As cancer treatments continue to advance and new therapies are introduced, it's easy to get lost in your search for information. To help you better understand the differences between specific cancer treatments and how they work, we spoke with medical oncologist Bhavina Sharma, MD, MPH.

"Chemotherapy are drugs designed to directly attack all rapidly dividing cells in the body, including cancer cells," explains Dr. Sharma. "It relies on the idea that cancer cells reproduce much faster than most healthy cells in our body."

Chemotherapy drugs can be given by infusion or in pill form. Unfortunately, these drugs can't tell the difference between cancerous cells and fast-growing healthy cells like the gastrointestinal tract and hair follicles, leading to side effects such as diarrhea and hair loss. Thankfully, recent advancements in chemotherapy have helped lessen side effects such as nausea, pain and lethargy.

Targeted therapy are special drugs designed to target differences within cancer cells that help them thrive. Unlike chemotherapy, targeted therapy drugs actually change the inner workings of the cancer cell. Because targeted therapy focuses on the part of the cancer cell that makes it different from the normal, healthy cell, it often has fewer side effects than standard chemotherapy treatments.

Immunotherapy is very different than chemotherapy in that it helps our immune system to find and kill cancer cells.

"Cancer cells are abnormal cells that have formed in our body because of cell damage or mutations," explains Dr. Sharma. "Cancer cells hide from your immune system by shutting down certain pathways of the immune response. Immunotherapy unlocks those pathways so your immune system can recognize and remove the cancer cells."

Cellular therapies are treatments that improve the body's ability to fight cancer. "Stem cell therapy falls under the umbrella of cellular therapy," explains Dr. Sharma. "It uses stem cells to mount an immune response to attack your cancer cells."

Stem cells from blood and bone marrow can be used in transplants. These stem cells can either come from a matched donor (allogeneic) or from the patient themselves (autologous).

Chimeric antigen receptor therapy or CAR T-cell, is a type of cellular therapy.

"T cells are white blood cells that help our bodies fight infection and cancer," explains Dr. Sharma. "With CAR T-cell therapy, your own T cells are collected from your blood. These T cells are modified to recognize cancer as a foreign cell and attack it."

CAR T-cell therapy has been approved by the Food and Drug Administration to treat lymphoma, leukemia and multiple myeloma.

Hormone therapy slows or stops the growth of cancer that uses hormones to grow. It is also called hormonal therapy, hormone treatment or endocrine therapy. Hormone therapy is recommended for cancers that are hormone-receptor positive, such as certain breast and prostate cancers. It can't be used in cancers that don't carry hormone receptors.

"Hormone therapy can be used for both early stage and metastatic hormone-receptor positive breast cancers," explains Dr. Sharma. "In patients with early-stage breast cancer, it is used after surgery to help reduce the risk of the cancer coming back."

Chemotherapy, immunotherapy, targeted therapy, and hormone therapy are just a few of the treatments we use to treat cancer. Many of these cancer treatments can be combined with others like cancer surgery and radiation therapy. Every person's journey through cancer is different. Your oncology team will help you sort through the best therapies available to create your treatment plan.

The information in this article is for information purposes only. For specific questions regarding your medical condition or treatment plan, please consult with your doctor directly. To schedule an appointment with a Nebraska Medicine cancer specialist, call 402.559.5600.

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Are immunotherapy and chemotherapy the same thing? How cancer treatments work - Nebraska Medicine

A new approach is paving the way for improved stem cell therapies and regenerative applications using cells from pigs. Led by Wan-Ju Li, a SCRMC researcher and associate professor in the Department of Orthopedics and Rehabilitation and the Department of Biomedical Engineering, this new study published in Scientific Reports offers a viable strategy to enhance the generation of induced pluripotent stem cellsfrom large animal cells and provides researchers with insight into the underlying mechanism controlling the reprogramming efficiency of cells. In turn, this approach will allow researchers to reprogram cells more efficiently into iPSCs which can be used to study regenerative therapies aimed at treating everything from osteoarthritis to heart disease.

While this approach can be applied to regenerative therapies targeting any organ or tissue, Li and his Musculoskeletal Biology and Regenerative Medicine Laboratory study cartilage, so he developed the model by deriving iPSCs from the fibroblast cells of three different breeds of miniature pigs including Wisconsin miniature swine, Yucatan miniature swineand Gttingen minipigs. Fibroblast cells are easily obtained for cellular reprogramming and Li is interested in using these cells to efficiently develop cartilage cells that can be used to help patients experiencing osteoarthritis. But, while his goal for the study was specific, the model has wide-reaching implications.

"This model we created can be used for many applications," says Li. "In successfully developing iPSCs from three different breeds of minipigs, we learned we can take somatic skin cells from these pigs that we programmed ourselves into iPSCs and then inject them back into the same animal to treat the disease. Or we can take the cell that carried the disease gene and put that into the culture dish and use that as a disease model to study disease formation."

Li explained that iPSCs can be created from nearly any type of somatic cell, such as skin or blood cells, that are reprogrammed back into an embryonic-like pluripotent cells. These pluripotent stem cells are the bodys master cells and are, therefore, able to become nearly any cell in the body. Harnessing the power of such a cell and being able to grow these versatile cells in the lab is invaluable to medicine as these cells can be used for the regeneration or repair of damaged tissue and in drug testing to see how medication will impact heart, liver, or other cells within the body.

Through this research, Li and his lab have provided researchers with insight into the underlying mechanism controlling the reprogramming efficiency of iPSCs, allowing researchers to harness to power of iPSCs and develop them more efficiently. Specifically, he discovered that the expression level of the switch/sucrose nonfermentable component BAF60A, which is essentially a protein that can remodel the way DNA is packaged, helps to determine the efficiency of iPSC generation. He also noted that the BAF60A is regulated by STAT3, a transcription factor protein that plays a role in cell growth and death. Through this, Li discovered that the efficiency of iPSC generation is based on the expression level of these proteins and that the expression levels vary among pig breeds.

"While we successfully developed iPSCs and programmed iPSCs from the three different strains of pig, we noticed that some pigs had a higher reprogramming efficiency,"says Li. "So, the second part of our findings, which is significant in biology, is understanding how these differences occur and why."

Li shared that understanding why different pig breeds have varying levels of reprogramming efficiency will directly translate to understanding differences in the effectiveness of iPSC generation between individual humans. In fact, a previous study by Mackey et al., has shown that a person's ethnicity may impact their cell's reprogramming efficiency. So, understanding what mechanisms control cellular reprogramming will be crucial to developing effective protocols of iPSC generation for individualized therapies.

"With this model, we can study musculoskeletal regeneration particularly cartilage regeneration for osteoarthritis patient,"says Li. "But we think the impact is way beyond the application of orthopedics because from now on, anybody on campus who is interested in using the technology we have developed for a minipig model, can reprogram their cells into iPSCs and then these cells and the animal can be used to investigate heart disease, kidney disease, neuronal diseaseor any type of a disease."

Translating this research to improve human health, is deeply important to Li. He has spent much of his career studying novel approaches to regenerate cartilage and bone for orthopedic applications and developing a translational model like this means that science is one step closer to healing more patients using stem cells.

"I feel really touched by the stories people share. You cannot imagine how many emails come in asking me if they can become the first human patient in our future clinical trial,"Li says. "People are in desperate need for something, especially when those people feel the current surgical procedure or intervention is not suitable for them. I have to keep saying, 'wait for another two, three years, maybe we'll be ready for a clinical trial,'but for me, it's time to move on and really do our larger animal studies to fulfill our promise. At least that way, I can fill the gap between the lab and clinical trials as the larger animals must be studied before you go into a clinical trial."

Li's development of a reliable and translational model for the generation of iPSCs in a large animal is critical as it has been a challenge to generate pig iPSCs with efficiency. The reprogramming efficiency of pig cells is relatively low compared to that of human or mouse cells, but large animal studies remain a crucial step in bringing treatments to clinical trials.

Interest in moving these treatments forward has grown and while this study was funded in part by NIH, Li also received support from the Plunkett Family Foundation in Milwaukee through their donation to the UW Stem Cell and Regenerative Medicine Center. After hearing of Li's research, Gwen Plunkett and her daughter Karen visited Li and his lab in 2019 to learn more and were inspired to support research into stem cells for cartilage regeneration.

"Innovation in medicine sparks critical change, for the world and the survival of our species and the Plunkett Family mission is to be a catalyst in stem cell and regenerative medicine research,"says Karen Plunkett. "We supported Jamie Thomson's lab in the early days when federal funding for human stem cell research was restricted. More recently, we continued our commitment to this research by supporting Dr. Wan-Ju Li's stem-cell based approaches for regenerating skeletal tissues, cartilageand bone for orthopedic applications. Additionally, it is personally gratifying to be able to support the SCRMC while my son completes his senior year studying neurobiology at UWMadison.We are happy to be part of the University of Wisconsin family."

Li shared that the donation was profoundly impactful and allowed him to further his goal of using stem cells to help patients struggling with osteoarthritis as well as other joint diseases.

"I want to make sure that our findings in stem cell research can be used to help people,"says Li. "I just feel this internal drive to study this area and I feel good knowing this model carries significant weight in terms of its potential for translational stem cell research and the development of therapeutic treatments."

This research was supported by grants from the National Institutes of Health (R01 AR064803) and the Plunkett Family Foundation. The UW Department of Pathology and Laboratory Medicine and UWCCC (P30 CA014520) and the Small Animal Imaging andRadiotherapy Facility and Flow Cytometry Laboratory, supported by UWCCC (P30 CA014520) also provided facilities and services.

Source: University of Wisconsin-Madison, whichis solely responsible for the information provided, and wholly owns the information. Informa Business Media and all its subsidiaries are not responsiblefor any of the contentcontained in this information asset.

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Reprogramming pig cells leads way for new regenerative therapies - National Hog Farmer

A breed of pigs called Wisconsin Miniature Swine created by a team of UWMadison scientists will help researchers better model and understand human diseases. Photo: Jeff Miller

Cells from miniature pigs are paving the way for improved stem cell therapies.

A team led by University of WisconsinMadison Stem Cell & Regenerative Medicine Center researcher Wan-Ju Li offers an improved way to create a particularly valuable type of stem cell in pigs a cell that could speed the way to treatments that restore damaged tissues for conditions from osteoarthritis to heart disease in human patients.

In a study published in Scientific Reports, Lis team also provides insights into the reprogramming process that turns cells from one part of the body into pluripotent stem cells, a type of building block cell that can transform into any type of tissue. These new insights will help researchers study treatments for a wide range of diseases.

The researchers turned to pigs, a well-established animal model for potential human treatments, because translating research to improve human health is deeply important to Li, a professor of Orthopedics and Rehabilitation and Biomedical Engineering. He has spent much of his career studying cartilage and bone regeneration to develop innovative therapies to help people.

Li and members of his Musculoskeletal Biology and Regenerative Medicine Laboratory obtained skin cells from the ears of three different breeds of miniature pigs Wisconsin miniature swine, Yucatan miniature swine and Gttingen minipigs.

University of WisconsinMadison Stem Cell & Regenerative Medicine Center researcher Wan-Ju Li (left) shows a collagen fiber sample to Gwen Plunkett and Karen Plunkett. Funding from the Plunkett Family Foundation has contributed to research on cartilage repair therapies in UWMadisons Musculoskeletal Research Program.

The researchers reprogrammed the cells to create induced pluripotent stem cells and demonstrated that they have the capacity to become different types of tissue cells. Pluripotent stem cells are the bodys master cells, and they are invaluable to medicine since they can be used for the regeneration or repair of damaged tissues.

Findings of this study suggest that the miniature pig is a promising animal model for pre-clinical research. The team plans to use the established pig model to reproduce their recent findings of cartilage regeneration in rats as reported in Science Advances. Regenerating cartilage in animals even more alike to humans moves science one step closer to helping patients experiencing joint diseases such as osteoarthritis.

In successfully developing induced pluripotent stem cells from three different breeds of minipigs, we learned we can take somatic skin cells from these pigs that we programmed ourselves and then inject them back into the same animal to repair cartilage defects, says Li. Or we can create induced pluripotent stem cells from the skin cell that carried the gene causing cartilage diseases such as chondrodysplasia and put that into the culture dish and use that as a disease model to study disease formation.

Li says the approach can be applied to regenerative therapies targeting any organ or tissue.

The team also found that a particular protein complex involved in managing the way genes are expressed, and tied to cellular growth and survival, could influence how efficiently induced pluripotent stem cells are generated. While we successfully created induced pluripotent stem cells from the three different strains of pig, we noticed that some pigs had a higher reprogramming efficiency, says Li. So, the second part of our findings, which is significant in biology, is understanding how these differences occur and why.

These findings, he says, may directly translate to understanding differences in the effectiveness of induced pluripotent stem cell generation between individual people one study has shown cellular reprogramming efficiency varying by age and ancestry and lead to better tailored therapies.

I want to make sure that our findings in stem cell research can be used to help people, says Li. I just feel this internal drive to study this area and I feel good knowing this model carries significant weight in terms of its potential for translational stem cell research and the development of therapeutic treatments.

Interest in moving these treatments forward has grown, and while the study was funded in part by the National Institutes of Health, Li also received support from the Milwaukee-based Plunkett Family Foundation through their donation to the UW Stem Cell & Regenerative Medicine Center. After hearing of Lis research, Gwen Plunkett and her daughter Karen visited Lis lab in 2019 to learn more. They were inspired to support research into stem cells for cartilage regeneration.

Innovation in medicine sparks critical change, for the world and the survival of our species, and the Plunkett Family mission is to be a catalyst in stem cell and regenerative medicine research, says Karen Plunkett.

The donation was profoundly impactful, says Li, allowed him to further his goal of using stem cells to help patients living with osteoarthritis and other joint diseases many of whom write his lab regularly in hope of finding a clinical trial opportunity.

I have to keep saying, Wait for another two, three years, maybe well be ready for a clinical trial, Li says. But for me, its time to move on and really do our larger animal studies to fulfill our promise. At least that way, I can fill the gap between the lab and clinical trials as the larger animals must be studied before you go into a clinical trial.

This research was supported by grants from the National Institutes of Health (R01 AR064803), the Plunkett Family Foundation and UW Carbon Cancer Center.

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Creating stem cells from minipigs offers promise for improved treatments - University of Wisconsin-Madison

PARIS Barbra Streisand loved her dog Samantha, aka Sammy. The white and fluffy purebred Coton of Tulear was even present on the steps of the Elyse Palace, the French Presidents official residence, when Streisand received the Legion of Honor in 2007.

As the singer and actress explained inThe New York Times in 2018, she loved Sammy so much that, unable to bring herself to see her pass away, she had the dog cloned by a Texas firm for the modest sum of 50,000 dollars just before she died in 2017, at the age of 14. And that's how Barbra Streisand became the happy owner of Miss Violet and Miss Scarlet, two puppies who are the spitting image of the deceased Samantha.

This may sound like a joke, but there is one deeply disturbing fact that Harvard Medical School genetics professor David A. Sinclair points out in his book Why We Age And Why We Dont Have To. It is that the cloning of an old dog has led to two young puppies.

This proves that DNA ours as well as that of Sammy has everything it takes to restore lost youth. This is a property that could be used to "reverse" aging without having to go through the problematic stage of cloning.

The idea rests on identifying the "reset" button of the organism. And aging specialists all have the same piece of good news to announce: this button has been found.

Its name sounds like a Japanese techno-thriller title: "The Yamanaka factors". But Shinya Yamanaka is not a fictional character. He is a scientist specialized in stem cell research who received the 2012 Nobel Prize in Medicine.

If all this sound a bit too science-fictional, you should know that the U.S. biotech company Altos Labs, which was just founded early this year, received a check of three billion dollars from billionaires Yuri Milner and Jeff Bezos. Not bad for a start-up. But this is a start-up with a very promising technology cellular reprogramming, which is nothing more than the name given by biologists to the famous "reset" button.

In 2006-2007, Yamanaka announced to the scientific community that he had discovered a combination of four genes Oct4, Klf4, Sox2 and c-Myc which, when injected into a cell, induces it to go from being a differentiated cell (nerve, blood, and so on) to being a pluripotent stem cell, i.e., one that can subsequently redevelop into any cell type.

It didn't take long for Yamanaka's colleagues to take advantage of his amazing discovery. In 2011, French researcher Jean-Marc Lematre, who worked at the Institute of Functional Genomics at the University of Montpellier (which never received the same financial support as American biotech company Altos Labs!) was the first to experimentally prove, on human tissues, that cellular aging was a reversible process. He and his team succeeded in transforming aging or senescent human skin cells back into young skin cells.

The process has since been improved, since it is no longer necessary to go through the stage of pluripotent cells which can degenerate into cancerous cells to reverse cellular aging. Interrupting the process before reaching this stage is enough to start the series of gene reactions that counter cellular aging.

But that's not all. Since Lematre's pioneering work, biologists from both sides of the Atlantic have shown that what was possible at the level of the cell is also possible at the level of the organism as a whole. As is often the case, they used mice as guinea pigs. At the end of 2016, in a famous study published by the "Cell" magazine, a professor at the Salk Institute (San Diego, California) Juan Carlos Izpisua Belmonte revealed the more than promising results recorded on genetically modified rodents.

The rodents' genome had been enriched with the Yamanaka factors as well as a small piece of additional genetic code, corresponding to a sort of on-off switch. Controlling the activation of the four genes, this "promoter" was itself activated only if the mouse ingested an antibiotic the doxycycline to be precise.

By prescribing this molecule (and thus activating the Yamanaka factors) two days a week throughout the life of the mice, Belmonte and his team increased their lifespan by 40%. "Aging is no longer a unidirectional process, as we thought. We can slow it down and even reverse it," he announced triumphantly. In a very similar experiment, Jean-Marc Lematre has obtained a more modest lengthening, of 15%, but thanks to a single dose of doxycycline. And above all, insists the French researcher, this "extra" lifespan proved to be free of all age-related diseases: osteoporosis, arthritis, pulmonary or renal fibrosis, etc.

The genetic modification of mice is common practice in labs. But should we do the same with humans to get the same result? There was public outcry in 2018 when Chinese researcher He Jiankui gave birth to twins with tampered genomes the first genetically modified children in history with the objective of giving them resistance to HIV.

How we view "GMO babies" may change over the next few decades. But whether it changes or not, it will not be necessary to go that far to do cell reprogramming in humans. A simple vaccine will probably do the trick.

The Covid-19 pandemic made the public aware that a vaccine whether RNA or DNA could be used as a vector to introduce genetic material into the human body. BioNTech's and Moderna's messenger RNA vaccines do this, but many other "viral vectors" exist, such as adeno-associated viruses (AAVs), small, non-pathogenic DNA viruses commonly used in molecular biology to carry one or more "genes of interest. On paper, there is nothing to prevent these genes of interest from being precisely those highlighted by Yamanaka.

And this is what our near future could look like. Around the age of 30, when we are alas, only temporarily! at the peak of our mental and physical fitness, we would receive one or more injections of this viral vector responsible for carrying Yamanaka's factors into us. Nothing would change in our body yet, as the Yamanaka factors have been programmed to remain silent until activated by the promoter. So we would continue to age normally. The passing of the years would no longer be irreparable!

Indeed, as soon as we would start to feel their first undesirable effects, let's say in our mid-forties, we would be prescribed a month's treatment with doxycycline. And then but only then would the youth therapy kick in. White hair disappearing, wounds healing faster, wrinkles fading, organs regenerating, glasses becoming useless... "Like Benjamin Button," writes David Sinclair, "you would experience the sensations of a 35-year-old. Then 30. Then 25. But unlike Benjamin Button, you would not go beyond that limit, because the statute of limitations would be interrupted... You would be about two decades younger biologically, physically and mentally, without having lost any of your knowledge, wisdom or memories."

Of course, such a possibility, if it becomes a reality and especially if it becomes widespread, will revolutionize large parts of society and will not be without its own tricky problems for a resource-limited planet. But who among us, once we reach a certain age, wouldn't dream of regaining our lost youth, while retaining the "benefits of experience"?

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Benjamin Button For Real? Scientists Are Close To Cracking The Code To Reverse Aging - Worldcrunch

Theaxolotl(Ambystoma mexicanum) is an aquatic salamander renowned for its ability toregenerate its spinal cord, heart and limbs. These amphibians alsoreadily make new neuronsthroughout their lives. In 1964, researchers observed that adult axolotls couldregenerate parts of their brains, even if a large section was completely removed. But one study found that axolotlbrain regenerationhas a limited ability to rebuild original tissue structure.

So how perfectly can axolotls regenerate their brains after injury?

As aresearcher studying regeneration at the cellular level, I and my colleagues in theTreutlein Labat ETH Zurich and theTanaka Labat the Institute of Molecular Pathology in Vienna wondered whether axolotls are able to regenerate all the different cell types in their brain, including the connections linking one brain region to another. In ourrecently published study, we created an atlas of the cells that make up a part of the axolotl brain, shedding light on both the way it regenerates and brain evolution across species.

Differentcell typeshave different functions. They are able to specialize in certain roles because they each express different genes. Understanding what types of cells are in the brain and what they do helps clarify the overall picture of how the brain works. It also allows researchers to make comparisons across evolution and try to find biological trends across species.

One way to understand which cells are expressing which genes is by using a technique calledsingle-cell RNA sequencing (scRNA-seq). This tool allows researchers to count the number of active genes within each cell of a particular sample. This provides a snapshot of the activities each cell was doing when it was collected.

This tool has been instrumental in understanding the types of cells that exist in the brains of animals. Scientists have used scRNA-seq infish,reptiles,miceand evenhumans. But one major piece of the brain evolution puzzle has been missing: amphibians.

Our team decided to focus on thetelencephalonof the axolotl. In humans, the telencephalon is the largest division of the brain and contains a region called theneocortex, which plays a key role in animal behavior and cognition. Throughout recent evolution, the neocortex hasmassively grown in sizecompared with other brain regions. Similarly, the types of cells that make up the telencephalon overall havehighly diversifiedand grown in complexity over time, making this region an intriguing area to study.

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We used scRNA-seq to identify the different types of cells that make up the axolotl telencephalon, including different types ofneuronsandprogenitor cells, or cells that can divide into more of themselves or turn into other cell types. We identified what genes are active whenprogenitor cells become neurons, and found that many pass through an intermediate cell type called neuroblasts previously unknown to exist in axolotls before becoming mature neurons.

We then put axolotl regeneration to the test by removing one section of their telencephalon. Using aspecialized method of scRNA-seq, we were able to capture and sequence all the new cells at different stages of regeneration, from one to 12 weeks after injury. Ultimately, we found that all cell types that were removed had been completely restored.

We observed that brain regeneration happens in three main phases. The first phase starts with a rapid increase in the number of progenitor cells, and a small fraction of these cells activate a wound-healing process. In phase two, progenitor cells begin to differentiate into neuroblasts. Finally, in phase three, the neuroblasts differentiate into the same types of neurons that were originally lost.

Astonishingly, we also observed that the severedneuronal connectionsbetween the removed area and other areas of the brain had been reconnected. This rewiring indicates that the regenerated area had also regained its original function.

Adding amphibians to the evolutionary puzzle allows researchers to infer how the brain and its cell types has changed over time, as well as the mechanisms behind regeneration.

When we compared our axolotl data with other species, we found that cells in their telencephalon show strong similarity to the mammalianhippocampus, the region of the brain involved in memory formation, and theolfactory cortex, the region of the brain involved in the sense of smell. We even found some similarities in one axolotl cell type to the neocortex, the area of the brain known for perception, thought and spatial reasoning in humans. These similarities indicate that these areas of the brain may be evolutionarily conserved, or stayed comparable over the course of evolution, and that the neocortex of mammals may have an ancestor cell type in the telencephalon of amphibians.

While our study sheds light on the process of brain regeneration, including which genes are involved and how cells ultimately become neurons, we still dont know whatexternal signalsinitiate this process. Moreover, we dont know if the processes we identified are still accessible to animals that evolved later in time, such as mice or humans.

But were not solving the brain evolution puzzle alone. TheTosches Labat Columbia University explored the diversity of cell types inanother species of salamander, Pleurodeles waltl, while the Fei lab at the Guangdong Academy of Medical Sciences in China and collaborators at life sciences companyBGIexplored how cell types arespatially arranged in the axolotl forebrain.

Identifying all the cell types in the axolotl brain also helps pave the way for innovative research in regenerative medicine. The brains of mice and humans havelargely lost their capacityto repair or regenerate themselves.Medical interventionsfor severe brain injury currently focus on drug and stem cell therapies to boost or promote repair. Examining the genes and cell types that allow axolotls to accomplish nearly perfect regeneration may be the key to improve treatments for severe injuries and unlock regeneration potential in humans.

This article is republished fromThe Conversationunder a Creative Commons license. Read theoriginalarticle.

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Axolotls can regenerate their brains - Big Think

IMAC Holdings, Inc.

BRENTWOOD, Tenn., Sept. 09, 2022 (GLOBE NEWSWIRE) -- IMAC Holdings, Inc. (Nasdaq: BACK) (IMAC or the Company), today announces it has completed the third cohort of its Phase 1 clinical trial for its investigational compound utilizing umbilical cord-derived allogenic mesenchymal stem cells for the treatment of bradykinesia due to Parkinsons disease.

The third cohort consists of five patients with bradykinesia due to Parkinsons disease receiving an intravenous infusion of a high concentration stem cell treatment. The third and final cohort of the Phase 1 clinical trial was completed on Tuesday, September 6, 2022.

About IMACs Phase 1 Clinical Trial

The Phase 1 clinical trial, consisting of a 15-patient dose escalation safety and tolerability study, is being conducted at three of IMACs clinical centers in Chesterfield, Missouri, Paducah, Kentucky, and Brentwood, Tennessee. The trial is divided into three groups: 1) five patients with bradykinesia due to Parkinsons disease received a low concentration dose, intravenous infusion of stem cells, 2) five received a medium concentration intravenous dose, 3) and five received a high concentration intravenous dose. All groups will be subsequently tracked for 12 months. IMACs medical doctors and physical therapists at the clinical sites have been trained to administer the treatment and manage the therapy. Ricardo Knight, M.D., M.B.A., who is medical director of the IMAC Regeneration Center of Chicago, is the trials principal investigator.

The Institute of Regenerative and Cellular Medicine serves as the trials independent investigational review board, while Regenerative Outcomes provides management of the study. Further details of the trial can be found at clinicaltrials.gov.

About Bradykinesia Due to Parkinsons Disease

In addition to unusually slow movements and reflexes, bradykinesia may lead to limited ability to lift arms and legs, reduced facial expressions, rigid muscle tone, a shuffling walk, and difficulty with repetitive motion tasks, self-care, and daily activities. Parkinsons disease is the typical culprit of bradykinesia, and as it progresses through its stages, a persons ability to move and respond declines.

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According to Zion Market Research, the global Parkinsons disease therapeutics market was $2.61 billion in 2018 and is expected to grow to $5.28 billion by 2025. The Parkinsons Disease Foundation estimates that nearly 10 million people are suffering from Parkinsons disease, and almost 60,000 new cases are reported annually in the U.S.

About IMAC Holdings, Inc.

IMAC Holdingsowns and manages health and wellness centers that deliver sports medicine, orthopedic care, and restorative joint and tissue therapies for movement restricting pain and neurodegenerative diseases.IMACis comprised of three business segments: outpatient medical centers, The Back Space, and a clinical research division. With treatments to address both young and aging populations,IMAC Holdingsowns or manages outpatient medical clinics that deliver regenerative rehabilitation services as a minimally invasive approach to acute and chronic musculoskeletal and neurological health problems. IMACs The Back Company retail spinal health and wellness treatment centers deliver chiropractic care within Walmart locations. IMACs research division is currently conducting a Phase I clinical trial evaluating a mesenchymal stem cell therapy candidate for bradykinesia due to Parkinsons disease. For more information visitwww.imacholdings.com.

# # #

Safe Harbor Statement

This press release contains forward-looking statements. These forward-looking statements, and terms such as anticipate, expect, believe, may, will, should or other comparable terms, are based largely on IMAC's expectations and are subject to a number of risks and uncertainties, certain of which are beyond IMAC's control. Actual results could differ materially from these forward-looking statements as a result of, among other factors, risks and uncertainties associated with its ability to raise additional funding, its ability to maintain and grow its business, variability of operating results, its ability to maintain and enhance its brand, its development and introduction of new products and services, the successful integration of acquired companies, technologies and assets, marketing and other business development initiatives, competition in the industry, general government regulation, economic conditions, dependence on key personnel, the ability to attract, hire and retain personnel who possess the skills and experience necessary to meet customers requirements, and its ability to protect its intellectual property. IMAC encourages you to review other factors that may affect its future results in its registration statement and in its other filings with the Securities and Exchange Commission. In light of these risks and uncertainties, there can be no assurance that the forward-looking information contained in this press release will in fact occur.

IMAC Press Contact:

Laura Fristoe

lfristoe@imacrc.com

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IMAC Holdings, Inc. Announces Completion of Third Cohort of its Phase 1 Clinical Study of Umbilical Cord-Derived Mesenchymal Stem Cells for the...

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Clinical translation of stem cell therapy for spinal cord injury still premature: results from a single-arm meta-analysis based on 62 clinical trials...

This months top grants in regenerative medicine, sourced from Dimensions, includes projects on: a novel platform to enhance single cell interrogation of nervous system development, human endothelial cell regulation of ossification and the development of a dynamic double network hydrogel for generating pancreatic organoids from induced pluripotent stem cells.

This project aims to investigate a strategy, which utilizes novel spatial transcriptomics approaches, integrated multiplexed RNA/protein detection and visualization and computational algorithms to identify and map molecular markers of the preganglionic neurons in the ventral spinal cord and progenitor cell populations of the sympathetic ganglia. If successful, the approach could provide a foundation for basic research of peripheral nervous system birth defects and repair using stem cell-based therapies, as well as future studies of neuroblastoma initiation.

Funding amount:US$206,000

Funding period: 8 August 2022 31 July 2024

Funder:Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD)

Research organization:Stowers Institute for Medical Research (MO, USA)

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Over one million patients undergo bone repair procedures in the USA annually, with autologous bone grafting remaining the preferred treatment for bone defects. The development of therapies that exploit the osteogenic potential of bone marrow-derived mesenchymal stem cells (bm-MSCs) has been limited due to limited understanding of the regulatory mechanisms of in vivo bm-MSC osteogenesis. Previous research from the group showed that the osteogenic potential of bm-MSCs is dependent on sustained proximity to endothelial cells. The goal of the present study is to elucidate the cellular and molecular mechanisms by which endothelial cells regulate the osteogenic differentiation of bm-MSCs and develop a foundation of knowledge upon which to build therapeutic strategies for bone regeneration utilizing autologous bm-MSCs.

Funding amount:US$442,000

Funding period: 10 August 2022 31 May 2027

Funder:National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)

Research organization:Boston Childrens Hospital (MA, USA)

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Human induced pluripotent stem cells provide a valuable source of cells for basic research and translational applications. While there have been advances in lineage-specific differentiation of human induced pluripotent stem cells, there remains limited understanding on the impact of matrix stiffness, viscoelasticity and integrin ligand presentation on the multi-stage development of exocrine pancreatic organoids. This research aims to define the influence of matrix properties on the generation of exocrine pancreatic organoids by developing a viscoelastic dynamic double network hydrogel platform with controllable matrix mechanical properties and biochemical motifs. This will advance the application of chemically defined matrices as xeno-free artificial stem cell niches for organoid growth and tissue regeneration applications.

Funding amount:US$468,000

Funding period: 1 August 2022 31 July 2026

Funder:National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Research organization: Indiana University Purdue University Indianapolis (IA, USA)

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Top 3 grants in regenerative medicine: July 2022 - RegMedNet

EARD2022 is over, but the research and events continue. Heres a summary of everything thats happened in August.

We are hiring! We are currently looking for a full-time chief of staff, a full-time data-driven Senior Marketing Manager, a part-time Youtube sponsorship/partnership acquisition lead, a social media intern, a part-time grant writer, and volunteers to support various programs. If you are interested in learning more about any of these positions, please contact us with your resume and salary expectations.

Announcing the Longevity Prize: The Longevity Prize is a series of prizes designed to honor the researchers who are helping to build a future in which age-related diseases are a thing of the past. This new initiative aims to accelerate progress in the rejuvenation biotechnology field and encourage innovation.

Stephanie Dainow to Present at the 9th ARDD Conference: On August 22, 2022, Lifespan.io Executive Director Stephanie Dainow participated in the Decentralized Science and Blockchain session as a part of the Emerging Tech Workshop at the worlds largest annual Aging Research and Drug Discovery conference (9th ARDD).

Longevity Camp: The Longevity Summer Camp is a four-day retreat featuring people from many longevity-related walks of life. Recently, somewhere between the former gold mining town of Nevada City and the infamous Donner Pass, a unique gathering took place.

Cells Return from Death: Cells, dead for an hour under warm conditions, have been revived. Questions about when life begins have been hot topics for awhile, but there is also debate about when life ends.

Rapamycin and Metformin: Rapamycin and metformin, two well-studied drugs in aging research, can be combined for synergistic effects in mice. Rapamycin and metformin are viewed by many as the two most promising anti-aging drugs, but now scientists have found that these drugs can work hand in hand.

Steve Horvath on the Present and Future of Epigenetic Clocks: Dr. Steve Horvath is the inventor of the epigenetic clock and, currently, principal investigator at Altos Labs. We talked about the recent developments in this immensely important field, including pan-mammalian clocks, two-species clocks, and single-cell clocks, along with the challenges the field faces.

Prof. Albert-Lszl Barabsi on Network Medicine: Albert-Lszl Barabsi is the Robert Gray Dodge Professor of Network Science at Northeastern University, and he also holds an appointment in the Department of Medicine at Harvard Medical School. We talked about a revolutionary network medicine approach that can greatly enhance our ability to understand biological processes and seek cures for disease.

Martin ODea Talks About the Longevity Summit: We recently had the opportunity to speak to Martin ODea about a new longevity-focused event happening in Irelands capital city on September 18th-20th. Martin holds an MBS and is a business lecturer at Dublin Business School in Dublin, Ireland. He is also the author of Beyond the Subjectivity Trap.

Dr. Aubrey de Grey Will Speak at the Longevity Summit Dublin: We recently caught up with Dr. Aubrey de Grey and talked to him about the upcoming Dublin Longevity Summit and how things are looking on the advocacy landscape.

Old Plasma Dilution Reduces Human Biological Age: The Journal Club has returned to our Facebook page with your host, Dr. Oliver Medvedik. This month, we have investigated a paper, Old plasma dilution reduces human biological age: a clinical study, in which Irina Conboy and her team investigated the effects of therapeutic plasma exchange on aging in people.

Vitamin D Fails to Improve Bone Health in Mega-Study: A high-quality, randomized, controlled trial found no effect of vitamin D supplementation or blood levels on the incidence of fractures in an aging population.

Hesperetin Upregulates Metabolism and Longevity in Mice: Researchers publishing in Journal of Biomedical Science have concluded that hesperetin, a compound found in various herbs, improves longevity in mice by promoting the expression of the pro-longevity gene Cisd2.

Caloric Restriction Improves Immune System Function: A new study published in Mechanisms of Aging and Development has shown that caloric restriction effectively restores T cell abundance in aged mice. Caloric restriction has become a well-known anti-aging intervention, as it can reverse several hallmarks of aging and extend lifespan in different animal models.

Ghrelin Is Associated with Worse Muscle Aging in Mice: A team of researchers publishing through Multidisciplinary Digital Publishing Institute has described an association between ghrelin and skeletal muscle aging in mice. Ghrelin is a peptide containing 28 amino acids. Its main function is to stimulate the appetite through receptors in the hypothalamus.

Sauna Combined with Exercise Improves Cardiovascular Health: In a randomized, controlled trial, scientists have shown that sauna and exercise, when taken together, might have a synergistic, beneficial effect on cardiovascular health and cholesterol levels. Sauna bathing has been credited with many health benefits, predominantly for the cardiovascular system.

Developing Nanobodies to Fight Parkinsons Disease: A team of researchers publishing in Nature Communications has described nanobodies that can destroy the -synuclein aggregates that characterize Lewy bodies, which are associated with dementia and Parkinsons disease. Traditional antibody therapies, while promising in some studies, are too large to enter cells in order to affect the aggregates there.

Scientists Move the Boundaries of Post-Mortem Recovery: Researchers have been able to achieve substantial recovery of cellular and organismal activity in pigs that had been dead for a full hour. Advances in resuscitation have already moved the boundaries of life and death, making it possible to revive a person several minutes after the heart stops beating.

An In-Depth Review of Skin Aging Genes: In a new systematic review published in Scientific Reports, multiple genes driving skin aging were identified. The authors start by explaining the intrinsic (genetic and chronological) and extrinsic (environmental) factors that drive skin aging.

Hypertension Is Associated with Brain Drainage Changes: Researchers publishing in Aging have found that enlarged perivascular spaces in the brain are correlated with vascular disorders. These spaces, which are part of the brains glymphatic system, allow for the drainage of potentially dangerous metabolites such as beta amyloid.

Rapamycin-Loaded Microneedles Reverse Hair Loss in Mice: Scientists have successfully regrown hair in a mouse model of hair loss using custom-made plastic microneedles loaded with rapamycin and epigallocatechin gallate (EGCG), an active ingredient in green tea.

Identifying Mitonuclear Genes for Longevity: Publishing in GeroScience, a team of researchers that included Nir Barzilai and Matt Kaeberlein examined genes that may affect both mitochondria and lifespan.

Dietary Restrictions Do Not Help Cognitive Function in Mice: A new study published in Neurobiology of Aging has shown that neither caloric restriction nor intermittent fasting improve late-life cognition in genetically diverse mice, but the effect depends on genetic composition.

Combining Senolytic Pathways Has Synergistic Effects: A team of researchers have explained in Aging how multiple compounds that target the BCL-2 protein family are considerably more effective against senescent cells than each compound by itself.

New Synthetic Molecule Alleviates Alzheimers in Mice: Scientists have synthesized a molecule that alleviates Alzheimers in a mouse model by targeting inflammation. Two of the most prominent and probably interconnected symptoms of Alzheimers disease are the accumulation of amyloid beta (A) and chronic neuroinflammation.

The Relationship Between Stroke and Inflammation: Publishing in Aging, a team of Chinese researchers has provided evidence showing a relationship between systemic inflammation and prognosis after a stroke. As the researchers point out, strokes are the leading cause of death in China.

Almost Half of Cancer Deaths Worldwide are Preventable: Researchers have shown that 44.4% of cancer deaths worldwide can be attributed to preventable risk factors, including behavioral and environmental ones. It is well known that many cancer cases occur due to behavioral and environmental and factors such as smoking and pollution, which makes them theoretically preventable.

Rapamycin and Metformin Show Synergy in Mice: Scientists have found that rapamycin and metformin work hand in hand in diabetes-prone mice, boosting each others effectiveness and blocking side effects. Both have been in use for various indications for decades and have decent safety profiles.

Plasma Dilution Appears to Rejuvenate Humans: Published in GeroScience, a groundbreaking study from the renowned Conboy lab has confirmed that plasma dilution leads to systemic rejuvenation against multiple proteomic aspects of aging in human beings. This paper takes the view that much of aging is driven by systemic molecular excess of signaling molecules, antibodies, and toxins.

Mitochondrial Drug Alleviates Atherosclerosis in Mice: Scientists have drastically improved various symptoms of atherosclerosis in mice by precisely targeting mitochondria with a plant-derived antioxidant. Atherosclerosis, the accumulation of plaques on arterial walls, is one of the deadliest age-related diseases.

Intravenous Stem Cells Alleviate Guinea Pig Osteoarthritis: Scientists have shown that intravenous delivery of mesenchymal stem cells, which has some advantages over the more conventional intra-articular injection, alleviates age-related osteoarthritis and decreases inflammation in guinea pigs. Osteoarthritis, a degenerative joint disease, is one of the most common causes of disability in old age.

Glycans as Biomarkers of Aging: In a new review published in Clinica Chimica Acta, researchers from the University of Zagreb discuss immunoglobulin G glycans, the changes that their composition undergoes with aging, and their potential as biomarkers of aging. One of the reviews co-authors is Prof. Gordan Lauc, who gave a presentation on them at EARD2022.

A wearable electrochemical biosensor for the monitoring of metabolites and nutrients: The monitoring of metabolites for the early identification of abnormal health conditions could facilitate applications in precision nutrition.

Epigenome-wide association study analysis of calorie restriction in humans, CALERIE TM Trial analysis: DNA methylation changes may contribute to caloric restrictions effects on aging.

Association of Leisure Time Physical Activity Types and Risks of All-Cause, Cardiovascular, and Cancer Mortality Among Older Adults: There were significant associations between participating in 7.5 to less than 15 MET hours per week of any activity and mortality risk.

Ginkgo biloba extract EGb 761 plus acetylcholinesterase inhibitors improved cognitive function in patients with mild cognitive impairment: These findings suggest that combined therapy with EGb 761 plus AChEI may provide added cognitive and functional benefits in patients with MCI.

Suppression of trimethylamine N-oxide with DMB mitigates vascular dysfunction, exercise intolerance, and frailty associated with a Western-style diet in mice: These therapies may be promising for mitigating the adverse effects of a Western diet on physiological function and thereby reducing the risk of chronic diseases.

Canagliflozin retards age-related lesions in heart, kidney, liver, and adrenal gland in genetically heterogenous male mice: Canagliflozin can be considered a drug that acts to slow aging and should be evaluated for potential protective effects against many other late-life conditions.

Fecal microbiota transplantation can improve cognition in patients with cognitive decline and Clostridioides difficile infection: This study revealed important interactions between the gut microbiome and cognitive function. Moreover, it suggested that FMT may effectively delay cognitive decline in patients with dementia.

Mitochondrial dynamics maintain muscle stem cell regenerative competence throughout adult life by regulating metabolism and mitophagy: As mitochondrial fission occurs less frequently in the satellite cells in older humans, these findings have implications for regeneration therapies in sarcopenia.

Long-lasting, dissociable improvements in working memory and long-term memory in older adults with repetitive neuromodulation: These findings demonstrate that the plasticity of the aging brain can be selectively and sustainably exploited using repetitive and highly focalized neuromodulation

Supplementing Glycine and N-Acetylcysteine (GlyNAC) in Older Adults Improves Aging Hallmarks: By combining the benefits of glycine, NAC and GSH, GlyNAC is an effective nutritional supplement that improves and reverses multiple age-associated abnormalities to promote health in aging humans.

VitaDAO Funds ApoptoSENS Project for $253,000: Preventing the dysfunction of natural killer cells may be a promising area to explore in the fight against cellular senescence. Researchers are hoping to define the correlation between the increase in senescent cells and the onset or worsening of disease in humans.

VitaDAO Backs Research into Chronic Oral Disease: Periodontal disease affects more than 47% of adults aged 30 and over. For people over 65 years of age, that number rises to over 70%, making periodontitis one of the most commonly observed age-related illnesses. Jonathan Ans lab seeks to research inflammation-targeting compounds that can help treat periodontal disease.

Researchers Propose Five New Hallmarks of Aging: Publishing in Aging five months after their panel discussion in Copenhagen, many well-known researchers have explained their reasons for wishing to add new hallmarks of aging to the existing paradigm.

SENS Research Foundation Announces Ending Aging Forum 2022: SENS Research Foundation has announced this years Ending Aging Forum, which will be held through a virtual conference platform with an immersive environment.

Longevity Investors Conference: Organized and sponsored by Maximon, the Longevity Investors Conference is focused on the investment aspects of longevity. The LIC welcomes everyone with an interest in the financial aspects of the longevity sector, including venture capitalists, asset managers, and managers of private equity funds and private banks.

Longevity Summit Dublin: This conference will feature two days of inspiring research developments along with top longevity entrepreneurs, biotech companies, longevity investors, and researchers from around the world.

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Rejuvenation Roundup August 2022 - Lifespan.io News

By Giles Campion, EVP, head of R&D and chief medical officer, Silence Therapeutics

siRNA is a gene-silencing technology with great potential for treating a wide range of rare diseases, as I discussed in my previous article, but its promise doesnt end there. In this last article in the series, I examine siRNAs potential for treating not-so-rare and even quite common diseases.

Unlike rare diseases, which are often caused by pathological genetic mutations, common diseases may be associated with genetic variants that are not pathological and therefore do not dysregulate a biological process. For example, variants of the LPA or PCSK9 gene can increase a persons risk of cardiovascular disease by affecting cholesterol levels, but these variants do not directly cause cardiovascular disease by disrupting a fundamental biological process. This contrasts with, for example, mutations in the HBB gene that cause beta thalassemia and disrupt the mechanisms that protect the body from toxic iron buildup.

Nevertheless, the approach to treating rare and common diseases with siRNA therapies is similar: silence a gene that has little or no effect on phenotypes outside the disease, thereby maximizing safety. This is an important factor in rare diseases, which often begin early in life and require lifelong treatment. But it is equally important in common chronic diseases, such as hyperlipidemia, in which a patient has abnormally high levels of fats in the blood, where patients may live for decades before they experience any overt symptoms from their condition and are not likely to tolerate a therapy with even minor side effects that interfere with their quality of life.

At the forefront of common conditions being targeted by gene silencing is elevated lipoprotein (a), or Lp(a), a cholesterol-rich particle closely related to the well-known cardiovascular risk factor LDL. High levels of Lp(a) are associated with high risk of cardiovascular events, such as heart attacks and strokes; low levels of Lp(a) are associated with a low risk of these events.

Unlike other types of cholesterol-carrying particles, Lp(a) levels are not significantly modifiable by lifestyle factors; levels are genetically determined by the variant of the LPA gene, which encodes apolipoprotein (a) a major protein component of Lp(a) that a person has. Because these variants are not pathological mutations, the person may not experience disease symptoms for years and may even be unaware of their elevated Lp(a) levels. Yet the condition is common: One in five people have high levels of Lp(a), defined as 50 mg/dl or 120 nmol/L. Other cholesterol-reducing medicines, such as statins, have no effect on Lp(a) and can even increase levels; currently there are no approved Lp(a)-reducing therapies.

However, assessments of human genetic databases, such as the UK Biobank, have revealed that cardiovascular risk is the only phenotype associated with Lp(a) levels. Some individuals have zero levels of Lp(a), and the only known phenotype in them is a much-reduced incidence of cardiovascular events. This indicates that silencing LPA with a properly designed siRNA therapy, such as Silences clinical-stage asset SLN360, could reduce the risk of cardiovascular disease in people with elevated Lp(a) while minimizing the risk of any unwanted or unexpected side effects.

The PCSK9 gene is another example of an siRNA target for the common condition of hyperlipidemia. The PCSK9 protein negatively regulates the cellular uptake of low-density lipoprotein-cholesterol (LDL-C) in the bloodstream by reducing the number of LDL receptors on the surface of cells. This means that high levels of PCSK9 decrease cellular uptake of LDL-C, leaving more of it in circulation.

High LDL-C levels in blood are associated with coronary artery disease (CAD). While not entirely determined by genetics, as Lp(a) levels are, some variants of the PCSK9 gene are associated with low levels of LDL-C and a reduced incidence of cardiovascular disease. Similar to the LPA gene, this suggests that silencing PCSK9 with an siRNA could reduce LDL-C levels in the blood to treat hyperlipidemia and reduce the risk of CAD. Indeed, the siRNA therapy inclisiran, which silences PCSK9, was approved by the European Union in December 2020 and in the United States in December 2021 for use in people with atherosclerotic cardiovascular disease (ASCVD), ASCVD risk equivalents, and heterozygous familial hypercholesterolemia (HeFH), in conjunction with lifestyle changes and other cholesterol-lowering medicines.

An important feature of siRNA therapies in the treatment of common chronic conditions such as elevated Lp(a) and elevated LDL-C is that they have long-lasting effects, and thus they require less frequent dosing than statins and other small molecule drugs, which must be taken daily. This in turn should increase patients compliance with the therapeutic regimen and thereby improve outcomes. In fact, a 2018 retrospective study found that hyperlipidemia patients who were prescribed the right intensity (level) of statin treatment and complied 100% with their therapy had a 40% lower risk of cardiovascular events than patients who received low-intensity statin treatment and had 5% compliance.1The study concluded that an optimal therapy could reduce the risk of cardiovascular events by 30% in three years.

Though published before any siRNA therapy was approved for hyperlipidemia, the studys implications are clear: Therapeutic intensity and patient compliance are important factors in saving peoples lives. With siRNA therapies, the intensity is known, and the compliance issues are likely to be less of an issue compared with oral drugs. This is just one aspect of siRNA that makes it as well-suited for treating common diseases as rare diseases.

siRNA also has the potential to improve outcomes in hematopoietic stem cell transplantation (HSCT). Though not a disease per se, HCST is a procedure commonly used to treat a range of blood cancers and, with increasing frequency, certain autoimmune disorders.

HCST involves ablating the existing bone marrow to make way for a healthy stem cell graft to repopulate the marrow. This ablation shifts an enormous load of dead iron-laden blood cells into the circulation. Retrospective studies suggest this acute release of toxic iron from ablated cells can adversely affect the survival of the stem cell graft and increase the risk of potentially lethal infections in HSCT patients.

As in the rare disease examples I mentioned previously, silencing TMPRSS6 with an siRNA could increase hepcidin to reduce iron levels in HSCT patients, potentially improving their survival and engraftment outcomes.

I am passionate about RNA technology and the benefits that targeted, precision siRNA medicines can bring to patients with rare diseases and not-so-rare diseases who need new therapeutic options. As both a physician and drug developer, I find it rewarding and exciting to witness this technology finally coming into its own, with the promise of delivering even greater benefits in the coming years.

Reference

About The Author:

Giles Campion, MD, joined Silence Therapeutics as head of R&D and chief medical officer in 2019 and was appointed as an executive director in 2020. He is an expert in translational medicine and an experienced biotech and pharmaceutical professional across many therapeutic areas, most recently in orphan neuromuscular disorders. He has held senior global R&D roles in several large pharma, diagnostics, and biotech companies, including as group vice president of the neuromuscular franchise at BioMarin Pharmaceutical Inc., and chief medical officer and senior vice president of R&D at Prosensa. He is also a co-founder of PepGen Ltd. He earned his bachelors and doctorate degrees in medicine from the University of Bristol and is listed on the General Medical Council (UK) Specialist Register (Rheumatology).

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The Promise Of Gene Silencing To Treat Not-So-Rare Diseases - BioProcess Online

Healthy fasting is therapeutic if appropriately done, and evidence supports this. Our body can cure itself if given the correct nourishment, movement, sleep, emotional wellness, and surroundings; fasting boosts its curing capabilities. Its vital for holistic health.

It has beneficial effects on physical, emotional, brain, and spiritual health. In fact, it exists as a practice in most religions (religious fasting). For example, Muslims reduce caloric intake for a period of time during Ramadan to cleanse the mind, body, and soul. Other religious fasts include Christians, Greek Orthodox Christians, Jews, Hindus, and Buddhists, reducing caloric intake on certain days of the week or year.

Fasting has been performed for millennia with favorable effects, but only lately have studies shown its significance in adaptive cellular responses that minimize oxidative damage and inflammation, optimize energy metabolism and heart health, and bolster cellular defense. Furthermore, it helps with weight loss because it depletes liver glycogen, causing lipolysis and ketone body production, which reduces body fat (fat percentage) and hip circumference.

Fasting is such a popular scientific research topic today that the number of these studies demonstrating how good it is for holistic health keeps growing. The outcomes of these studies show that it can make you smarter, increase longevity by slowing down the aging process, and heal diseases, digestive issues, neurodegenerative disorders, and neurological disorders (mood disorders). Other health effects include the prevention of cardiovascular disease and chronic diseases.

Fasting activates our inner intelligence via calorie restriction. Its straightforward science. Fasting lets the digestive system rest by halting calorie intake. This break saves energy that would have gone toward digesting food. This conserved energy is used for repair, recovery, development, rejuvenation, and healing, which are needed for curing every human disease.

What happens first when were sick? Reduced appetite. So, what does this tell us? Our body reduces appetite to save energy that would have gone to digestion for mending and repair instead. Fasting does the same thing. It activates good genes with protective mechanisms, such as the SIRT1 gene, which regulates longevity, inflammation, fat and glucose metabolism, and other health effects.

A PLOS One study found that fasting reduces hunger hormones, improves metabolism, and helps people lose weight. Chicago researchers tested intermittent fasting on 20 obese adults for eight weeks. It enhanced the participants insulin resistance and glucose regulation, reduced cravings, and increased the feeling of fullness. Furthermore, they felt better overall and experienced no side effects.

Most people today overeat by incessantly munching and nibbling. Constant and excessive eating and out-of-balance dietary intake can overload the digestive system, leading to illness and a majority of health-related problems. Fasting helps mend this damage.

Chronic fasting (long-term fasting) enhances the lower eukaryote lifetime by altering metabolic and stress resistance pathways. Intermittent fasting (short-term fasting) protects against diabetes, malignancies, heart disease, neurodegeneration, obesity, hypertension, asthma, and rheumatoid arthritis.

Most people fast by only drinking water, dubbed water fasting. Other versions include juice fasting (apple cider vinegar, lemonade, carrot juice, celery juice, etc.) and eating light, where participants primarily eat vegetables, fruits, and lean meats like fish and chicken. However, real fasting involves going without food, solid, and liquid (aside from water) for at least 12 hours.

Several variations exist. Sometimes spiritual disciplines like prayer and meditation are included, turning it into a ritual. These disciplines make the process easier by calming the psyche.

As mentioned, various methods (diets) exist; all deliver positive effects. Here are a few examples:

This is the most common style of fasting and the most accurate form. Except for water, no solids or liquids are consumed. For those doing an extended water fast (over three days), sometimes herbal teas, tonics, and broths are consumedbut absolutely no caffeine or alcohol.

People following this diet will only drink vegetable and fruit juices for the duration of the fast.

This variation allows anything liquid, like broth or pureed soups, smoothies, and juices.

Its odd to call this one a fast because you can eat. Nevertheless, this diet is for people looking to purify their bodies. They must eliminate all non-plant-based foods (only things like fruits, vegetables, nuts, seeds, and legumes are allowed).

Skipping meals regularly, known as intermittent fasting or partial fasting, is becoming increasingly popular worldwide. People realize its physical and mental health benefits. It enhances energy, moods, sleep, and sex life. However, it involves a set daily fasting time.

Intermittent fasting also has the following benefits:

There are over twenty variations of intermittent fasting. The most popular include:

This strategy entails daily periods of fastingof 18 hours and then eating a light meal every other day. On alternate days you can eat healthy things like vegetables, berries, nuts, lean protein, etc.

Every day, you consume within specific periods of time. For example, your daily fast may be limited to eating from midday to 8:00 p.m..

You follow a schedule of regular eating for five days, then two days of fasting (preferably water fasting).

This fast allows one meal a day, but not breakfast. It is also commonly referred to as the One Meal a Day diet (OMAD).

You designate a six-hour window per day in which you can eat.

Most people fast to shed weight, regulate blood sugar, cleanse themselves of toxins, or regain mental clarity and emotional stability. However, it is a difficult thing to do alone. For those that need a little motivation, inspiration, and guidance, there are many fasting or detox retreats worldwide.

In addition, a growing number of medical clinics are offering guided fasting treatments. During these rehabilitation sessions, physicians supervise patients while undertaking water-only or very low-calorie (less than 200 kcal/day) fasting periods of one week or more. People participate for help in weight management or disease treatment and prevention.

Mexico has fasting pods, aka Fast incubators. These locations surround individuals with nature and block out food odors and noise. One can fast for 10 to 30 days. As a result, various disorders have reportedly healed faster. Many even experience improved eyesight and hearing.

While fasting is a simple concept, it can perplex many people due to the abundance of claims, methods, and precautions floating around the internet. However, it does not have to be challenging. On the contrary, it should be second nature to us.

Circadian rhythm fasting is the most natural and realistic technique to fast. In laymans terms, sunset to sunrise fasting involves eating ones last meal of the day early (near to or with sundown) and breaking it after sunrise. This provides for a minimum of 12-hour fasting and is one of the most efficient strategies to incorporate the practice into your lifestyle.

If you are still not hungry after 12 hours, gently extend your fast until you experience actual physical hunger, and then break youre fast correctly. You are not required to have breakfast if you arent hungry. Not feeling hungry in the morning indicates that your body is still detoxifying and processing your evening meal. Respect your body by fasting accordingly.

Fasting while sleeping is ideal since all critical detoxification, repair, and recovery processes occur during deep sleep. Our bodies detoxify at night, and the physical health benefits are more noticeable when fasting.

When you want to break the fast, however, it is entirely up to you and the signs your body is sending. Some people wake up hungry, while others do not till the afternoon. Pay attention to your body. There is a distinct distinction between fasting and starvation. If you are not hungry, respect your hunger and continue your fast for a few more hours.

Breaking a fast gently awakens your digestive system. So, gorging after a fast is terrible. It could overwhelm your stomach. Water breaks a dry fast best. Take a few sips, then eat fruit or 1-2 fresh dates. After 30-40 minutes, cook a wholesome meal. This is particularly important for long fasts.

Some fasters drink tea, coffee, or juice. Acidic drinks can damage stomach linings. Therefore, one should fast appropriately or not at all. If opting for juice fast, stick with vegetable juice like celery, green juice, or non-acidic fruits. Likewise, teas should be caffeine-free and herbal only (lavender, jasmine, etc.).

Theres no one-size-fits-all answer. Some find fasted workouts beneficial, while others find them hazardous. Fasted workouts depend on objectives, energy and hunger levels, training, and health conditions. However, do it if you can because fasted workouts are fantastic for insulin resistance, weight loss, and abdominal fat.

Note: Your body needs time to acclimate to a fast before you experience mental changes. You may get headaches or discomfort early on. Your brain is granted a cleaner bloodstream after your body eliminates toxins. This improves your thoughts, emotions, memory, and other senses.

Fasting causes ketogenesis, promotes potent changes in metabolic pathways and cellular processes such as stress resistance, lipolysis, and autophagy, and can have medical applications that are as effective as approved drugs, such as dampening seizures and seizure-associated brain damage, alleviating rheumatoid arthritis, and maximizing holistic health, as explained in the rest of this page.

Fasting uses up excess carbohydrates. The body burns fat. The metabolic rate rises, unlike with caloric restrictionweight loss results.

Half of our energy goes into digestion. This energy can be used to heal and regenerate, which happens during a fast. The human body recognizes what needs mending.

Sick and weaker cells are killed after 24-36 hours via apoptosis and autophagy, then recycled into new cells. Its natural. Apoptosis kills 50 to 70 billion human cells daily. Fasting boosts this rate.

Stem cell production and activation rise after fasting. The number of new stem cells and HGH peak during days 3-5 of a fast, then fall. Additional research shows that new white blood cells are created with increased stem cell growth, boosting the immune system.

Besides fat burning and strengthening the immune system, it reduces inflammation, rebalances the gut microbiome and hormones, protects the brain from neurological diseases, reduces cancer risk, slows aging, and promotes cell maintenance and repair.

Fasting is the best medicine, and its free!

Fasting has many powerful benefits, but its not for everyone. It should be avoided or done only under medical supervision in the following situations. People who are:

If you think you can do it, go for it! Fasting is the bodys natural stem cell therapy, renewing and regenerating the body. It is the ultimate biohack. Theres no better method to restore cells, improve healing, and increase energy and focus.

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Discover the Mental and Physical Health Benefits of Fasting - Intelligent Living

Clogging a proteins active site is a straightforward way to take it offline. Thats why the active site is often the first place drug designers look when designing new drugs, Reich explained. However, about eight years ago he decided to investigate compounds that could bind to other sites in an effort to avoid off-target effects.

As the group was investigating DNMT3A, they noticed something peculiar. While most of these epigenetic-related enzymes work on their own, DNMT3A always formed complexes, either with itself or with partner proteins. These complexes can involve more than 60 different partners, and interestingly, they act as homing devices to direct DNMT3A to control particular genes.

Early work in the Reich lab, led by former graduate student Celeste Holz-Schietinger, showed that disrupting the complex through mutations did not interfere with its ability to add chemical markers to the DNA. However, the DNMT3A behaved differently when it was on its own or in a simple pair; it wasnt to stay on the DNA and mark one site after another, which is essential for its normal cellular function.

Around the same time, the New England Journal of Medicine ran a deep dive into the mutations present in leukemia patients. The authors of that study discovered that the most frequent mutations in acute myeloid leukemia patients are in theDNMT3Agene. Surprisingly, Holz-Schietinger had studied the exact same mutations. The team now had a direct link between DNMT3A and the epigenetic changes leading to acute myeloid leukemia.

Reich and his group became interested in identifying drugs that could interfere with the formation of DNMT3A complexes that occur in cancer cells. They obtained a chemical library containing 1,500 previously studied drugs and identified two that disrupt DNMT3A interactions with partner proteins (protein-protein inhibitors, or PPIs).

Whats more, these two drugs do not bind to the proteins active site, so they dont affect the DNMT1 at work in all of the bodys other cells. This selectivity is exactly what I was hoping to discover with the students on this project, Reich said.

These drugs are more than merely a potential breakthrough in leukemia treatment. They are a completely new class of drugs: protein-protein inhibitors that target a part of the enzyme away from its active site. An allosteric PPI has never been done before, at least not for an epigenetic drug target, Reich said. It really put a smile on my face when we got the result.

This achievement is no mean feat. Developing small molecules that disrupt protein-protein interactions has proven challenging, noted lead authorJonathan Sandovalof UC San Francisco, a former doctoral student in Reichs lab. These are the first reported inhibitors of DNMT3A that disrupt protein-protein interactions.

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A new kind of chemo - University of California

SOMERVILLE, Mass.--(BUSINESS WIRE)--Cellarity, a life sciences company founded by Flagship Pioneering to transform the way medicines are created, announced today the release of a unique single-cell dataset to accelerate innovation in mapping multimodal genetic information across cell states and over time. This dataset will be used to power a competition hosted by Open Problems in Single-Cell Analysis.

Cells are among the most complex and dynamic systems and are regulated by the interplay of DNA, RNA, and proteins. Recent technological advances have made it possible to measure these cellular features and such data provide, for the first time, a direct and comprehensive view spanning the layers of gene regulation that drive biological systems and give rise to disease.

Advancements in single-cell technologies now make it possible to decode genetic regulation, and we are excited to generate another first-of-its-kind dataset to support Open Problems in Single Cell Analysis, said Fabrice Chouraqui, PharmD, CEO of Cellarity and a CEO-Partner at Flagship Pioneering. Developing new machine learning algorithms that can predict how a single-cell genome can drive a diversity of cellular states will provide new insights into how cells and tissues move from health to disease and support informed design of new medicines.

To drive innovation for such data, Cellarity generated a time course profiling in vitro differentiation of blood progenitors, a dataset designed in collaboration with scientists at Yale University, Chan Zuckerberg Biohub, and Helmholtz Munich. This time course will be used to power a competition to develop algorithms that learn the underlying relationships between DNA, RNA, and protein modalities across time. Solving this open problem will help elucidate complex regulatory processes that are the foundation for cell differentiation in health and disease.

While multimodal single-cell data is increasingly available, methods to analyze these data are still scarce and often treat cells as static snapshots without modeling the underlying dynamics of cell state, said Daniel Burkhardt, Ph.D., cofounder of Open Problems in Single-Cell Analysis and Machine Learning Scientist at Cellarity. New machine learning algorithms are needed to learn the rules that govern complex cell regulatory processes so we can predict how cell state changes over time. We hope these new algorithms can augment the value of existing or future single-modality datasets, which can be cost effectively generated at higher quality to streamline and accelerate research.

In 2021, Cellarity partnered with Open Problems collaborators to develop the first benchmark competition for multimodal single-cell data integration using a first-of-its-kind multi-omics benchmarking dataset (NeurIPS 2021). This dataset was the largest atlas of the human bone marrow measured across DNA, RNA, and proteins and was used to predict one modality from another and learn representations of multiple modalities measured in the same cells. The 2021 competition saw winning submissions from both computational biologists with deep single-cell expertise and machine learning practitioners for whom this competition marked their first foray into biology. This translation of knowledge across disciplines is expected to drive more powerful algorithms to learn fundamental rules of biology.

For 2022, Cellarity and Open Problems are extending the challenge to drive innovation in modeling temporal single-cell data measured in multiple modalities at multiple time points. For this years competition, Cellarity generated a 300,000-cell time course dataset of CD34+ hematopoietic stem and progenitor cells (HSPC) from four human donors at five time points. HSPCs are stem cells that give rise to all other cells in the blood throughout adult life, and a 10-day time course captures important biology in CD34+ HSPCs. Being able to solve the prediction problems over time is expected to yield new insights into how gene regulation influences differentiation.

Entries to the competition will be accepted until November 15, 2022. For more information, visit the competition page on Kaggle.

About Open Problems in Single Cell Analysis

Open Problems in Single-Cell Analysis was founded in 2020 bringing together academic, non-profit, and for-profit institutions to accelerate innovation in single-cell algorithm development. An explosion in single-cell analysis algorithms has resulted in more than 1,200 methods published in the last five years. However, few standard benchmarks exist for single-cell biology, both making it difficult to identify top performing algorithms and hindering collaboration with the machine learning community to accelerate single-cell science. Open Problems is a first-of-its-kind international consortium developing a centralized, open-source, and continuously updated framework for benchmarking single-cell algorithms to drive innovation and alignment in the field. For more information, visit https://openproblems.bio/.

About Cellarity

Cellaritys mission is to fundamentally transform the way medicines are created. Founded by Flagship Pioneering in 2017, Cellarity has developed unique capabilities combining high-resolution data, single cell technologies, and machine learning to encode biology, predict interventions, and purposefully design breakthrough medicines. By focusing on the cellular changes that underlie disease instead of a single target, Cellaritys approach uncovers new biology and treatments and is applicable to a vast array of disease areas. The company currently has programs underway in metabolic disease, hematology, immuno-oncology, and respiratory disease. For more info, visit http://www.cellarity.com.

About Flagship Pioneering

Flagship Pioneering conceives, creates, resources, and develops first-in-category bioplatform companies to transform human health and sustainability. Since its launch in 2000, the firm has, through its Flagship Labs unit, applied its unique hypothesis-driven innovation process to originate and foster more than 100 scientific ventures, resulting in more than $100 billion in aggregate value. To date, Flagship has deployed over $2.9 billion in capital toward the founding and growth of its pioneering companies alongside more than $19 billion of follow-on investments from other institutions. The current Flagship ecosystem comprises 41 transformative companies, including Denali Therapeutics (NASDAQ: DNLI), Evelo Biosciences (NASDAQ: EVLO), Foghorn Therapeutics (NASDAQ: FHTX), Moderna (NASDAQ: MRNA), Omega Therapeutics (NASDAQ: OMGA), Rubius Therapeutics (NASDAQ: RUBY), Sana Biotechnology (NASDAQ: SANA), and Seres Therapeutics (NASDAQ: MCRB).

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Cellarity Releases Novel, Open-Source, Single-Cell Dataset and Invites the Machine Learning and Computational Biology Communities to Develop New...

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that targets motor neurons, gradually bereaving patients of their ability to control muscle movements. Scientists discovered more than 50 potential disease-causing genes and linked several cellular pathways to ALS, but the syndromes diverse clinical and genetic nature make it difficult to predict and interfere with disease progression.1

Researchers discovered a T cell population in mice that mirrors ALS-4 disease progression.

In a recent study published in Nature, Laura Campisi, Ivan Marazzi, and colleagues at Icahn School of Medicine at Mount Sinai discovered an immune cell signature in patients with early onset ALS (ALS-4) that mirrors disease progression and may contribute to neuronal death.2 These findings could have significant implications for ALS diagnostics, prognostics, and therapeutics.

Laura Campisi joined Marazzis laboratory wanting to better understand how the body mounts immune responses. She set out to molecularly profile activated immune cells and discovered several immunity regulators, including SENATAXIN (SETX). Because SETX mutations cause ALS-4, Campisi wondered if ALS might join the suite of other neurodegenerative diseases such as narcolepsy, Alzheimers disease, and Parkinsons disease that scientists recently connected to the immune system.3,4,5,6

To test whether the immune system plays a role in ALS-4 disease progression, Campisi turned to a mouse model that carries the most common human SETX mutation.7 She replaced their mutated hematopoietic stem cells (HSCs)progenitors that form immune cellswith wildtype ones and found that they protected against disease. In contrast, replacing healthy HSCs with SETXmutant ones in wildtype mice did not cause disease. This set of experiments showed that mutant HSCs and their progeny contribute to disease, but do not cause disease on their own. This is extremely strong preclinical evidence that forms a basis for pharmaceutically targeting these cells, said David Gate, an assistant professor of neurology at Northwestern University, who was not involved in this study.

Campisi and her colleagues next characterized the immune system in pre-symptomatic mice and discovered an ALS-specific immune cell signature: ALS-4 mice contained more CD8+ T cells in their blood and cerebrospinal fluid (CSF) prior to symptom onset, and this cell population continued to expand as the disease progressed. While Campisis team faced pandemic-related difficulties in recruiting enough ALS-4 patients to confirm these findings, they are now teaming up with clinicians to expand their preclinical trials. We want to follow this [T cell] population in patients to see if they express specific markers that can predict if and when the disease progresses, Campisi said.

My hypothesis is that the T cells are autoreactive, so they are reacting against a cellular antigen.Laura Campisi, Icahn School of Medicine at Mount Sinai

To find what these T cells responded to, Campisi sequenced them and found that nearly all cells expressed the same T cell receptor, suggesting they bind the same antigen. The problem is that it is very difficult to find the antigen. I dont think it is an infection because [the] mice live in a pathogen-free facility. My hypothesis is that the T cells we found are autoreactive, so they are reacting against a cellular antigen, Campisi said.

Given that ALS targets motor neurons, Campisi wondered if the ALS-4 T cells promoted disease progression because they react to and are activated by a protein in the brain. To test this hypothesis, Campisi injected ALS-4mice with brain cancer cells that express neuronal antigens to see if the T cell population would react and confer protection against the cancer type. It was pretty striking: the tumors became so big in wildtype mice that I had to stop the experiment, but the [mutant] mice that were in the same cage were completely fine, their tumor was not growing, Campisi said. In contrast, there was no protection against skin-related cancer cells that she injected as a control. The T cells that infiltrated the ALS-4 mices brain tumors expressed the same T cell receptor as cells found in their CSF. While Gate cautions that cancer cells typically express many newly created neoantigens, Campisis data suggests that the T cell population likely recognizes a brain cell-related antigen.

Campisis challenge now lies in identifying the actual antigen and therapeutically targeting these T cells to slow and restrict the disease course. In ALS, you probably have a defect that starts with neurons, triggering a cascade of events. So, even if you restore what is wrong in neurons, we have to [also] target the other players, Campisi said.

References

Excerpt from:
Mutant T Cells That Drive Amyotrophic Lateral Sclerosis (ALS) Progression May React To a Brain Antigen - The Scientist

Raising the dead sounds like science fiction, but a team of medical scientists at Yale University have managed to achieve just thatat least on a cellular level. They successfully revived cells from pigs that were dead for an hour, as a Nature study published August 3 reports. While the study authors emphasize the technology is ages away from being used on people, the work could eventually help keep human tissues alive longer, increasing the supply of viable organs for transplants.

These cells are functioning hours after they should not be, said Nenad Sestan, a professor of neuroscience and comparative medicine at Yale and lead author of the study, in a news briefing per CNN. And what this tells us is that the demise of cells can be halted. And their functionality restored in multiple vital organs. Even one hour after death.

Sestan and his colleagues received 100 pigs from a local breeder. They placed the pigs on ventilators and shocked the animals hearts to induce cardiac arrest. An hour after confirmed death, the Yale scientists used two systems to pump blood back into the bodiesan ECMO machine removed carbon dioxide and added oxygenated blood to one group, while another device, called OrganEx, pumped artificial blood back into the other. That fluid entered the blood vessels of the dead pigs, where synthetic forms of hemoglobin and other molecules protected cells from degradation and stopped blood clots.

After six hours, the researchers recorded signs of oxygen recirculating into the pigs tissues. A heart scan confirmed signs of electrical activity in the heart of pigs on the OrganEx machine, though those organs did not fully restart. Elsewhere, there were signs of business as usual, too: The livers of the deceased pigs resumed production of a protein called albumin. Additionally, the cells of other vital organs were responsive to glucose, suggesting the pigs metabolic processes were working again.

The experiment is not the first time scientists have tried to redefine life and death. In the early 20th century, there were attempts to reboot the brains of deceased monkeys. And in 2019, neuroscientists reanimated the brains of decapitated pigs four hours after they died in a slaughterhouse.

Studies such as these raise questions about what it means to be dead. We presume death is a thing, it is a state of being, Nita Farahany, a Duke law professor who studies ethical, legal and social implications of emerging technologies, told The New York Times. Are there forms of death that are reversible? Or not?

The findings also call into question who is considered legally dead, especially as medicine adapts to make cardiac death one day reversible. People tend to focus on brain death, but theres not much consensus on when cardiac death occurs, Arthur Caplan, a bioethicist at New York University told Nature News. This paper brings that home in an important way.

Ethical challenges abound if technology such as this were applied to people. In 2016 Indias medical research council, citing ethical concerns, blocked a planned clinical trial that aimed to revive brain-dead people to a minimally conscious state using a mix of stem cells and other techniques.

While the current study showed no signs of brain activity in the pigs, the researchers observed the heads, necks, and torsos moved. If brain activity was restored, there is no telling how functional or conscious the pigs would be, making it one of a slew of ethical questions scientists will need to answer as they breach this murky area of science.

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Pigs died after heart attacks. Scientists brought their cells back to life. - Popular Science

Fibrosis is the thickening of various tissues caused by the deposition of fibrillar extracellular matrix (ECM) in tissues and organs as part of the bodys wound healing response to various forms of damage. When accompanied by chronic inflammation, fibrosis can go into overdrive and produce excess scar tissue that can no longer be degraded. This process causes many diseases in multiple organs, including lung fibrosis induced by smoking or asbestos, liver fibrosis induced by alcohol abuse, and heart fibrosis often following heart attacks. Fibrosis can also occur in the bone marrow, the spongy tissue inside some bones that houses blood-producing hematopoietic stem cells (HSCs) and can lead to scarring and the disruption of normal functions.

Chronic blood cancers known as myeloproliferative neoplasms (MPNs) are one example, in which patients can develop fibrotic bone marrow, or myelofibrosis, that disrupts the normal production of blood cells. Monocytes, a type of white blood cell belonging to the group of myeloid cells, are overproduced from HSCs in neoplasms and contribute to the inflammation in the bone marrow environment, or niche. However, how the fibrotic bone marrow niche itself impacts the function of monocytes and inflammation in the bone marrow was unknown.

Now, a collaborative team from Penn, Harvard, the Dana-Farber Cancer Institute (DFCI), and Brigham and Womens Hospital has created a programmable hydrogel-based in vitro model mimicking healthy and fibrotic human bone marrow. Combining this system with mouse in vivo models of myelofibrosis, the researchers demonstrated that monocytes decide whether to enter a pro-inflammatory state and go on to differentiate into inflammatory dendritic cells based on specific mechanical properties of the bone marrow niche with its densely packed ECM molecules. Importantly, the team found a drug that could tone down these pathological mechanical effects on monocytes, reducing their numbers as well as the numbers of inflammatory myeloid cells in mice with myelofibrosis. The findings are published in Nature Materials.

We found that stiff and more elastic slow-relaxing artificial ECMs induced immature monocytes to differentiate into monocytes with a pro-inflammatory program strongly resembling that of monocytes in myelofibrosis patients, and the monocytes to differentiate further into inflammatory dendritic cells, says co-first author Kyle Vining, who recently joined Penn. More viscous fast-relaxing artificial ECMs suppressed this myelofibrosis-like effect on monocytes. This opened up the possibility of a mechanical checkpoint that could be disrupted in myelofibrotic bone marrow and also may be at play in other fibrotic diseases. Vining will be appointed assistant professor of preventive and restorative sciences in the School of Dental Medicine and the Department of Materials Sciences in the School of Engineering and Applied Science, pending approval by Penn Dental Medicines personnel committees and the Provosts office.

Vining worked on the study as a postdoctoral fellow at Harvard in the lab of David Mooney. Our study shows that the differentiation state of monocytes, which are key players in the immune system, is highly regulated by mechanical changes in the ECM they encounter, says Mooney, who co-led the study with DFCI researcher Kai Wucherpfennig. Specifically, the ECMs viscoelasticity has been a historically under-appreciated aspect of its mechanical properties that we find correlates strongly between our in vitro and the in vivo models and human disease. It turns out that myelofibrosis is a mechano-related disease that could be treated by interfering with the mechanical signaling in bone marrow cells.

Mooney is also the Robert P. Pinkas Family Professor of Bioengineering at Harvard and leads the Wyss Institutes Immuno-Materials Platform. Wucherpfennig is director of DFCIs Center for Cancer Immunotherapy Research, professor of neurobiology at Brigham and Harvard Medical School, and an associate member of the Broad Institute of MIT and Harvard. Mooney, together with co-senior author F. Stephen Hodi, also heads the Immuno-engineering to Improve Immunotherapy (i3) Center, which aims to create new biomaterials-based approaches to enhance immune responses against tumors. The new study follows the Centers road map. Hodi is director of the Melanoma Center and The Center for Immuno-Oncology at DFCI and professor of medicine at Harvard Medical School.

Gleaning mechanical bone marrow failureThe mechanical properties of most biological materials are determined by their viscoelastic characteristics. Unlike purely elastic substances like a vibrating quartz, which store elastic energy when mechanically stressed and quickly recover to their original state once the stress is removed, slow-relaxing viscoelastic substances also have a viscous component. Like the viscosity of honey, this allows them to dissipate stress under mechanical strain by rapid stress relaxation. Viscous materials are thus fast-relaxing materials in contrast to slow-relaxing purely elastic materials.

The team developed an alginate-based hydrogel system that mimics the viscoelasticity of natural ECM and allowed them to tune the elasticity independent from other physical and biochemical properties. By tweaking the balance between elastic and viscous properties in these artificial ECMs, they could recapitulate the viscoelasticity of healthy and scarred fibrotic bone marrow, whose elasticity is increased by excess ECM fibers. Human monocytes placed into these artificial ECMs constantly push and pull at them and in turn respond to the materials mechanical characteristics.

Next, the team investigated how the mechanical characteristics of stiff and elastic hydrogels compared to those in actual bone marrow affected by myelofibrosis. They took advantage of a mouse model in which an activating mutation in a gene known as Jak2 causes MPN, pro-inflammatory signaling in the bone marrow, and development of myelofibrosis, similar to the disease process in human patients with MPN. When they investigated the mechanical properties of bone marrow in the animals femur bones, using a nanoindentation probe, the researchers measured a higher stiffness than in non-fibrotic bone marrow. Importantly, we found that the pathologic grading of myelofibrosis in the animal model was significantly correlated with changes in viscoelasticity, said co-first author Anna Marneth, who spearheaded the experiments in the mouse model as a postdoctoral fellow working with Ann Mullally, a principal investigator at Brigham and DFCI, and another senior author on the study.

Targeting dysregulated bone marrow mechanicsAn important question was whether monocytes response to the mechanical impact of the fibrotic bone marrow niche could be therapeutically targeted. The researchers focused on an isoform of the phosphoinositide 3-kinase (PI3K)-gamma protein, which is specifically expressed in monocytes and closely related immune cells. PI3K-gamma is known for regulating the assembly of a cell-stiffening filamentous cytoskeleton below the cell surface that expands in response to mechanical stress, which the team also observed in monocytes encountering a fibrotic ECM. When they added a drug that inhibits PI3K-gamma to stiff elastic artificial ECMs, it toned down their pro-inflammatory response and, when given as an oral treatment to myelofibrosis mice, significantly lowered the number of monocytes and dendritic cells in their bone marrow.

This research opens new avenues for modifying immune cell function in fibrotic diseases that are currently difficult to treat. The results are also highly relevant to human cancers with a highly fibrotic microenvironment, such as pancreatic cancer, says Wucherpfennig.

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University of Pennsylvania: Deconstructing the mechanics of bone marrow disease | India Education - India Education Diary

Cell Culture Media, Sera, and Reagents Market: Introduction

According to the report, the globalcell culture media, sera, and reagents marketwas valued at US$6.1 Bnin 2020 and is projected to expand at a CAGR of10.3%from 2021 to 2031. Cell culture media, also known as growth media, is an umbrella term that encompasses any gel or liquid created to support cellular growth in an artificial environment. It is a combination of compounds and nutrients designed to support cellular growth.

Cell culture reagents include cell culture media, media supplements, and sterile reagents. Common cell culture reagents are antibiotics and amino acid supplements. Serum is a key component for growing and maintaining cells in culture. It contains a mixture of proteins, hormones, minerals, and other growth factors. It is added to media as a growth supplement, and specialized forms can be used for different experimental conditions.

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Increase in Demand for Cost-effective and Highly Efficient Cell Culture Products to Drive Global Market

Cell culture technology is applied in various domains such as research, academics, bioprocessing & manufacturing, cell therapy, and regenerative medicines. Leading pharmaceutical companies are expanding their capabilities into biopharmaceutical manufacturing in order to leverage high market potential and due to increase in demand for these products.

Rise in demand for cost-effective and highly efficient cell culture products such as bioreactors, media, reagents, and sera for the production of high-yield cell lines has led to an increase in the number of new product launches. This factor is anticipated to provide lucrative opportunities in the global cell culture market during the forecast period.

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Contract Research & Manufacturing and Focus on Stem Cell Research to Propel Market

The cell culture media, sera, and reagents market is witnessing a shift toward contract manufacturing & research, primarily due to significant capital investment and specificity of each biomanufacturing process. For instance, cell cultures could be 2D, 3D, rotating, continuously stirred, batch-fed, and several other types. The expanding scope of cell culture into areas such as stem cell research is boosts the growth of the global market. Rise in importance of stem cell therapy is underlined by the fact that these therapies help treat the cause of the disease, while conventional treatment methods help in managing only the symptoms. This requires advanced capabilities in terms of capital, equipment, and resources; hence, contract manufacturing presents an economically beneficial solution.

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Major Players in Global Cell Culture Media, Sera, and Reagents Market

Key players operating in the global cell culture media, sera, and reagents market include Thermo Fisher Scientific, Inc., Merck KGaA, Cytiva (Danaher Corporation), Becton, Dickinson and Company, Corning Incorporated, HiMedia Laboratories, FUJIFILM Irvine Scientific, Inc., InvivoGen, SeraCare (LGC Clinical Diagnostics, Inc.), and Lonza. Each of these players has been profiled in the cell culture media, sera, and reagents market report based on parameters such as company overview, financial overview, business strategies, application portfolio, business segments, and recent developments.

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The Role of Cell Culture Media, Sera, and Reagents Market Industry Growth, Competitors Analysis, New Technology, Trends and Forecast 2021 2031 -...

In short, stem cells initiate the production of new tissue cells, which can then replace their diseased counterparts.

Mesenchymal stem cells (MSCs) are adult stem cells found in many areas of the body such as bone marrow. The unique thing about these cells is their compatibility with a range of tissues such as bone, cartilage, muscle, or fat. MSCs respond to injury or disease by migrating to these damaged areas, where they restore tissue function by replacing the damaged cells.

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It has recently been shown that the success of MSCs relies on their ability to release cell signals their mechanism to initiate tissue regeneration. These signals are packaged into extracellular vehicles (EVs) which are essentially bubbles of information. These are released by MSCs and taken up by the injured or diseased tissue cells to kickstart their inbuilt process of regeneration.

Through funding from the Royal Society of Edinburgh, research has started into the development of artificial EVs as a viable alternative to cell therapy. These EVs will contain the key molecules released by stem cells when they are responding to injury cues in the body.

The power to induce tissue regeneration would provide a significant new tool in biomedical treatment, such as incorporating EVs into synthetic hydrogels within a wound dressing to encourage and accelerate healing.

Within the lab setting, we have been able to manipulate stem cell cultures to produce EVs with different signal make-ups, and accurately identify their properties.

Controlling and identifying the different make-ups contained in EV signals which in turn induce different cell responses is crucial if we want to operationalise their use in medicine.

We now aim to synthesise artificial vesicles, or bubbles, for different clinical problems, such as, for example, bubbles with potent wound-healing properties that would help our ability to use new artificial stem cell therapy.

The research is underway and it is showing promise that we may be able to harness the regenerative power of stem cells in the near future.

An artificial EV-based approach also has several advantages over stem cell-based therapies, such as having increased potency and greater consistency in treatment, and at a lower cost to carry out.

Both inside and on the surface of the body, we would have the ability to induce a process vital to medical treatment we work with every day and, in turn, open a whole new avenue of possibilities in biomedical science.

Dr Catherine Berry is a reader in the Centre for the Cellular Microenvironment at the University of Glasgow, and a recipient of the Royal Society of Edinburghs personal research fellowship in 2021. This article expresses her own views. The RSE is Scotland's national academy, bringing great minds together to contribute to the social, cultural and economic well-being of Scotland. Find out more at rse.org.uk and @RoyalSocEd.

Link:
Stem cells: Could we gain the power to induce cell regeneration? Dr Catherine Berry - The Scotsman

Stem Cells Market: Introduction

According to the report, the globalstem cells marketwas valued at US$11.73Bn in 2020 and is projected to expand at a CAGR of10.4%from 2021 to 2028. Stem cells are defined as specialized cells of the human body that can develop into various different kinds of cells. Stem cells can form muscle cells, brain cells and all other cells in the body. Stem cells are used to treat various illnesses in the body.

North America was the largest market for stem cells in 2020. The region dominated the global market due to substantial investments in the field, impressive economic growth, increase in incidence of target chronic diseases, and technological progress. Moreover, technological advancements, increase in access to healthcare services, and entry of new manufacturers are the other factors likely to fuel the growth of the market in North America during the forecast period.

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Asia Pacific is projected to be a highly lucrative market for stem cells during the forecast period. The market in the region is anticipated to expand at a high CAGR during the forecast period. High per capita income has increased the consumption of diagnostic and therapy products in the region. Rapid expansion of the market in the region can be attributed to numerous government initiatives undertaken to improve the health care infrastructure. The market in Asia Pacific is estimated to expand rapidly compared to other regions due to shift in base of pharmaceutical companies and clinical research industries from developed to developing regions such as China and India. Moreover, changing lifestyles and increase in urbanization in these countries have led to a gradual escalation in the incidence of lifestyle-related diseases such as cancer, diabetes, and heart diseases.

Technological Advancements to Drive Market

Several companies are developing new approaches to culturing or utilizing stem cells for various applications. Stem cell technology is a rapidly developing field that combines the efforts of cell biologists, geneticists, and clinicians, and offers hope of effective treatment for various malignant and non-malignant diseases. The stem cell technology is progressing as a result of multidisciplinary effort, and advances in this technology have stimulated a rapid growth in the understanding of embryonic and postnatal neural development.

Adult Stem Cells Segment to Dominate Global Market

In terms of product type, the global stem cells market has been classified into adult stem cells, human embryonic stem cells, and induced pluripotent stem cells. The adult stem cells segment accounted for leading share of the global market in 2020. The capability of adult stem cells to generate a large number of specialized cells lowers the risk of rejection and enables repair of damaged tissues.

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Autologous Segment to Lead Market

Based on source, the global stem cells market has been bifurcated into autologous and allogenic. The autologous segment accounted for leading share of the global market in 2020. Autologous stem cells are used from ones own body to replace damaged bone marrow and hence it is safer and is commonly being practiced.

Regenerative Medicines to be Highly Lucrative

In terms of application, the global stem cells market has been categorized into regenerative medicines (neurology, oncology, cardiology, and others) and drug discovery & development. The regenerative medicines segment accounted for major share of the global market in 2020, as regenerative medicine is a stem cell therapy and the medicines are made using stem cells in order to repair an injured tissue. Increase in the number of cardiac diseases and other health conditions drive the segment.

Therapeutics Companies Emerge as Major End-users

Based on end-user, the global stem cells market has been divided into therapeutics companies, cell & tissue banks, tools & reagents companies, and service companies. The therapeutics companies segment dominated the global stem cells market in 2020. The segment is driven by increase in usage of stem cells to treat various illnesses in the body. Therapeutic companies are increasing the utilization of stem cells for providing various therapies. However, the cell & tissue banks segment is projected to expand at a high CAGR during the forecast period. Increase in number of banks that carry out research on stem cells required for tissue & cell growth and elaborative use of stem cells to grow various cells & tissues can be attributed to the growth of the segment.

Regional Analysis

In terms of region, the global stem cells market has been segmented into North America, Europe, Asia Pacific, Latin America, and Middle East & Africa. North America dominated the global stem cells market in 2020, followed by Europe. Emerging markets in Asia Pacific hold immense growth potential due to increase in income levels in emerging markets such as India and China leading to a rise in healthcare spending.

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Competition Landscape

The global stem cells market is fragmented in terms of number of players. Key players in the global market include STEMCELL Technologies, Inc., Astellas Pharma, Inc., Cellular Engineering Technologies, Inc., BioTime, Inc., Takara Bio, Inc., U.S. Stem Cell, Inc., BrainStorm Cell Therapeutics, Inc., Cytori Therapeutics, Inc., Osiris Therapeutics, Inc., and Caladrius Biosciences, Inc.

Stem Cells Market, by Application

Stem Cells Market, by End-user

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Stem Cells Market to Expand at a CAGR of 10.4% from 2021 to 2028 Travel Adventure Cinema - Travel Adventure Cinema

Wilmington, Delaware, United States, July 18, 2022 (GLOBE NEWSWIRE) -- Transparency Market Research Inc.: The market value of the global cell separation technologies market is estimated to be over US$ 20.3 Bn by 2031, according to a research report by Transparency Market Research (TMR). Hence, the market is expected expand at a CAGR of 11.9% during the forecast period, from 2022 to 2031.

According to the TMR insights on the cell separation technologies market, the prevalence of chronic disorders including obesity, diabetes, cardiac diseases, cancer, and arthritis is being increasing around the world. Some of the key reasons for this situation include the sedentary lifestyle of people, increase in the older population, and rise in cigarette smoking and alcohol consumption across many developed and developing nations. These factors are expected to help in the expansion of the cell separation technologies market during the forecast period.

Players in the global cell separation technologies market are increasing focus on the launch of next-gen products. Hence, they are seen increasing investments in R&Ds. Moreover, companies are focusing on different strategies including acquisitions and strengthening their distribution networks in order to stay ahead of the competition.

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As per the Imperial College London, chronic diseases are expected to account for approximately 41 million deaths per year, which seven out of 10 demises worldwide. Of these deaths, approximately 17 million are considered to be premature. Hence, surge in cases of chronic diseases globally is resulting into increased need for cellular therapies in order to treat such disease conditions, which, in turn, is boosting the investments toward R&Ds, creating sales opportunities in the cell separation technologies market.

Cell Separation Technologies Market: Key Findings

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Cell Separation Technologies Market: Growth Boosters

Cell Separation Technologies Market: Regional Analysis

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Cell Separation Technologies Market: Key Players

Some of the key players profiled in the report are:

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Cell Separation Technologies Market Segmentation

Modernization of healthcare in terms of both infrastructure and services have pushed the healthcare industry to new heights, Stay Updated with Latest Healthcare Research Reports by Transparency Market Research:

Cell Culture Market: Rise in outsourcing activities and expansion of biopharmaceutical manufacturers are expected to drive the cell culture market during the forecast period

Cell Culture Media, Sera, and Reagents Market: The global cell culture media, sera, and reagents market is majorly driven by growth and expansion of biotechnology & pharmaceutical companies and academic & research institutes.

Stem Cells Market: The global stem cells market is majorly driven by rising applications of stem cells in regenerative medicines. Increase in the number of chronic diseases such as cardiac diseases, diabetes, cancer, etc.

Cell Line Authentication and Characterization Tests Market: Increase in the geriatric population and surge in incidence of chronic diseases are projected to drive the global cell line authentication and characterization tests market.

CAR T-cell Therapy Market: The CAR T-cell therapy market is expected to clock a CAGR of 30.6% during the assessment period. The CAR T-cell therapy is known as a revolutionary treatment option for cancer, owing to its remarkably effective and durable clinical responses.

Cell & Tissue Preservation Market: Rise in investments in the field of regenerative medicine research is estimated to propel the market. Human blood, tissues, cells, and organs own the capability to heal damaged tissues and organs with long-term advantages.

Placental Stem Cell Therapy Market: Placental stem cell therapy market is driven by prominence in treatment of age-related disorders/diseases and increase in awareness about stem cell therapies are projected to drive the global market in the near future.

Biotherapeutics Cell Line Development Market: The market growth will be largely driven by research and development activities due to which, new solutions and technologies have gradually entered the market.

About Transparency Market Research

Transparency Market Research, a global market research company registered at Wilmington, Delaware, United States, provides custom research and consulting services. Our exclusive blend of quantitative forecasting and trends analysis provides forward-looking insights for thousands of decision makers. Our experienced team of Analysts, Researchers, and Consultants use proprietary data sources and various tools & techniques to gather and analyze information.

Our data repository is continuously updated and revised by a team of research experts, so that it always reflects the latest trends and information. With a broad research and analysis capability, Transparency Market Research employs rigorous primary and secondary research techniques in developing distinctive data sets and research material for business reports.

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Cell Separation Technologies Market Expands with Rise in Prevalence of Chronic Diseases, States TMR Study - GlobeNewswire