Li et al. report that Edwardsiella piscicida employs HigA, an anti-toxin protein, to facilitate the diversion of tryptophan metabolism to the kynurenine pathway, rather than the serotonin pathway, by directly activating IDO1 in a T6SS-dependent manner as a cross-kingdom effector. The serotonin-level fluctuation modulates host intestinal histological damage and bacterial infection.
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The Janus kinase (Jak)/signal transducer and activating protein (STAT) pathways mediate the intracellular signaling of cytokines in a wide spectrum of cellular processes. They participate in physiologic and inflammatory cascades and have become a major focus of research, yielding novel therapies for immune-mediated inflammatory diseases (IMID). Genetic linkage has related dysfunction of Tyrosine kinase 2 (Tyk2)—the first member of the Jak family that was described—to protection from psoriasis. Furthermore, Tyk2 dysfunction has been related to IMID prevention, without increasing the risk of serious infections; thus, Tyk2 inhibition has been established as a promising therapeutic target, with multiple Tyk2 inhibitors under development.
October 21–22, 2025 (Online) 🌿
Dear colleagues and friends.
We are pleased to invite you to the International Scientific Conference “Anti-Aging: Science and Practice of Healthy Longevity”, organized by the Gerontology Section of the Moscow Society of Naturalists (MOIP) at Lomonosov Moscow State University, with the support of the Gerontology Society of the Ural Branch of the Russian Academy of Sciences (URAN).
📅 Dates: October 21–22, 2025 🕛 Time: 12:00–16:00 (Moscow time) 💻 Format: Online participation (free of charge) 🗣️ Working language: Russian.
🔹 October 21 — “Hypoxic Training (Therapy): Modern Aspects of Healthy Longevity Medicine” 🔹 October 22 — “Fundamental and Clinical Gerontology as the Basis of Healthy Longevity Medicine”
The conference will feature leading scientists from Russia, Germany, Belarus, Kyrgyzstan and other countries. Topics include: • Hypoxic therapy and adaptive mechanisms; • Geroprotection and the biology of aging; • Epigenetic reprogramming and cellular rejuvenation; • Applied aspects of active and healthy longevity.
🔗 Connection links: • Day 1 (October 21): https://my.mts-link.ru/j/38630705/5798697072
In a study published in Neuron, a research team at the Department of Neurology at Massachusetts General Hospital, aimed to understand how immune cells of the brain, called microglia, contribute to Alzheimer’s disease (AD) pathology. It’s known that subtle changes, or mutations, in genes expressed in microglia are associated with an increased risk for developing late-onset AD.
The study focused on one such mutation in the microglial gene TREM2, an essential switch that activates microglia to clean up toxic amyloid plaques (abnormal protein deposits) that build up between nerve cells in the brain. This mutation, called T96K, is a “gain-of-function” mutation in TREM2, meaning it increases TREM2 activation and allows the gene to remain super active.
The researchers explored how this mutation impacts microglial function to increase risk for AD. The team generated a mutant mouse model carrying the mutation, which was bred with a mouse model of AD to have brain changes consistent with AD. They found that in female AD mice exclusively, the mutation strongly reduced the capability of microglia to respond to toxic amyloid plaques, making these cells less protective against brain aging.
The genus Tobamovirus belongs to the family Virgaviridae, and the genome consists of monopartite, positive, single-strand RNA. Most species contain four open reading frames encoding four essential proteins. Transmission occurs primarily through mechanical contact between plants, and in some cases, via seed dispersal. Tobamovirus fructirugosum (tomato brown rugose fruit virus, ToBRFV), the most recently described species in the genus, was first reported in 2015. It overcame genetic resistance that had been effective in tomato for sixty years, causing devastating losses in tomato production worldwide, and highlights the importance of understanding Tobamovirus genomic variation and evolution. In this study, we measured and characterized nucleotide variation for the entire genome and for all species in the genus Tobamovirus.
Cancer cells are known to reawaken embryonic genes to grow. A new study reveals the disease also hijacks the proteins, or “editors,” that control how those genes are read.
The findings, published in the journal Nucleic Acids Research, help explain why tumors grow so fast and adapt so well, and may point the way to new treatments.
Embryonic cells have to grow fast and must be able to transform into many different tissue types. The cells rely on genetic programs that are eventually switched off as tissues mature. Cancer reawakens these programs, giving the disease embryonic-like potential to fuel growth.
Modern toads (Bufonidae) are among the most successful amphibians on the planet, a diverse group of more than 600 species that are found on every continent except Antarctica. But just how did they conquer the world? An international team of researchers set out to find the answer and discovered the toads’ global success was due to their toxic glands and geological timing.
Modern toads are a type of frog with a stout, squat body, relatively short legs, toothless mouths and a thick, dry, warty skin. One of their most distinctive features is a large gland behind each eye that secretes a poison to deter predators. They originated in South America and are found in diverse habitats like deserts and rainforests.
To find out how they got from South America to almost every other continent, the scientists analyzed fresh DNA samples from 124 species from Africa, Asia, Europe, South America, North America and Oceania. They combined this with existing genetic data from hundreds of other species. Using powerful computer models to process the genetic information, they traced the geological spread of toads over millions of years, identifying when survival features like their poisonous glands evolved and when they branched out to form new species.
Approximately 20% of American adolescents experience a mental health disorder each year, a number that has been on the rise. Genetics and life events contribute, but because so many factors are involved, and because their influence can be subtle, it’s been difficult for researchers to generate effective models for predicting who is most at risk for mental health problems.
A new study from researchers at Washington University School of Medicine in St. Louis provides some answers. Published Sept. 15 in Nature Mental Health, it mined an enormous set of data collected from pre-teens and teens across the U.S. and found that social conflicts—particularly family fighting and reputational damage or bullying from peers—were the strongest predictors of near-and long-term mental health issues.
The research also revealed sex differences in how boys and girls experience stress from peer conflict, suggesting that nuance is needed when assessing social stressors in teens.