By preventing ice formation while cooling human livers below freezing, researchers have managed to extend the viable lifespan of donated livers threefold.
Telomerase's reputation is that it has an important role in maintaining the ability of stem cells to divide through maintaining telomeres, the structures at the tips of chromosomes that shorten with each replication cycle.
Researchers at the University of California at San Diego have used a strategy of "rock-paper-scissors" to engineer more durable synthetic circuits into bacteria.
Three separate research teams have failed to replicate a 2016 primate study showing that treatment with a primate version of monoclonal antibody Entyvio (vedolizumab, Takeda Pharmaceutical Co. Ltd.), led to prolonged suppression of viremia in SHIV-infected monkeys.
Researchers at the Christian Albrechts University of Kiel and the MRC London Institute of Medical Science have developed a way to screen four-way interactions between genetically simple hosts, their microbiome, nutrients and drugs.
The hype surrounding artificial intelligence (AI) can make it sound like the technology has all the answers. But from a scientific perspective, one of the technology's biggest strengths is that it can ask better questions.
TRK inhibitors, like essentially all targeted therapies, are vulnerable to resistance mutations, and several resistance mutations to Vitrakvi and the recently approved Rozlytrek have been described. The most common form of resistance to targeted therapies, and the only mechanisms that have been described for TRK inhibitors to date, are due to mutations in the target itself. Now, researchers at Memorial Sloan-Kettering Cancer Center have described resistance to TRK inhibitors that occurred due to activation of the MAP kinase (MAPK) pathway.
Investigators at Stanford University have created a panel of isogenic iPSC-derived neurons with various mutations of amyloid precursor protein (APP) and presenilin (PSEN), and used it to demonstrate that accumulation of APP beta C-terminal fragments (beta-CTFs), but not of amyloid beta, correlated with endosomal dysfunction and could be improved by inhibiting beta-secretase (BACE-1). Genetic evidence clearly implicates APP misprocessing in Alzheimer's disease (AD), and amyloid beta plaques are the disease's major anatomical calling card, which has led to a focus on therapeutic targeting of the latter. However, that therapeutic targeting has failed multiple times, and the evidence linking amyloid beta to AD is weaker than that for APP. Recently, endosomal dysfunction has been proposed as "another plausible underlying pathological mechanism," leading the authors to investigate the causes of endosomal dysfunction in their cell lines. They showed that endosomal dysfunction, which leads to deficits in intracellular transport, was correlated with changes in beta-CTF but not amyloid beta.
