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Category: biotech/medical – Page 651

This is a SURVEY result of Rapamycin users. Overall, it’s really good for you. It has not had a true trial as it is off-patent so it’s harder to get rich from it. Low dose use has minimal side effects if any at all. Many patients can get off-label prescription from their doctor.

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Here Prof Kaeberlein provides some updates on rapamycin, in particular the results from the survey based trial that his team ran and thoughts on next steps for the supplement.

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According to new research in the journal Immunity, T cells have a nuclear receptor doing something very odd—but very important—to help them fight pathogens and destroy cancer cells. This receptor, called retinoic acid receptor alpha (RARα), is known to control gene expression programs in the nucleus, but it also now appears to operate outside the cell nucleus to coordinate the early events triggered at the cell surface that lead to T cell activation.

Scientists wouldn’t normally expect to see a nuclear receptor such as RARα playing this role outside the cell nucleus. And yet the new findings suggest T cells cannot begin to fight disease without a form of RARα on the scene in the cytoplasm.

“Cytoplasmic retinoic acid receptors turn out to be central for a T cell to link sensing at the with downstream signaling cascades and gene expression programs that transform the T cell to become an active fighter,” says Professor Hilde Cheroutre, Ph.D., who led the new study at La Jolla Institute for Immunology (LJI) with LJI Assistant Professor Samuel Myers, Ph.D., LJI Professor Mitchell Kronenberg, Ph.D., and LJI Professor Emeritus Amnon Altman, Ph.D.

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Researchers from Monash University in Melbourne and The University of Western Australia have demonstrated how a reprogramming method imitates embryonic epigenetic reset. Transient naive treatment (TNT) reprogrammed human induced pluripotent stem (hiPS) cells that are molecularly and functionally more similar to human embryonic stem (hES) cells than primed hiPS cells, which are more like cells in the post-implantation embryo. This research suggests that TNT reprogramming has the potential to set a new standard for therapeutic and biomedical uses.

The research article “Transient naive reprogramming corrects hiPS cells functionally and epigenetically” was published online today in Nature.

“Our work shows that TNT reprogramming is a practical and scalable approach to overcome these intrinsic characteristics of hiPS cells, which is important for the clinical delivery of this technology,” stated the authors. “We foresee TNT reprogramming becoming a new standard for biomedical and therapeutic applications.”

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DISCLOSURE: Longevity. Technology (a brand of First Longevity Limited) has been contracted by the company featured in this article to support its current funding round. Qualifying investors can find out more via the Longevity. Technology investor portal.

This week’s Longevity Summit Dublin is in full swing, bringing together experts from around the world, fostering collaboration and knowledge exchange in the pursuit of solutions to extend human healthspan. One of the speakers during today’s sessions was Stanford professor and surgeon, Dr Vinit Mahajan, who is also Chief Medical Advisor for longevity biotech startup Mitrix Bio.

In his address to summit delegates in Dublin, Mahajan presented the company’s fascinating preclinical technology: bioreactor-grown mitochondria designed to be transplanted into the human body to regenerate organs, reverse age-related disease, and support other longevity therapies.

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Since 2014, the ALS Ice Bucket Challenge has inspired more than 17 million people to raise $115 million for The ALS Association, which has funded over 500 research projects with the money. Because of that boost, the first drug to treat ALS has been approved by the FDA, other new treatments are in testing, and scientists have been able to identify several genes that are connected to the disease.

While mutations in a gene called NEK1 have only been associated with around two percent of ALS cases, it is one of the primary genetic causes of ALS that have been revealed so far. Now investigators have learned more about how NEK1 mutations can lead to ALS, a disease in which the motor neurons that control movement degenerate and die, which causes paralysis and eventually, death. The work has been reported in Science Advances.

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Researchers at the National Heart, Lung, and Blood Institute at NIH, Bethesda, have discovered a potential breakthrough for people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), marked by extreme exhaustion, post-exertional malaise and cognitive issues.

In a paper, “WASF3 disrupts and may mediate exercise intolerance in /,” published in PNAS, the team details the influence of increased WASF3 proteins on the assembly of mitochondrial proteins, hampering energy production.

The study focused on a woman (S1) who experienced severe long-term fatigue. Measuring her muscles for phosphocreatine regeneration after exercise revealed a significant delay in mitochondrial ATP synthesis capacity. This discovery was followed up with a cell assay which found increased phospho-activation of an enzyme in a signaling pathway (MPAK).

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A recent study published in Nature Machine Intelligence examines a novel deep-learning method known as BigMHC, which can predict when the immune system will respond to triggers from cancer-related protein fragments, thus killing the tumors. This study was led and conducted by a team of researchers at Johns Hopkins University and holds the potential to develop personalized cancer immunotherapies and vaccines.

Rendition of cytotoxic CD8+ T-cells identifying cancer cells via receptor binding neoantigens. (Credit: Image generated by DALL-E 2 from OpenAI)

“Cancer immunotherapy is designed to activate a patient’s immune system to destroy cancer cells,” said Dr. Rachel Karchin, who is a professor of biomedical engineering, oncology and computer science at Johns Hopkins University, and a co-author on the study. “A critical step in the process is immune system recognition of cancer cells through T-cell binding to cancer-specific protein fragments on the cell surface.”

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A new study led by University of Maryland physicists sheds light on the cellular processes that regulate genes. Published in the journal Science Advances, the paper explains how the dynamics of a polymer called chromatin—the structure into which DNA is packaged—regulate gene expression.

Through the use of machine learning and statistical algorithms, a research team led by Physics Professor Arpita Upadhyaya and National Institutes of Health Senior Investigator Gordon Hager discovered that can switch between a lower and higher mobility state within seconds. The team found that the extent to which chromatin moves inside cells is an overlooked but important process, with the lower mobility state being linked to gene expression.

Notably, (TFs)—proteins that bind specific DNA sequences within the chromatin polymer and turn on or off—exhibit the same mobility as that of the piece of chromatin they are bound to. In their study, the researchers analyzed a group of TFs called , which are targeted by drugs that treat a variety of diseases and conditions.

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We’ve explored bioelectricity in cells. We’ve looked at bioelectricity within the human body. Now, functional use of “electrical engineering” is being found in the realms between.

Physicists learn about electrostatics, the laws governing stationary charges. Then they learn about electrodynamics, the laws governing moving charges. Biologists are finding that life utilizes both systems of laws at all scales, from within the cell to tissues, organs, and entire organisms. Here are some recent discoveries in the emerging science of bioelectricity.

How does that tick jump from its twig onto your clothing as you walk through brush? The answer, says Current Biology, is by hopping on an electrostatic bullet train. A cow or other host animal walking through the bushes carries a net static charge. The tick, regardless of its own charge polarity, is “pulled by these electric fields across air gaps of several body lengths.”

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Researchers have determined a new feature of how the natural ends of our chromosomes are protected from harmful outcomes.

In a new study, University of Michigan researchers looked at how the DNA damage recognition process seems to know the difference between harmful DNA breaks that need repair versus the natural ends of chromosomes, called , that need to be left alone.

“If possible, you repair it, and if you can’t repair it, then the cell dies. You don’t want to keep dividing with broken DNA. That’s what happens in a normal cell, and that’s a good thing,” said Jayakrishnan Nandakumar, a professor of molecular, cellular and developmental biology.

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