Category Health/Medical

A schematic showing how a human monoclonal antibody containing a loop structure (CDR-H3) inspired by antibodies found naturally in camels can bind to matrix metalloproteinase 14, which has been shown to play a significant role in several types of cancer.

Researchers at the University of California, Riverside have camels and llamas to thank for their development of a new cancer treatment that is highly selective in blocking the action of faulty matrix metalloproteinases (MMPs). MMPs are a group of 26 closely related proteinases (enzymes that break down other proteins) that are essential in tissue regeneration and other normal cellular processes. However, when a tumor grows, certain MMPs are over-produced, allowing cancer cells to spread to other parts of the body.

Assistant professor Xin Ge...

Reductions in Atherogenic Lipids and Major Cardiovascular Events A Pooled Analysis of 10 ODYSSEY Trials Comparing Alirocumab With Control Credit: Imperial College London

Although previous studies have suggested lowering cholesterol levels may be associated with a lower risk of heart attack, recent evidence has questioned whether very low levels are beneficial.
In the latest study, led by scientists at Imperial College London, researchers analysed data from over 5,000 people taking part in cholesterol-lowering trials. These studies utilised a new therapy to reduce cholesterol to much lower levels than previously possible.

The scientists found that dropping cholesterol to the lowest level possible – to levels similar to those we were born with – reduced the risk of heart attack, stroke or fa...

Highlights •Systems-level approach reveals GATA4 roles in human cardiac development and function •Heterozygous GATA4 missense mutation impairs cardiac gene program •GATA4 G296S mutation disrupts TBX5 genome occupancy at cardiac super-enhancers •PI3K signaling is a key “hub” in the GATA4 gene regulatory network

Scientists linked a single gene mutation to 2 types of heart disease: one causes a hole in the heart of infants, and the other causes heart failure. Using cells donated by a family with the mutation, the researchers gained insight into congenital heart disease, heart development, and healthy heart function...

Highlights •Partial reprogramming erases cellular markers of aging in mouse and human cells •Induction of OSKM in progeria mice ameliorates signs of aging and extends lifespan •In vivo reprogramming improves regeneration in 12-month-old wild-type mice

In mice carrying a mutation leading to premature aging, reprogramming of chemical marks in the genome, ie epigenetic marks, reduced many signs of aging in the mice and extended their lifespan on average from 18 weeks to 24. The study suggests epigenetic changes drive the aging process, and that those changes may be malleable. “We did not correct the mutation that causes premature aging in these mice,” says Juan Carlos Izpisua Belmonte, a professor in the Salk Institute of Biological Science’s Gene Expression Laboratory...