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Category: genetics – Page 15

In a shocking turn of events, a surgeon operating on a cancer patient managed to contract the deadly disease in what is believed to be an unprecedented case. The doctor was performing surgery on a 32-year-old German man suffering from a rare type of cancer when he accidentally “transplanted” the disease into himself.

This occurred when cells from the patient’s tumor seeped into a cut on the surgeon’s hand. Despite immediate disinfection and bandaging, the 53-year-old medic noticed a hard lump developing at the base of his middle finger five months later.

A hand specialist identified the lump as a malignant tumor genetically identical to cancer suffered by his former patient. Doctors treating him concluded that he had contracted cancer when his patient’s tumor cells seeped into the cut.

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Image credit: GrumpyBeere – Pixabay

Researchers used a refined method of ancestry analysis utilizing ancient DNA. This study represents a significant advancement in our understanding of historical population movements.

Researchers can trace human migration through DNA changes, but it’s challenging when historical groups are genetically similar.

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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.

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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.

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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.

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

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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.

Continue reading “Bedbugs Are Stronger Than Ever and Scientists Just Found Out Why” | >

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.

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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.

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