AFib ablation promotes LA/LV reverse remodeling.
Read this study about how combined assessment better stratifies distinct trajectories in systolic dysfunction. @MasatoOkada1105
BackgroundCatheter ablation of atrial fibrillation (AF) is an effective treatment to achieve left atrial (LA) and left ventricular (LV) reverse remodeling in patients with systolic dysfunction. However, the relationship between LA and LV reverse remodeling (LARR and LVRR) and their clinical implications remains unclear.
Liquid crystal monomers (LCMs), critical substances of liquid crystal displays in consumer electronics, are persistent pollutants, posing potential threats to marine ecosystems. Despite their bioaccumulative potential, their occurrence and possible biological impacts on marine megafauna remain understudied. We investigated LCM occurrence in Indo-Pacific humpback dolphins (Sousa chinensis) and finless porpoises (Neophocaena phocaenoides) collected from the South China Sea (2007–2021) and assessed their toxicity through in vitro assays using established dolphin cell lines. By employing robust source-tracing methodologies, we provide the first evidence that LCMs from household electronics and coastal e-waste accumulate in cetacean tissues, including blubber, muscle, and, critically, brain tissues, demonstrating blood–brain barrier penetration, a previously undocumented phenomenon of LCMs in mammalian wildlife. The temporal trend of LCM burden in porpoise blubber is correlated with shifts in global liquid crystal display production. Transcriptomic profiling revealed LCM-induced DNA damage, cell cycle arrest, and impaired cell division in cetacean cells. These findings suggest that LCMs may pose potential risks to the nervous system and other organs of marine mammals, warranting further investigation into their toxicological effects and possible implications for human health. By bridging critical gaps among everyday electronics, LCM contamination, and marine conservation, this study highlights the need for urgent regulatory actions and improved e-waste governance to mitigate ecological and public health risks.
Researchers at the Weill Institute for Cell and Molecular Biology have uncovered new evidence that two major types of gene-controlling DNA sequences, promoters and enhancers, operate with a shared logic and often perform the same jobs. The finding, made possible through a high-throughput assay they developed called QUASARR-seq, could reshape how scientists design gene therapies, interpret disease-related mutations, and understand cancer genetics.
New research from the lab of Haiyuan Yu, Tisch University Professor of Computational Biology at Cornell University’s College of Agriculture and Life Sciences (CALS) and faculty at the Weill Institute, reveals that drawing a distinction between the two classes gene controllers may be too black and white—they seem to respond to the same biological rules and act in concert.
In a study published in Nature Communications on Jan. 30 and led by Mauricio Paramo, a graduate student at the Weill Institute, the team developed a technology capable of measuring an element’s promoter and enhancer activity simultaneously, in close collaboration with the lab of John Lis, Barbara McClintock Professor of Molecular Biology & Genetics. This is significant because, until now, most technologies could measure only one function at a time, leaving open the question of whether—and how—the two activities interact inside the same DNA sequence.
Our bodies are home to millions of fungi that, for the most part, are completely harmless. However, they can sometimes change from peaceful residents into dangerous invaders. One such is Candida parapsilosis, which normally lives on our skin or in our intestinal tract but can also be found on medical devices and hospital surfaces. If it gets into a wound or onto a catheter, it can cause a serious blood infection.
Treatments typically include a class of medicines called echinocandins, but the fungus is increasingly developing resistance to them. In a new study published in the journal Microbiology Spectrum, scientists describe how it can resist our strongest drugs and evade the immune system—by undergoing cell wall remodeling.
The researchers collected four separate samples of the fungus at different stages of a persistent blood infection. They were taken from a patient who was undergoing treatment with echinocandins but was failing to get better.
Phosphoric acid is vital in both biology and modern technology because of its exceptional ability to move electrical charge. Inside the human body and in devices such as fuel cells, this small molecule helps drive essential chemical reactions.
Scientists at the Department of Molecular Physics at the Fritz Haber Institute have now uncovered new details about how it performs this task at the molecular level.
A privacy-first AI can diagnose a life-shortening hormone disorder—just from a photo of your hand.
Researchers at Kobe University have developed an artificial intelligence system that can identify a rare endocrine disorder by examining photos of the back of a person’s hand and their clenched fist. By avoiding facial images, the approach was designed with privacy in mind. The team believes this tool could help doctors refer patients to specialists more efficiently and help narrow gaps in access to care.
Acromegaly and Delayed Diagnosis.
Purified diets offer compositionally defined platforms that improve causal inference in nutrition studies. When aligned with the biological question, they enable targeted nutrient loss- and gain-of-function experiments, systematic lipid-source swaps, and the discovery of diet-microbiome-drug interactions. We recommend complementary validation in grain-based chow or human-relevant diets to maximize translational relevance.
Researchers at Stanford University engineered a modified version of the immune protein interleukin-10 (IL-10) that retains only its anti-inflammatory properties while eliminating its pro-inflammatory ones. When injected into aged mice, this modified protein stimulated the growth of new neurons and improved performance on memory and learning tasks, such as maze navigation and object recognition. The study, published in Immunity, suggests that age-related cognitive decline is linked to the accumulation of exhausted T-lymphocytes in the brain, chronic inflammation, and impaired microglial function — all of which reduce neurogenesis. The findings indicate that selectively modulating immune signaling could open new avenues for treating neurodegenerative diseases. The team plans to further investigate the protein’s mechanisms and explore ways to target specific cell types more precisely to minimize potential side effects.
A modified immune protein developed by Stanford researchers points to a novel strategy for combating age-related cognitive decline.
