Scientists have identified a critical breakdown in the cellular machinery that produces proteins in aging brains.
Category: biotech/medical – Page 283
Malicious npm Package Posing as OpenClaw Installer Deploys RAT, Steals macOS Credentials
Cybersecurity researchers have discovered a malicious npm package that masquerades as an OpenClaw installer to deploy a remote access trojan (RAT) and steal sensitive data from compromised hosts.
The package, named “@openclaw-ai/openclawai,” was uploaded to the registry by a user named “openclaw-ai” on March 3, 2026. It has been downloaded 178 times to date. The library is still available for download as of writing.
JFrog, which discovered the package, said it’s designed to steal system credentials, browser data, crypto wallets, SSH keys, Apple Keychain databases, and iMessage history, as well as install a persistent RAT with remote access capabilities, SOCKS5 proxy, and live browser session cloning.
Chemistry in Pictures: Glowing with pride
“It looks like a tiny solar system. But instead of planets, it’s a snapshot of my research journey in the lab,” says Sadiya Tanga, a chemistry graduate student at Ashoka University. Tanga’s work has focused on a type of drug molecule called proteolysis-targeting chimeras, or PROTACs for short. PROTACs have two active ends, one that grabs a target protein and another that grabs a molecular flag that tells the cell to break down the whole assembly as waste. “Each glowing flask and sphere holds a different compound I worked hard to design and synthesize,” Tanga says. “The colors you see are from parts of the molecules that shine under UV light.”
Scientists discover hidden brain cells that may stop Alzheimer’s tau buildup
Scientists have uncovered a surprising new role for little-known brain cells called tanycytes that may influence the development of Alzheimer’s disease. These specialized cells appear to help remove toxic tau protein from the brain by transporting it from the cerebrospinal fluid into the bloodstream. When tanycytes become damaged or dysfunctional, tau can accumulate in the brain, a hallmark of Alzheimer’s.
Circulating MALAT1 in Preeclampsia and Association With Cardiometabolic Risk
RESEARCH ARTICLE: Circulating MALAT1 in Preeclampsia and Association With Cardiometabolic Risk @tovelekva
BACKGROUND: Preeclampsia is a hypertensive disorder affecting 2% to 8% of pregnancies. Women with a history of preeclampsia have an increased risk of cardiovascular disease. The long noncoding RNA MALAT1 is shown to regulate inflammatory responses linked to cardiovascular disease. MALAT1 is decreased in preeclampsia placentas and may have a cis-regulatory function on neighboring RNAs. METHODS: Expression of MALAT1, NEAT1, mascRNA, SCYL1, and FRMD8 was assessed in peripheral blood mononuclear cells, and MALAT1 in plasma and extracellular vesicles, at 22 to 24 and 36 to 38 weeks of gestation in healthy (n=214) and preeclampsia (n=37) women from the STORK cohort study (STORe barn og Komplikasjoner, translated as Large Babies and Complications) and at 5-year follow-up in women with and without history of preeclampsia (n=29; n=271).
Recent pandemic viruses jumped to humans without prior adaptation, study finds
A new University of California San Diego study published in Cell challenges a long-standing assumption about how animal viruses become capable of sparking human epidemics and pandemics. Using a phylogenetic, genome-wide analysis across multiple viral families, researchers report that most zoonotic viruses—infectious pathogens that spread from animals to humans, including the cause of COVID-19—do not show evidence of special evolutionary adaptation before spilling over into humans.
“This work has direct relevance to the ongoing controversy around COVID-19 origins,” said Joel Wertheim, Ph.D., senior author and professor of medicine in the Division of Infectious Diseases and Global Public Health at UC San Diego School of Medicine.
“From an evolutionary perspective, we find no evidence that SARS-CoV-2 was shaped by selection in a laboratory or prolonged evolution in an intermediate host prior to its emergence. That absence of evidence is exactly what we would expect from a natural zoonotic event—and it represents another nail in the coffin for theories invoking laboratory manipulation.”
Present state and future of screening for atrial fibrillation: a state-of-the-art review
AFib AF
Atrial fibrillation (AF) is the most common arrhythmia and is a leading cause of stroke and heart failure yet often remains undiagnosed. Screening has been proposed to identify asymptomatic AF and initiate preventive treatment, but evidence for reduction in hard clinical endpoints such as stroke and heart failure remains inconclusive. In this state-of-the-art review, we critically examine major AF screening trials across opportunistic, systematic and consumer-driven strategies, focusing on design features, population selection, monitoring strategies and outcomes. Variability in trial design, particularly in randomisation timing, participation rates and intensity of monitoring, significantly affects both AF detection and clinical outcomes. Systematic screening shows promise, but many trials were underpowered for hard outcomes.
Understanding the Role of Gut Microbial Enzyme in CMD
Studies of the putative functional relationships between the gut microbiota and host cardiometabolic diseases (CMDs), including atherosclerosis, diabetes, and metabolic dysfunction-associated steatohepatitis (MASH), have garnered unprecedented attention in recent years.1,2 Although causality has not yet been unequivocally established, interventions targeting the gut microbiota, such as antibiotics and fecal microbiota transplantation, have been demonstrated to improve health.3 Although such interventions show unique clinical value in specific scenarios such as recurrent Clostridioides difficile infection,4 they typically show interindividual variability in efficacy and raise safety concerns, altogether underscoring the need for safer, more precise, and targeted strategies.5 A deeper understanding of the molecular mechanisms by which gut microbiota exert their functions in health and disease will be crucial to such goals.
Enzymes are intracellular proteins that perform defined biological processes, and enzyme-targeting drugs constitute a significant proportion of current therapeutics.6 In recent years, growing evidence has indicated that gut microbial enzymes are key mediators of microbiota-derived functions.7 Such enzymes contribute to CMDs pathogenesis primarily through 3 mechanisms: generating bioactive metabolites that influence intestinal barrier integrity, inflammation, and other essential physiological processes; regulating the homeostasis of critical host metabolites, such as ceramides and cholesterol; and metabolizing xenobiotics derived from diet and drugs, thereby modulating nutrient absorption and drug efficacy.
Given the complexity of the functions of gut microbiota, it is arguably overly simplistic to categorize them as symbionts that are probiotic or pathogenic. Rather, by identifying and characterizing key microbial enzymes, we will be able to precisely modulate gut microbiota functions in health and disease. When a clear enzymatic cause is identified, therapies targeting microbial enzymes capitalize on a function-driven mechanism. This allows for precision that is independent of taxonomy and avoids off-target consequences stemming from compositional heterogeneity of the functional microbes across individuals. The operational feasibility and druggability of these therapies are further supported by mature enzyme-based therapy development paradigms. Ultimately, enzyme-targeted interventions are expected to work alongside conventional whole-microbiota or strain-level approaches, thereby enriching the toolkit for developing gut microbiome-based therapeutics.
Why lungs age unevenly: Vulnerable cells may guide new therapies
Aging is associated with increased risk for nearly every lung disease, including acute conditions like pneumonia and chronic diseases like chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and lung cancer. Now, one of the most comprehensive analyses of human lung aging has found that not all cells age equally.
The study, published in Nature Communications, has found that certain types of lung cells are especially vulnerable to aging. The findings could inform treatments that target the defective cells, say the researchers.
“This data allows us to start thinking about lung aging not as a passive state that we have to accept, but as something that we may be able to modify with therapies and interventions,” says senior author Naftali Kaminski, MD, Boehringer Ingelheim Pharmaceuticals, Inc. Professor of Medicine (Pulmonary) at Yale School of Medicine and chief of pulmonary, critical care and sleep medicine at Yale.