Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: genetics – Page 67

A Genetic Deficiency That Raises Susceptibility to Many Types of Flu

There are many processes and proteins that help the body fight a flu infection. One of them is known as IFITM3. Researchers have now shown that this protein can help prevent viruses from mutating after they have infected a new host. But some people are deficient in IFITM3, which can raise their risk of a severe flu infection. That deficiency is not unusual in some groups. For example, around twenty percent of Chinese people and four percent of people with European ancestry carry variants in IFITM3 that can interfere with the protein’s expression. This study has shown that these genetic variants can allow flu viruses to establish infections even when the virus is present at very low levels that would not usually cause infection. The findings have been reported in Nature Communications.

The IFITM3 (interferon-induced transmembrane protein 3) protein is part of the innate immune system, and is generated at high levels after the detection of a flu infection. It can sequester viral particles so that they are not able to replicate, which reduces the severity of flu infections. Mouse models that are IFITM3 deficient are extremely vulnerable to the flu.

Sunlight Deficiency As A Contributor To Poor Health: Roger Seheult, M.D. (‪@Medcram‬)

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD

Discount Links/Affiliates:
Blood testing (where I get my labs): https://www.ultalabtests.com/partners/michaellustgarten.

Clearly Filtered Water Filter: https://get.aspr.app/SHoPY

At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgarten.
Use Code: CONQUERAGING At Checkout.

Epigenetic, Telomere Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ6…M0&irgwc=1
Use Code: CONQUERAGING

NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/

Continue reading “Sunlight Deficiency As A Contributor To Poor Health: Roger Seheult, M.D. (‪@Medcram‬)” | >

Gene Repair Restores Brain Signal Efficiency in Autism

Summary: Autism-linked SHANK3 gene mutations disrupt not only neurons but also oligodendrocytes, essential for producing myelin, which insulates nerve fibers. This damage reduces brain signal efficiency and impairs behavior.

Using gene therapy, researchers successfully repaired these cells in a mouse model, restoring their function and myelin production. They validated their findings with human-derived stem cells, confirming similar impairments and repair mechanisms.

This discovery highlights a significant role for oligodendrocytes in autism and opens the door for innovative treatments targeting myelin dysfunction. The study underscores both the biological complexity of autism and the promise of genetic therapies for intervention.

Free Biological Age Calculator

We converted the calculations in Morgan Levine and Steve Horvath’s famous research paper on phenotypic age into a free biological age calculator.

It’s a great (cheap) alternative to $400 epigenetic age tests and means you can test more frequently to see if longevity interventions are actually…

This free biological age calculator is based on a pioneering paper by longevity experts Dr. Morgan Levine and Dr. Steve Horvath.

The paper, titled “An epigenetic biomarker of aging for lifespan and healthspan,” used some super-advanced machine learning techniques to find blood biomarkers which are significantly correlated with aging-related health outcomes, including mortality.

Essentially, they are able to use the results from this test to predict how near (or far away) you are from death.

Advances in Y chromosome analysis aid in horse breeding and conservation

Researchers at the Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) are helping uncover new information about the Y chromosome in horses, which will help owners identify optimal lineages for breeding and help conservationists preserve breed diversity.

“Because of its complex structure, the Y chromosome is much harder to sequence, making our knowledge of it far from complete,” said Dr. Gus Cothran, a professor emeritus in the VMBS’ Department of Veterinary Integrative Biosciences (VIBS). “In fact, scientists used to believe that the Y chromosome lacked genetic variety, which we believed meant that it didn’t contribute much to species diversity.”

However, Cothran’s new research collaboration, led by the University of Veterinary Medicine Vienna, has uncovered that the Y chromosome does have meaningful variation and is important for species diversity.

Humans are walking ecosystems and microbes rule their evolution

We might like to think of ourselves as autonomous entities but, in reality, we’re more like walking ecosystems, teeming with bacteria, viruses, and other microbes. It turns out that differences in these microbes might be as crucial to evolution and natural variation as genetic mutations are.

This novel perspective was discussed in a recent publication by Seth Bordenstein, director of Penn State’s One Health Microbiome Center, who is a professor of biology and entomology and holds the Dorothy Foehr Huck and J. Lloyd Huck Endowed Chair in Microbiome Sciences.

He, along with 21 colleagues from around the globe, collectively known as the Holobiont Biology Network, propose that understanding the relationships between microbes and their hosts will lead to a more profound understanding of biological variation.

Ancient Gene Reprograms Stem Cells to Create a Living Mouse

Summary: Scientists have reprogrammed mouse cells into pluripotent stem cells using a gene from choanoflagellates, single-celled organisms related to animals. This breakthrough demonstrates that key genes driving stem cell formation existed in unicellular ancestors nearly a billion years ago.

The resulting stem cells were used to create a chimeric mouse, showcasing how ancient genetic tools can integrate with modern mammalian biology. This discovery redefines the evolutionary origins of stem cells and may inform regenerative medicine advancements.

Fat cells have epigenetics-based memory: Researchers discover mechanism behind weight loss yo-yo effect

Can weight loss leave a lasting imprint on our fat cells?

Losing weight is often touted as a cornerstone of better health, particularly for people dealing with obesity and its associated health risks.

Anyone who has ever tried to get rid of a few extra kilos knows the frustration: the weight drops initially, only to be back within a matter of weeks—the yo-yo effect has struck. Researchers at ETH Zurich have now been able to show that this is all down to epigenetics.

Epigenetics is the part of genetics that’s based not on the sequence of genetic , but on small yet characteristic chemical markers on these building blocks. The sequence of building blocks has evolved over a long period of time; we all inherit them from our parents.

Epigenetic markers, on the other hand, are more dynamic: , our and the condition of our body—such as obesity—can change them over the course of a lifetime. But they can remain stable for many years, sometimes decades, and during this time, they play a key role in determining which genes are active in our cells and which are not.

A ChatGPT-Like AI Can Now Design Whole New Genomes From Scratch

Called Evo, the AI was inspired by the large language models, or LLMs, underlying popular chatbots such as OpenAI’s ChatGPT and Anthropic’s Claude. These models have taken the world by storm for their prowess at generating human-like responses. From simple tasks, such as defining an obtuse word, to summarizing scientific papers or spewing verses fit for a rap battle, LLMs have entered our everyday lives.

If LLMs can master written languages—could they do the same for the language of life?

This month, a team from Stanford University and the Arc Institute put the theory to the test. Rather than training Evo on content scraped from the internet, they trained the AI on nearly three million genomes—amounting to billions of lines of genetic code—from various microbes and bacteria-infecting viruses.

Researchers uncover new role of mutant proteins in some of the deadliest cancers

Researchers at the National Institutes of Health (NIH) and their collaborators have discovered a new way in which RAS genes, which are commonly mutated in cancer, may drive tumor growth beyond their well-known role in signaling at the cell surface.

Mutant RAS, they found, helps to kick off a series of events involving the transport of specific nuclear proteins that lead to uncontrolled , according to a study published November 11, 2024, in Nature Cancer.

RAS are the second most frequently mutated genes in cancer, and mutant RAS proteins are key drivers of some of the deadliest cancers, including nearly all , half of colorectal cancers, and one-third of lung cancers.