Category Health/Medical

How ‘Superbug’ E. coli clones take over human Gut

The researchers investigated how and why a clone of E. coli called ST131 – dubbed a ‘superbug’ because it is resistant to multiple drugs – has become the major cause of drug resistant E. coli infections

A ‘superbug’ clone of E. coli has evolved to prevent itself from becoming so dominant that it could potentially wipe out the bacteria from existence, scientists led by the University of Birmingham have discovered.

The researchers investigated how and why a clone of E. coli called ST131 – dubbed a ‘superbug’ because it is resistant to multiple drugs – has become the major cause of drug resistant E. coli infections, but not so dominant that it has wiped out other clones that do not have multi-drug resistance.

Escherichia coli (E...

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Proofreading the book of life: Gene Editing made Safer

The graphic illustrates the technique described in the new study. A version of the Cas9 protein used in CRISPR gene editing has been mutated. While this protein, seen in blue, retains its proper functioning, it remains “immunosilent”–hidden from predation as a foreign entity by the immune system’s T cells (seen in brown).
Credit: Graphic by Jason Drees

Scientists describe a method of rendering the gene editing tool CRISPR-Cas9 ‘immunosilent,’ potentially allowing the editing and repair of genes to be accomplished reliably and stealthily...

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Protecting Damaged Hearts with microRNAs

Fig. 4
\miR-19a/19b promotes cardiomyocyte proliferation after myocardial infarction.

New research advances the possibility of regenerating cardiac tissue after a heart attack. Once the heart is fully formed, the cells that make up heart muscle, known as cardiomyocytes, have very limited ability to reproduce themselves. After a heart attack, cardiomyocytes die off; unable to make new ones, the heart instead forms scar tissue. Over time, this can set people up for heart failure.

New work published April 17th in Nature Communications advances the possibility of reviving the heart’s regenerative capacities using microRNAs – small molecules that regulate gene function and are abundant in developing hearts.

In 2013, Da-Zhi Wang, PhD, a cardiology researcher at Boston Children’s Hospital an...

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Synthetic Peptide can Inhibit Toxicity, Aggregation of protein in Alzheimer’s disease

a chemical structure of a peptide

Ball-and-stick model of the structure of AP407, one of the synthetic alpha sheet peptides designed by the research team to inhibit toxic oligomers of amyloid beta.Shea et al., PNAS, 2019

Researchers have developed synthetic peptides that target and inhibit the small, toxic protein aggregates that are thought to trigger Alzheimer’s disease. Neurons in the human brain make a protein called amyloid beta. Such proteins on their own, called monomers of amyloid beta, perform important tasks for neurons. But in the brains of people with Alzheimer’s disease, amyloid beta monomers have abandoned their jobs and joined together. First, they form oligomers – small clumps of up to a dozen proteins – then longer strands and finally large deposits called plaques...

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