Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: genetics – Page 36

Meanwhile, scientists dug into how psychedelics and MDMA fight off depression and post-traumatic stress disorders. The year was a relative setback for the psychedelic renaissance, with the FDA rejecting MDMA therapy. But the field is still gaining recognition for its therapeutic potential.

Then there’s lenacapavir, a shot that protects people from HIV. Named “breakthrough of the year” by Science, the shot completely protected African teenage girls and women against HIV infection. Another trial supported the results, showing the drug protected people who have sex with men at nearly 100 percent efficacy. The success stems from a new understanding of the protein “capsule” guarding the virus’ genetic material. Many other viruses have a similar makeup—meaning the strategy could help researchers design new drugs to fight them off too.

So, what’s poised to take the leap from breakthrough to clinical approval in 2025? Here’s what to expect in the year ahead.

Read more | >

Research reveals distinct mechanisms underlying neonatal and post-pubertal social behaviors, providing valuable insights for developing targeted early interventions.

Researchers from the University of Texas Health Science Center at San Antonio and Hirosaki University have unveiled significant findings on the development of social behaviors in fragile X syndrome, the most common genetic cause of autism spectrum disorder. The study, published in Genomic Psychiatry, highlights the effects of a specific prenatal treatment on social behaviors in mice.

The researchers found that administering bumetanide—a drug that regulates chloride levels in neurons—to pregnant mice restored normal social communication in newborn pups with the fragile X mutation. However, they also discovered an unexpected outcome: the same treatment reduced social interaction after puberty in both fragile X and typical mice. These findings shed light on the complex and developmental-stage-specific effects of interventions for fragile X syndrome.

Read more | >

We termed enhancers that gained (and maintained) H3K4me1 in obesity and WL ‘new enhancers’. Most of these ‘new enhancers’ were also active (that is, marked by H3K27ac) during obesity and/or WL (Fig. 4D). We then annotated the enhancers to their closest gene and performed a GSEA. In agreement with the promoter GSEA above, we found that the ‘new active enhancers’ were related to inflammatory signalling, lysosome activity and extracellular matrix remodelling (Fig. 4e and Extended Data Fig. 9i), indicating a persistent shift of adipocytes towards a more inflammatory and less adipogenic identity. Corroborating these results, Roh et al. had analysed H3K27ac in adipocytes of obese mice and reported impaired identity maintenance during obesity25.

To combine our findings regarding retained translational changes and epigenetic memory, we investigated whether epigenetic mechanisms, such as differentially marked promoters or enhancers, could explain the persistent translational obesity-associated changes after WL. Notably, 57–62% of downregulated and 68–75% of upregulated persistent translational DEGs after WL could be accounted for by one or more of the analysed epigenetic modalities (Fig. 4f). Overall, these results strongly suggest the presence of stable cellular, epigenetic and transcriptional memory in mouse adipocytes that persists after WL.

Read more | >

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

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

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

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

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 “Dasatinib + Quercetin: Longevity Biohacker Kenneth Scott’s Experience” | >

Link :

Ever since then, researchers have marveled at the bedbug’s resilience. No matter what kind of chemical insecticide we throw at it, they manage to survive. This is due in large part to its development of insecticide resistance. Recent research conducted by Hidemasa Bono at Hiroshima University found that a series of genetic mutations explain the bedbug’s resistance to insecticides.

To figure that out, Bono and his team took a peek at the genome of an insecticide-resistant bedbug. They then compared it to bedbug samples collected in 2010 from a hotel in Hiroshima, along with wild bedbugs dating back to the 1950s. They used a technique called long-read sequencing to create nearly free and nearly error-free genomic maps to compare the various bedbugs across time. This allowed them to see several different mutations across the three types of bedbugs.

They found that the bedbug that came from the hotel had 19,895 times more resistance to one of the most common types of insecticide, pyrethroids, than the nonresistant genome. All told, they identified 729 resistant specific mutations. Some of these mutations are related directly to DNA damage response, cell cycle regulation, and insulin metabolism.

Read more | >

Summary: A new “molecular lantern” technique allows researchers to monitor molecular changes in the brain non-invasively using a thin light-emitting probe. This innovative tool utilizes Raman spectroscopy to detect chemical changes caused by tumors, injuries, or other pathologies without altering the brain beforehand.

Unlike prior methods requiring genetic modifications, this approach analyzes natural brain tissue with high precision, offering significant potential for diagnosing and studying brain diseases. Future developments aim to integrate artificial intelligence to enhance diagnostic accuracy and explore diverse biomedical applications.

Read more | >

Background and objectives: Aging clocks are computational models designed to measure biological age and aging rate based on age-related markers including epigenetic, proteomic, and immunomic changes, gut and skin microbiota, among others. In this narrative review, we aim to discuss the currently available aging clocks, ranging from epigenetic aging clocks to visual skin aging clocks.

Methods: We performed a literature search on PubMed/MEDLINE databases with keywords including: “aging clock,” “aging,” “biological age,” “chronological age,” “epigenetic,” “proteomic,” “microbiome,” “telomere,” “metabolic,” “inflammation,” “glycomic,” “lifestyle,” “nutrition,” “diet,” “exercise,” “psychosocial,” and “technology.”

Results: Notably, several CpG regions, plasma proteins, inflammatory and immune biomarkers, microbiome shifts, neuroimaging changes, and visual skin aging parameters demonstrated roles in aging and aging clock predictions. Further analysis on the most predictive CpGs and biomarkers is warranted. Limitations of aging clocks include technical noise which may be corrected with additional statistical techniques, and the diversity and applicability of samples utilized.

Read more | >

A new study by Tel Aviv University reveals how bacterial defense mechanisms can be neutralized, enabling the efficient transfer of genetic material between bacteria. The researchers believe this discovery could pave the way for developing tools to address the antibiotic resistance crisis and promote more effective genetic manipulation methods for medical, industrial, and environmental purposes.

The study was led by Ph.D. student Bruria Samuel from the lab of Prof. David Burstein at the Shmunis School of Biomedicine and Cancer Research at Tel Aviv University’s Wise Faculty of Life Sciences. Other contributors to the research include Dr. Karin Mittelman, Shirly Croitoru, and Maya Ben-Haim from Prof. Burstein’s lab. The findings were published in the journal Nature.

The researchers explain that genetic diversity is essential for the survival and adaptation of different species in response to environmental changes. For humans and many other organisms, sexual reproduction is the primary driver of the genetic diversity required for survival. However, bacteria and other microorganisms lack such a reproduction mechanism.

Read more | >

Researchers have developed an innovative therapeutic platform by mimicking the intricate structures of viruses using artificial intelligence (AI). Their pioneering research was published in Nature on December 18.

Viruses are uniquely designed to encapsulate genetic material within spherical shells, enabling them to replicate and invade host cells, often causing disease. Inspired by these complex structures, researchers have been exploring artificial proteins modeled after viruses.

These “nanocages” mimic viral behavior, effectively delivering therapeutic genes to target cells. However, existing nanocages face significant challenges: their small size restricts the amount of genetic material they can carry, and their simple designs fall short of replicating the multifunctionality of natural viral proteins.

Read more | >