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The distinct population of endothelial cells that line blood vessels in the insulin-producing “islets” of the human pancreas have been notoriously difficult to study, but Weill Cornell Medicine investigators have now succeeded in comprehensively detailing the unique characteristics of these cells.

The resulting atlas advances basic research on the biology of the pancreas and could lead to new treatment strategies for diabetes and other pancreatic diseases.

In the study, published in Nature Communications, the researchers devised a set of methods for rapidly isolating and profiling endothelial cells called ISECs (islet-specific endothelial cells) from donor pancreases.

Vimentin is a type III intermediate filament (IF) protein normally expressed in cells that develop into connective tissue, blood vessels, and lymphatic tissue (mesenchymal cells). Despite being widely studied, its role in tumor growth and progression remains unexplored.

A team of researchers at Queen Mary University of London have discovered how a small change in the vimentin protein can make more aggressive. The work is published in the journal eLife.

By modifying a specific amino acid cysteine to serine residue at position 328 in vimentin, they discovered that this mutation disrupted the protein’s interaction with the cell’s structural network. Remarkably, the mutated vimentin induced aggressive cancer-like behavior in breast cancer cells, including faster cell growth, migration, and invasion accompanied by reduced .

Harvard University and the Chinese University of Hong Kong researchers have developed a technique that increases the solubility of drug molecules by up to three orders of magnitude. This could be a breakthrough in drug formulation and delivery.

Over 60% of pharmaceutical drug candidates suffer from poor water solubility, which limits their bioavailability and therapeutic viability. Conventional techniques such as particle-size reduction, solid dispersion, lipid-based systems, and mesoporous confinement often have drug-specific limitations, can be costly to implement, and are prone to stability issues.

The newly developed approach addresses these issues by leveraging the competitive adsorption mechanism of drug molecules and water on engineered silica surfaces. It avoids chemical modification of drug molecules or using additional solubilizing agents to achieve solubility, potentially replacing multiple drug delivery technologies.

A joint research team from the LKS Faculty of Medicine (HKUMed) and the Faculty of Science at the University of Hong Kong has uncovered an unexpected interaction between chemotherapeutic agents and a crucial efficacy marker.

Sylvain Lesné, a neuroscientist accused of image manipulation in a seminal Alzheimer’s disease paper in, resigned last week from his tenured professorship at the University of Minnesota Twin Cities (UMN). The move follows a 2.5-year investigation in which the university found problems with several other papers on which Lesné is an author. The study has already been pulled, but the school has asked that four more of Lesné’s papers be retracted.

The resignation, effective 1 March, was first reported by the. Lesné did not respond to a request for comment. UMN spokesperson Jake Ricker said, “The university has identified data integrity concerns impacting several publications and has been in touch with those journals to recommend retraction of the publications, where appropriate.”

As a postdoc, Lesné worked in the lab of neuroscientist Karen Ashe. In 2006, they published a study in that seemed to show a cause-effect relationship between a protein—amyloid-beta *56—and memory loss in rats. Those symptoms seemed to resemble the memory problems that afflict Alzheimer’s patients.

Mitochondria are well known as the powerhouses of the cell. These crucial, energy generating organelles even have their own little genomes, and make their own proteins. Mutations in mitochondrial DNA (mtDNA) can cause some serious diseases, and dysfunctional mitochondria have been associated with a wide variety of health disorders. Researchers have also found links between mitochondrial defects and diabetes.

There are special cells in the pancreas known as beta cells, which is where insulin is generated. When these cells are lost due to an autoimmune attack, type 1 diabetes arises. Some studies have determined that there are abnormal mitochondria in the beta cells of some diabetes patients.