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Who has heard of mitochondrial medicine?


“We know that increased rates of mtDNA mutation cause premature aging,” said Bruce Hay, Professor of biology and biological engineering at the California Institute of Technology. “This, coupled with the fact that mutant mtDNA accumulates in key tissues such as neurons and muscle that lose function as we age, suggests that if we could reduce the amount of mutant mtDNA, we could slow or reverse important aspects of aging.”

This brings us to the second major development relevant to mitochondria in disease — that genetic technology is now at a point where the targeted removal of the problem mitochondrial genes can become the basis for clinical intervention. This is the implication of research that Hay and colleagues both at Caltech and the University of California at Los Angeles described in a paper published in the journal Nature Communications.

Fixing body tissues by knocking out genes that prevent bad mitochondrial from being ousted in a timely fashion might sound like science fiction, but that’s where things are going and it’s part of a growing trend of what’s being described as mitochondrial medicine.

Summary: Study reports SARS-CoV-2, the virus that causes COVID-19, was well suited to making the jump from animals to humans by shapeshifting as it gained the ability to infect human cells. The virus’s ability to infect humans occurred via exchanging gene fragments from a coronavirus that infected pangolins. The species-to-species transmission was a result of the ability of SARS-CoV-2 to bind to host cells through alterations to its genetic material.

Source: Duke University

A team of scientists studying the origin of SARS-CoV-2, the virus that has caused the COVID-19 pandemic, found that it was especially well-suited to jump from animals to humans by shapeshifting as it gained the ability to infect human cells.

VIENNA — We all know that one person who can eat whatever they like and never gain a pound. Ice cream at 2 in the morning? Bring it on. A third, or fourth, slice of pizza? Sure, why not. For the rest of us, the genetic perks that these individuals enjoy can be frustrating to say the least. Now, a groundbreaking new international study appears to have zeroed in on the so-called “skinny gene” that help keep such individuals thin.

Scientists from Austria, Canada, and Estonia say that lower, or deficient, levels of the gene Anaplastic Lymphoma Kinase (ALK) are significantly linked to skinniness and bodily resistance to weight gain.

Most research projects focusing on weight loss and gain search for genes that cause obesity. This study is novel due to the fact that it focuses specifically for a gene linked to thinness instead.

The most common organism in the oceans, and possibly on the entire planet, is a family of single-celled marine bacteria called SAR11. These drifting organisms look like tiny jelly beans and have evolved to outcompete other bacteria for scarce resources in the oceans.

We now know that this group of thrives despite—or perhaps because of—the ability to host viruses in their DNA. A study published in May in Nature Microbiology could lead to new understanding of viral survival strategies.

University of Washington oceanographers discovered that the that dominate seawater, known as Pelagibacter or SAR11, hosts a unique virus. The virus is of a type that spends most of its time dormant in the host’s DNA but occasionally erupts to infect other cells, potentially carrying some of its host’s along with it.

Circa 2017 face_with_colon_three


For the first time, scientists have found a genetic mutation that appears to offer a measure of protection against some of the biological effects of ageing.

And, as far as we know, it looks like the only community in the world known to harbour it is an Old Order Amish community living in Indiana.

The mutation can occur on one or both copies of a gene called SERPINE1. It’s known that when both gene copies are mutated, it can lead to a rare genetic bleeding disorder — and the Amish community in question is susceptible to it.

Whereas textbooks depict metabolism in perfect homeostasis, disturbances occur in real life. One particularly relevant disturbance, caused by excess food and alcohol consumption and exacerbated by genetics, is reductive stress. New work by Goodman et al. identifies a biomarker of reductive stress and uses a gene therapy solution in mice. This work suggests how exercise and an accessible nutritional technology can synergistically increase catabolism and relieve reductive stress.

Sirtuins, telomeres, A.I. experiment with vitamin A and personalized medicine, a bit of everything here.


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Not all viruses set out to cause widespread death and sickness — some have the potential to fight cancer, according to new research.

Researchers from Hokkaido University in Japan have genetically engineered adenoviruses, which is a family of viruses that cause mild symptoms, to replicate inside cancer cells and kill them, according to a new paper in the journal Cancers.

To do this, Fumihiro Higashino, a molecular oncologist, and his team inserted adenylate-uridylate-rich elements (AREs) from two human genes — a stabilizing element found in a type of macromolecule present in all biological cells — into two strains of the virus to help specifically attack cancer cells.