozygous (Het) embryos at E9.5 with hematoxylin and eosin (H&E) staining. Homozygous embryos that had defective brain development indicated by open arrows. (D) Brain cross section of WT, homozygous, and heterozygous embryos at E9.5 with H&E staining. Homozygous embryos that had unclosed neural tube in forebrain, midbrain, and hindbrain were indicated by arrows; WT and heterozygous E9.5 embryos with closed neural tube were indicated by arrowhead. (E) Morphological comparison of WT and Na/K-ATPase 1 (+/) embryos at E9.5. White bars, 0.3 mm (n = 5 to 7). Photo credit: Xiaoliang Wang, Marshall Institute for Interdisciplinary Research at Marshall University.

There is evidence that endogenous ouabain is important in animal physiology because of its role in stimulating the signaling function of the NKA (10, 19, 20). Because the loss of the CBM abolishes ouabain-induced signal transduction in vitro, we tested whether administration of pNaKtide, a specific inhibitor of the receptor NKA/Src complex (21), would cause the same embryonic lethality as we observed in mCBM mice. As depicted in fig. S3, we observed no change in fetal survival after administration of pNaKtide to female mice before mating and continued until the end of pregnancy. It is important to mention that pNaKtide has been proven to be specific and effective in blocking the NKA/Src receptor signaling in vivo (2226), and our control experiments showed that pNaKtide could cross the placental barrier. Moreover, this lack of pNaKtide effect on mouse embryogenesis appears to be consistent with a previous report demonstrating that neutralization of endogenous ouabain by injection of an anti-ouabain antibody did affect the kidney development of neonatal mice but did not affect their overall survival (20). On the basis of these, we concluded that the NKA/Src receptor function in the CBM mutant embryo was not the direct cause of lethality and set out to identify a hitherto unrecognized NKA CBM-dependent yet NKA-Srcindependent underlying mechanism.

Embryo implantation within mice occurs around embryonic day 4.5 (E4.5) (27), followed by gastrulation around E5.5 to E7.5 (28), when the simple embryo develops into an organized and patterned structure with three germ layers (29). Subsequently, organogenesis takes place at E8.0 and onward; the patterned embryo starts to develop its organ systems including the brain, heart, limbs, and spinal cord.

To further analyze and explore the molecular mechanisms of the CBM mutation in the embryonic development of mice, we harvested the fertilized eggs at E1.5, and cultured them in vitro. It has previously been demonstrated that 1 knockout results in the failure of blastocyst formation (13). In contrast, we found that eggs from mCBM heterozygous parents developed into morphologically normal blastocysts. These findings indicate that loss of the CBM does not affect the molecular mechanisms necessary for blastocyst formation. Thus, a loss of functional 1 CBM and complete knockout of 1 NKA both result in embryonic lethality but differ by their specific mechanisms. Knockout of 1 NKA inevitably causes the loss of NKA enzymatic function, which is incompatible with life (13), and results in the failure of blastocyst formation in mice. In contrast, our in vitro data indicate that a loss of the CBM does not cause any notable alteration in NKA enzymatic activity, which is supported by the observation that mCBM mice are still capable of producing morphologically normal blastocysts. Consequently, CBM role in development appears to be critical at a developmental stage beyond blastocyst stage, and we further set out to identify this stage.

To this end, we collected and genotyped embryos or yolk sacs from mCBM heterozygous mice at different days of gestation. We first dissected 31 embryos at E12.5 from three different mice (Fig. 3A). Reabsorption and empty deciduae were observed in six implantation sites with only the mothers genotype detectable. At E9.5, we were able to dissect a total of 303 embryos. Sixty-four of them were mCBM homozygous (21%), 71 were wild-type (23%), and 168 were mCBM heterozygous (55%) (Fig. 3A).

To further analyze the embryonic developmental defects, we examined mCBM embryos at E7.5, E8.5, and E9.5. The embryos looked similar between wild-type and mCBM homozygous mice at E7.5 and E8.5 under dissection microscopy. However, we found several severe morphological defects in homozygous embryos at E9.5 (Fig. 3, C and D). First, the overall size of embryos was considerably reduced in mCBM homozygous embryos (about 35% the size of the wild-type embryos). In addition, the observed effect of the CBM mutant on embryonic size was gene dose dependent, as the mCBM heterozygous embryos were significantly smaller than those of wild-type embryos but much bigger than the homozygous embryos. Second, most homozygous embryos did not turn, a process normally initiated at E8.5, suggesting that the loss of a functional CBM was responsible for a developmental arrest at an early stage of organogenesis. Last, the most severe morphological defects were observed in the heads of the mCBM homozygous embryos. In addition to the reduced size (about 25% of the size of wild-type embryos), we observed that mCBM homozygous embryos failed to close their cephalic neural folds (anterior neuropore) as indicated by the arrow in Fig. 3B. This phenotype more closely resembled wild-type embryos at E8.0 to E8.5, suggesting again that the loss of CBM arrested organogenesis in its early stages. On the other hand, all heterozygous embryos, although smaller than wild-type embryos, showed normal head morphology (Fig. 3B).

To follow up on the above observations, we collected and made histological sections of wild-type, heterozygous, and homozygous embryos at E9.5 (Fig. 3, C and D). Normally, formation and closure of the anterior neuropore occurs at E9.5 (Fig. 3D). In sharp contrast, mCBM homozygous embryos developed defects in neural closure. Specifically, failure of neural tube closure at the level of forebrain, midbrain, and hindbrain was prominent in homozygous embryos (Fig. 3D).

To further explore the molecular mechanism by which the loss of the CBM led to defects in organogenesis, we next conducted RNA sequencing analyses (RNAseq) in wild-type and mCBM homozygous embryos. More than 17,000 genes were read out in either mCBM homozygous or wild-type samples. Data analyses indicated that 214 and 208 genes from mCBM homozygous embryos were significantly down- and up-regulated, respectively (fig. S4). Among them, the expression of a cluster of transcriptional factors important for neurogenesis was significantly reduced. As depicted in Fig. 4A, the expression of neurogenin 1 and 2 (Ngn1/2), two basic helix-loop-helix (bHLH) transcriptional factors (30), was significantly down-regulated in homozygous embryos. Ngn1/2 are considered to be determination factors for neurogenesis, while members of the NeuroD family of bHLH work downstream to promote neuronal differentiation (31). We found that the expression of NeuroD1/4 was further reduced in mCBM homozygous embryos. As expected from these findings, the marker of neural stem cells nestin (Nes) and other genes related to neurogenesis including huntington-associated protein 1 (Hap1), nuclear receptor subfamily 2 group E members 1 (Nr2e1), and adhesion G protein (heterotrimeric guanine nucleotidebinding protein)coupled receptor (Adgrb1) were all down-regulated in mCBM homozygous embryos (Fig. 4A). To verify these data, we performed reverse transcription quantitative PCR (RT-qPCR) analyses of both wild-type and mCBM homozygous embryos collected at E9.5. As depicted in Fig. 4 (B to D), the aforementioned transcriptional factors were all down-regulated in a cascade fashion. While a modest reduction was found with Ngn1/2, the expression of NeuroD1/4 was almost completely inhibited. To test whether the effects of the CBM mutation on the expression levels of these transcriptional factors were gene dose dependent, we also examined mRNA levels of Ngn1/2 and NeuroD1/4 in mCBM heterozygous embryos. As depicted in Fig. 4 (B and C), the expression of these genes followed the pattern found in homozygous embryos. The expression level in heterozygous embryos was significantly reduced compared to wild-type embryos but was much higher than that of mCBM homozygous embryos. These gene dosingdependent cascade effects suggest that the 1 NKA is an important upstream regulator but not a determinant of neurogenesis like Ngn1/2 (32) or a key receptor mechanism like Wnt is.

(A) RNAseq results of several neurogenesis and neural stem cell markers. Log2 ratio = 1 means twofold of change. *P < 0.05 compared to WT. (B and C) RT-qPCR analysis of selected gene expression in WT, heterozygous, and homozygous mCBM embryos at E9.5. (D) RT-qPCR analysis of neural stem cell marker gene expression in WT and homozygous mCBM E9.5 embryos. (E) RT-qPCR analysis of neurogenesis marker genes in WT and NKA 1+/ mouse E9.5 embryos. Quantitative data are presented as means SEM from at least six independent experiments. *P < 0.05, **P < 0.01 versus WT control.

As a control, we also assessed the expression of different isoforms of NKA and caveolin-1. As depicted in fig. S5, no changes were detected in the expression of the 1 isoform of the NKA. This is expected, as the mutations were only expressed on exon 4. Previous reports have demonstrated that, in addition to the 1 isoform, neurons also express the 3 isoform, while muscle and glial cells express the 2 isoform of the NKA (9). No difference was observed in the expression of 3, while the expression of 2 was too low to be measured. We were also unable to detect any change in the expression of caveolin-1.

The total amount of protein recognized by the anti-NKA 1 antibody is unchanged in mCBM heterozygous mouse tissues compared to that of the wild type, albeit with changes in distribution in caveolar versus noncaveolar fractions. This indicates that the CBM mutant protein is fully expressed, as observed in cells (fig. S1), and further demonstrates that a reduction of enzymatic activity is not responsible for the observed phenotype in mCBM homozygous embryos. However, because the expression of wild-type 1 in mCBM heterozygous animals is most likely reduced, the phenotypic changes we observed in these mice could be due to the reduction of wild-type 1 expression rather than the expression of CBM mutant 1. To address this important issue, we collected embryos from 1 NKA heterozygous (1+/) mice and their littermate controls (33). In contrast to mCBM heterozygotes, reduction of 1 expression alone did not change the size of embryos (Fig. 3D), head morphology, or the expression of neuronal transcriptional factors (Fig. 4E). Because NKA 1 haploinsufficiency did not phenocopy mCBM heterozygosity, it was concluded that the mCBM allele was responsible for the observed changes.

The CBM in NKA has a consensus sequence of FCxxxFGGF (fig. S6). To assess the generality of CBM-mediated regulation, we first turned to the conserveness of the CBM in animal NKA. A database search reveals that, like Wnt, the mature form of NKA (i.e., containing CBM, Na+/K+ binding sites, and subunit) is absent in unicellular organisms but present in all multicellular organisms within animal kingdom (fig. S6). Further analysis of published data confirms the coevolutionary nature of the CBM and the binding sites for Na+ and K+ in the NKA. The first indication is from the analysis of single-cell organisms. No mature form of NKA is found in these organisms (fig. S6A). However, Salpingoeca rosetta, a marine eukaryote belonging to the Choanoflagellates class, undergoes a very primitive level of cell differentiation and specialization in their life cycle and expresses a putative NKA with several conserved motifs involved in the binding of Na+/K+. On the other hand, it contains no CBM (fig. S6) and there is also no evidence that it expresses a subunit.

Second, as depicted in figs. S6 and S7, Caenorhabditis elegans, an example of a metazoan organism, expresses a mature form of NKA (eat-6) that contains binding sites for Na+ and K+ as well as the N-terminal CBM. It also expresses a couple of putative NKA such as catp-2 (34). However, they contain neither the CBM nor Na+ and K+ binding sites.

Third, although the X amino acids in the NKA CBM in invertebrates vary, only conserved substitutions occurred in this motif. This is in sharp contrast to many other membrane receptors/transducers such as Patched and G that also contain a consensus CBM (figs. S6 and S7). Within vertebrates, the CBM sequence FCRQLFGGF in NKA remains completely conserved across all species. Moreover, this sequence remains conserved in all isoforms of the subunit except for the 4 isoform, which is exclusively expressed in sperm. The 4 isoform in some species still adapts the CBM sequence found in invertebrates (fig. S6). Moreover, of a total of nine subunits found in zebrafish (35), five appear to be 1 homologs that, like the 4 isoform, contain both vertebrate and invertebrate CBM sequences.

Last, turning to the evolutionary aspect of the receptor NKA/Src complex, we found that the Src-binding NaKtide and Y260 sequences, in sharp contrast to the CBM, are only conserved in mammalian ATP1A1 (fig. S7). Therefore, the NKA/Src receptor may have evolved after the acquisition of the CBM, and hence is not a part of the fundamental regulation of animal organogenesis (fig. S3).

In short, the N-terminal CBM, like the binding sites for Na+ and K+, is conserved in all subunits of NKA in animals, even after taking into consideration gene duplications and the generation of different isoforms or homologs. Thus, we postulate that this CBM must be evolutionally conserved to enable the NKA, in parallel with its enzymatic function, to serve an important role in the origination of multicellular organisms within the animal kingdom.

Organogenesis represents a unique feature of multicellular organisms. In considering the preceding findings, we reasoned that the loss of NKA CBM would also affect embryonic development in invertebrates such as C. elegans. To test our hypothesis, we used CRISPR-Cas9 to knock in the equivalent CBM double mutations of F75A and F78A in C. elegans NKA gene eat-6 (named as syb575) (fig. S8). Similar to the impact of the expression of CBM mutant 1 NKA in mice, no homozygous worms were produced, whereas the heterozygous worms hatched normally. Moreover, by using the gene balancer nT1, we confirmed that the F75A and F78A double mutations induced embryonic lethality in syb575 homozygotes secondary to L1 arrest (Fig. 5A). Furthermore, the observed larval arrest due to the loss of the eat-6 CBM was rescued by a transgene expressing a wild-type eat-6 complementary DNA (cDNA) through an extrachromosomal array (Fig. 5B). The lethality phenotype in syb575 mutants was different from those of the eat-6 mutants defective in enzymatic (transport) activity, because while the eat-6 mutants had growth defects, they were able to grow past the L1 stage (36). An exception to this was a cold-sensitive eat-6 (ad792) mutant with severely reduced transport activity, which exhibited L1 arrest at lower temperatures similarly to the syb575 mutant worms (36). Overall, those data suggest that both CBM-mediated signaling and ion transport activity by the NKA are essential to full-scale organogenesis in C. elegans.

(A) Heterozygous CBM mutant (mCBM) worms syb575/nT1 have GFP signals in pharynx (pointed with the arrowhead), while mCBM homozygous worms are GFP negative and arrested at larval stage (pointed with an arrow). (B) Rescue with a WT eat-6 gene showing a mCBM homozygous worm with a transgenic marker sur-5::GFP. Arrow points the somatic GFP signals. (C) Mutation of CBM1 NKA (F97A; F100A) results in reduced colony formation in human iPSC (mCBM iPSC). (D) RT-qPCR analysis of stem cell markers and primary germ layer markers in WT and mCBM iPSC. *P < 0.05 compared to WT. n = 7. Photo credit: Liquan Cai, Marshall Institute for Interdisciplinary Research at Marshall University.

In short, our data indicate that loss of the NKA CBM results in defective organogenesis in both mice and C. elegans. This, together with our finding that the NKA CBM is conserved in all NKA regardless of isoform or homolog, indicates that the NKA was originally evolved as a dual functional protein in multicellular organisms, and that it represents a primordial and common mechanism for regulating stem cell differentiation and early stage of organogenesis in animals.

Turning now to even more general features of the CBM in organogenesis, we searched for the plant plasma membrane H-ATPase that functions equivalently to the animal NKA. Like the NKA, the plant plasma membrane H-ATPase also contains a sequence motif at the first transmembrane segment that is in accordance with the consensus CBM. This motif is completely conserved from blue algae to land plants but does not exist within yeast and bacteria (fig. S6).

To assess the human relevance of our findings, we used CRISPR-Cas9 gene editing to generate the same mutations in human induced pluripotent stem cells (iPSCs) (fig. S9). As depicted in Fig. 5C, the expression of mutant CBM 1 reduced the colony formation ability of human iPSCs. Concomitantly, this was accompanied by a significant reduction in the expression of stemness markers (both Nanog and Oct4), and transcriptional factors controlling germ layer differentiation (gene MIXL and T for mesoderm, OTX2 and SOX1 for ectoderm, and GATA4 and SOX17 for endoderm) (Fig. 5D). These findings confirm an essential role of the NKA CBM in the regulation of stem cell differentiation and suggest the potential utility of targeting the NKA for improving tissue regeneration.

The canonical Wnt pathway is made of multiple components localized in the plasma membrane and cytosol (2, 3). Functionally, this pathway is critically important in animal organogenesis (2, 37). For example, it plays an essential role in the establishment of neurogenic niches and regulates the differentiation of neural stem cells into neuroblasts during organogenesis by regulating the expression of transcriptional factors Ngn and NeuroD (37, 38). Thus, we were prompted by the observed neural defects in mice to test whether the expression of the CBM mutant 1 NKA affects Wnt/-catenin signaling.

In the first set of studies, we examined the cellular distribution of -catenin in LW-mCBM cells. As depicted in Fig. 6A, confocal imaging analysis showed that -catenin was distributed away from the plasma membrane in a vesicle-like form in LW-mCBM cells. To verify this finding, we fractionated the cell lysates as performed in Fig. 3B and observed that -catenin, like Src and caveolin-1, moved from the low-density fractions to high-density fractions when compared to control cells (Fig. 6B). Control experiments showed no changes in the expression of E-cadherin, glycogen synthase kinase3 (GSK-3), LRP5/6 (Low-density lipoprotein receptor-related protein 5 and 6), and -catenin in LW-mCBM cells (Fig. 6C).

(A) -Catenin staining of AAC-19 and LW-mCBM at basal level (n = 5). Blue arrow indicated -catenin signal in the cytoplasm of cells. (B) Sucrose gradient fractionation of -catenin in AAC-19 and LW-mCBM cells (n = 3). **P < 0.01. (C) Western blot analysis of Wnt/-catenin signaling proteins in AAC-19, LX-2, and LW-mCBM cells from at least six independent experiments. Two samples from each cell lines are presented. (D) Wnt3a induced TOPFlash luciferase report assay in AAC-19 and LW-mCBM (n = 8). ***P < 0.01. (E) Wnt3a induced expression of Wnt/-catenin targeting genes (n = 8). **P < 0.01. (F) Wnt3a induced TOPFlash luciferase report assay in AAC-19, LX-2, and LW-mCBM cells (n = 4). ***P < 0.01.

To test whether these changes in -catenin distribution alter the function of canonical Wnt signaling, we conducted a TOPFlash luciferase activity assay (39). Cells were transiently transfected with the reporter plasmid, exposed to Wnt3a conditional medium, and then subjected to TOPFlash luciferase assays. As shown in Fig. 6D, while Wnt3a induced a greater than 35-fold increase in luciferase activity in AAC-19 cells, it only produced a fourfold increase in LW-mCBM cells, which equates to an approximate 90% reduction in the dynamics of Wnt activation. To further test the impact of the CBM mutation on Wnt signaling, we examined the effects of Wnt3a on the expression of Wnt target genes. Cells were exposed to Wnt3a for 6 hours and subjected to RT-qPCR analysis. As depicted in Fig. 6E, while Wnt3a increased the expression of c-Myc, Lef, and NKD1 expression in AAC-19 cells, it failed to do so in LW-mCBM cells.

On the basis of the above observations, we reasoned that the NKA CBM might play an essential role in the dynamic regulation of Wnt signaling. We therefore analyzed Wnt signaling in our LX-2 cell line. This cell line was made by the same strategy used for the generation of LW-mCBM cells, and it expresses essentially just the 2 isoform (40). We have observed that 2 NKA, like CBM mutant 1, maintains cellular pumping capacity but is unable to signal via Src like a wild-type 1 NKA (40). However, unlike CBM mutant 1, 2 does contain the same CBM at the N terminus (fig. S6). As depicted in Fig. 6F, expression of the 2 isoform produced a rescue of Wnt signaling dynamics when compared to that in LW-mCBM cells, which reinforces the idea that the NKA CBM is key to the dynamics of Wnt signaling. Like in LW-mCBM cells, no change in -catenin expression was noted in LX-2 cells. However, compared to LW-mCBM cells, caveolin-1 expression was decreased in LX-2 cells, while ERK activity was increased (Fig. 6C). Together, these findings suggest that the conserved NKA CBM is essential for regulating Wnt signaling, which is independent of the pumping or CTS (ardiotonic steroid)activated Src-dependent signaling transduction.

To see whether there is evidence of Wnt signaling defects in mCBM homozygous embryos, we examined the RNAseq data using a tool kit of pathway analysis. As depicted in fig. S10, Wnt signaling appears to be defective at the transcriptional level. First, the expression of one of the Wnt receptors [Frizzled homolog 5 (Fzd5)] and one of the Wnt ligands (Wnt7b) was down-regulated (fig. S10A). Second, the Wnt/-catenin signaling inhibitor, secreted frizzled-related protein 5 (Sfrp5), was up-regulated in mCBM homozygous embryos. Third, the -catenin destruction complex component adenomatosis polyposis coli (APC) was down-regulated in mCBM homozygous embryos. All these defects in Wnt signaling were confirmed by RT-qPCR analysis of both wild-type and mCBM homozygous embryos at E9.5 (fig. S10B). In addition, APC down-regulation was also observed at the protein level in mCBM iPSCs (fig. S10C). Last, the defect in Wnt signaling was further substantiated by the altered expression of Wnt downstream target genes. As shown in fig. S10B, the expression of Lef and NKD1 was significantly reduced in mCBM homozygous embryos. The expression of c-Myc was too low to be detected.

Together, these data provide strong support to the notion that the CBM is a key to the regulation of Wnt by the NKA. We hypothesize that this critical function of the NKA CBM may explain why the CBM is conserved in all four subunit isoforms of the NKA. It is important to mention that the specific molecular defects in Wnt signaling that we have identified were tested in epithelial cells, a model we have previously used to characterize 1-specific signaling functions (16, 41). In view of the cell/tissue specificity of both NKA expression and subunit assemble (42) and Wnt signaling (13, 37), it is likely that this mechanism does not fully explain the Wnt signalingrelated defects in embryogenesis.

The enzymatic function of NKA coordinates the transmembrane movement of Na+/K+, which is essential for the survival of individual animal cells. At the tissue/organ level, the ATP-powered transport of Na+/K+ by the NKA is required for neuronal firing, muscle contraction, and the formation and functionality of epithelia and endothelia. The NKA was found to be essential for forming septate junction in Drosophila melanogaster (43, 44) via a regulatory mechanism independent of its ion-pumping activity. Here, we reveal an additional fundamentally important role of NKA in the regulation of signal transduction through a separate functional domain (CBM) unrelated to its enzymatic activity.

Our findings raise the question of why NKA acquired the CBM in addition to its binding sites for Na+ and K+. One possible explanation for this is that the additional functionality in NKA (fulfilled by the CBM) evolved for the purpose of regulating stem cell differentiation and organogenesis in multicellular organisms. Two observations support this hypothesis. First, both Wnt and NKA are present in the first multicellular organisms within the animal kingdom and are evolutionally conserved ever since. Thus, it is likely that the NKA and Wnt work in concert to enable stem cell differentiation and organogenesis in animals. Second, while Wnt is key to the cellular programs of stemness and cell lineage specification (2), it does not directly participate in cell lineagespecific activities of newly differentiated cells. Instead, this particular function might be fulfilled by the NKA. Conceivably, the NKA could have been evolved, as exemplified by the mitochondrial cytochrome c in ATP generation, to bring together two seemingly unrelated processes (i.e., Wnt signaling regulation via the CBM and ion transport through Na+ and K+ binding) into one signaling circuitry, which is critical to the dynamic regulation of transcriptional factors that are required for organogenesis in a temporally and spatially organized manner. Needless to say, this hypothesis remains to be tested. In addition, other important signaling pathways such as Notch and Sonic Hedgehog may also be regulated by NKA.

It is also of interest to note the evolutionary conserveness of the CBM in the plant plasma membrane H-ATPase. Like its counterpart within the animal kingdom, the plasma membrane H-ATPase is essential for plant organogenesis (45). Unlike the NKA, the plasma membrane H-ATPase exists in single-celled organisms such as yeast, and their ion-pumping function is regulated by similar mechanisms (46). However, yeast, with no use for cellular machinery needed for organogenesis, does not contain the H-ATPase with conserved CBM. Moreover, we also observed that no CBM exists in the plasma membrane Ca-ATPase (fig. S6), both of which belong to the same type II P-type ATPase family as the NKA. While the Ca-ATPase is a more ancient protein than the NKA, as its expression can be found in unicellular organisms, the H/K-ATPase appeared later than the NKA, at some point during the development of vertebrates. Thus, we suggest that the NKA may have evolved from a P-ATPase of unicellular organisms via the gain of both the CBM and Na+/K+ binding sites. In contrast, the H/K-ATPase may have evolved from the NKA, losing not only the Na+ binding site but also the CBM.

We have shown a direct interaction between the NKA and caveolin-1 (8, 17), which has been independently confirmed (47). The loss of the CBM significantly reduced the interaction between NKA and caveolin-1 as revealed by multiple assays. In addition to caveolin-1, we and others have reported several signal transductionrelated interactions (48). Of these, the potential interaction between 1 NKA and Src has attracted the most attention, especially in the past 10 years (7). While most studies indicated an important role of Src in CTS-activated signal transduction via 1 NKA, several publications have questioned whether 1 NKA interacts with Src directly to regulate Src functionality (49, 50). While this important difference remains to be experimentally addressed, we would like to point out the following facts. First, while we recognize the merit of using purified protein preparation to study protein interaction, it is important to recognize the limitation of using purified Src from bacterial expression system because they are heterogeneously phosphorylated. Second, we have reported multiple lines of evidence that support a direct interaction between 1 NKA and Src, including the identification of isoform-specific Src interaction, the mapping of potential Src-interacting sites in the 1 isoform, and the development of pNaKtide as Src inhibitor and receptor antagonist. These findings have substantially increased our understanding of 1 NKA/Src interaction in cell biology and animal physiology. It is important to mention that several groups not associated with us have successfully used pNaKtide to block ouabain and NKA signaling in vitro and in vivo (2326, 51). While our group and others continue to characterize the molecular basis and biological function of the NKA/Src receptor complex, we propound that the question of NKA/caveolin-1 interaction is a more pressing one in the context of this study. The role of CBM in caveolin-protein interaction and caveolae-related signaling is still debated (41, 52, 53).

Last, we conclude from these interesting findings that the NKA is not just an ion pump or a CBM-directed regulator but a critical multifunctional protein. This whole functionality underlies a hitherto unrecognized common mechanism essential for stem cell differentiation and organogenesis in multicellular organisms within the animal kingdom. Moreover, many recent studies also support the concept that the 1 NKA has acquired more functional motifs (e.g., Src-binding sites for the formation of NKA/Src receptor complex) during evolution. In addition, we have demonstrated that either knockdown of 1 NKA or the expression of an N-terminal fragment containing the CBM of the 1 subunit was sufficient to attenuate purinergic calcium signaling in renal epithelial cells (54). The 1 NKA is also found to be essential for CD36 and CD40 signaling in macrophages and renal epithelial cells (55, 56). Aside from the profound biological and fundamental implications, the previously unidentified NKA-mediated regulation of Wnt signaling through its N-terminal CBM may have substantial implications in our understanding of disease progression. The rapidly increasing appreciation of Wnt signaling in the pathogenesis of cancer and cardiovascular diseases (2, 3, 38) underlies the potential utility of NKA as a multidrug target (12, 22, 57, 58).

Acknowledgments: Funding: This work was supported by grants from: National Institutes of Health (NIH) Research Enhancement Award (R15) (R15 HL 145666); American Heart Association (AHA) Scientist Development Grant (#17SDG33661117); Brickstreet Foundation and the Huntington Foundation, which provide discretionary funds to the Joan C. Edwards School of Medicine. (These funds are both in the form of endowments that are held by Marshall University). Author contributions: Conceptualization: Z.X., X.W., J.X.X., L.C., G.-Z.Z., S.V.P., and J.I.S.; methodology: X.W., L.C., I.L., D.W., and G.-Z.Z.; investigation: X.W., L.C., X.C., J.W., Y.C., and J.Z.; writing (original draft): X.W., J.X.X., and Z.X.; writing (review and editing): Z.X., J.X.X., L.C., J.I.S., S.V.P., D.W., G.-Z.Z., and X.W.; funding acquisition: Z.X.; visualization: X.W. and Z.X. Competing interests: The authors declare that they have no competing interests. Data and materials availability: All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. Additional data related to this paper may be requested from the authors.

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Rheumatoid Arthritis Stem Cell Therapy Market to Register Substantial Expansion by Fact.MR – The Cloud Tribune

By daniellenierenberg

The global Rheumatoid Arthritis Stem Cell Therapy market study presents an all in all compilation of the historical, current and future outlook of the market as well as the factors responsible for such a growth. With SWOT analysis, the business study highlights the strengths, weaknesses, opportunities and threats of each Rheumatoid Arthritis Stem Cell Therapy market player in a comprehensive way. Further, the Rheumatoid Arthritis Stem Cell Therapy market report emphasizes the adoption pattern of the Rheumatoid Arthritis Stem Cell Therapy across various industries.Request Sample Reporthttps://www.factmr.com/connectus/sample?flag=S&rep_id=1001The Rheumatoid Arthritis Stem Cell Therapy market report highlights the following players:The global market for rheumatoid arthritis stem cell therapy is highly fragmented. Examples of some of the key players operating in the global rheumatoid arthritis stem cell therapy market include Mesoblast Ltd., Roslin Cells, Regeneus Ltd, ReNeuron Group plc, International Stem Cell Corporation, TiGenix and others.

The Rheumatoid Arthritis Stem Cell Therapy market report examines the operating pattern of each player new product launches, partnerships, and acquisitions has been examined in detail.Important regions covered in the Rheumatoid Arthritis Stem Cell Therapy market report include:

North America (U.S., Canada)Latin America (Mexico, Brazil)Western Europe (Germany, Italy, U.K., Spain, France, Nordic countries, BENELUX)Eastern Europe (Russia, Poland, Rest Of Eastern Europe)Asia Pacific Excluding Japan (China, India, Australia & New Zealand)JapanMiddle East and Africa (GCC, S. Africa, Rest Of MEA)

The Rheumatoid Arthritis Stem Cell Therapy market report takes into consideration the following segments by treatment type:

Allogeneic Mesenchymal stem cellsBone marrow TransplantAdipose Tissue Stem Cells

The Rheumatoid Arthritis Stem Cell Therapy market report contain the following distribution channel:

HospitalsAmbulatory Surgical CentersSpecialty ClinicsHave Any Query? Ask our Industry Experts-https://www.factmr.com/connectus/sample?flag=AE&rep_id=1001

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The Rheumatoid Arthritis Stem Cell Therapy market report offers a plethora of insights which include:

Changing consumption pattern among individuals globally.Historical and future progress of the global Rheumatoid Arthritis Stem Cell Therapy market.Region-wise and country-wise segmentation of the Rheumatoid Arthritis Stem Cell Therapy market to understand the revenue, and growth lookout in these areas.Accurate Year-on-Year growth of the global Rheumatoid Arthritis Stem Cell Therapy market.Important trends, including proprietary technologies, ecological conservation, and globalization affecting the global Rheumatoid Arthritis Stem Cell Therapy market.

The Rheumatoid Arthritis Stem Cell Therapy market report answers important questions which include:

Which regulatory authorities have granted approval to the application of Rheumatoid Arthritis Stem Cell Therapy in Health industry?How will the global Rheumatoid Arthritis Stem Cell Therapy market grow over the forecast period?Which end use industry is set to become the leading consumer of Rheumatoid Arthritis Stem Cell Therapy by 2028?What manufacturing techniques are involved in the production of the Rheumatoid Arthritis Stem Cell Therapy?Which regions are the Rheumatoid Arthritis Stem Cell Therapy market players targeting to channelize their production portfolio?Get Full Access of the Report @https://www.factmr.com/report/1001/rheumatoid-arthritis-stem-cell-therapy-market

Pertinent aspects this study on the Rheumatoid Arthritis Stem Cell Therapy market tries to answer exhaustively are:

What is the forecast size (revenue/volumes) of the most lucrative regional market? What is the share of the dominant product/technology segment in the Rheumatoid Arthritis Stem Cell Therapy market? What regions are likely to witness sizable investments in research and development funding? What are Covid 19 implication on Rheumatoid Arthritis Stem Cell Therapy market and learn how businesses can respond, manage and mitigate the risks? Which countries will be the next destination for industry leaders in order to tap new revenue streams? Which new regulations might cause disruption in industry sentiments in near future? Which is the share of the dominant end user? Which region is expected to rise at the most dominant growth rate? Which technologies will have massive impact of new avenues in the Rheumatoid Arthritis Stem Cell Therapy market? Which key end-use industry trends are expected to shape the growth prospects of the Rheumatoid Arthritis Stem Cell Therapy market? What factors will promote new entrants in the Rheumatoid Arthritis Stem Cell Therapy market? What is the degree of fragmentation in the Rheumatoid Arthritis Stem Cell Therapy market, and will it increase in coming years?Why Choose Fact.MR?

Fact.MR follows a multi- disciplinary approach to extract information about various industries. Our analysts perform thorough primary and secondary research to gather data associated with the market. With modern industrial and digitalization tools, we provide avant-garde business ideas to our clients. We address clients living in across parts of the world with our 24/7 service availability.

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14-year-old girl is only chance to save dad’s life – Chinchilla News

By daniellenierenberg

IN A stark hospital room, Damian Cross waits for his 14-year-old daughter to save his life.

Shauna is less than 10km away at the Queensland Children's Hospital having her bone marrow extracted.

Despite only being a half match for her father, it was the best solution during a time when full match bone marrow was difficult to come by due to COVID-19 travel restrictions.

The family are a long way from their Coraki home where for a year Damian has been in remission from leukaemia after five rounds of chemotherapy.

"Leukaemia has come back and my only hope for cure now is my 14-year-old daughter," he said.

At Royal Brisbane Hospital with his partner Amy Rolfe by his side, the 33-year-old was under sedation for a bone marrow biopsy.

Shauna's bone marrow will be collected through a needle in her neck.

"Shauna has a fear of needles but hasn't batted an eye at the catheter in her neck," Amy said.

Coraki's Damian Cross in hospital in Brisbane waiting for a bone marrow transplant from his 14 year old daughter. PIC: AMY ROLFE Amy Rolfe

In preparation to receive his daughter's bone marrow, Damian will undergo three days of chemotherapy and four days of radiation to wipe out his cells.

"Then he gets her cells," Amy said.

Donor cells, especially when they are a half match, could attack Damian's cells.

"He'll be here for 100 days after the transplant," Amy said.

"Three to four weeks in hospital and then we have to stay in Brisbane for three months."

Damian will be on anti-rejection drugs and the procedure can fail within a three-year period.

The family is hopeful though and urge Australians to consider registering for bone marrow donation through the Australian Bone Marrow Donor Registry.

The World Marrow Donor Association operates a global database to find the best stem cell

source with a database of 36,214,535 donors from 98 different registries in 53 different countries.

Amy said Germany had the best bone marrow donor rate.

The WMDA said COVID-19 infection had the potential to impact and interfere with the timely provision of cells across international borders.

It is currently uncertain whether COVID-19 is transmissible parenterally, and it seems prudent to defer donors from countries with a high rate of COVID-19 infection, WMDA said.

Support the family through their crowdfunding campaign.

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Imago BioSciences To Present Update on Phase 2 results of Bomedemstat (IMG-7289), a Lysine Specific Demethylase-1 (LSD1) Inhibitor for the Treatment…

By daniellenierenberg

SOUTH SAN FRANCISCO--(BUSINESS WIRE)--Imago BioSciences, Inc. (Imago), a clinical stage biopharmaceutical company developing innovative treatments for myeloid diseases, today announced that positive Phase 2 data from its lead pipeline program bomedemstat (IMG-7289), will be presented at the Virtual Edition of the 25th EHA Annual Congress beginning June 12, 2020.

Title: A PHASE 2 STUDY OF BOMEDEMSTAT (IMG-7289), A LYSINE-SPECIFIC DEMETHYLASE-1 (LSD1) INHIBITOR, FOR THE TREATMENT OF LATER-STAGE MYELOFIBROSIS (MF)

Session Topic: 16. Myeloproliferative Neoplasms

Final Abstract Code: EP1080

The data demonstrates the potential of bomedemstat as a monotherapy in intermediate-2 and high-risk patients with myelofibrosis who have become intolerant of, or resistant to, or are ineligible for a Janus Kinase (JAK) inhibitor.

Imago is currently conducting a Phase 2 study of bomedemstat in five countries. Clinical endpoints include spleen volume reduction, reduction in total symptom scores, and improvement in circulating inflammatory cytokines, anemia, bone marrow fibrosis and blast count. For additional information, visit cliniciatrials.gov (NCT03136185).

About Bomedemstat (IMG-7289)

Bomedemstat is being evaluated in an open-label Phase 2 clinical trial for the treatment of advanced myelofibrosis (MF), a bone marrow cancer that interferes with the production of blood cells. The endpoints include spleen volume reduction and symptom improvement at 12 and 24 weeks of treatment. Bomedemstat is used as monotherapy in patients who are resistant to, intolerant of, or ineligible for a Janus Kinase (JAK) inhibitor.

Bomedemstat is a small molecule developed by Imago BioSciences that inhibits lysine-specific demethylase 1 (LSD1 or KDM1A), an enzyme shown to be vital in cancer stem/progenitor cells, particularly neoplastic bone marrow cells. In non-clinical studies, IMG-7289 demonstrated robust in vivo anti-tumor efficacy across a range of myeloid malignancies as a single agent and in combination with other chemotherapeutic agents. Bomedemstat (IMG-7289) is an investigational agent currently being evaluated in ongoing clinical trials (ClinicalTrials.gov Identifier: NCT03136185 and NCT02842827). Bomedemstat has FDA Orphan Drug and Fast Track Designation for the treatment of myelofibrosis and essential thrombocythemia, and Orphan Drug Designation for treatment of acute myeloid leukemia.

About Imago BioSciences

Imago BioSciences is a clinical-stage biopharmaceutical company focused on discovering and developing novel anti-cancer therapeutics targeting epigenetic enzymes. Imago has developed a series of compounds that inhibit LSD1, an epigenetic enzyme critical for cancer stem cell function and differentiation. Imago is advancing the clinical development of its first LSD1 inhibitor, bomedemstat, for the treatment of myeloid neoplasms including myelofibrosis and essential thrombocythemia. Imago BioSciences is backed by leading strategic and venture investors including a fund managed by Blackstone Life Sciences, Frazier Healthcare Partners, Omega Funds, Amgen Ventures, MRL Ventures Fund, HighLight Capital, Pharmaron, Greenspring Associates and Xeraya Capital. The company is based in South San Francisco, California. To learn more, visit http://www.imagobio.com.

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Autologous Stem Cell Based Therapies Market Segmentation Along With Regional Outlook, Competitive Strategies, Factors Contributing To Growth 2020-2026…

By daniellenierenberg

QY Research as of late produced a research report titled, Autologous Stem Cell Based Therapies . The research report speak about the potential development openings that exist in the worldwide market. The report is broken down on the basis of research procedures procured from historical and forecast information. The global Autologous Stem Cell Based Therapies market is relied upon to develop generously and flourish as far as volume and incentive during the gauge time frame. The report will give a knowledge about the development openings and controls that will build the market. Pursuers can increase important perception about the eventual fate of the market.

Key companies that are operating in the global Autologous Stem Cell Based Therapies market are: Regeneus, Mesoblast, Pluristem Therapeutics Inc, US STEM CELL, INC., Brainstorm Cell Therapeutics, Tigenix, Med cell Europe, etc.

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https://www.qyresearch.com/sample-form/form/1787822/covid-19-impact-on-autologous-stem-cell-based-therapies-market

Segmental Analysis

The report incorporates significant sections, for example, type and end user and a variety of segments that decide the prospects of the market. Each type provide data with respect to the business esteem during the conjecture time frame. The application area likewise gives information by volume and consumption during the estimate time frame. The comprehension of this segment direct the readers in perceiving the significance of variables that shape the market development.

Global Autologous Stem Cell Based Therapies Market Segment By Type:

, Embryonic Stem Cell, Resident Cardiac Stem Cells, Umbilical Cord Blood Stem Cells

Global Autologous Stem Cell Based Therapies Market Segment By Application:

, Neurodegenerative Disorders, Autoimmune Diseases, Cardiovascular Diseases

Competitive Landscape

The report incorporates various key players and producers working in the local and worldwide market. This segment shows the procedures received by players in the market to remain ahead in the challenge. New patterns and its reception by players assist readers with understanding the elements of the business and how it very well may be utilized to their own benefit. The readers can likewise recognize the strides of players to comprehend the global market better.

Key companies operating in the global Autologous Stem Cell Based Therapies market include Regeneus, Mesoblast, Pluristem Therapeutics Inc, US STEM CELL, INC., Brainstorm Cell Therapeutics, Tigenix, Med cell Europe, etc.

Key questions answered in the report:

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TOC

1.1 Research Scope1.2 Market Segmentation1.3 Research Objectives1.4 Research Methodology1.4.1 Research Process1.4.2 Data Triangulation1.4.3 Research Approach1.4.4 Base Year1.5 Coronavirus Disease 2019 (Covid-19) Impact Will Have a Severe Impact on Global Growth1.5.1 Covid-19 Impact: Global GDP Growth, 2019, 2020 and 2021 Projections1.5.2 Covid-19 Impact: Commodity Prices Indices1.5.3 Covid-19 Impact: Global Major Government Policy1.6 The Covid-19 Impact on Autologous Stem Cell Based Therapies Industry1.7 COVID-19 Impact: Autologous Stem Cell Based Therapies Market Trends 2 Global Autologous Stem Cell Based Therapies Quarterly Market Size Analysis2.1 Autologous Stem Cell Based Therapies Business Impact Assessment COVID-192.1.1 Global Autologous Stem Cell Based Therapies Market Size, Pre-COVID-19 and Post- COVID-19 Comparison, 2015-20262.2 Global Autologous Stem Cell Based Therapies Quarterly Market Size 2020-20212.3 COVID-19-Driven Market Dynamics and Factor Analysis2.3.1 Drivers2.3.2 Restraints2.3.3 Opportunities2.3.4 Challenges 3 Quarterly Competitive Assessment, 20203.1 By Players, Global Autologous Stem Cell Based Therapies Quarterly Market Size, 2019 VS 20203.2 By Players, Autologous Stem Cell Based Therapies Headquarters and Area Served3.3 Date of Key Players Enter into Autologous Stem Cell Based Therapies Market3.4 Key Players Autologous Stem Cell Based Therapies Product Offered3.5 Mergers & Acquisitions, Expansion Plans 4 Impact of Covid-19 on Autologous Stem Cell Based Therapies Segments, By Type4.1 Introduction1.4.1 Embryonic Stem Cell1.4.2 Resident Cardiac Stem Cells1.4.3 Umbilical Cord Blood Stem Cells4.2 By Type, Global Autologous Stem Cell Based Therapies Market Size, 2019-2021 5 Impact of Covid-19 on Autologous Stem Cell Based Therapies Segments, By Application5.1 Overview5.5.1 Neurodegenerative Disorders5.5.2 Autoimmune Diseases5.5.3 Cardiovascular Diseases5.2 By Application, Global Autologous Stem Cell Based Therapies Market Size, 2019-20215.2.1 By Application, Global Autologous Stem Cell Based Therapies Market Size by Application, 2019-2021 6 Geographic Analysis6.1 Introduction6.2 North America6.2.1 Macroeconomic Indicators of US6.2.2 US6.2.3 Canada6.3 Europe6.3.1 Macroeconomic Indicators of Europe6.3.2 Germany6.3.3 France6.3.4 UK6.3.5 Italy6.4 Asia-Pacific6.4.1 Macroeconomic Indicators of Asia-Pacific6.4.2 China6.4.3 Japan6.4.4 South Korea6.4.5 India6.4.6 ASEAN6.5 Rest of World6.5.1 Latin America6.5.2 Middle East and Africa 7 Company Profiles7.1 Regeneus7.1.1 Regeneus Business Overview7.1.2 Regeneus Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.1.3 Regeneus Autologous Stem Cell Based Therapies Product Introduction7.1.4 Regeneus Response to COVID-19 and Related Developments7.2 Mesoblast7.2.1 Mesoblast Business Overview7.2.2 Mesoblast Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.2.3 Mesoblast Autologous Stem Cell Based Therapies Product Introduction7.2.4 Mesoblast Response to COVID-19 and Related Developments7.3 Pluristem Therapeutics Inc7.3.1 Pluristem Therapeutics Inc Business Overview7.3.2 Pluristem Therapeutics Inc Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.3.3 Pluristem Therapeutics Inc Autologous Stem Cell Based Therapies Product Introduction7.3.4 Pluristem Therapeutics Inc Response to COVID-19 and Related Developments7.4 US STEM CELL, INC.7.4.1 US STEM CELL, INC. Business Overview7.4.2 US STEM CELL, INC. Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.4.3 US STEM CELL, INC. Autologous Stem Cell Based Therapies Product Introduction7.4.4 US STEM CELL, INC. Response to COVID-19 and Related Developments7.5 Brainstorm Cell Therapeutics7.5.1 Brainstorm Cell Therapeutics Business Overview7.5.2 Brainstorm Cell Therapeutics Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.5.3 Brainstorm Cell Therapeutics Autologous Stem Cell Based Therapies Product Introduction7.5.4 Brainstorm Cell Therapeutics Response to COVID-19 and Related Developments7.6 Tigenix7.6.1 Tigenix Business Overview7.6.2 Tigenix Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.6.3 Tigenix Autologous Stem Cell Based Therapies Product Introduction7.6.4 Tigenix Response to COVID-19 and Related Developments7.7 Med cell Europe7.7.1 Med cell Europe Business Overview7.7.2 Med cell Europe Autologous Stem Cell Based Therapies Quarterly Revenue, 20207.7.3 Med cell Europe Autologous Stem Cell Based Therapies Product Introduction7.7.4 Med cell Europe Response to COVID-19 and Related Developments 8 Key Findings 9 Appendix9.1 About US9.2 Disclaimer

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QYResearch always pursuits high product quality with the belief that quality is the soul of business. Through years of effort and supports from huge number of customer supports, QYResearch consulting group has accumulated creative design methods on many high-quality markets investigation and research team with rich experience. Today, QYResearch has become the brand of quality assurance in consulting industry.

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Regenerative Medicine Market to Witness a Pronounce Growth During 2017 to 2025 – 3rd Watch News

By daniellenierenberg

Regenerative Medicine Market: Snapshot

Regenerative medicine is a part of translational research in the fields of molecular biology and tissue engineering. This type of medicine involves replacing and regenerating human cells, organs, and tissues with the help of specific processes. Doing this may involve a partial or complete reengineering of human cells so that they start to function normally.

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Regenerative medicine also involves the attempts to grow tissues and organs in a laboratory environment, wherein they can be put in a body that cannot heal a particular part. Such implants are mainly preferred to be derived from the patients own tissues and cells, particularly stem cells. Looking at the promising nature of stem cells to heal and regenerative various parts of the body, this field is certainly expected to see a bright future. Doing this can help avoid opting for organ donation, thus saving costs. Some healthcare centers might showcase a shortage of organ donations, and this is where tissues regenerated using patients own cells are highly helpful.

There are several source materials from which regeneration can be facilitated. Extracellular matrix materials are commonly used source substances all over the globe. They are mainly used for reconstructive surgery, chronic wound healing, and orthopedic surgeries. In recent times, these materials have also been used in heart surgeries, specifically aimed at repairing damaged portions.

Cells derived from the umbilical cord also have the potential to be used as source material for bringing about regeneration in a patient. A vast research has also been conducted in this context. Treatment of diabetes, organ failure, and other chronic diseases is highly possible by using cord blood cells. Apart from these cells, Whartons jelly and cord lining have also been shortlisted as possible sources for mesenchymal stem cells. Extensive research has conducted to study how these cells can be used to treat lung diseases, lung injury, leukemia, liver diseases, diabetes, and immunity-based disorders, among others.

Global Regenerative Medicine Market: Overview

The global market for regenerative medicine market is expected to grow at a significant pace throughout the forecast period. The rising preference of patients for personalized medicines and the advancements in technology are estimated to accelerate the growth of the global regenerative medicine market in the next few years. As a result, this market is likely to witness a healthy growth and attract a large number of players in the next few years. The development of novel regenerative medicine is estimated to benefit the key players and supplement the markets growth in the near future.

Global Regenerative Medicine Market: Key Trends

The rising prevalence of chronic diseases and the rising focus on cell therapy products are the key factors that are estimated to fuel the growth of the global regenerative medicine market in the next few years. In addition, the increasing funding by government bodies and development of new and innovative products are anticipated to supplement the growth of the overall market in the next few years.

On the flip side, the ethical challenges in the stem cell research are likely to restrict the growth of the global regenerative medicine market throughout the forecast period. In addition, the stringent regulatory rules and regulations are predicted to impact the approvals of new products, thus hampering the growth of the overall market in the near future.

Global Regenerative Medicine Market: Market Potential

The growing demand for organ transplantation across the globe is anticipated to boost the demand for regenerative medicines in the next few years. In addition, the rapid growth in the geriatric population and the significant rise in the global healthcare expenditure is predicted to encourage the growth of the market. The presence of a strong pipeline is likely to contribute towards the markets growth in the near future.

Global Regenerative Medicine Market: Regional Outlook

In the past few years, North America led the global regenerative medicine market and is likely to remain in the topmost position throughout the forecast period. This region is expected to account for a massive share of the global market, owing to the rising prevalence of cancer, cardiac diseases, and autoimmunity. In addition, the rising demand for regenerative medicines from the U.S. and the rising government funding are some of the other key aspects that are likely to fuel the growth of the North America market in the near future.

Furthermore, Asia Pacific is expected to register a substantial growth rate in the next few years. The high growth of this region can be attributed to the availability of funding for research and the development of research centers. In addition, the increasing contribution from India, China, and Japan is likely to supplement the growth of the market in the near future.

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Global Regenerative Medicine Market: Competitive Analysis

The global market for regenerative medicines is extremely fragmented and competitive in nature, thanks to the presence of a large number of players operating in it. In order to gain a competitive edge in the global market, the key players in the market are focusing on technological developments and research and development activities. In addition, the rising number of mergers and acquisitions and collaborations is likely to benefit the prominent players in the market and encourage the overall growth in the next few years.

Some of the key players operating in the regenerative medicine market across the globe areVericel Corporation, Japan Tissue Engineering Co., Ltd., Stryker Corporation, Acelity L.P. Inc. (KCI Licensing), Organogenesis Inc., Medtronic PLC, Cook Biotech Incorporated, Osiris Therapeutics, Inc., Integra Lifesciences Corporation, and Nuvasive, Inc.A large number of players are anticipated to enter the global market throughout the forecast period.

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Cancer Stem Cells Reliance on a Key Amino Acid Could Be an Exploitable Weakness – On Cancer – Memorial Sloan Kettering

By daniellenierenberg

By Matthew Tontonoz Tuesday, May 26, 2020

Starving skin cancer tumors of serine increases cancer stem cell differentiation in mice. In this image, skin stem cells undergoing differentiation are magenta and those remaining as stem cells are green.

Summary

A team of scientists at the Sloan Kettering Institute and The Rockefeller University has discovered that cancer stem cells rely on a steady external supply of the amino acid serine. This dependency makes them vulnerable to restrictions on this supply, a discovery that could potentially be exploited therapeutically.

In recent years, cancer biologists have come to understand that metabolism the way that cells acquire and use nutrients can directly affect their tendency to become cancerous.

SKI cell biologist Lydia Finley and colleagues in the Elaine Fuchs lab at The Rockefeller University have now deepened knowledge of this relationship in the context of squamous cell carcinoma, a cancer that arises from stem cells in the skin. Using mouse models and cells growing in tissue culture, they found that the amount of the amino acid serine present in a stem cells environment influences its decision to keep dividing or to grow up (differentiate). Differentiated cells generally do not form cancer.

The stem cells that give rise to squamous cell carcinoma seem to be highly dependent on extracellular serine for their growth, Dr. Finley says. Trying to starve these cells of this source of serine could be a strategy to try to curb their growth by forcing them to differentiate.

A normal stem cell will respond to a shortage of extracellular serine by synthesizing more. Atthe same time, they will begin differentiating: The biochemical pathways involved with serine synthesis interact with proteins called histones that wrap DNA like a spool of thread and allow specific genes to be turned on. Stem cells with cancer-predisposing mutations, on the other hand, seem intent onavoiding new serine synthesis.

Cancer stem cells heightened reliance on extracellular serine reflects what Dr. Finley calls metabolic rewiring: By relying on extracellular serine, the cancer stem cells can avoid serine synthesis, with the happy side effect (for the cancer cell) that the path toward differentiation is blocked.

Our findings link the nutrients that a skin stem cell consumes to their identity and their ability to initiate a tumor, says Sanjeethan Baksh, a Tri-Institutional MD/PhD student in the Fuchs lab and the papers first author. Not only do nutrients allow stem cells and cancer cells to grow, but our study also shows that metabolism directly regulates gene expression programs important for cancer stem cell identity.

Although restricting serine in the diet is not feasible in humans, the team is currently looking for ways that they might be able to interfere with cancer stem cells ability to take up serine in the hope of curbing cancer growth.

The findings were reported on May 25 in the journal Nature Cell Biology.

This study received financial support from the Howard Hughes Medical Institute, the National Institutes of Health (grants R01-AR31737, F31CA236465, F30CA236239-01, and 1F32AR073105), the Human Frontiers Science Program, the European Molecular Biology Organization, NYSTEM (CO29559), The Starr Foundation, the Damon Runyon Cancer Research Foundation, the Concern Foundation, the Anna Fuller Fund, The Edward Mallinckrodt, Jr. Foundation, and the Memorial Sloan Kettering Cancer Center Support Grant P30 CA008748. The study authors declare no competing interests.

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‘The Alchemy Of Us’ Examines Inventions And How They’ve Shaped Human Life – WSHU

By daniellenierenberg

Science has fascinated Ainissa Ramirez ever since she watched her very first episode of the PBS kids science show 3-2-1 Contact. It changed the way she looked at the world and put her on a career path.

Today Ramirez is a materials scientist. Shes done research at Bell Labs and has taught at Yale and MIT. Shes also on a quest to transform our understanding of inventions: how they came to be and how they've changed our lives. In her new book, The Alchemy of Us, she writes, In order to create the finest version of ourselves we need to think critically about the tools that surround us.

WSHUs Morning Edition Host Tom Kuser recently spoke to Ainissa Ramirez. Below is a transcript of their conversation.

I understand you were inspired to write this book after a particularly challenging glass blowing class.What happened during that class?

Well theres a wonderful studio not far from me, in Branford. I live in New Haven, and I wanted to take some glass blowing classes, just on my bucket list. It was fun but I was also very scared. Usually I would take a small amount of glass and make a small vase.

But one day I came in in a very bad mood and actually took a lot of glass on the end of my pipe. As I was making this piece, all I had to do was one last step.But I wasnt really paying attention because I was talking to a friend.And the glass piece fell on the floor.My instructor came by and he fixed it, he reattached it to my pipe.And we were able to put it back together, although it now had a flattened side.

But as it was cooling and as I was calming down, I thought a little bit about what had happened. I was shaping the glass but the glass was actually shaping me.I came to the class in a bad mood and I was leaving in a better mood.It might feel a little existential, but I just said, I wonder how materials and humans have been shaping each other over the eons.So thats what compelled me to write my book, The Alchemy of Us.

Its clear in reading your book that this is not a dry scientific tome.You tell some very compelling stories about fascinating characters who played very significant roles in innovations that changed and are still changing our culture for better and for worse.

The eight chapters highlightspecific innovations. The chapter called CONVEY explores the development of the telegraph.SEE is all about the invention of artificial light and in CAPTURE, you focus on photography.With so many inventions over the millennia, how did you focus on just eight?

[Laugh] Yeah.It could have been much, much longer. In the architecture of the book, I was looking for stories and they had to show how humans changed.And as you mentioned the chapters are given titles that are verbs. So when I was hunting for various stories, I found eight very compelling stories to do that.There are other materials that I could have focused on but these seem to sing the loudest.So thats how I selected it.Each material had to show how it impacted culture by changing the human experience.

In your first chapter INTERACT, you take on time itself through clocks and how they now control our sleep.How did that happen?

INTERACT is one of my favorite chapters because it starts off with a woman who sold time.

Yes. I never heard that story before and I found it fascinating.

In the 19th century, when we became more and more obsessed with time, someone actually had a job where they would walk around with a watch that was certified from the Royal Observatory and show it to different businesses.Now before Ruth Bellville had her business, people slept differently.We used to sleep in two different segments.We would go to bed at 9:00. Go to sleep for about 3 1/2 hours, wake up for about an hour, do something around the house, read, talk to our neighbors who were also up, and then go back to sleep for another 3 1/2 hours.

These segments were called first and second sleep, and everyone slept that way. And if you read old books, youll see words like first sleep and second sleep and thats what they mean. As we became more obsessed with time, we had to wake up earlier so one of those segments got truncated and also with the development of electrical lights the first segment got truncated and they consolidated and that type of sleep is how we sleep today.

And that, you point out, has an impact on health.

Oh absolutely.A lot of people say they have a form of insomnia, and historians actually think its harkening back to this old way of sleeping. And also in terms of our health, the artificial light also seems to be also impacting our health because our bodies actually have two modes.We have a daytime mode and a nighttime mode.

How the body knows which mode to be in is based on blue light.Now when our ancestors were alive they lived by sunlight, which has a lot of blue in it, and candlelight which has less. But we live under artificial lights all the time.And when we're in daytime mode our bodies are actually in growth mode and thats actually impacting us because our cells will respond to that growth mode in ways that we dont necessarily want.

You bring up the chapter about the electric light or artificial light, and of course you include Thomas Edison in the chapter which is called SEE. But it seems that your protagonist, I guess I can call him that, is really an inventor named William Wallace of Ansonia, Connecticut.Why is he a player in this story?

Well, I really loved William Wallace because if you read books about Edison, very thick books, youll always see William Wallace as a footnote. And I said, Who is this guy? I found out that Edison actually came to Ansonia and he met William Wallace.Wallace had created an early version of the electric light, it was an arc light so it was very, very bright, it was like a searchlight, so it wasnt really useful for the home, but Edison saw this and said, Hey, I think Ill start working on electric lights.And then he went back to Menlo Park in New Jersey and created his incandescent bulb. But he wouldnt have had that idea if he didnt come to Connecticut. And most people in Connecticut dont know this. That Edison came up here. So thats why I highlighted William Wallace. I wanted this little known inventor to get his moment in the sun.

You mention the day Thomas Edison came to meet Wallace in Ansonia was really the beginning of a period of darkness for Wallace because he was cut out of the invention process from beyond that time.

That is absolutely right.Wallace thought his moment had come.The great Wizard of Menlo Park came to visit him to see what he had created.And Wallace had created not only this fantastic light, he created a special generator which transmitted the water power from the Naugatuck River into electricity because there wasnt any electricity in the homes yet. And so Edison said well I want one of these electrical systems.He brought it back to his place in Menlo Park and he cut Wallace out of the deal.He just bought the units from Wallace and never included Wallace in his inventions moving forward.

You also talk about the things that weve lost along with what we gained through these innovations. For example with the light bulb, we lost darkness.Tell us about that down side.

Well our ancestors used to look and see thousands of stars.Now if you and I look up, well see about fifty. Recently I went on a trip and I went to a place that was very, very dark.And the starred sky is amazing.You feel very small and you feel connected to nature.So I do talk about how that has happened.As a result of having all these lights, this abundance of lights, it really disconnects us from really seeing how beautiful the night sky is.

And one of the illustrations you use, when talking about the effect on the environment is the life cycle of the lighting bug or the firefly.

Yeah, well on the East Coast were very lucky.We have this wonderful bug, the lightning bug or firefly. But it ends up on the West Coast the fireflies dont make it that far. And the number of fireflies has been decreasing and the reason is because of the lights. Fireflies speak to each other through a Morse code of flashes but its really important that they see each other in a dark sky. They can see each other, connect, and make future fireflies.But when theres a street light overhead, the female firefly doesnt know to flash back to the male firefly so they dont meet. So thats why their numbers are decreasing.Even though artificial lights are convenient for us, for humans, theyre really making things difficult for fireflies.

Since you mentioned the Morse Code that the fireflies use,Id like to jump over to CONVEY, the third chapter in the book about telegraph wires and the invention of the telegraph with Samuel B. Morse.You connect Morse with a number of things in culture that have changed over the years, including the way we write and also, a lack of personal social interaction due to things like texting and emails.Could you connect those dots for us?

Sure.When Morse was first making his telegraph he would work with his assistant (Alfred Vail). And he would chide him and say, condense your language, which was harsh language back in those days.And what he was trying to tell Vail is to not write so much when sending a message.

What Vail would do or what Morse would do, is they would write their letters by longhand and then convertall the letters in the alphabet in the word to dots and dashes, and type in those dots and dashes, figure out what those dots and dashes mean and then write out the word. That took a lot of time.

And so Morse would get a message from Vail and it would be dash, four dots and another dot and youd convert it and youd seek the word the. Thats a lot of work for a word that doesnt do very much.So he was telling Vail to shorten what youre saying in the message that youre transmitting.

It ends up that telegraphs become very popular in society and telegraph officers would tell customers to be brief because the telegraph was great at sending information long distances but it couldnt handle a lot of messages. And so the officers wanted customers to just send very short messages so they could keep it available for the next set of customers.

Telegraphs became popular in newsrooms and editors would tell their reporters to be succinct, again one of the limitation of their prose was because of the telegraph. Now there was one reporter that really loved this style of writing with short declarative sentences. His name was Earnest Hemingway.So the way that he writes is a style that was designed by the use of the telegraph. So this is how one technology, this technology of the telegraph has changed language.

Now the other thing that you mention is about how the telegraph has squeezed out the human part. Morse use to write very, very long letters and used wonderful prose that described everything around him. But when you use the telegraph, you dont have that luxury.

And so the progeny of the telegraph is text messages.

And again when we as humans communicate, we use a lot of different ways of getting a message across besides words.We can look at body language, we can look at peoples eyes.And as a result of communicating in this one-dimensional way, what historians, linguists and scholars are concerned with is that were reducing our ability to empathize.

So thats one of the things that I also point to in The Alchemy of Us, is that this technology is useful in getting information across but its deteriorating our ability to be human with each other, that is to empathize and relate to one another.

Your chapter about photography, called CAPTURE explores several stories and several dimensions of how photography affected culture in the years following its invention and development.One Id like to talk about, you explaining how the development of film actually contributed to the stereotyping of African Americans. Can you please connect those dots for us.

Well it ends up that the most photographed person in the world at one point was Frederick Douglass.Not Lincoln, not Twain. Frederick Douglass. Now why was he so crazy about getting selfies of himself? Well he was trying to use his image as a way to combat the negative stereotypes about African Americans. here were a lot of characters that were hand-drawn and they would show people with exaggerated expressions, with eyes that were white and were bugging out and wide smiles.And if youve ever seen a photograph of Frederick Douglass he looks so regal, hes a handsome looking guy he wanted to combat that image.And so thats the reason why every time he went by a portraiture place for pictures, he would go in to take his pictures because those pictures would also be sold.And so he wanted to use this as a way to combat that stereotype.

Maybe you could talk a bit more about the technical issue that resulted in film really all the way into the later part of the 20th century resulting in film that did not expose correctly darker skin.

Ok thats a very good question.In the 1950s, 1960s, African American mothers were looking at class photos of their children and they saw something that didnt look right. The black children did not come out as well as the white children.And African American mothers they asked manufactures of film to fix this. What they had seen is that actually there was a bias in the film. The film was tailormade or was optimized for people with lighter skin because the main customer were people of lighter complexion.Initially camera film was egalitarian because it was homemade chemistry that you could do in your kitchen. Whoever took a picture, their likeness would be depicted.But as it became manufactured by companies, they tailored the process so that it was optimized for a certain population.And this is what these African American mothers saw in the 1950s.

And so after some chiding, not from these African American mothers, even though they wrote letters. It was only when two businesses, furniture manufacturers and confectioners that made chocolate, when they told this manufacturer that they had to change their film, that changes happened.

Because they wanted their chocolates of different flavors, you know, white chocolate, milk chocolate, dark chocolate.They wanted people to be able to discern those different types of chocolate and in the current form of the film.That wasnt happening. So eventually the formulation was changed so that the film was democratic and could pick up different hues of chocolate as well as different hues of skin.

And I cant let you go without asking for your perspective on the COVID-19 pandemic.Im wondering if theres an innovation from our past that might have created this unfortunate situation?

I dont know if theres an innovation in our past.Weve benefited from not having pandemics because weve got tremendous medicines.And weve got new technologies that can do things that couldnt happen as quickly in the past.We can trace. We can test.So weve got things to combat it a little bit better. Were not actually using them as well as we could, but technologies can definitely help.

From your vantage point as a scientist and a science communicator, how do you see this pandemictransforming perhaps science and our culture looking forward?

This pandemic is also because people feel disconnected from science.I think if people were a little bit more informed about how things work, they would adhere, they would comply a little bit more.Because weve had a little bit of a breakdown with how we teach science, STEM in particular, we dont see how were part of a global system, that what you do affects me.As scientists we forgot to teach that and so as a result, people dont see that their actions actually have some ripple effect outward.

So thats kind of what I see as the impact.And I hope that going forward science, science communicators and also society in general will just realize that theres an ecology, that what you do affects other people although you may not be able to see them.

My ignorance is showing here now.You are a materials scientist.Can you explain just what that is?

I tell people Im an atom whisperer. Materials science sits where chemistry and physics overlap. So chemistry is interested in how things bond and physicists are interested in how materials behave in different situations and I want to show how one thing is linked to the other.So that is what materials science is. Its not very well-known but a lot of the things you take for granted like the cell phone and the fact that this phone call being made by microphone, thats all materials science.

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Global Myelofibrosis Treatment Market to Register Growth in Incremental Opportunity During the Forecast Period 2016 2022 – Cole of Duty

By daniellenierenberg

In the current situation of restricted movement and reduced workforce, (due to COVID-19 Pandemic) new technologies have been developed to provide end-to-end automation in different sectors such as food processing. Automated systems are hired by the companies to ensure continued supply and manufacturing of products with the least manual interference

The advent of Health Information Technology (HIT) components such as electronic health records (EHR), hospital information systems (HIS), picture archiving and communication systems (PACS), and vendor neutral archives (VNA) has had just as transformational an impact on the overall healthcare sector as the concerns regarding security and privacy. Data theft, undue access to personal health records, and cyber-attacks are very real threats that the healthcare sector faces today.

Myelofibrosis or osteomyelofibrosis is a myeloproliferative disorder which is characterized by proliferation of abnormal clone of hematopoietic stem cells. Myelofibrosis is a rare type of chronic leukemia which affects the blood forming function of the bone marrow tissue. National Institute of Health (NIH) has listed it as a rare disease as the prevalence of myelofibrosis in UK is as low as 0.5 cases per 100,000 population. The cause of myelofibrosis is the genetic mutation in bone marrow stem cells. The disorder is found to occur mainly in the people of age 50 or more and shows no symptoms at an early stage. The common symptoms associated with myelofibrosis include weakness, fatigue, anemia, splenomegaly (spleen enlargement) and gout. However, the disease progresses very slowly and 10% of the patients eventually develop acute myeloid leukemia. Treatment options for myelofibrosis are mainly to prevent the complications associated with low blood count and splenomegaly.

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The global market for myelofibrosis treatment is expected to grow moderately due to low incidence of a disease. However, increasing incidence of genetic disorders, lifestyle up-gradation and rise in smoking population are the factors which can boost the growth of global myelofibrosis treatment market. The high cost of therapy will the growth of global myelofibrosis treatment market.

The global market for myelofibrosis treatment is segmented on basis of treatment type, end user and geography:

As myelofibrosis is considered as non-curable disease treatment options mainly depend on visible symptoms of a disease. Primary stages of the myelofibrosis are treated with supportive therapies such as chemotherapy and radiation therapy. However, there are serious unmet needs in myelofibrosis treatment market due to lack of disease modifying agents. Approval of JAK1/JAK2 inhibitor Ruxolitinib in 2011 is considered as a breakthrough in myelofibrosis treatment. Stem cell transplantation for the treatment of myelofibrosis also holds tremendous potential for market growth but high cost of therapy is foreseen to limits the growth of the segment.

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On the basis of treatment type, the global myelofibrosis treatment market has been segmented into blood transfusion, chemotherapy, androgen therapy and stem cell or bone marrow transplantation. Chemotherapy segment is expected to contribute major share due to easy availability of chemotherapeutic agents. Ruxolitinib is the only chemotherapeutic agent approved by the USFDA specifically for the treatment of myelofibrosis, which will drive the global myelofibrosis treatment market over the forecast period.

Geographically, global myelofibrosis treatment market is segmented into five regions viz. North America, Latin America, Europe, Asia Pacific and Middle East & Africa. Northe America is anticipated to lead the global myelofibrosis treatment market due to comparatively high prevalence of the disease in the region.

Some of the key market players in the global myelofibrosis treatment market are Incyte Corporation, Novartis AG, Celgene Corporation, Mylan Pharmaceuticals Ulc., Bristol-Myers Squibb Company, Eli Lilly and Company, Taro Pharmaceuticals Inc., AllCells LLC, Lonza Group Ltd., ATCC Inc. and others.

The report covers exhaustive analysis on:

Regional analysis includes

Report Highlights:

Our unmatched research methodologies set us apart from our competitors. Heres why:PMRs set of research methodologies adhere to the latest industry standards and are based on sound surveys.We are committed to preserving the objectivity of our research.Our analysts customize the research methodology according to the market in question in order to take into account the unique dynamics that shape the industry.Our proprietary research methodologies are designed to accurately predict the trajectory of a particular market based on past and present data.PMRs typical operational model comprises elements such as distribution model, forecast of market trends, contracting and expanding technology applications, pricing and transaction model, market segmentation, and vendor business and revenue model.

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Silver Nanoparticle-Induced Apoptosis in ARPE-19 Cells Is Inhibited by | IJN – Dove Medical Press

By daniellenierenberg

Juan-Hua Quan,1,* Fei Fei Gao,2,* Hassan Ahmed Hassan Ahmed Ismail,3,* Jae-Min Yuk,2 Guang-Ho Cha,2 Jia-Qi Chu,4 Young-Ha Lee2

1Department of Gastroenterology, The Affiliated Hospital of Guangdong Medical University, Zhanjiang 524-001, Peoples Republic of China; 2Department of Infection Biology and Department of Medical Science, Chungnam National University College of Medicine, Daejeon 301-131, Korea; 3Communicable and Non-Communicable Diseases Control Directorate, Federal Ministry of Health, Khartoum, Sudan; 4Stem Cell Research and Cellular Therapy Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong Province 524-001, Peoples Republic of China

*These authors contributed equally to this work

Correspondence: Young-Ha LeeDepartment of Infection Biology and Department of Medical Science, Chungnam National University College of Medicine 6 Munhwa-Dong, Jung-Gu, Daejeon 35015, KoreaTel +82-42-580-8273Fax +82-42-583-8216Email yhalee@cnu.ac.kr

Purpose: External and internal stimuli easily affect the retina. Studies have shown that cells infected with Toxoplasma gondii are resistant to multiple inducers of apoptosis. Nanoparticles (NPs) have been widely used in biomedical fields; however, little is known about cytotoxicity caused by NPs in the retina and the modulators that inhibit nanotoxicity.Materials and Methods: ARPE-19 cells from human retinal pigment epithelium were treated with silver nanoparticles (AgNPs) alone or in combination with T. gondii. Then, the cellular toxicity, apoptosis, cell cycle analysis, autophagy, ROS generation, NOX4 expression, and MAPK/mTOR signaling pathways were investigated. To confirm the AgNP-induced cytotoxicity in ARPE-19 cells and its modulatory effects caused by T. gondii infection, the major experiments carried out in ARPE-19 cells were performed again using human foreskin fibroblast (HFF) cells and bone marrow-derived macrophages (BMDMs) from NOX4/ mice.Results: AgNPs dose-dependently induced cytotoxicity and cell death in ARPE-19 cells. Apoptosis, sub-G1 phase cell accumulation, autophagy, JNK phosphorylation, and mitochondrial apoptotic features, such as caspase-3 and PARP cleavages, mitochondrial membrane potential depolarization, and cytochrome c release into the cytosol were observed in AgNP-treated cells. AgNP treatment also increased the Bax, Bik, and Bim protein levels as well as NOX4-dependent ROS generation. However, T. gondii-infected ARPE-19 cells inhibited AgNP-induced apoptosis, JNK phosphorylation, sub-G1 phase cell accumulation, autophagy, NOX4-mediated ROS production, and mitochondrial apoptosis. Furthermore, mitochondrial apoptosis was found in AgNP-treated HFF cells and BMDMs, and AgNP-induced mitochondrial apoptosis inhibition via NOX4-dependent ROS suppression in T. gondii pre-infected HFF cells and BMDMs was also confirmed.Conclusion: AgNPs induced mitochondrial apoptosis in human RPE cells combined with cell cycle dysregulation and autophagy; however, these effects were significantly inhibited by T. gondii pre-infection by suppression of NOX4-mediated ROS production, suggesting that T. gondii is a strong inhibitory modulator of nanotoxicity in in vitro models.

Keywords: silver nanoparticles, Toxoplasma gondii, mitochondrial apoptosis, human retinal pigment epithelium, reactive oxygen species, NADPH oxidase 4

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Revenue from the Sales of Neuroprosthetics Market to Surge Exponentially Owing To High Demand During COVID-19 Lockdown and Forecast 2015 to 2021 -…

By daniellenierenberg

The impact of COVID-19 pandemic can be felt across the Healthcare Industry The growing inability in the production and manufacturing processes, in the light of the self-quarantined workforce has caused a major disruption in the supply chain across the sector. Restrictions encouraged by this pandemic are obstructing the production of essentials such as life-saving drugs.

The nature of operation in Pharmaceuticals plants that cannot be easily stopped and started, makes the operational restrictions in these plants a serious concern for the industry leaders. Restricted and delayed shipments from China have created a price hike in the raw materials, affecting the core of the Healthcare Industry.

Central nervous system comprises brain and spinal cord, and is responsible for integration of sensory information. Brain is the largest and one of the most complex organs in the human body. It is made up of 100 billion nerves that communicate with 100 trillion synapses. It is responsible for the thought and movement produced by the body. Spinal cord is connected to a section of brain known as brain stem and runs through the spinal canal. The brain processes and interprets sensory information sent from the spinal cord. Brain and spinal cord serve as the primary processing centers for the entire nervous system, and control the working of the body.

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Neuroprosthetics improves or replaces the function of the central nervous system. Neuroprosthetics, also known as neural prosthetics, are devices implanted in the body that stimulate the function of an organ or organ system that has failed due to disease or injury. It is a brain-computer interface device used to detect and translate neural activity into command sequences for prostheses. Its primary aim is to restore functionality in patients suffering from loss of motor control such as spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosis, and stroke. The major types of neuroprosthetics include sensory implants, motor prosthetics, and cognitive prosthetics. Motor prosthetics support the autonomous system and assist in the regulation or stimulation of affected motor functions.

Similarly, cognitive prosthetics restore the function of brain tissue loss in conditions such as paralysis, Parkinsons disease, traumatic brain injury, and speech deficit. Sensory implants pass information into the bodys sensory areas such as sight or hearing, and it is further classified as auditory (cochlear implant), visual, and spinal cord stimulator. Some key functions of neuroprosthetics include providing hearing, seeing, feeling abilities, pain relief, and restoring damaged brain cells. Cochlear implant is among the most popular neuroprosthetics. In addition, auditory brain stem implant is also a neuroprosthetic meant to improve hearing damage.

North America dominates the global market for neuroprosthetics due to the rising incidence of neurological diseases and growth in geriatric population in the region. Asia is expected to display a high growth rate in the next five years in the global neuroprosthetics market, with China and India being the fastest growing markets in the Asia-Pacific region. Among the key driving forces for the neuroprosthetics market in developing countries are the large pool of patients, increasing awareness about the disease, improving healthcare infrastructure, and rising government funding in the region.

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Increasing prevalence of neurological diseases such as traumatic brain injury, stroke and Parkinsons disease, rise in geriatric population, increase in healthcare expenditure, growing awareness about healthcare, rapid progression of technology, and increasing number of initiatives by various governments and government associations are some key factors driving growth of the global neuroprosthetics market. However, factors such as high cost of devices, reimbursement issues, and adverse effects pose a major restraint to the growth of the global neuroprosthetics market.

Innovative self-charging neural implants that eliminate the need for high risk and costly surgery to replace the discharge battery and controlling machinery with thoughts would help to develop opportunities for the growth of the global neuroprosthetics market.

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The major companies operating in the global neuroprosthetics market are ,

Key geographies evaluated in this report are:

Key features of this report

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Revenue from the Sales of Neuroprosthetics Market to Surge Exponentially Owing To High Demand During COVID-19 Lockdown and Forecast 2015 to 2021 -...

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Clinical Outcomes Using RYONCIL (remestemcel-L) in Children and Adults With Severe Inflammatory Graft Versus Host Disease Published in Three Articles…

By daniellenierenberg

Key points:

NEW YORK, May 25, 2020 (GLOBE NEWSWIRE) -- Mesoblast Limited (Nasdaq:MESO; ASX:MSB), global leader in cellular medicines for inflammatory diseases, today announced that clinical outcomes of its allogeneic mesenchymal stem cell (MSC) medicine RYONCIL (remestemcel-L) in children and adults with steroid-refractory acute graft versus host disease (GVHD) have been published in three peer-reviewed articles and an accompanying editorial in the May issue of Biology of Blood and Marrow Transplantation, the official publication of the American Society for Transplantation and Cellular Therapy.

Mesoblast Chief Medical Officer Dr Fred Grossman said: Results from these three trials show a consistent pattern of safety and efficacy for RYONCIL (remestemcel-L) in patients with the greatest levels of inflammation and the most severe grades of acute GVHD. These clinical outcomes provide a compelling rationale for use of remestemcel-L in children and adults with other conditions associated with severe inflammation and cytokine release, including acute respiratory distress syndrome (ARDS) and systemic vascular manifestations of COVID-19 infection.

In the accompanying editorial, Dr Jacques Galipeau, Professor and Assistant Dean of Medicine at the Stem Cell & Regenerative Medicine Center at the University of WisconsinMadison and Chair of the International Society of Cell and Gene Therapy (ISCT) MSC Committee, concluded that after more than a decade of clinical study involving three distinct advanced trials, it appears that remestemcel-L might well have finally met the regulatory requirements for marketing approval in the United States for steroid refractory acute GVHD in children, and it is to be determined whether this industrial MSC product will find utility for adults afflicted by acute GVHD or other indications.

The trials highlighted in the three articles all evaluated the same treatment regimen of RYONCIL, with patients receiving twice weekly intravenous infusions of 2 million cells per kg body weight over a four-week period. RYONCIL was well-tolerated in all studies with no identified safety concerns. The three trials were:

1. Study 275: An Expanded Access Program in 241 children across 50 centers in eight countries where RYONCIL was used as salvage therapy for steroid-refractory acute GVHD in patients who failed to respond to steroid therapy as well as multiple other agents.

2. Study GVHD001/002: A Phase 3 single-arm trial in 55 children across 20 centers in the United States where RYONCIL was used as the first line of treatment for children who failed to respond to steroids for acute GVHD.

3. Study 280: A Phase 3 randomized placebo-controlled trial in 260 patients, including 28 children, across 72 centers in seven countries where RYONCIL or placebo were added to second line therapy in patients with steroid-refractory acute GVHD who failed to respond to steroid treatment.

About Acute Graft Versus Host Disease Acute GVHD occurs in approximately 50% of patients who receive an allogeneic bone marrow transplant (BMT). Over 30,000 patients worldwide undergo an allogeneic BMT annually, primarily during treatment for blood cancers, and these numbers are increasing.1 In patients with the most severe form of acute GVHD (Grade C/D or III/IV) mortality is as high as 90% despite optimal institutional standard of care.2,3 There are currently no FDA-approved treatments in the United States for children under 12 with steroid-refractory acute GVHD.

About RYONCILTM Mesoblasts lead product candidate, RYONCIL (remestemcel-L), is an investigational therapy comprising culture-expanded mesenchymal stem cells derived from the bone marrow of an unrelated donor. It is administered to patients in a series of intravenous infusions. RYONCIL is believed to have immunomodulatory properties to counteract the inflammatory processes that are implicated in SR-aGVHD by down-regulating the production of pro-inflammatory cytokines, increasing production of anti-inflammatory cytokines, and enabling recruitment of naturally occurring anti-inflammatory cells to involved tissues.

References 1. Niederwieser D, Baldomero H, Szer J. Hematopoietic stem cell transplantation activity worldwide in 2012 and a SWOT analysis of the Worldwide Network for Blood and Marrow Transplantation Group including the global survey. Bone Marrow Transplant 2016; 51(6):778-85.2. Westin, J., Saliba, RM., Lima, M. (2011) Steroid-refractory acute GVHD: predictors and outcomes. Advances in Hematology 2011;2011:601953.3. Axt L, Naumann A, Toennies J (2019) Retrospective single center analysis of outcome, risk factors and therapy in steroid refractory graft-versus-host disease after allogeneic hematopoietic cell transplantation. Bone Marrow Transplantation 2019;54(11):1805-1814.

About MesoblastMesoblast Limited (Nasdaq:MESO; ASX:MSB) is a world leader in developing allogeneic (off-the-shelf) cellular medicines. The Company has leveraged its proprietary mesenchymal lineage cell therapy technology platform to establish a broad portfolio of commercial products and late-stage product candidates. The Companys proprietary manufacturing processes yield industrial-scale, cryopreserved, off-the-shelf, cellular medicines. These cell therapies, with defined pharmaceutical release criteria, are planned to be readily available to patients worldwide.

Mesoblasts Biologics License Application to seek approval of its product candidate RYONCIL (remestemcel-L) for pediatric steroid-refractory acute graft versus host disease (acute GVHD) has been accepted for priority review by the United States Food and Drug Administration (FDA), and if approved, product launch in the United States is expected in 2020. Remestemcel-L is also being developed for other inflammatory diseases in children and adults including moderate to severe acute respiratory distress syndrome. Mesoblast is completing Phase 3 trials for its product candidates for advanced heart failure and chronic low back pain. Two products have been commercialized in Japan and Europe by Mesoblasts licensees, and the Company has established commercial partnerships in Europe and China for certain Phase 3 assets.

Mesoblast has a strong and extensive global intellectual property (IP) portfolio with protection extending through to at least 2040 in all major markets. This IP position is expected to provide the Company with substantial commercial advantages as it develops its product candidates for these conditions.

Mesoblast has locations in Australia, the United States and Singapore and is listed on the Australian Securities Exchange (MSB) and on the Nasdaq (MESO). For more information, please see http://www.mesoblast.com, LinkedIn: Mesoblast Limited and Twitter: @Mesoblast

Forward-Looking StatementsThis announcement includes forward-looking statements that relate to future events or our future financial performance and involve known and unknown risks, uncertainties and other factors that may cause our actual results, levels of activity, performance or achievements to differ materially from any future results, levels of activity, performance or achievements expressed or implied by these forward-looking statements. We make such forward-looking statements pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995 and other federal securities laws. Forward-looking statements include, but are not limited to, statements about the initiation, timing, progress and results of Mesoblast and its collaborators clinical studies; Mesoblast and its collaborators ability to advance product candidates into, enroll and successfully complete, clinical studies; the timing or likelihood of regulatory filings and approvals; and the pricing and reimbursement of Mesoblasts product candidates, if approved; the potential benefits of strategic collaboration agreements and Mesoblasts ability to maintain established strategic collaborations; Mesoblasts ability to establish and maintain intellectual property on its product candidates and Mesoblasts ability to successfully defend these in cases of alleged infringement; the scope of protection Mesoblast is able to establish and maintain for intellectual property rights covering its product candidates and technology. You should read this press release together with our risk factors, in our most recently filed reports with the SEC or on our website. Uncertainties and risks that may cause Mesoblasts actual results, performance or achievements to be materially different from those which may be expressed or implied by such statements, and accordingly, you should not place undue reliance on these forward-looking statements. We do not undertake any obligations to publicly update or revise any forward-looking statements, whether as a result of new information, future developments or otherwise.

Release authorized by the Chief Executive.

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Impact of Covid-19 on Stem Cell Banking Market 2020: Remarking Enormous Growth with Recent Trends | Cord Blood Registry (CBR) Systems (US), Cordlife…

By daniellenierenberg

Market Expertz has very recently published a report on the Stem Cell Banking market, which delves deeper into a bunch of insightful as well as comprehensive information about the Stem Cell Banking industrys ecosystem. The research report on the Stem Cell Banking market covers both qualitative as well as quantitative details that focus entirely on the various parameters such as Stem Cell Banking market risk factors, challenges, industrial developments, new opportunities available in the Stem Cell Banking report. These factors are the ones that determine the functioning and trends in the forecasted period for the market.

This is the most recent report inclusive of the COVID-19 effects on the functioning of the market. It is well known that some changes, for the worse, were administered by the pandemic on all industries. The current scenario of the business sector and pandemics impact on the past and future of the industry are covered in this report.

Avail your copy of the sample of the report on the global Stem Cell Banking [emailprotected] https://www.marketexpertz.com/sample-enquiry-form/122606

With the growing number of new players entering the Stem Cell Banking market, expansion in businesses is also improving. Then Stem Cell Banking report focuses on boosting a series of parameters such as revenue shares, optimizing cost structure, offering better services, Stem Cell Banking market demand or supply chain, development policies, which mainly maps to streamline business processes during the projected timeline.

The fundamental drivers, as well as restraints, are identified by the recent trends and historical milestones gathered by the Stem Cell Banking market. It also demonstrates the brief evaluation of the investments, Stem Cell Banking production, innovative technologies, and growth rate of the specific businesses.

Leading Stem Cell Banking manufacturers/companies operating at both regional and global levels:

Cord Blood Registry (CBR) Systems (US), Cordlife Group Limited (Singapore), Cryo-Cell International (US), ViaCord (US), Cryo-Save AG (Netherlands), LifeCell International (India), StemCyte (US), Global Cord Blood Corporation (China), Smart Cells International (UK), Vita34 AG (Germany), and CryoHoldco (Mexico).

The report also inspects the financial standing of the leading companies, which includes gross profit, revenue generation, sales volume, sales revenue, manufacturing cost, individual growth rate, and other financial ratios.

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The creative advancements are investigated widely to understand the probable impact on the growth of the global Stem Cell Banking market.

The Stem Cell Banking market has been segmented into key segments such as product types, end-users, leading regions, and noteworthy players. The readers can assess detailed and strategical information about each segment. The Stem Cell Banking market report also includes a blend of statistics about sales, consumption rate, volume, value, gross margin, and more.

The segmentation included in the report is beneficial for readers to capitalize on the selection of appropriate segments for the Stem Cell Banking sector and can help companies in deciphering the optimum business move to reach their desired business goals.

product landscape:

Placental Stem Cells (PSCS), Adipose Tissue-Derived Stem Cells (ADSCS), Bone Marrow-Derived Stem Cells (BMSCS), Human Embryo-Derived Stem Cells , (HESCS), Dental Pulp-Derived Stem Cells (DPSCS)

Application landscape:

Sample Preservation and Storage, Sample Analysis, Sample Processing, Sample Collection and Transportation

End user landscape:

Personalized Banking Applications, Research, Clinical Application

The report includes accurately drawn facts and figures, along with graphical representations of vital market data. The research report sheds light on the emerging market segments and significant factors influencing the growth of the industry to help investors capitalize on the existing growth opportunities.

To get in-depth insights into the global Stem Cell Banking market, reach out to us @ https://www.marketexpertz.com/customization-form/122606

Thus, with the rising adoption of the Stem Cell Banking market in the international sector, the industry for the global Stem Cell Banking market is expected to represent a predicted outlook during the forecast phase from 2020-2027. Additionally, the report on the Stem Cell Banking market delivers a systematic representation of the growth opportunities, Stem Cell Banking market dynamics, and the existing trends are anticipated to shape the growth of the Stem Cell Banking market across the globe.

Geographically, this report studies the top producers and consumers in these key regions:

North America

Europe

China

Japan

Southeast Asia

India

A conscious effort is made by the subject matter experts to analyze how some business owners succeed in maintaining a competitive edge while the others fail to do so makes the research interesting. A quick review of the realistic competitors makes the overall study a lot more interesting. Opportunities that are helping product owners size up their business further add value to the overall study.

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The Stem Cell Banking Market Research/Analysis Report addresses the following questions:

Read the full Research Report along with a table of contents, facts and figures, charts, graphs, etc. @ https://www.marketexpertz.com/industry-overview/2020-stem-cell-banking-global-market

To summarize, the global Stem Cell Banking market report studies the contemporary market to forecast the growth prospects, challenges, opportunities, risks, threats, and the trends observed in the market that can either propel or curtail the growth rate of the industry. The market factors impacting the global sector also include provincial trade policies, international trade disputes, entry barriers, and other regulatory restrictions.

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Coronavirus isnt the killer, our immune response is – ThePrint

By daniellenierenberg

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The killer is not the virus but the immune response.

The current pandemic is unique not just because it is caused by a new virus that puts everyone at risk, but also because the range of innate immune responses is diverse and unpredictable. In some it is strong enough to kill. In others it is relatively mild.

My research relates to innate immunity. Innate immunity is a persons inborn defense against pathogens that instruct the bodys adaptive immune system to produce antibodies against viruses. Those antibody responses can be later used for developing vaccination approaches. Working in the lab of Nobel laureate Bruce Beutler, I co-authored the paper that explained how the cells that make up the bodys innate immune system recognize pathogens, and how overreacting to them in general could be detrimental to the host. This is especially true in the COVID-19 patients who are overreacting to the virus.

Also read: All the Covid-19 symptoms you didnt know about

I study inflammatory response and cell death, which are two principal components of the innate response. White blood cells called macrophages use a set of sensors to recognize the pathogen and produce proteins called cytokines, which trigger inflammation and recruit other cells of the innate immune system for help. In addition, macrophages instruct the adaptive immune system to learn about the pathogen and ultimately produce antibodies.

To survive within the host, successful pathogens silence the inflammatory response. They do this by blocking the ability of macrophages to release cytokines and alert the rest of the immune system. To counteract the viruss silencing, infected cells commit suicide, or cell death. Although detrimental at the cellular level, cell death is beneficial at the level of the organism because it stops proliferation of the pathogen.

For example, the pathogen that caused the bubonic plague, which killed half of the human population in Europe between 1347 and 1351, was able to disable, or silence, peoples white blood cells and proliferate in them, ultimately causing the death of the individual. However, in rodents the infection played out differently. Just the infected macrophages of rodents died, thus limiting proliferation of the pathogen in the rodents bodies which enabled them to survive.

The silent response to plague is strikingly different from the violent response to SARS-CoV-2, the virus that causes COVID-19. This suggests that keeping the right balance of innate response is crucial for the survival of COVID-19 patients.

Also read: If I had Covid-19 am I immune? This is what scientists know so far

Heres how an overreaction from the immune system can endanger a person fighting off an infection.

Some of the proteins that trigger inflammation, named chemokines, alert other immune cells like neutrophils, which are professional microbe eaters to convene at the site of infections where they can arrive first and digest the pathogen.

Others cytokines such as interleukin 1b, interleukin 6 and tumor necrosis factor guide neutrophils from the blood vessels to the infected tissue. These cytokines can increase heartbeat, elevate body temperature, trigger blood clots that trap the pathogen and stimulate the neurons in the brain to modulate body temperature, fever, weight loss and other physiological responses that have evolved to kill the virus.

When the production of these same cytokines is uncontrolled, immunologists describe the situation as a cytokine storm. During a cytokine storm, the blood vessels widen further (vasolidation), leading to low blood pressure and widespread blood vessel injury. The storm triggers a flood of white blood cells to enter the lungs, which in turn summon more immune cells that target and kill virus-infected cells. The result of this battle is a stew of fluid and dead cells, and subsequent organ failure.

The cytokine storm is a centerpiece of the COVID-19 pathology with devastating consequences for the host.

When the cells fail to terminate the inflammatory response, production of the cytokines make macrophages hyperactive. The hyperactivated macrophages destroy the stem cells in the bone marrow, which leads to anemia. Heightened interleukin 1b results in fever and organ failure. The excessive tumor necrosis factor causes massive death of the cells lining the blood vessels, which become clotted. At some point, the storm becomes unstoppable and irreversible.

One strategy behind the treatments for COVID is, in part, based in part on breaking the vicious cycle of the cytokine storm. This can be done by using antibodies to block the primary mediators of the storm, like IL6, or its receptor, which is present on all cells of the body.

Inhibition of tumor necrosis factor can be achieved with FDA-approved antibody drugs like Remicade or Humira or with a soluble receptor such as Enbrel (originally developed by Bruce Beutler) which binds to tumor necrosis factor and prevents it from triggering inflammation. The global market for tumor necrosis factor inhibitors is US$22 billion.

Drugs that block various cytokines are now in clinical trials to test whether they are effective for stopping the deadly spiral in COVID-19.

Alexander (Sasha) Poltorak, Professor of Immunology, Tufts University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Also read: Covid vaccine research in India at nascent stage, breakthrough unlikely this year: Experts

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Advancements in Medical Skin Care Products Market to boost Revenues Through COVID-19 Crisis Phase and Forecast 2017 2025 – WaterCloud News

By daniellenierenberg

New York City, United States The change during the COVID-19 pandemic has overhauled our dependence on pattern setting developments, for instance, expanded reality, computer generated reality, and the Healthcare web of things. The unfulfilled cash related targets are persuading the relationship to grasp robotization and forefront advancements to stay ahead in the market competition. Associations are utilizing this open entryway by recognizing step by step operational needs and showing robotization in it to make an automated structure as far as might be feasible

Medical skin care products are used for beautifying or to address some other skin care problems. The cosmetic industry is booming and skin care forms a very huge part of this industry. The aesthetic appearance is so important that people spend a lot on skin care products and treatment. People being more technologically aware of the various new skin care products trending in the market. In addition to the aesthetic application, the medical skin care products are also used to address issues such as acne, pimples or scars.

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Medical Skin Care Products Market: Drivers and Restraints

The medical skin care products is primarily driven by the need of natural based active ingredients products which are now trending in the market. Consumers demand medical skin care products which favor health and environment. Moreover, the consumers are updated with the trends so that various companies end up providing such products to satisfy the customers. For instance, a single product face mask has thousands of different variants. This offers consumers different options to select the product depending on the skin type. Moreover, the market players catering to the medical skin care products are offering products with advanced technologies. For instance, Santinov launched the CICABEL mask using stem cell material based on advanced technologies. The stem cells used in the skin care product helps to to protect and activate the cells and promote the proliferation of skin epidermal cells and the anagenesis of skin fibrosis.

Medical Skin Care Products Market: Segmentation

On the basis of product type the medical skin care products market can be segmented as:

On the basis of application, the medical skin care products market can be segment as:

On the basis of distribution channel, the medical skin care products market can be segment as:

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Medical Skin Care Products Market: Overview

Medical skin care products are used to address basic skin problems ranging from acne to scars. There are various advancements in the ingredients used to offer skin care products to the consumers. For instance, the use of hyaluronic acid and retinoids is the latest development in the industry. The anti-aging creams are at the forefront as the help treating issues such as wrinkles, scars, acne, and sun damage. Another, product in demand is the probiotic skincare which include lactobacillus and bifidobacterium.

Medical Skin Care Products Market: Region-wise Outlook

In terms of geography, medical skin care products market has been divided into five regions including North- America, Asia- Pacific, Middle-East & Africa, Latin America and Europe. North America dominated the global medical skin care products market as international players are acquiring domestic companies to make their hold strong in the U.S. LOral is accelerating its U.S. market by signing a definitive agreement with Valeant Pharmaceuticals International Inc. to acquire CeraVe, AcneFree and Ambi skin-care brands for US$ 1.3 billion. The acquisition is expected LOreal to get hold of the brands in the price-accessible segment. Asia Pacific is expected to be the fastest growing region owing to the increasing disposable income and rising awareness towards the skin care products.

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Medical Skin Care Products Market: Key Market Participants

Some of the medical skin care products market participants are ,

Report Highlights:

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