Monday, January 27, 2020

Cancer patients could be treated with a one-size-fits-all therapy, following the discovery of an immune cell which kills all forms of the disease.

Researchers at Cardiff University have found a new type of killer T-cell, capable of recognising and destroying most human cancers while preserving healthy cells. The scientists discovered a method of killing prostate, breast, lung and other cancers in lab tests and say there is enormous potential for immunotherapies not previously thought to be possible.

Cardiff Universitys cancer findings came from scientists looking for unconventional ways in which the immune system naturally attacks tumours. They found, inside human blood, a T-cell that can scan the body for a threat, such as cancerous cells, and eliminate the danger while leaving healthy cells alone. The team described the work as at an early stage, but exciting.

T-cell cancer therapies are where immune cells are removed, modified and returned to the patients blood to seek and destroy cancer cells. The most widely-used, known as CAR-T, is personalised to the patient but combats only a handful of cancers and has not been successful in eliminating solid tumours - which account for the vast majority of cancers.

The Cardiff teams discovery involves a new type of T-cell receptor (TCR), which recognises a molecule present on the surface of a wide range of cancer cells as well as in many of the bodys normal cells and is, remarkably, able to distinguish between the two. In tests, T-cells equipped with the new TCR killed lung, skin, blood, colon, breast, bone, prostate, ovarian, kidney and cervical cancer cells.

Professor Andrew Sewell, the lead author on the study and an expert in T-cells from Cardiff Universitys School of Medicine, said it was highly unusual to find a TCR with such broad cancer specificity, raising the prospect of universal cancer therapy.

Prof Sewell said: We hope this new TCR may provide us with a different route to target and destroy a wide range of cancers in all individuals. Current TCR-based therapies can only be used in a minority of patients with a minority of cancers.

Cancer-targeting via MR1-restricted T-cells is an exciting new frontier - it raises the prospect of a one-size-fits-all cancer treatment; a single type of T-cell that could be capable of destroying many different types of cancers across the population. Previously nobody believed this could be possible.

Further experiments and safety testing are now underway, with the hope of trialling this new approach in patients towards the end of 2020. Prof Sewell added: There are plenty of hurdles to overcome; however, if this testing is successful, then I would hope this new treatment could be in use in patients in a few years time.

Cancer is the leading cause of all avoidable deaths in the UK. Breast cancer is the most common, followed jointly by prostate and lung cancer and then by bowel cancer. Obesity is now a bigger cause than smoking of some cancers, namely bowel, kidney, liver and ovarian cancer.

According to financial information business Defaqto*, 38 out of 51 health insurance products include cancer cover, with benefits ranging from breakthrough treatment not otherwise available on the NHS to hormone therapy, reconstructive surgery and stem cell therapy. To find the right cancer cover for your family, use our online comparison tool or speak with our team on 0800 862 0373.

Photo:Cardiff Universitys Professor Andrew Sewell, left, with Research Fellow Garry Dolton.

Credit: Cardiff University

* Data sourced on January 2, 2020.

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When Marie Antoinette was captured during the French Revolution, her hair reportedly turned white overnight. In more recent history, former U.S. Senator John McCain experienced severe injuries as a prisoner during the Vietnam Warand lost color in his hair.

For a long time, anecdotes have connected stressful experiences with hair-graying.

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Now, for the first time, Harvard University scientists have discovered exactly how the process plays out: stress activates nerves that are part of the fight-or-flight response, which in turn cause permanent damage to pigment-regenerating stem cells in hair follicles.

The work, published inNature, details the molecular mechanisms behind the longstanding biological puzzle.

Everyone has an anecdote to share about how stress affects their body, particularly in their skin and hairthe only tissues we can see from the outside, said senior authorYa-Chieh Hsu, the Alvin and Esta Star Associate Professor of Stem Cell and Regenerative Biology at Harvard. We wanted to understand if this connection is true, and if so, how stress leads to changes in diverse tissues. Hair pigmentation is such an accessible and tractable system to start with, and besides, we were genuinely curious to see if stress indeed leads to hair-graying.

Fingering the culprit

Because stress affects the whole body, researchers first had to narrow down which body system was responsible for connecting stress to hair color. The team first hypothesized that stress causes an immune attack on pigment-producing cells. However, when mice lacking immune cells still showed hair-graying, researchers turned to the hormone cortisol. Once more, it was a dead end.

Stress always elevates levels of the hormone cortisol in the body, so we thought that cortisol might play a role, Hsu said. But surprisingly, when we removed the adrenal gland from the mice so that they couldnt produce cortisol-like hormones, their hair still turned gray under stress.

After systematically eliminating different possibilities, researchers homed in on the sympathetic nervous system, which is responsible for the bodys fight-or-flight response.

Sympathetic nerves branch out into each hair follicle on the skin. The researchers found that stress causes these nerves to release the chemical norepinephrine, which gets taken up by nearby pigment-regenerating stem cells.

Permanent damage

In the hair follicle, certain stem cells act as a reservoir of pigment-producing cells. When hair regenerates, some of the stem cells convert into pigment-producing cells that color the hair.

Researchers found that the norepinephrine from sympathetic nerves causes the stem cells to activate excessively. The stem cells all convert into pigment-producing cells, prematurely depleting the reservoir.

When we started to study this, I expected that stress was bad for the body, but the detrimental impact of stress that we discovered was beyond what I imagined, Hsu said. After just a few days, all of the pigment-regenerating stem cells were lost. Once theyre gone, you cant regenerate pigments anymore. The damage is permanent.

The finding underscores the negative side effects of an otherwise protective evolutionary response, the researchers said.

Acute stress, particularly the fight-or-flight response, has been traditionally viewed to be beneficial for an animals survival. But in this case, acute stress causes permanent depletion of stem cells, said postdoctoral fellow Bing Zhang, the lead author of the study.

Answering a fundamental question

To connect stress with hair-graying, the researchers started with a whole-body response and progressively zoomed into individual organ systems, cell-to-cell interaction and, eventually, all the way down to molecular dynamics. The process required a variety of research tools along the way, including methods to manipulate organs, nerves and cell receptors.

To go from the highest level to the smallest detail, we collaborated with many scientists across a wide range of disciplines, using a combination of different approaches to solve a very fundamental biological question, Zhang said.

One of the study collaborators wasIsaac Chiu, assistant professor of immunology in the Blavatnik Institute at Harvard Medical School, who studies the interplay between the nervous and immune systems.

We know that peripheral neurons powerfully regulate organ function, blood vessels and immunity, but less is known about how they regulate stem cells, Chiu said.With this study, we now know that neurons can control stem cells and their function and can explain how they interact at the cellular and molecular levels to link stress with hair-graying.

The findings can help illuminate the broader effects of stress on various organs and tissues. This understanding will pave the way for new studies that seek to modify or block the damaging effects of stress.

By understanding precisely how stress affects stem cells that regenerate pigment, weve laid the groundwork for understanding how stress affects other tissues and organs in the body, Hsu said. Understanding how our tissues change under stress is the first critical step towards eventual treatment that can halt or revert the detrimental impact of stress. We still have a lot to learn in this area.

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CHICAGO - Brian Wallach wasn't supposed to live to see his younger daughter's first birthday.

Diagnosed with amyotrophic lateral sclerosis (ALS), a terminal disease with no cure, doctors told him in 2017 that he might have six months to live.

Today, he's focused on being there for his daughter's future firsts: kindergarten drop-off, middle school dance, wedding day.

More than two years after his diagnosis, he has been lucky, he said, to experience relatively limited progression of his disease. After some balance issues, the Kenilworth resident now uses a cane - or, as he is careful to specify, a "cool walking stick" - to get around.

When Wallach was diagnosed, neither he nor his wife, Sandra Abrevaya, knew much about ALS, a neurodegenerative disease that affects nerve cells in the brain and the spinal cord, eventually paralyzing even the body's ability to breathe.

In response to Wallach's diagnosis, the couple, both 39, launched I AM ALS in 2019. Former staffers in the Obama White House, they marshaled lessons learned while campaigning - gathering information, forming consensus, considering the impossible possible - to build a force to mobilize hope and change for those facing a disease they say can and should be cured.

Rays of hope are beginning to emerge through an innovative trial that received FDA approval last week to test several drugs at the same time, a bipartisan congressional caucus, doubled federal funding, and support from groups like the Chan Zuckerberg Initiative, which gave the couple's organization a $453,000 grant in September.

"Last year we made hope a word that was OK to use," Wallach said. "This year we have to make hope real."

Audaciousness is the only option, the couple says, in their race against the clock.

Wallach logged 120,000 miles in the air last year, including traveling to Washington, D.C., in April, where he testified before Congress and asked legislators to amp up funding.

"Last year, every time someone said, 'Do you want to speak to us,' I said, 'yes.' Every time someone said, 'There's a meeting,' I said, 'I'm going.'" he said. "Every time there was anything, I said, 'Great, I'm on the plane.'"

Until October, when Wallach fell while exiting a Lyft in Boston after swinging a heavy backpack onto his back. Thirteen staples in his head later, and after terrifying Abrevaya with a phone call, the two agreed he wouldn't travel alone anymore. He's maintaining momentum for the cause with more hours in his home office and fewer in airports.

In December, I AM ALS debuted billboards around Times Square as part of its #CuresForAll campaign aimed at informing the public about the impact a cure or better treatment for a neurodegenerative disease can have on other diseases such as multiple sclerosis, Alzheimer's and Parkinson's. ALS patients and their families from states including Michigan, Maine and Colorado were in New York for the launch.

The billboards noted the number of people lost to ALS each day - 16 - with photographs of those who died in 2019. Days earlier, Pete Frates, a founder of the viral fundraiser the Ice Bucket Challenge, which raised $115 million, had died. He was 34.

The campaign was also shared on social media. The posts expressed the suffering and loss nationwide: a mother wrote about her son who was diagnosed at 20 and died at 28; a son posted in honor of his dad; Colorado Rep. Jason Crow posted a message honoring his cousin.

It's time, the couple said, to switch ALS conversations from a diagnosis rooted in darkness to the faces of people bravely moving forward. They want to speed development of potential cures and give patients more access to experimental treatments.

That's not an unreasonable goal, said Sabrina Paganoni, a faculty member at The Sean M. Healey & AMG Center for ALS at Mass General in Boston, which plans to test at least five different medications for ALS at the same time, a first for the disease and something she said could be a huge turning point.

On Wednesday, the Healey Center announced it received FDA approval to move forward with testing the first three drugs: Zilucoplan, Verdiperstat and CNM-Au8. Similar to how cancer drugs are already tested, this gives patients access to more treatments and allows researchers to quickly collect data and accelerate the pace toward a cure.

"This is a very exciting time in the history of ALS," Paganoni said. "I think this is going to be the decade when ALS is changed from a rapidly fatal disease to a more chronic disease that we can manage."

For years, Steve Perrin, the chief executive officer at the ALS Therapy Development Institute, has monitored clinical trials for ALS. So far, he said, the two drugs approved by the FDA, Radicava and Rilutek, are "a very marginal slowing down of disease."

This year, he said the quality of drugs going into trials seems improved. He is excited about several trials, including one studying stem cells and another testing a drug to potentially slow progression in some patients.

"As a patient you want to see something measurable, and I don't mean measurable in days," he said. "If I'm a patient, I want to see something, and I want hope for myself and my family. I want something that is going to slow the disease down so I can watch my kids growing up, I can watch them graduate from college, I can watch them marry."

But that takes resources.

"We are in a time when we can reasonably say that there's going to be new treatments available," Paganoni said. "But we need more funding and support, so all of this can happen, and happen soon."

Nearly every moment feels like a push-pull for Wallach and Abrevaya.

Do they spend more precious minutes with their two daughters, ages 4 and 2, or do they spend time away, among strangers - on a plane, in a researcher's office, walking the halls of Congress - with the hope that those minutes will, someday, result in time banked to create more family memories.

"The hardest balance, if I'm honest, is, I love every minute I have with them," Wallach said about his daughters, "but I also feel this pressing sense of, I need to be working towards a goal of actually finding a cure."

"We're doing that so we have a shot at a real future together," Abrevaya said about their time spent traveling and advocating.

At home, when the family heads for the door, the toddlers reach for their father's shoes, and they get his walking stick.

"While that both fills your heart with joy and appreciation, it's also painful that your toddlers are being put in this position," Abrevaya said.

The parents guard normalcy. They take their daughters to swim at the neighborhood pool and on vacation with friends. Wallach wishes he could lift them above his head to touch the ceiling, like their uncle can. But he can lie on the floor and play with them; he can listen to them belt out songs on their purple karaoke machine.

They find ways to lighten a heavy subject. On New Year's Eve, the two danced in a video on the foundation's Instagram, singing into hairbrushes, and Wallach promised to get an "ALS: You Gone" tattoo if 20,000 people donated $10 to a Healey Center research fundraiser. It raised $40,000 in 24 hours, Wallach said. No matter the outcome, he plans to get the tattoo.

The couple, who both work full-time jobs - Abrevaya is the president of nonprofit Thrive, Wallach works at law firm Skadden, Arps, Slate, Meagher & Flom - want more research, to create a patient navigation system, and to gather signatures for a letter asking new FDA commissioner Stephen Hahn to speed ALS patients' access to possible treatments.

And they keep looking for light. But it takes work.

Changing life with ALS for Wallach, and for other patients and their families, requires bold action from people with the power to make change: politicians, researchers, philanthropists.

As they meet others with ALS, they welcome new friends and face the pain of losing some.

"It does make you uniquely urgent in what you do," Wallach said. "You push because you have to. You push because you know that the time that we have is precious, and that you want to see 20 years from now. And know that you can make that happen."

Wallach often shares moments about his ALS journey on Twitter with his 40,000 followers. Recently, he shared something he wasn't sure he should. It was a time he was unable to find light.

On a recent night, he woke up to pain he's had for the past few months, radiating from his right hip to his right calf.

He clutched a stuffed llama his daughter gave him. And he began to cry.

"I cried because of the pain. I cried because I couldn't be the father to my girls I dreamed of being," he wrote. "I cried because I couldn't be the husband to my wife I dream of being. Because I saw the future zooming ahead, and for a brief moment I wondered if I would be a part of it."

His wife heard him crying that night. She asked what was wrong. And he said maybe they would be better off if he left, living instead in an assisted living facility. Their daughters, he told her, could have a dad who could do everything he dreamed of doing.

She looked at him in the dark. "You are my light," she said. "You are their light. The only way you are leaving us is if you die in my arms, and we aren't going to let that happen for a long, long, long time."

Distributed by Tribune Content Agency, LLC.

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In a race against terminal illness, former Obama staffer with ALS and his wife find new hope a year later - PostBulletin.com

Spinal Cord Stem Cells Comments Off on In a race against terminal illness, former Obama staffer with ALS and his wife find new hope a year later – PostBulletin.com | January 27th, 2020

Submerged in liquid nitrogen vapor at a temperature of minus 175 degrees Celsius, hundreds of thousands of stem cells from all over Europe bide their time in large steel barrels on the outskirts of Warsaw.

Present in blood drawn from the umbilical cord of a newborn baby, stem cells can help cure serious blood-related illnesses like leukemias and lymphomas, as well as genetic conditions and immune system deficits.

Polish umbilical cord blood bank PBKM/FamiCord became the industrys leader in Europe after Swiss firm Cryo-Save went bankrupt early last year.

It is also the fifth largest in the world, according to its management, after two companies in the United States, a Chinese firm and one based in Singapore.

Since the first cord blood transplant was performed in France in 1988, the sector has significantly progressed, fuelling hopes.

Health insurance

Mum-of-two Teresa Przeborowska has firsthand experience.

At five years old, her son Michal was diagnosed with lymphoblastic leukemia and needed a bone marrow transplant, the entrepreneur from northern Poland said.

The most compatible donor was his younger sister, Magdalena.

When she was born, her parents had a bag of her cord blood stored at PBKM.

More than three years later, doctors injected his sisters stem cells into Michals bloodstream.

It was not quite enough for Michals needs but nicely supplemented harvested bone marrow.

As a result, Michal, who is nine, is now flourishing, both intellectually and physically, his mum told AFP.

A cord blood transplant has become an alternative to a bone marrow transplant when there is no donor available, with a lower risk of complications.

Stem cells taken from umbilical cord blood are like those taken from bone marrow, capable of producing all blood cells: red cells, platelets and immune system cells.

When used, stem cells are first concentrated, then injected into the patient. Once transfused, they produce new cells of every kind.

At the PBKM laboratory, each container holds up to 10,000 blood bags Safe and secure, they wait to be used in the future, its head, Krzysztof Machaj, said.

The bank holds around 440,000 samples, not including those from Cryo-Save, he said.

If the need arises, the blood will be ready to use without the whole process of looking for a compatible donor and running blood tests, the biologist told AFP.

For families who have paid an initial nearly 600 euros (around P34,000) and then an annual 120 euros (around P7,000) to have the blood taken from their newborns umbilical cords preserved for around 20 years, it is a kind of health insurance promising faster and more effective treatment if illness strikes.

But researchers also warn against unrealistic expectations.

Beauty products

Hematologist Wieslaw Jedrzejczak, a bone marrow pioneer in Poland, describes promoters of the treatment as sellers of hope, who make promises that are either impossible to realize in the near future or downright impossible to realize at all for biological reasons.

He compares them to makers of beauty products who swear their cream will rejuvenate the client by 20 years.

Various research is being done on the possibility of using the stem cells to treat other diseases, notably nervous disorders. But the EuroStemCell scientist network warns that the research is not yet conclusive.

There is a list of almost 80 diseases for which stem cells could prove beneficial, U.S. hematologist Roger Mrowiec, who heads the clinical laboratory of the cord blood program Vitalant in New Jersey, told AFP.

But given the present state of medicine, they are effective only for around a dozen of them, like leukemia or cerebral palsy, he said.

Its not true, as its written sometimes, that we can already use them to fight Parkinsons disease or Alzheimers disease or diabetes.

EuroStemCell also cautions against private blood banks that advertise services to parents suggesting they should pay to freeze their childs cord blood in case its needed later in life.

Studies show it is highly unlikely that the cord blood will ever be used for their child, the network said.

It also pointed out that there could be a risk of the childs cells not being useable anyway without reintroducing the same illness.

Some countries, such as Belgium and France, are cautious and ban the storage of cord blood for private purposes. Most E.U. countries however permit it while imposing strict controls.

Rapid growth

In the early 2000s, Swiss company Cryo-Save enjoyed rapid growth.

Greeks, Hungarians, Italians, Spaniards and Swiss stored blood from their newborns with the company for 20 years on payment of 2,500 euros (around P140,000) upfront.

When the firm was forced to close in early 2019, clients were left wondering where their stem cells would end up.

Under a kind of back-up agreement, the samples of some 250,000 European families were transferred for storage at PBKM.

The Polish firm, founded in 2002 with 2 million zlotys (around P26 million), has also grown quickly.

Present under the FamiCord brand in several countries, PBKM has some 35% of the European market, excluding Cryo-Save assets.

Over the last 15 months, outside investors have contributed 63 million euros to the firm, PBKMs chief executive Jakub Baran told AFP.

But the company has not escaped controversy: the Polityka weekly recently published a critical investigative report on several private clinics that offer what was described as expensive treatment involving stem cells held by PBKM.IB/JB

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Europe's guardian of stem cells and hopes, real and unrealistic - INQUIRER.net

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Global Cell Therapy Technologies Marketwas valued US$ 12 billion in 2018 and is expected to reach US$ 35 billion by 2026, at CAGR of 12.14 %during forecast period.

The objective of the report is to present comprehensive assessment projections with a suitable set of assumptions and methodology. The report helps in understanding Global Cell Therapy Technologies Market dynamics, structure by identifying and analyzing the market segments and projecting the global market size. Further, the report also focuses on the competitive analysis of key players by product, price, financial position, growth strategies, and regional presence. To understand the market dynamics and by region, the report has covered the PEST analysis by region and key economies across the globe, which are supposed to have an impact on market in forecast period. PORTERs analysis, and SVOR analysis of the market as well as detailed SWOT analysis of key players has been done to analyze their strategies. The report will to address all questions of shareholders to prioritize the efforts and investment in the near future to the emerging segment in the Global Cell Therapy Technologies Market.

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Global Cell Therapy Technologies Market: OverviewCell therapy is a transplantation of live human cells to replace or repair damaged tissue and/or cells. With the help of new technologies, limitless imagination, and innovative products, many different types of cells may be used as part of a therapy or treatment for different types of diseases and conditions. Celltherapy technologies plays key role in the practice of medicine such as old fashioned bone marrow transplants is replaced by Hematopoietic stem cell transplantation, capacity of cells in drug discovery. Cell therapy overlap with different therapies like, gene therapy, tissue engineering, cancer vaccines, regenerative medicine, and drug delivery. Establishment of cell banking facilities and production, storage, and characterization of cells are increasing volumetric capabilities of the cell therapy market globally. Initiation of constructive guidelines for cell therapy manufacturing and proven effectiveness of products, these are primary growth stimulants of the market.

Global Cell Therapy Technologies Market: Drivers and RestraintsThe growth of cell therapy technologies market is highly driven by, increasing demand for clinical trials on oncology-oriented cell-based therapy, demand for advanced cell therapy instruments is increasing, owing to its affordability and sustainability, government and private organization , investing more funds in cell-based research therapy for life-style diseases such as diabetes, decrease in prices of stem cell therapies are leading to increased tendency of buyers towards cell therapy, existing companies are collaborating with research institute in order to best fit into regulatory model for cell therapies.Moreover, Healthcare practitioners uses stem cells obtained from bone marrow or blood for treatment of patients with cancer, blood disorders, and immune-related disorders and Development in cell banking facilities and resultant expansion of production, storage, and characterization of cells, these factors will drive the market of cell therapy technologies during forecast period.

On the other hand, the high cost of cell-based research and some ethical issue & legally controversial, are expected to hamper market growth of Cell Therapy Technologies during the forecast period

AJune 2016, there were around 351 companies across the U.S. that were engaged in advertising unauthorized stem cell treatments at their clinics. Such clinics boosted the revenue in this market.in August 2017, the U.S. FDA announced increased enforcement of regulations and oversight of clinics involved in practicing unapproved stem cell therapies. This might hamper the revenue generation during the forecast period; nevertheless, it will allow safe and effective use of stem cell therapies.

Global Cell Therapy Technologies Market: Segmentation AnalysisOn the basis of product, the consumables segment had largest market share in 2018 and is expected to drive the cell therapy instruments market during forecast period at XX % CAGR owing to the huge demand for consumables in cell-based experiments and cancer research and increasing number of new product launches and consumables are essential for every step of cell processing. This is further expected to drive their adoption in the market. These factors will boost the market of Cell Therapy Technologies Market in upcoming years.

On the basis of process, the cell processing had largest market share in 2018 and is expected to grow at the highest CAGR during the forecast period owing to in cell processing stage,a use of cell therapy instruments and media at highest rate, mainly in culture media processing. This is a major factor will drive the market share during forecast period.

Global Cell Therapy Technologies Market: Regional AnalysisNorth America to held largest market share of the cell therapy technologies in 2018 and expected to grow at highest CAGR during forecast period owing to increasing R&D programs in the pharmaceutical and biotechnology industries. North America followed by Europe, Asia Pacific and Rest of the world (Row).

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Scope of Global Cell Therapy Technologies Market

Global Cell Therapy Technologies Market, by Product

Consumables Equipment Systems & SoftwareGlobal Cell Therapy Technologies Market, by Cell Type

Human Cells Animal CellsGlobal Cell Therapy Technologies Market, by Process Stages

Cell Processing Cell Preservation, Distribution, and Handling Process Monitoring and Quality ControlGlobal Cell Therapy Technologies Market, by End Users

Life Science Research Companies Research InstitutesGlobal Cell Therapy Technologies Market, by Region

North America Europe Asia Pacific Middle East & Africa South America

Key players operating in the Global Cell Therapy Technologies Market

Beckman Coulter, Inc. Becton Dickinson and Company GE Healthcare Lonza Merck KGaA MiltenyiBiotec STEMCELL Technologies, Inc. Terumo BCT, Inc. Thermo Fisher Scientific, Inc. Sartorius AG

Browse Full Report with Facts and Figures of Cell Therapy Technologies Market Report at:https://www.maximizemarketresearch.com/market-report/global-cell-therapy-technologies-market/31531/

MAJOR TOC OF THE REPORT

Chapter One: Cell Therapy Technologies Market Overview

Chapter Two: Manufacturers Profiles

Chapter Three: Global Cell Therapy Technologies Market Competition, by Players

Chapter Four: Global Cell Therapy Technologies Market Size by Regions

Chapter Five: North America Cell Therapy Technologies Revenue by Countries

Chapter Six: Europe Cell Therapy Technologies Revenue by Countries

Chapter Seven: Asia-Pacific Cell Therapy Technologies Revenue by Countries

Chapter Eight: South America Cell Therapy Technologies Revenue by Countries

Chapter Nine: Middle East and Africa Revenue Cell Therapy Technologies by Countries

Chapter Ten: Global Cell Therapy Technologies Market Segment by Type

Chapter Eleven: Global Cell Therapy Technologies Market Segment by Application

Chapter Twelve: Global Cell Therapy Technologies Market Size Forecast (2019-2026)

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Global Cell Therapy Technologies Market : Industry Analysis and Forecast (2018-2026) - Expedition 99

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UCLA Broad Stem Cell Research Center/Nature Medicine

At left, image shows white blood cells (red) from one of the X-CGD clinical trial participants before gene therapy. At right, after gene therapy, white blood cells from the same patient show the presence of the chemicals (blue) needed to attack and destroy bacteria and fungus.

UCLA researchers are part of an international team that reported the use of a stem cell gene therapy to treat nine people with the rare, inherited blood disease known as X-linked chronic granulomatous disease, or X-CGD. Six of those patients are now in remission and have stopped other treatments. Before now, people with X-CGD which causes recurrent infections, prolonged hospitalizations for treatment, and a shortened lifespan had to rely on bone marrow donations for a chance at remission.

With this gene therapy, you can use a patients own stem cells instead of donor cells for a transplant, said Dr. Donald Kohn, a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and a senior author of the new paper, published today in the journal Nature Medicine. This means the cells are perfectly matched to the patient and it should be a much safer transplant, without the risks of rejection.

People with chronic granulomatous disease, or CGD, have a genetic mutation in one of five genes that help white blood cells attack and destroy bacteria and fungus using a burst of chemicals. Without this defensive chemical burst, patients with the disease are much more susceptible to infections than most people. The infections can be severe to life-threatening, including infections of the skin or bone and abscesses in organs such as lungs, liver or brain. The most common form of CGD is a subtype called X-CGD, which affects only males and is caused by a mutation in a gene found on the X-chromosome.

Other than treating infections as they occur and taking rotating courses of preventive antibiotics, the only treatment option for people with CGD is to receive a bone marrow transplant from a healthy matched donor. Bone marrow contains stem cells called hematopoietic, or blood-forming, stem cells, which produce white blood cells. Bone marrow from a healthy donor can produce functioning white blood cells that effectively ward off infection. But it can be difficult to identify a healthy matched bone marrow donor and the recovery from the transplant can have complications such as graft versus host disease, and risks of infection and transplant rejection.

Patients can certainly get better with these bone marrow transplants, but it requires finding a matched donor and even with a match, there are risks, Kohn said. Patients must take anti-rejection drugs for six to 12 months so that their bodies dont attack the foreign bone marrow.

In the new approach, Kohn teamed up with collaborators at the United Kingdoms National Health Service, France-based Genethon, the U.S. National Institute of Allergy and Infectious Diseases at the National Institutes of Health, and Boston Childrens Hospital. The researchers removed hematopoietic stem cells from X-CGD patients and modified the cells in the laboratory to correct the genetic mutation. Then, the patients own genetically modified stem cells now healthy and able to produce white blood cells that can make the immune-boosting burst of chemicals were transplanted back into their own bodies. While the approach is new in X-CGD, Kohn previously pioneered a similar stem cell gene therapy to effectively cure a form of severe combined immune deficiency (also known as bubble baby disease) in more than 50 babies.

The viral delivery system for the X-CGD gene therapy was developed and fine-tuned by Professor Adrian Thrashers team at Great Ormond Street Hospital, or GOSH, in London, who collaborated with Kohn. The patients ranged in age from 2 to 27 years old; four were treated at GOSH and five were treated in the U.S., including one patient at UCLA Health.

Two people in the new study died within three months of receiving the treatment due to severe infections that they had already been battling before gene therapy. The seven surviving patients were followed for 12 to 36 months after receiving the stem cell gene therapy. All remained free of new CGD-related infections, and six of the seven have been able to discontinue their usual preventive antibiotics.

None of the patients had complications that you might normally see from donor cells and the results were as good as youd get from a donor transplant or better, Kohn said.

An additional four patients have been treated since the new paper was written; all are currently free of new CGD-related infections and no complications have arisen.

Orchard Therapeutics, a biotechnology company of which Kohn is a scientific co-founder, acquired the rights to the X-CGD investigational gene therapy from Genethon. Orchard will work with regulators in the U.S. and Europe to carry out a larger clinical trial to further study this innovative treatment. The aim is to apply for regulatory approval to make the treatment commercially available, Kohn said.

Kohn and his colleagues plan to develop similar treatments for the other forms of CGD caused by four other genetic mutations that affect the same immune function as X-CGD.

Beyond CGD, there are also other diseases caused by proteins missing in white blood cells that could be treated in similar ways, Kohn said.

The research was supported by grants from the California Institute for Regenerative Medicine; the National Heart, Lung and Blood Institute and the National Institute of Allergy and Infectious Diseases, both at the National Institutes of Health; the Wellcome Trust; Boston Childrens Hospital; the National Institute for Health Research Great Ormond Street Hospital Biomedical Research Centre; the Institute for Health Research Biomedical Research Centre at University College London Hospitals NHS Foundation Trust and University College London; the Great Ormond Street Hospital Childrens Charity; the AFM-Tlthon, French Muscular Dystrophy Association; and the European Commission through the Net4CGDconsortium.

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Biomedical researchers from Texas Tech University Health Sciences Center El Paso (TTUHSC El Paso) and The University of Texas at El Paso (UTEP) are collaborating to develop artificial mini-hearts using 3D bioprinting technology for space.

These heart-tissue structures will be sent to the International Space Station (ISS) to gain insight into how microgravity affects the function of the human heart, particularly in regards to the health condition known as cardiac atrophy.

The artificial mini-heart, otherwise known as a cardiac organoid, will be produced using a combination of human stem cells and 3D bioprinting. The project, which began in September 2019, will take course over the next three years. It is funded by the National Science Foundation (NSF) and the space stations U.S. National Laboratory.

TTUHSC El Paso faculty scientist Munmun Chattopadhyay, Ph.D., a researcher on the project, states:

Knowledge gathered from this study could be used to develop technologies and therapeutic strategies to better combat tissue atrophy experienced by astronauts, as well as open the door for improved treatments for people who suffer from serious heart issues due to illness.

How does microgravity affect our hearts?

Researchers taking part in the project are Dr. Chattopadhyay and UTEP biomedical engineer Binata Joddar, Ph.D. Dr. Chattopadhyay is an assistant professor in TTUHSC El Pasos Center of Emphasis in Diabetes and Metabolism, part of the Paul L. Foster School of Medicines Department of Molecular and Translational Medicine. Dr. Joddar is an assistant professor in the UTEP College of Engineering and leads research in the universitys Inspired Materials and Stem Cell-Based Tissue Engineering Laboratory.

Together, the researchers will collaborate to 3D bioprint small cardiac organoids using human stem cells. These heart-tissue structures will then be sent to the ISS, where they will be exposed to the near-weightless environment of the orbiting space station. The researchers hope that this will provide a better understanding of cardiac atrophy, which is a reduction and weakening of heart tissue, leading to difficulty pumping blood to the body. This condition commonly affects astronauts who spend long periods of time in microgravity, which causes significant problems as a weakened heart muscle can lead to symptoms such as fainting, irregular heartbeat, heart valve problems, and even heart failure.

Cardiac atrophy and a related condition, cardiac fibrosis, is a very big problem in our community. People suffering from diseases such as diabetes, muscular dystrophy and cancer, and conditions such as sepsis and congestive heart failure, often experience cardiac dysfunction and tissue damage, comments Dr. Chattopadhyay.

The first phase of the project will focus on research design. During this stage, taking place over the first year, Dr. Joddar will use 3D printing to fabricate the cardiac organoids. This will be achieved by coupling cardiac cells in physiological ratios to mimic heart tissue. Moving on to the second year, the researchers will be preparing the organoid payload for a rocket launch and mission in space. The third and final year of the project will center on analyzing the data from the experiment once the organoids have been returned to Earth.

Additionally, Dr. Chattopadhyay and Dr. Joddars project will provide an educational opportunity for the El Paso community. A workshop for K-12 students will be set up engaging young minds in the local area around the subject of tissue engineering, with focus placed on projects taking place on the space station. A seminar will also be provided for medical students, interns and residents to enable a discussion regarding the benefits and challenges of transitioning research from Earth-based laboratories into space.

3D bioprinting aboard the ISS

The TTUHSC El Paso and UTEP collaborative research project is one of just five research proposals selected by the NSF and ISS National Lab in 2019 as part of the organizations collaboration on tissue-engineering research funding. The NSF awarded Dr. Chattopadhyay $256,892 and Dr. Joddar $259,350 for their roles in the project.

A number of 3D bioprinting research projects have taken place aboard the ISS, as companies and organizations seek further understanding of how space flight affects astronauts.

For example, Russian bio-technical research laboratory 3D Bioprinting Solutions developed its Organ.Aut magnetic 3D bioprinter to study how living organisms are affected by long flights in outer space. In 2018, it was delivered to the ISS onboard the Soyuz MS-11 manned spacecraft following a previous failed launch from the Soyuz MS-10 spaceflight. In late 2019 it was announced that the company was able to 3D bioprint bone tissue in zero gravity aboard the ISS using the Organ.Aut. The experiment is part of a plan to create bone implants for astronaut transplantation during long-term interplanetary expeditions.

Additionally, the 3D BioFabrication Facility (BFF) bioprinter from nScrypt, a Florida-based 3D printing system manufacturer, and spaceflight equipment developer Techshot is also onboard the ISS. Delivered to the ISS aboard the SpaceX CRS-18 cargo mission in 2019, the system is capable of manufacturing human tissue in microgravity conditions. It was sent to the ISS in order to facilitate the production of self-supporting tissues that could lead to the development of therapeutic treatments.

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Featured image shows the ISS Exterior. Photo via Roscosmos/ NASA/TTUHSC El Paso.

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The hearts ability to beat normally over a lifetime is predicated on the synchronized work of proteins embedded in the cells of the heart muscle.

Like a fleet of molecular motors that get turned on and off, these proteins cause the heart cells to contract, then force them to relax, beat after life-sustaining beat.

Now a study led by researchers at Harvard Medical School, Brigham and Womens Hospital and the University of Oxford shows that when too many of the hearts molecular motor units get switched on and too few remain off, the heart muscle begins to contract excessively and fails to relax normally, leading to its gradual overexertion, thickening and failure.

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Results of the work, published Jan. 27 inCirculation,reveal that this balancing act is an evolutionary mechanism conserved across species to regulate heart muscle contraction by controlling the activity of a protein called myosin, the main contractile protein of the heart muscle.

The findingsbased on experiments with human, mouse and squirrel heart cellsalso demonstrate that when this mechanism goes awry it sets off a molecular cascade that leads to cardiac muscle over-exertion and culminates in the development of hypertrophic cardiomyopathy (HCM), the mostcommon genetic diseaseof the heartand aleading causeof sudden cardiac death in young people and athletes.

Our findings offer a unifying explanation for the heart muscle pathology seen in hypertrophic cardiomyopathy that leads to heart muscle dysfunction and, eventually, causes the most common clinical manifestations of the condition, said senior authorChristine Seidman, professor of genetics in the Blavatnik Institute at Harvard Medical School, a cardiologist at Brigham and Womens Hospital and a Howard Hughes Medical InstituteInvestigator.

Importantly, the experiments showed that treatment with an experimental small-molecule drug restored the balance of myosin arrangements and normalized the contraction and relaxation of both human and mouse cardiac cells that carried the two most common gene mutations responsible for nearly half of all HCM cases worldwide.

If confirmed in further experiments, the results can inform the design of therapies that halt disease progression and prevent complications.

Correcting the underlying molecular defect and normalizing the function of heart muscle cells could transform treatment options, which are currently limited to alleviating symptoms and preventing worst-case scenarios such as life-threatening rhythm disturbances and heart failure, said study first authorChristopher Toepfer,who performed the work as a postdoctoral researcher in Seidmans lab and is now a joint fellow in the Radcliffe Department of Medicine at the University of Oxford.

Some of the current therapies used for HCM include medications to relieve symptoms, surgery to shave the enlarged heart muscle or the implantation of cardioverter defibrillators that shock the heart back into rhythm if its electrical activity ceases or goes haywire. None of these therapies address the underlying cause of the disease.

Imbalance in the motor fleet

Myosin initiates contraction by cross-linking with other proteins to propel the cell into motion. In the current study, the researchers traced the epicenter of mischief down to an imbalance in the ratio of myosin molecule arrangements inside heart cells. Cells containing HCM mutations had too many molecules ready to spring into action and too few myosin molecules idling standby, resulting in stronger contractions and poor relaxation of the cells.

An earlier study by the same team found that under normal conditions, the ratio between on and off myosin molecules in mouse heart cells is around 2-to-3. However, the new study shows that this ratio is off balance in heart cells that harbor HCM mutations, with disproportionately more molecules in active versus inactive states.

In an initial set of experiments, the investigators analyzed heart cells obtained from a breed of hibernating squirrel as a model to reflect extremes in physiologic demands during normal activity and hibernation. Cells obtained from squirrels in hibernationwhen their heart rate slows down to about six beats per minutecontained 10 percent more off myosin molecules than the heart cells of active squirrels, whose heart rate averages 340 beats per minute.

We believe this is one example of natures elegant way of conserving cardiac muscle energy in mammals during dormancy and periods of deficient resources, Toepfer said.

Next, researchers looked at cardiac muscle cells from mice harboring the two most common gene defects seen in HCM. As expected, these cells had altered ratios of on and off myosin reserves.The researchers also analyzed myosin ratios in two types of human heart cells: Stem cell-derived human heart cells engineered in the lab to carry HCM mutations and cells obtained from the excised cardiac muscle tissue of patients with HCM. Both had out-of-balance ratios in their active and inactive myosin molecules.

Further experiments showed that this imbalance perturbed the cells normal contraction and relaxation cycle. Cells harboring HCM mutations contained too many on myosin molecules and contracted more forcefully but relaxed poorly. In the process, the study showed, these cells gobbled up excessive amounts of ATP, the cellular fuel that sustains the work of each cell in our body. And because oxygen is necessary for ATP production, the mutated cells also devoured more oxygen than normal cells, the study showed. To sustain their energy demands, these cells turned to breaking down sugar molecules and fatty acids, which is a sign of altered metabolism, the researchers said.

Taken together, our findings map out the molecular mechanisms that give rise to the cardinal features of the disease, Seidman said. They can help explain how chronically overexerted heart cells with high energy consumption in a state of metabolic stress can, over time,lead to a thickened heart muscle that contracts and relaxes abnormally and eventually becomes prone to arrhythmias, dysfunction and failure.

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Bones are an important part of the musculoskeletal system. This article, the first in a two-part series on the skeletal system, reviews the anatomy and physiology of bone

The skeletal system is formed of bones and cartilage, which are connected by ligaments to form a framework for the remainder of the body tissues. This article, the first in a two-part series on the structure and function of the skeletal system, reviews the anatomy and physiology of bone. Understanding the structure and purpose of the bone allows nurses to understand common pathophysiology and consider the most-appropriate steps to improve musculoskeletal health.

Citation: Walker J (2020) Skeletal system 1: the anatomy and physiology of bones. Nursing Times [online]; 116: 2, 38-42.

Author: Jennie Walker is principal lecturer, Nottingham Trent University.

The skeletal system is composed of bones and cartilage connected by ligaments to form a framework for the rest of the body tissues. There are two parts to the skeleton:

As well as contributing to the bodys overall shape, the skeletal system has several key functions, including:

Bones are a site of attachment for ligaments and tendons, providing a skeletal framework that can produce movement through the coordinated use of levers, muscles, tendons and ligaments. The bones act as levers, while the muscles generate the forces responsible for moving the bones.

Bones provide protective boundaries for soft organs: the cranium around the brain, the vertebral column surrounding the spinal cord, the ribcage containing the heart and lungs, and the pelvis protecting the urogenital organs.

As the main reservoirs for minerals in the body, bones contain approximately 99% of the bodys calcium, 85% of its phosphate and 50% of its magnesium (Bartl and Bartl, 2017). They are essential in maintaining homoeostasis of minerals in the blood with minerals stored in the bone are released in response to the bodys demands, with levels maintained and regulated by hormones, such as parathyroid hormone.

Blood cells are formed from haemopoietic stem cells present in red bone marrow. Babies are born with only red bone marrow; over time this is replaced by yellow marrow due to a decrease in erythropoietin, the hormone responsible for stimulating the production of erythrocytes (red blood cells) in the bone marrow. By adulthood, the amount of red marrow has halved, and this reduces further to around 30% in older age (Robson and Syndercombe Court, 2018).

Yellow bone marrow (Fig 1) acts as a potential energy reserve for the body; it consists largely of adipose cells, which store triglycerides (a type of lipid that occurs naturally in the blood) (Tortora and Derrickson, 2009).

Bone matrix has three main components:

Organic matrix (osteoid) is made up of approximately 90% type-I collagen fibres and 10% other proteins, such as glycoprotein, osteocalcin, and proteoglycans (Bartl and Bartl, 2017). It forms the framework for bones, which are hardened through the deposit of the calcium and other minerals around the fibres (Robson and Syndercombe Court, 2018).

Mineral salts are first deposited between the gaps in the collagen layers with once these spaces are filled, minerals accumulate around the collagen fibres, crystallising and causing the tissue to harden; this process is called ossification (Tortora and Derrickson, 2009). The hardness of the bone depends on the type and quantity of the minerals available for the body to use; hydroxyapatite is one of the main minerals present in bones.

While bones need sufficient minerals to strengthen them, they also need to prevent being broken by maintaining sufficient flexibility to withstand the daily forces exerted on them. This flexibility and tensile strength of bone is derived from the collagen fibres. Over-mineralisation of the fibres or impaired collagen production can increase the brittleness of bones as with the genetic disorder osteogenesis imperfecta and increase bone fragility (Ralston and McInnes, 2014).

Bone architecture is made up of two types of bone tissue:

Also known as compact bone, this dense outer layer provides support and protection for the inner cancellous structure. Cortical bone comprises three elements:

The periosteum is a tough, fibrous outer membrane. It is highly vascular and almost completely covers the bone, except for the surfaces that form joints; these are covered by hyaline cartilage. Tendons and ligaments attach to the outer layer of the periosteum, whereas the inner layer contains osteoblasts (bone-forming cells) and osteoclasts (bone-resorbing cells) responsible for bone remodelling.

The function of the periosteum is to:

It also contains Volkmanns canals, small channels running perpendicular to the diaphysis of the bone (Fig 1); these convey blood vessels, lymph vessels and nerves from the periosteal surface through to the intracortical layer. The periosteum has numerous sensory fibres, so bone injuries (such as fractures or tumours) can be extremely painful (Drake et al, 2019).

The intracortical bone is organised into structural units, referred to as osteons or Haversian systems (Fig 2). These are cylindrical structures, composed of concentric layers of bone called lamellae, whose structure contributes to the strength of the cortical bone. Osteocytes (mature bone cells) sit in the small spaces between the concentric layers of lamellae, which are known as lacunae. Canaliculi are microscopic canals between the lacunae, in which the osteocytes are networked to each other by filamentous extensions. In the centre of each osteon is a central (Haversian) canal through which the blood vessels, lymph vessels and nerves pass. These central canals tend to run parallel to the axis of the bone; Volkmanns canals connect adjacent osteons and the blood vessels of the central canals with the periosteum.

The endosteum consists of a thin layer of connective tissue that lines the inside of the cortical surface (Bartl and Bartl, 2017) (Fig1).

Also known as spongy bone, cancellous bone is found in the outer cortical layer. It is formed of lamellae arranged in an irregular lattice structure of trabeculae, which gives a honeycomb appearance. The large gaps between the trabeculae help make the bones lighter, and so easier to mobilise.

Trabeculae are characteristically oriented along the lines of stress to help resist forces and reduce the risk of fracture (Tortora and Derrickson, 2009). The closer the trabecular structures are spaced, the greater the stability and structure of the bone (Bartl and Bartl, 2017). Red or yellow bone marrow exists in these spaces (Robson and Syndercombe Court, 2018). Red bone marrow in adults is found in the ribs, sternum, vertebrae and ends of long bones (Tortora and Derrickson, 2009); it is haemopoietic tissue, which produces erythrocytes, leucocytes (white blood cells) and platelets.

Bone and marrow are highly vascularised and account for approximately 10-20% of cardiac output (Bartl and Bartl, 2017). Blood vessels in bone are necessary for nearly all skeletal functions, including the delivery of oxygen and nutrients, homoeostasis and repair (Tomlinson and Silva, 2013). The blood supply in long bones is derived from the nutrient artery and the periosteal, epiphyseal and metaphyseal arteries (Iyer, 2019).

Each artery is also accompanied by nerve fibres, which branch into the marrow cavities. Arteries are the main source of blood and nutrients for long bones, entering through the nutrient foramen, then dividing into ascending and descending branches. The ends of long bones are supplied by the metaphyseal and epiphyseal arteries, which arise from the arteries from the associated joint (Bartl and Bartl, 2017).

If the blood supply to bone is disrupted, it can result in the death of bone tissue (osteonecrosis). A common example is following a fracture to the femoral neck, which disrupts the blood supply to the femoral head and causes the bone tissue to become necrotic. The femoral head structure then collapses, causing pain and dysfunction.

Bones begin to form in utero in the first eight weeks following fertilisation (Moini, 2019). The embryonic skeleton is first formed of mesenchyme (connective tissue) structures; this primitive skeleton is referred to as the skeletal template. These structures are then developed into bone, either through intramembranous ossification or endochondral ossification (replacing cartilage with bone).

Bones are classified according to their shape (Box1). Flat bones develop from membrane (membrane models) and sesamoid bones from tendon (tendon models) (Waugh and Grant, 2018). The term intra-membranous ossification describes the direct conversion of mesenchyme structures to bone, in which the fibrous tissues become ossified as the mesenchymal stem cells differentiate into osteoblasts. The osteoblasts then start to lay down bone matrix, which becomes ossified to form new bone.

Box 1. Types of bones

Long bones typically longer than they are wide (such as humerus, radius, tibia, femur), they comprise a diaphysis (shaft) and epiphyses at the distal and proximal ends, joining at the metaphysis. In growing bone, this is the site where growth occurs and is known as the epiphyseal growth plate. Most long bones are located in the appendicular skeleton and function as levers to produce movement

Short bones small and roughly cube-shaped, these contain mainly cancellous bone, with a thin outer layer of cortical bone (such as the bones in the hands and tarsal bones in the feet)

Flat bones thin and usually slightly curved, typically containing a thin layer of cancellous bone surrounded by cortical bone (examples include the skull, ribs and scapula). Most are located in the axial skeleton and offer protection to underlying structures

Irregular bones bones that do not fit in other categories because they have a range of different characteristics. They are formed of cancellous bone, with an outer layer of cortical bone (for example, the vertebrae and the pelvis)

Sesamoid bones round or oval bones (such as the patella), which develop in tendons

Long, short and irregular bones develop from an initial model of hyaline cartilage (cartilage models). Once the cartilage model has been formed, the osteoblasts gradually replace the cartilage with bone matrix through endochondral ossification (Robson and Syndercombe Court, 2018). Mineralisation starts at the centre of the cartilage structure, which is known as the primary ossification centre. Secondary ossification centres also form at the epiphyses (epiphyseal growth plates) (Danning, 2019). The epiphyseal growth plate is composed of hyaline cartilage and has four regions (Fig3):

Resting or quiescent zone situated closest to the epiphysis, this is composed of small scattered chondrocytes with a low proliferation rate and anchors the growth plate to the epiphysis;

Growth or proliferation zone this area has larger chondrocytes, arranged like stacks of coins, which divide and are responsible for the longitudinal growth of the bone;

Hypertrophic zone this consists of large maturing chondrocytes, which migrate towards the metaphysis. There is no new growth at this layer;

Calcification zone this final zone of the growth plate is only a few cells thick. Through the process of endochondral ossification, the cells in this zone become ossified and form part of the new diaphysis (Tortora and Derrickson, 2009).

Bones are not fully developed at birth, and continue to form until skeletal maturity is reached. By the end of adolescence around 90% of adult bone is formed and skeletal maturity occurs at around 20-25 years, although this can vary depending on geographical location and socio-economic conditions; for example, malnutrition may delay bone maturity (Drake et al, 2019; Bartl and Bartl, 2017). In rare cases, a genetic mutation can disrupt cartilage development, and therefore the development of bone. This can result in reduced growth and short stature and is known as achondroplasia.

The human growth hormone (somatotropin) is the main stimulus for growth at the epiphyseal growth plates. During puberty, levels of sex hormones (oestrogen and testosterone) increase, which stops cell division within the growth plate. As the chondrocytes in the proliferation zone stop dividing, the growth plate thins and eventually calcifies, and longitudinal bone growth stops (Ralston and McInnes, 2014). Males are on average taller than females because male puberty tends to occur later, so male bones have more time to grow (Waugh and Grant, 2018). Over-secretion of human growth hormone during childhood can produce gigantism, whereby the person is taller and heavier than usually expected, while over-secretion in adults results in a condition called acromegaly.

If there is a fracture in the epiphyseal growth plate while bones are still growing, this can subsequently inhibit bone growth, resulting in reduced bone formation and the bone being shorter. It may also cause misalignment of the joint surfaces and cause a predisposition to developing secondary arthritis later in life. A discrepancy in leg length can lead to pelvic obliquity, with subsequent scoliosis caused by trying to compensate for the difference.

Once bone has formed and matured, it undergoes constant remodelling by osteoclasts and osteoblasts, whereby old bone tissue is replaced by new bone tissue (Fig4). Bone remodelling has several functions, including mobilisation of calcium and other minerals from the skeletal tissue to maintain serum homoeostasis, replacing old tissue and repairing damaged bone, as well as helping the body adapt to different forces, loads and stress applied to the skeleton.

Calcium plays a significant role in the body and is required for muscle contraction, nerve conduction, cell division and blood coagulation. As only 1% of the bodys calcium is in the blood, the skeleton acts as storage facility, releasing calcium in response to the bodys demands. Serum calcium levels are tightly regulated by two hormones, which work antagonistically to maintain homoeostasis. Calcitonin facilitates the deposition of calcium to bone, lowering the serum levels, whereas the parathyroid hormone stimulates the release of calcium from bone, raising the serum calcium levels.

Osteoclasts are large multinucleated cells typically found at sites where there is active bone growth, repair or remodelling, such as around the periosteum, within the endosteum and in the removal of calluses formed during fracture healing (Waugh and Grant, 2018). The osteoclast cell membrane has numerous folds that face the surface of the bone and osteoclasts break down bone tissue by secreting lysosomal enzymes and acids into the space between the ruffled membrane (Robson and Syndercombe Court, 2018). These enzymes dissolve the minerals and some of the bone matrix. The minerals are released from the bone matrix into the extracellular space and the rest of the matrix is phagocytosed and metabolised in the cytoplasm of the osteoclasts (Bartl and Bartl, 2017). Once the area of bone has been resorbed, the osteoclasts move on, while the osteoblasts move in to rebuild the bone matrix.

Osteoblasts synthesise collagen fibres and other organic components that make up the bone matrix. They also secrete alkaline phosphatase, which initiates calcification through the deposit of calcium and other minerals around the matrix (Robson and Syndercombe Court, 2018). As the osteoblasts deposit new bone tissue around themselves, they become trapped in pockets of bone called lacunae. Once this happens, the cells differentiate into osteocytes, which are mature bone cells that no longer secrete bone matrix.

The remodelling process is achieved through the balanced activity of osteoclasts and osteoblasts. If bone is built without the appropriate balance of osteocytes, it results in abnormally thick bone or bony spurs. Conversely, too much tissue loss or calcium depletion can lead to fragile bone that is more susceptible to fracture. The larger surface area of cancellous bones is associated with a higher remodelling rate than cortical bone (Bartl and Bartl, 2017), which means osteoporosis is more evident in bones with a high proportion of cancellous bone, such as the head/neck of femur or vertebral bones (Robson and Syndercombe Court, 2018). Changes in the remodelling balance may also occur due to pathological conditions, such as Pagets disease of bone, a condition characterised by focal areas of increased and disorganised bone remodelling affecting one or more bones. Typical features on X-ray include focal patches of lysis or sclerosis, cortical thickening, disorganised trabeculae and trabecular thickening.

As the body ages, bone may lose some of its strength and elasticity, making it more susceptible to fracture. This is due to the loss of mineral in the matrix and a reduction in the flexibility of the collagen.

Adequate intake of vitamins and minerals is essential for optimum bone formation and ongoing bone health. Two of the most important are calcium and vitamin D, but many others are needed to keep bones strong and healthy (Box2).

Box 2. Vitamins and minerals needed for bone health

Key nutritional requirements for bone health include minerals such as calcium and phosphorus, as well as smaller qualities of fluoride, manganese, and iron (Robson and Syndercombe Court, 2018). Calcium, phosphorus and vitamin D are essential for effective bone mineralisation. Vitamin D promotes calcium absorption in the intestines, and deficiency in calcium or vitamin D can predispose an individual to ineffective mineralisation and increased risk of developing conditions such as osteoporosis and osteomalacia.

Other key vitamins for healthy bones include vitamin A for osteoblast function and vitamin C for collagen synthesis (Waugh and Grant, 2018).

Physical exercise, in particular weight-bearing exercise, is important in maintaining or increasing bone mineral density and the overall quality and strength of the bone. This is because osteoblasts are stimulated by load-bearing exercise and so bones subjected to mechanical stresses undergo a higher rate of bone remodelling. Reduced skeletal loading is associated with an increased risk of developing osteoporosis (Robson and Syndercombe Court, 2018).

Bones are an important part of the musculoskeletal system and serve many core functions, as well as supporting the bodys structure and facilitating movement. Bone is a dynamic structure, which is continually remodelled in response to stresses placed on the body. Changes to this remodelling process, or inadequate intake of nutrients, can result in changes to bone structure that may predispose the body to increased risk of fracture. Part2 of this series will review the structure and function of the skeletal system.

Bartl R, Bartl C (2017) Structure and architecture of bone. In: Bone Disorder: Biology, Diagnosis, Prevention, Therapy.

Danning CL (2019) Structure and function of the musculoskeletal system. In: Banasik JL, Copstead L-EC (eds) Pathophysiology. St Louis, MO: Elsevier.

Drake RL et al (eds) (2019) Grays Anatomy for Students. London: Elsevier.

Iyer KM (2019) Anatomy of bone, fracture, and fracture healing. In: Iyer KM, Khan WS (eds) General Principles of Orthopedics and Trauma. London: Springer.

Moini J (2019) Bone tissues and the skeletal system. In: Anatomy and Physiology for Health Professionals. Burlington, MA: Jones and Bartlett.

Ralston SH, McInnes IB (2014) Rheumatology and bone disease. In: Walker BR et al (eds) Davidsons Principles and Practice of Medicine. Edinburgh: Churchill Livingstone.

Robson L, Syndercombe Court D (2018) Bone, muscle, skin and connective tissue. In: Naish J, Syndercombe Court D (eds) Medical Sciences. London: Elsevier

Tomlinson RE, Silva MJ (2013) Skeletal blood flow in bone repair and maintenance. Bone Research; 1: 4, 311-322.

Tortora GJ, Derrickson B (2009) The skeletal system: bone tissue. In: Principles of Anatomy and Physiology. Chichester: John Wiley & Sons.

Waugh A, Grant A (2018) The musculoskeletal system. In: Ross & Wilson Anatomy and Physiology in Health and Illness. London: Elsevier.

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MAPLE GROVE, Minn., Jan. 27, 2020 /PRNewswire/ --StemoniX, a biotech company revolutionizing how new medicines are discovered, announced today that its Director of Applications, Oivin Guichert, Ph.D., will deliver a podium presentation highlighting the company's microBrain technology at the SLAS (Society for Laboratory Automation and Screening) 2020 International Conference & Exhibition at the San Diego Convention Center, Jan. 27-29, 2020. The presentation will be featured as part of the Assay Development and Screening Session during the annual meeting.

During the podium presentation, entitled "New innovation to solve unmet needs: Implementing human induced pluripotent stem cell-derived neural spheroids as a robust screening platform for phenotypic-based central nervous system drug discovery," Dr. Guichert will detail how performing a high-throughput functional screening assay on StemoniX's human induced pluripotent stem cell (iPSC)-derived 3D neural spheroid platform demonstrated the ability to identify a wide range of hits spanning multiple target areas. He will highlight how this model could provide relevant human platforms for disease-specific drug discovery to help overcome traditional hurdles of CNS-targeted drug discovery and development efforts.

Ping Yeh, co-founder and CEO of StemoniX, said: "The SLAS 2020 International Conference & Exhibitionis an ideal event to showcase the value potential of our microOrgan platform and AnalytiX data management and analytical software. As presented by Dr. Guichert and in the six posters, microBrain, microHeart, microPancreas and AnalytiX offer the potential to reshape how drugs are discovered and developed by providing the opportunity to go from model to molecule to validated drug in a fraction of the time and cost required with traditional methods. This includes the near-term potential to identify and advance novel therapeutic targets for Rett syndrome by leveraging our groundbreaking in vitro microBrain model in partnership with AI drug discovery pioneer, Atomwise."

Podium Presentation Details

Title:

New innovation to solve unmet needs: Implementing human induced pluripotent stem cell-derived neural spheroids as a robust screening platform for phenotypic-based central nervous system drug discovery

Session:

Assay Development and Screening

Event

SLAS 2020 International Conference & Exhibition

Date:

Tuesday, January 28, 2020

Time:

4:00 4:30 p.m. PST

Location:

San Diego Convention Center

Room/Location:

6C

Poster Presentations:

About StemoniXStemoniX is accelerating the discovery of new medicines to treat challenging diseases via the world's first ready-to-use assay plates containing living human microOrgans, including electrophysiologically active neural (microBrain) and cardiac (microHeart) cells. Predictive, accurate, and consistent, StemoniX's products combined with its proprietary data management and analytical tools (AnalytiX) are revolutionizing traditional drug discovery and development by radically improving the speed, accuracy and costs required to identify new drugs and conduct initial human cell toxicity and efficacy testing. Through its Discovery as a Service offering, the company partners with organizations to screen compounds as well as to create customized microOrgan models and assays tailored to specific discovery and toxicity needs. Visit http://www.stemonix.com to learn how StemoniX is helping global institutions humanize drug discovery and development to bring the most promising medicines to patients.

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Investor Contact:Maureen McEnroe, CFA+1.212.375.2664mmcenroe@tiberend.com

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StemoniX's microBrain to be Featured in Podium Presentation at SLAS 2020 International Conference & Exhibition - Crow River Media

Cardiac Stem Cells Comments Off on StemoniX’s microBrain to be Featured in Podium Presentation at SLAS 2020 International Conference & Exhibition – Crow River Media | January 27th, 2020

OSAKA An Osaka University team said it has carried out the worlds first transplant of cardiac muscle cells created from iPS cells in a physician-initiated clinical trial.

In the clinical project to verify the safety and efficacy of the therapy using induced pluripotent stem cells, Yoshiki Sawa, a professor in the universitys cardiovascular surgery unit, and colleagues aim to transplant heart muscle cell sheets into 10 patients suffering from serious heart malfunction caused by ischemic cardiomyopathy.

The cells on the degradable sheets attached to the surface of the patients hearts are expected to grow to secrete a protein that can regenerate blood vessels and improve cardiac function. The iPS cells have already been derived from healthy donors blood cells and stored.

The researchers said Monday they decided to conduct a clinical trial instead of a clinical study in hopes of obtaining approval from the health ministry for clinical applications as soon as possible.

The trial involves stringently evaluating risks, particularly cancer possibilities, and the efficacy of transplanting some 100 million cells per patient that may include tumor cells.

This is the second iPS cell-based clinical trial in Japan. The first was conducted on eye disease patients by the Riken research institute.

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Osaka University transplants iPS cell-based heart cells in world's first clinical trial - The Japan Times

IPS Cell Therapy Comments Off on Osaka University transplants iPS cell-based heart cells in world’s first clinical trial – The Japan Times | January 27th, 2020

CHICAGO Brian Wallach wasnt supposed to live to see his younger daughters first birthday.

Diagnosed with amyotrophic lateral sclerosis (ALS), a terminal disease with no cure, doctors told him in 2017 that he might have six months to live.

Today, hes focused on being there for his daughters future firsts: kindergarten drop-off, middle school dance, wedding day.

More than two years after his diagnosis, he has been lucky, he said, to experience relatively limited progression of his disease. After some balance issues, the Kenilworth resident now uses a cane or, as he is careful to specify, a cool walking stick to get around.

When Wallach was diagnosed, neither he nor his wife, Sandra Abrevaya, knew much about ALS, a neurodegenerative disease that affects nerve cells in the brain and the spinal cord, eventually paralyzing even the bodys ability to breathe.

In response to Wallachs diagnosis, the couple, both 39, launched I AM ALS in 2019. Former staffers in the Obama White House, they marshaled lessons learned while campaigning gathering information, forming consensus, considering the impossible possible to build a force to mobilize hope and change for those facing a disease they say can and should be cured.

Rays of hope are beginning to emerge through an innovative trial that received FDA approval last week to test several drugs at the same time, a bipartisan congressional caucus, doubled federal funding, and support from groups like the Chan Zuckerberg Initiative, which gave the couples organization a $453,000 grant in September.

Last year we made hope a word that was OK to use, Wallach said. This year we have to make hope real.

Audaciousness is the only option, the couple says, in their race against the clock.

Wallach logged 120,000 miles in the air last year, including traveling to Washington, D.C., in April, where he testified before Congress and asked legislators to amp up funding.

Last year, every time someone said, Do you want to speak to us, I said, yes. Every time someone said, Theres a meeting, I said, Im going. he said. Every time there was anything, I said, Great, Im on the plane.

Until October, when Wallach fell while exiting a Lyft in Boston after swinging a heavy backpack onto his back. Thirteen staples in his head later, and after terrifying Abrevaya with a phone call, the two agreed he wouldnt travel alone anymore. Hes maintaining momentum for the cause with more hours in his home office and fewer in airports.

In December, I AM ALS debuted billboards around Times Square as part of its #CuresForAll campaign aimed at informing the public about the impact a cure or better treatment for a neurodegenerative disease can have on other diseases such as multiple sclerosis, Alzheimers and Parkinsons. ALS patients and their families from states including Michigan, Maine and Colorado were in New York for the launch.

The billboards noted the number of people lost to ALS each day 16 with photographs of those who died in 2019. Days earlier, Pete Frates, a founder of the viral fundraiser the Ice Bucket Challenge, which raised $115 million, had died. He was 34.

The campaign was also shared on social media. The posts expressed the suffering and loss nationwide: a mother wrote about her son who was diagnosed at 20 and died at 28; a son posted in honor of his dad; Colorado Rep. Jason Crow posted a message honoring his cousin.

Its time, the couple said, to switch ALS conversations from a diagnosis rooted in darkness to the faces of people bravely moving forward. They want to speed development of potential cures and give patients more access to experimental treatments.

Thats not an unreasonable goal, said Sabrina Paganoni, a faculty member at The Sean M. Healey & AMG Center for ALS at Mass General in Boston, which plans to test at least five different medications for ALS at the same time, a first for the disease and something she said could be a huge turning point.

On Wednesday, the Healey Center announced it received FDA approval to move forward with testing the first three drugs: Zilucoplan, Verdiperstat and CNM-Au8. Similar to how cancer drugs are already tested, this gives patients access to more treatments and allows researchers to quickly collect data and accelerate the pace toward a cure.

This is a very exciting time in the history of ALS, Paganoni said. I think this is going to be the decade when ALS is changed from a rapidly fatal disease to a more chronic disease that we can manage.

For years, Steve Perrin, the chief executive officer at the ALS Therapy Development Institute, has monitored clinical trials for ALS. So far, he said, the two drugs approved by the FDA, Radicava and Rilutek, are a very marginal slowing down of disease.

This year, he said the quality of drugs going into trials seems improved. He is excited about several trials, including one studying stem cells and another testing a drug to potentially slow progression in some patients.

As a patient you want to see something measurable, and I dont mean measurable in days, he said. If Im a patient, I want to see something, and I want hope for myself and my family. I want something that is going to slow the disease down so I can watch my kids growing up, I can watch them graduate from college, I can watch them marry.

But that takes resources.

We are in a time when we can reasonably say that theres going to be new treatments available, Paganoni said. But we need more funding and support, so all of this can happen, and happen soon.

Nearly every moment feels like a push-pull for Wallach and Abrevaya.

Do they spend more precious minutes with their two daughters, ages 4 and 2, or do they spend time away, among strangers on a plane, in a researchers office, walking the halls of Congress with the hope that those minutes will, someday, result in time banked to create more family memories.

The hardest balance, if Im honest, is, I love every minute I have with them, Wallach said about his daughters, but I also feel this pressing sense of, I need to be working towards a goal of actually finding a cure.

Were doing that so we have a shot at a real future together, Abrevaya said about their time spent traveling and advocating.

At home, when the family heads for the door, the toddlers reach for their fathers shoes, and they get his walking stick.

While that both fills your heart with joy and appreciation, its also painful that your toddlers are being put in this position, Abrevaya said.

The parents guard normalcy. They take their daughters to swim at the neighborhood pool and on vacation with friends. Wallach wishes he could lift them above his head to touch the ceiling, like their uncle can. But he can lie on the floor and play with them; he can listen to them belt out songs on their purple karaoke machine.

They find ways to lighten a heavy subject. On New Years Eve, the two danced in a video on the foundations Instagram, singing into hairbrushes, and Wallach promised to get an ALS: You Gone tattoo if 20,000 people donated $10 to a Healey Center research fundraiser. It raised $40,000 in 24 hours, Wallach said. No matter the outcome, he plans to get the tattoo.

The couple, who both work full-time jobs Abrevaya is the president of nonprofit Thrive, Wallach works at law firm Skadden, Arps, Slate, Meagher & Flom want more research, to create a patient navigation system, and to gather signatures for a letter asking new FDA commissioner Stephen Hahn to speed ALS patients access to possible treatments.

And they keep looking for light. But it takes work.

Changing life with ALS for Wallach, and for other patients and their families, requires bold action from people with the power to make change: politicians, researchers, philanthropists.

As they meet others with ALS, they welcome new friends and face the pain of losing some.

It does make you uniquely urgent in what you do, Wallach said. You push because you have to. You push because you know that the time that we have is precious, and that you want to see 20 years from now. And know that you can make that happen.

(EDITORS: STORY CAN END HERE)

Wallach often shares moments about his ALS journey on Twitter with his 40,000 followers. Recently, he shared something he wasnt sure he should. It was a time he was unable to find light.

On a recent night, he woke up to pain hes had for the past few months, radiating from his right hip to his right calf.

He clutched a stuffed llama his daughter gave him. And he began to cry.

I cried because of the pain. I cried because I couldnt be the father to my girls I dreamed of being, he wrote. I cried because I couldnt be the husband to my wife I dream of being. Because I saw the future zooming ahead, and for a brief moment I wondered if I would be a part of it.

His wife heard him crying that night. She asked what was wrong. And he said maybe they would be better off if he left, living instead in an assisted living facility. Their daughters, he told her, could have a dad who could do everything he dreamed of doing.

She looked at him in the dark. You are my light, she said. You are their light. The only way you are leaving us is if you die in my arms, and we arent going to let that happen for a long, long, long time.

Finally, he smiled.

2020 Chicago Tribune

Visit the Chicago Tribune at http://www.chicagotribune.com

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In a race against terminal illness, former Obama staffer with ALS and his wife find new hope a year later - Bryan-College Station Eagle

Spinal Cord Stem Cells Comments Off on In a race against terminal illness, former Obama staffer with ALS and his wife find new hope a year later – Bryan-College Station Eagle | January 26th, 2020

(MENAFN - Gulf Times) The Foot and Ankle sub-specialty at Hamad General Hospital (HGH), part of Hamad Medical Corporation (HMC), will soon introduce the latest medical procedure, BMAC, to treat various illnesses related to foot and ankle.'Bone marrow aspirate concentrate (BMAC) is a regenerative therapy procedure that uses stem cells from a patient's bone marrow to initiate healing for a number of orthopaedic conditions, such as tendinopathy, osteoarthritis and cartilage injuries, said Dr Mohamed Maged Mekhaimar, senior consultant and orthopaedic surgeon at HGH.'This will help treating patients with tendon inflation. It can also be used to treat inflammation on the bottom of the foot as well as for traumatic conditions of the ankle. These services will soon be available at Hamad General Hospital, explained Dr Mekhaimar.Foot and ankle services were started at HGH in 2012. 'Now, there is a great demand for these services in the country as more and more people are approaching us for various issues. The centre provides treatment for several problems such as flat foot problems, among other issues. We also provide treatment for diabetic foot people, he continued.The centre currently performs about five surgeries per day and takes care for all different injuries, including sport injuries.According to the official, the centre also makes use of PRP (Platelet Rich Plasma) machine by which blood is taken from people and then separated. 'Using the PRP machine, we can inject the blood particles to the joints. This facility is available in HGH and the Bone and Joint Center, part of HMC, he noted.'Our clinics are at the Bone and Joint Center. All our patients come through the Bone and Joint Center. We are also in the process of introducing the weight-bearing CT scan machine. With this, we can scan the foot and ankle of the patient while he or she is standing on it. This can give better impression of the condition of the patients, he highlighted.'Some deformity can be better measured through this CT scan machine. It will also be used for treating the knee joint as it is one of the most advanced treatment options available now, he added.

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Qatar- HMC to introduce regenerative therapy to treat foot and ankle illnesses - MENAFN.COM

Bone Marrow Stem Cells Comments Off on Qatar- HMC to introduce regenerative therapy to treat foot and ankle illnesses – MENAFN.COM | January 26th, 2020

Many folks all over the world will be seen troubled by ache within the veins. And many occasions, even after an excessive amount of therapy, this ache shouldnt be relieved. But within the coming days youll be able to do away with neuralgia utterly, that too with none unwanted side effects. Researchers on the University of Sydney have used human stem cells for excessive ache reduction in mice. Now, theyre shifting in the direction of human trials.

Greg Nelly, senior researcher on the Charles Perkins Center, stated that at occasions, extreme stress on the nerves causes them to get broken. For instance, carpal tunnel syndrome is the median nerve within the fingers ( median nerve ) Due to extreme stress.

->As youll be able to think about, nerve accidents can result in insufferable neuropathic ache. There can also be no efficient therapy to alleviate ache in most sufferers.

Therefore, Nelly and colleagues on the University of Sydney developed an efficient remedy. Researchers have been in a position to create pain-relieving neurons utilizing human stem cells.

Nelly stated that this success implies that for some sufferers affected by nerve ache, we are able to carry out pain-relieving implants from our cells, which might cease the ache.

In the research, researchers collected stem cells from grownup blood samples. Then, used human-induced pluripotent stem cells (iPSCs) from the bone marrow to create pain-relieving cells within the laboratory.

To check the efficacy of the therapy, the group injected neurons that abolished spinal ache in mice affected by extreme neuropathic ache. It was revealed that this therapy supplied full reduction from ache to the mice with none unwanted side effects.

Co-senior creator Dr. Leslie Caron stated that because of this transplant remedy is prone to be an efficient and long-lasting therapy for neuropathic ache.

After shut therapy in mice, the University of Sydney group is shifting ahead for extra intensive research in pigs. Within the following 5 years, theyll check people who are suffering from power ache.

Researchers stated {that a} move check in people will probably be a giant success. This could point out the event of latest non-opioid, non-addictive ache administration methods for sufferers.

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If youre troubled by ache within the nerves, comply with the following tips, know - Sahiwal Tv

Bone Marrow Stem Cells Comments Off on If youre troubled by ache within the nerves, comply with the following tips, know – Sahiwal Tv | January 26th, 2020

Sorry Mom and Dad: It turns out you might not have been exaggerating when you told us your children made your hair turn gray.

Stress may play a key role in just how quickly hair goes from colored to ashen, a study published this past week in the journal Nature suggests.

Scientists have long understood some link is possible between stress and gray hair, but this new research from Harvard University in Massachusetts more deeply probes the exact mechanisms at play.

The researchers initial tests looked closely at cortisol, the stress hormone that surges in the body when a person experiences a fight or flight response.

Its an important bodily function, but the long-term presence of heightened cortisol is linked to a host of negative health outcomes.

But the culprit ended up being a different part of the bodys fight or flight response the sympathetic nervous system.

These nerves are all over the body, including making inroads to each hair follicle, the researchers reported.

Chemicals released during the stress response specifically norepinephrine causes pigment producing stem cells to activate prematurely, depleting the hairs reserves of color.

The detrimental impact of stress that we discovered was beyond what I imagined, Ya-Chieh Hsu, PhD, a lead study author and an associate professor of stem cell and regenerative biology at Harvard, said in a press release. After just a few days, all of the pigment-regenerating stem cells were lost. Once theyre gone, you cant regenerate pigments anymore. The damage is permanent.

But stress isnt the only or even the primary reason that most people get gray hair.

In most cases, its simple genetics.

Gray hair is caused by loss of melanocytes (pigment cells) in the hair follicle. This happens as we age and, unfortunately, there is no treatment that can restore these cells and the pigment they produce, melanin, Dr. Lindsey A. Bordone, a dermatologist at ColumbiaDoctors and an assistant professor of dermatology at Columbia University Medical Center in New York, told Healthline. Genetic factors determine when you go gray. There is nothing that can be done medically to prevent this from happening when it is genetically predetermined to happen.

That doesnt mean environmental factors such as stress dont play a role.

Smoking, for instance, is a known risk factor for premature graying, according to a 2013 study. So kick the habit if you want to keep that color a little longer.

Other contributing factors to premature graying include deficiencies in protein, vitamin B-12, copper, and iron as well as aging due in part to an accumulation of oxidative stress.

That stress is prompted by an imbalance between free radicals and antioxidants in your body that can damage tissue, proteins, and DNA, Kasey Nichols, NMD, an Arizona physician and a health expert at Rave Reviews, told Healthline.

And some degree of oxidative stress is a natural part of life.

We would expect increasing gray hair as we advance in age, and we see about a 10 percent increase in the chance of developing gray hair for every decade after age 30, Nichols said.

Changes you can pursue to delay premature grays include eating a diet high in omega-3 fatty acids such as walnuts and fatty fish, not spending too much time in the skin-damaging and hair-damaging ultraviolet light of the sun, and taking vitamin B-12 and vitamin B-6 supplements.

That said, if you are going gray prematurely, it wouldnt hurt to go have a checkup just in case natural genetic factors arent the sole culprit.

The new Harvard research is only a mouse study, so replicating the same results in a human study would be necessary to strengthen the findings.

But the Harvard research has implications far beyond graying hair, with the hair color change merely one obvious sign of other internal changes as a result of prolonged stress.

By understanding precisely how stress affects stem cells that regenerate pigment, weve laid the groundwork for understanding how stress affects other tissues and organs in the body, said Hsu. Understanding how our tissues change under stress is the first critical step towards eventual treatment that can halt or revert the detrimental impact of stress.

Might that also mean someday halting and reverting the march of premature gray hair? Its too soon to tell.

We still have a lot to learn in this area, Hsu said.

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Scientists Think They Know How Stress Causes Gray Hair - Healthline

Skin Stem Cells Comments Off on Scientists Think They Know How Stress Causes Gray Hair – Healthline | January 26th, 2020

If you havent chanced upon a gua sha stone facial or a jade roller video on your social media, are you even on it? The ancient Chinese technique of face massaging is gaining traction thanks to beauty bloggers sharing their basic kneads. If you have stumbled upon these videos but have no clue whats going on, read on. Dermatologist Dr Nirupama Parwanda says that the basics come from traditional Chinese wisdom: improper blood circulation and stagnant blood flow is one of the main reasons behind various diseases. To improve circulation and drain toxins, you can try jade rollers and gua sha an alternative therapy that involves massaging your skin using special tools. Parwanda says, Our bodies have a source of energy known as chi flowing through it. And to ensure good health and prosperity, we must balance it. Dr Rinky Kapoor, dermatologist and dermato-surgeon, explains, Both rollers and gua sha are made of stones such as quartz, jade, rose quartz and amethyst known for their healing properties. Gua sha is also known as coining, skin scrapping or pressure stroking. FLOW AND GLOWBoth work on the principle of improving blood flow under the skin and enhancing lymphatic drainage. This helps carry the oxygen to the skin cells, which in turn makes the skin tissues healthy, and reduces fine lines and wrinkles. Parwanda says that gua sha is also called natural botox as it helps in controlling signs of ageing. The proven benefits are: pain reduction in muscles and joints; reduction in perimenopause symptoms like anxiety, insomnia, hot flashes; improved blood circulation, removal of toxins. It also treats musculoskeletal disorders and reduces wrinkles.

TOO GOOD TO BE TRUE?Kapoor cautions that just looking at videos online doesnt mean you know the proper way to use it. You need to follow the process to reap the maximum benefits. Also, theres not one simple process for both jade roller and gua sha. Think of it as driving while the basics of accelerator, brake and clutch remain the same, driving styles are different, she says. Start both facials from the neck and then move upwards and with upward strokes. Rollers are simpler to use as you can just start massaging on the outward and upward direction from one point, except for the neck, where the massaging motion is downwards. Gua sha facials require more technique. Tip: you can learn from a practitioner.

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Roll play: Jade rollers and gua sha stone are making waves in skincare - Times of India

Skin Stem Cells Comments Off on Roll play: Jade rollers and gua sha stone are making waves in skincare – Times of India | January 26th, 2020

Marie Antoinette's hair suddenly turned white before the ill-fated French queen was taken to the guillotine to have her head chopped off, according to some historical accounts.

More modern reports refer to hair turning prematurely white in survivors of bomb attacks during World War II, while an Australian airline pilot saw his hair go grey in the months after landing a plane following a failure of all four engines in the early 1980s.

While there's been plenty of anecdotal evidence suggesting premature greying can be caused by extreme stress -- whether this is true and how this happens isn't widely understood.

Now, Harvard University scientists think they have the answer -- at least in mice.

The group of researchers believe it's down to the animal's sympathetic nervous system -- which is best known for activating our "fight or flight" response to danger, they say.

"Under stress, our sympathetic nerve becomes highly activated," said Ya-Chieh Hsu, associate professor of stem cell and regenerative biology at Harvard, in an email. "And actually, activation of the sympathetic nervous system under stress is supposed to be a good thing."

Its activation triggers the "fight or flight" response through the neurotransmitter norepinephrine, or noradrenaline, explained Hsu, a senior author of the study published Wednesday in the scientific journal Nature. "Noradrenaline raises our heartbeat and allows us to react quickly to danger without having to think about it," he said.

"However, it is the same noradrenaline that turns out to be bad for melanocyte stem cells at a high level, and triggers their loss."

Melanocyte stem cells are found in hair follicles and determine hair colour. In people, the pool of these cells deplete as they age, turning hair grey as pigment depletes. Their loss from excessive noradrenaline could be causing this to happen prematurely, the team suggest.

Loss of pigment

The team had thought that acute stress might trigger an immune attack on pigment-producing stem cells or that the blame lied with the hormone cortisol because cortisol levels are elevated under stress. Hsu said they went through many different possibilities before focusing on the sympathetic nervous system.

"We were really surprised to find that it was the culprit, because it is normally seen as a beneficial system, or at least transient and reversible," she said.

The team put mice under three different types of stress through what Hsu described as established standard protocols. These included a single injection of a chemical to activate the mouse's pain fiber, cage tilting and rapid changes between light and dark.

Changes were observed in all mice but there was some variability, with white hair only coming out after all the stem cells are gone.

"Some hair follicles have reduced levels of melanocyte stem cells so they can still make pigment, while others have lost all stem cells and can't make pigment anymore, so the hair becomes white," she said.

Pigment-producing stem cells and the sympathetic nervous system are very similar in mice and humans, explained Hsu who was hopeful that the mechanisms would be related. But future studies would be needed to provide definitive evidence, she said.

"Everyone has an anecdote to share about how stress affects their body, particularly in their skin and hair the only tissues we can see from the outside," Hsu said in a news release.

"We wanted to understand if this connection is true, and if so, how stress leads to changes in diverse tissues. Hair pigmentation is such an accessible and tractable system to start with and besides, we were genuinely curious to see if stress indeed leads to hair greying."

Hsu said the findings may also help shed light on the effects of stress on various organs and tissues, and pave the way for new studies that seek to modify or block the damaging effects of stress.

In an accompanying article, Shayla Clark and Christopher Deppmann, researchers from the Neuroscience Graduate Program at the University of Virginia, who were not involved in the study, said it was interesting to consider what possible evolutionary advantage might be conferred by stress-induced greying.

"Because grey hair is most often linked to age, it could be associated with experience, leadership and trust. Perhaps an animal that has endured enough stress to 'earn' grey hair has a higher place in the social order than would ordinarily be conferred by that individual's age," they wrote.

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Scientists prove link between stress and prematurely greying hair - Newstalk ZB

Skin Stem Cells Comments Off on Scientists prove link between stress and prematurely greying hair – Newstalk ZB | January 26th, 2020

Everyone sheds about 100 hairs each day as part of the normal hair growth cycle, but excess loss is usually a distressing development.(iStock)

Hair loss is typically considered the domain of aging men, but this equal-opportunity condition which has many causes can affect virtually anyone.

Alopecia is the medical term for hair loss, and it doesnt only happen on the scalp. Some illnesses and medications can trigger balding over the entire body, though genetics account for most cases on the head, according to theCleveland Clinic.

PARTY DRUG MDMA A STEP CLOSER TO LEGALIZATION FOR PTSD THERAPY

Everyone sheds about 100 hairs each day as part of the normal hair growth cycle, but excess loss is usually a distressing development. Americans spend more than $3.5 billion each year trying to treat it, according to theAmerican Hair Loss Association.

Most peoples hair grows about a half-inch per month, and about 90 percentof your hair is actively growing at any given time, with the other 10 percentin dormant phase. After two or three months, this dormant hair falls out and its follicles begin growing new hair as other follicles begin a dormant phase.

Shedding hair is different from hair loss, when a hair falls out and doesnt grow back. People often shed hair during stressful events, such aschildbirth, a breakup or divorce or during times of grief.

It still doesnt feel good, and it takes the hair [awhile] to reach a certain length where you perceive its presence, said Doris Day, a board-certified dermatologist New York City and an attending physician at Lenox Hill Hospital, also in New York. So it feels like a hair loss, but its not a hair loss.

Aside from heredity, noticeable hair loss can be caused by wide variety of factors, including:

Harsh hairstyles or treatments: Hairstyles that consistently use rubber bands, rollers or barrettes, or pull hair into tight styles such as cornrows, can inflame and scar hair follicles. So can incorrectly used chemical products such as dyes, bleaches, straighteners or permanent wave solutions. Depending on the degree of damage, resulting hair loss can be permanent.

Hormone imbalances: In women, hormonal shifts from birth control pills,pregnancy, childbirth, menopause or hysterectomy can induce more hair follicles than normal to enter the dormant phase.

Illness or surgery: The stress from sickness or surgery may prompt the body to temporarily cease nonessential tasks such as hair production. Specific conditions can also trigger it, including thyroid disorders,syphilis, iron deficiency,lupusor severe infection. An autoimmune condition called alopecia areata, which has no cure, causes rapid body-wide hair loss.

Medications and vitamins: Cancer chemotherapy, which attacks hair follicles in its attempt to kill all fast-growing cells around the body, is a well-known reason for hair loss. Other medications side effects include hair shedding as well, such as some that treat high blood pressure andgout(a painful joint condition caused by a buildup of uric acid). Excessive levels of vitamin A also contribute.

Nutritional deficits: Heavy dieting or eating disorders such asbulimiaandanorexiacan temporarily stun hair follicles to cease growth. This can also occur from insufficient protein, vitamin or mineral intake.

Aging: A natural effect of growing older is slowed hair growth.

Women usually dont go completely bald, but lose hair on the top of the head or the temples. Men tend to lose hair on their temples, and are more likely than women to go completely bald, Day said.

Dermatologists will examine the persons scalp and take a history of medical or stressful events to see whats been going on in their life and their world, Day said.

HELICOPTER-SHARING APP BLADE PAIRS WITH NYU LANGONE TO SPEED TRANSPLANT ORGANS

The dermatologist may take a biopsy a small patch of skin that includes the hair follicle and send it to a pathologist to determine if an autoimmune disease, such as lupus, is the cause of the hair loss.

Examining the hair and follicle can also determine whether someone has a bacterial or fungal infection, Day said.

Hair loss remedies range from the mild to the extreme and the inexpensive to the costly. Much depends on how much hair is gone and how high a priority it is to mask its absence or replace it.

According to the Cleveland Clinic, treatments include:

Hair weaves or wigs: Typically expensive, wigs and hair weaves either completely cover the head or add to existing hair, restoring the appearance of a full head of hair. They are especially practical for cancer patients and those whose hair loss is temporary.

Topical creams and lotions: Over-the-counter minoxidil (also known as the brand name Rogaine) can restore some hair growth, especially in those with hereditary hair loss. It is applied directly to the scalp. Prescription-strength finasteride (Propecia) comes in pill form and is only for men. According to theAmerican Academy of Family Physicians(AFP), it may take up to six months to tell if these medications are working.

Anti-inflammatory medications: Prescription steroid-based creams or injections can calm follicles damaged or inflamed by harsh chemicals or excessive pulling.

Surgery: Men tend to be better candidates for surgical hair-replacement techniques because their hair loss is often limited to one or two areas of the scalp. Procedures include grafting, which transplants from one to 15 hairs per disc-shaped graft to other locations. Scalp reduction removes bald skin from the scalp so hair-covered scalp can be stretched to fill in the bald areas. Side effects include swelling, bruising and headaches.

Hair-growth laser treatment can also help stimulate hair follicles and improve growth, Day said. People often see results when they combine laser treatment with another intervention, she said. Treatments range in price from $30 and up for Rogaine to about $3,000 for laser treatment, she added.

According to theNational Institute of Arthritis and Musculoskeletal and Skin Diseases(NIAMSD), alternative therapies may not help hair regrow and many are not supported by medical research. However, other treatments that reportedly improve alopecia areata include Chinese herbs, acupuncture, zinc and vitamin supplements, evening primrose oil and aroma therapy.

Viviscal, a natural supplement, has also shownmore hair growthin men compared to those who took fish extract in clinical trials, Day said.

The NIAMSD recommends discussing any alternative treatments with physicians before use.

The drug Tofacitinib is approved to treat adults witharthritis, but a growing number of cases suggest that it can also treat alopecia universalis, a condition in which people lose all of the hair on their body because theirimmune systemattacks hair follicles,Live Science previously reported.

The finding occurred after doctors prescribed a 25-year-old man with alopecia universalis the drug because they had heard it had treated a similar condition in mice,according to a statement from Yale University. After three months of treatment, the man had completely regrown the hair on his scalp, and he had visible eyebrows, eyelashes, facial hair, as well as hair elsewhere on his body.

Its exciting, said Day, who did not treat this particular patient. There seems to be a real effect here.

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Its unclear how Tofacitinib (brand name Xeljanz) works, but researchers hope to determine its mechanism soon. This data may help them learn which biological pathways lead to hair loss.

There are now clinical trials taking place around the country to test the safety and efficacy of the drug for hair loss conditions. One such study lasting 3 months gave Tofacitinib to 66 people with alopecia areata (an immune system condition that causes hair to fall out in patches). Half of the people regrew some hair, and one-third had more than 50 percentof the hair on their scalp grow back, according to the 2016 study, published in the journalJCI Insight.

However, researchers are still working to determine the best dose needed, whether the results are lasting, and whether they can develop a topical form of the drug, Day said. She added that patients should be aware that Tofacitinib has side effects. Its already associated with an increased risk of serious infections, as well as stomach and intestinal tears, according to Pfizer, the manufacturer.

Besides investigating Tofacitinib, researchers are also looking at ways to clone hair or use stem cell therapy to treat alopecia, Day said.

This article first appeared on LiveScience.

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With so many groundbreaking medical advances being revealed to the world every single day, you would imagine there would be some advancement on the plethora of many female-prevalent diseases (think female cancers, Alzheimer's, depression, heart conditions etc.) that women are fighting every single day.

For Anna Villarreal and her team, there frankly wasn't enough being done. In turn, she developed a method that diagnoses these diseases earlier than traditional methods, using a pretty untraditional method in itself: through your menstrual blood.

Getting from point A to point B wasn't so easy though. Villarreal was battling a disease herself and through that experience. I wondered if there was a way to test menstrual blood for female specific diseases," she says. "Perhaps my situation could have been prevented or at least better managed. This led me to begin researching menstrual blood as a diagnostic source. For reasons the scientific and medical community do not fully understand, certain diseases impact women differently than men. The research shows that clinical trials have a disproportionate focus on male research subjects despite clear evidence that many diseases impact more women than men."

There's also no denying that gap in women's healthcare in clinical research involving female subjects - which is exactly what inspired Villarreal to launch her company, LifeStory Health. She says that, with my personal experience everything was brought full circle."

There is a challenge and a need in the medical community for more sex-specific research. I believe the omission of females as research subjects is putting women's health at risk and we need to fuel a conversation that will improve women's healthcare.,"

-Anna Villarreal

Her brand new biotech company is committed to changing the women's healthcare market through technology, innovation and vocalization and through extensive research and testing. She is working to develop the first ever, non-invasive, menstrual blood diagnostic and has partnered with a top Boston-area University on research and has won awards from The International Society for Pharmaceutical Engineering and Northeastern University's RISE.

How does it work exactly? Proteins are discovered in menstrual blood that can quickly and easily detect, manage and track diseases in women, resulting in diseases that can be earlier detected, treated and even prevented in the first place. The menstrual blood is easy to collect and since it's a relatively unexplored diagnostic it's honestly a really revolutionary concept, too.

So far, the reactions of this innovative research has been nothing but excitement. The reactions have been incredibly positive." she shares with SWAAY. Currently, menstrual blood is discarded as bio waste, but it could carry the potential for new breakthroughs in diagnosis. When I educate women on the lack of female subjects used in research and clinical trials, they are surprised and very excited at the prospect that LifeStory Health may provide a solution and the key to early detection."

To give a doctor's input, and a little bit more of an explanation as to why this really works, Dr. Pat Salber, MD, and Founder of The Doctor Weighs In comments: researchers have been studying stem cells derived from menstrual blood for more than a decade. Stem cells are cells that have the capability of differentiating into different types of tissues. There are two major types of stem cells, embryonic and adult. Adult stem cells have a more limited differentiation potential, but avoid the ethical issues that have surrounded research with embryonic stem cells. Stem cells from menstrual blood are adult stem cells."

These stem cells are so important when it comes to new findings. Stem cells serve as the backbone of research in the field of regenerative medicine the focus which is to grow tissues, such as skin, to repair burn and other types of serious skin wounds.

A certain type of stem cell, known as mesenchymal stem cells (MenSCs) derived from menstrual blood has been found to both grow well in the lab and have the capability to differentiate in various cell types, including skin. In addition to being used to grow tissues, their properties can be studied that will elucidate many different aspects of cell function," Dr. Salber explains.

To show the outpour of support for her efforts and this major girl power research, Villarreal remarks, women are volunteering their samples happily report the arrival of their periods by giving samples to our lab announcing de-identified sample number XXX arrived today!" It's a far cry from the stereotype of when it's that time of the month."

How are these collections being done? Although it might sound odd to collect menstrual blood, plastic cups have been developed to use in the collection process. This is similar to menstrual products, called menstrual cups, that have been on the market for many years," Dr. Salber says.

Equally shocking and innovative, this might be something that becomes more common practice in the future. And according to Dr. Salber, women may be able to not only use the menstrual blood for early detection, but be able to store the stem cells from it to help treat future diseases. Companies are working to commercialize the use of menstrual blood stem cells. One company, for example, is offering a patented service to store menstrual blood stem cells for use in tissue generation if the need arises."

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The first symposium of the South West Brain Tumour Centre was held on Thursday at Derriford Hospital in Plymouth. During a fascinating and very well attended event, topics covered included the mechanism of tumour development, new drug targets, new biomarkers and brain tumour imaging. The South West Brain Tumour centre is of course one of the UK Centres of Excellence funded by Brain Tumour Research.

A really big cancer wide story this week is here Immune discovery 'may treat all cancer' applicable to some solid tumours but not yet brain it really shows the direction of travel toward immunotherapy I have recommended this book before but if interested please do read The Breakthrough by Charles Graeber it is available on Amazon and you can read reviews here - http://www.charlesgraeber.com.Researchers uncover novel drug target for glioblastoma by revealing a cellular pathway that appears to contribute to glioma stem cell spread and proliferation. This pathway shows that glioma stem cells ability to access key nutrients in their surrounding microenvironment is integral for their maintenance and spread. Finding a way to interrupt this feedback loop will be important for treating glioblastoma.

An intelligent molecule could significantly extend the lives of patients with glioblastoma, research finds. The molecule, called ZR2002, which can be administered orally and is capable of penetrating the blood-brain barrier, could delay the multiplication of glioblastoma stem cells resistant to standard treatment. According to scientists in the Metabolic Disorders and Complications Program at the Research Institute of the McGill University Health Centre (RI-MUHC) the ZR2002 molecule is designed to kill two birds with one stone: on top of attacking the tumour, it destroys its defence system.

Researchers find clues to drug resistance in medulloblastoma subtype.US scientists have identified specific types of cells that cause targeted treatment to fail in a subtype of medulloblastoma. They found while the majority of cells responded to treatment, diverse populations within the tumour continue to grow leadingto treatment resistance. They concluded that the diversity of cells within tumours allow them to become rapidly resistant to precisely targeted treatments," and that due to this tumour cell diversity, molecularly precise therapies should be used in combinations to be effective."

Nanoparticles deliver 'suicide gene' therapy to paediatric brain tumours growing in mice So-called "suicide genes" have been studied and used in cancer treatments for more than 25 years. Researchers report here that a type of biodegradable, lab-engineered nanoparticle they fashioned can successfully deliver a ''suicide gene'' to paediatric brain tumour cells implanted in the brains of mice.

According to a study that uncovers an unexpected connection between gliomas and neurodegenerative diseases a protein typically associated with neurodegenerative diseases like Alzheimers might help scientists explore how gliomas become so aggressive. The new study, in mouse models and human brain tumour tissues, was published in Science Translational Medicine and found a significant expression of the protein TAU in glioma cells, especially in those patients with better prognoses. Patients with glioma are given a better prognosis when their tumour expresses a mutation in a gene called isocitrate dehydrogenase 1 (IDH1). In this international collaborative study led by the Instituto de Salud Carlos III-UFIEC in Madrid, Spain, those IDHI mutations stimulated the expression of TAU. Then, the presence of TAU acted as a brake for the formation of new blood vessels, which are necessary for the aggressive behaviour of the tumours.

'Innovative research award' helps Colorado scientists block brain cancer escape routes Cancers used to be defined by where they grow in the body - lung cancer, skin cancer, brain cancer, etc. But work in recent decades has shown that cancers sharing specific genetic changes may have more in common than cancers that happen to grow in an area of the body. For example, lung cancers, skin cancers, and brain cancers may all be caused by mutation in a gene called BRAF. Drugs targeting BRAF have changed the treatment landscape for melanoma, an aggressive form of skin cancer, and are also in use against lung cancers and brain cancers with BRAF mutations. It is really worth clicking through to read more on this and the ultimate goal of identifying new potential targets for combination therapy and new agents that could be added to BRAF inhibiting drugs in brain cancer to keep the cancer from developing resistance.

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