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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.

Customizable magnetic iron nanowires pinpoint and track the movements of target cells.

Living cells inside the body could be placed under surveillance—their location and migration noninvasively tracked in real time over many days—using a new method developed by researchers at KAUST.

The technique uses magnetic core-shell iron nanowires as nontoxic contrast agents, which can be implanted into live cells, lighting up those cells’ location inside a living organism when scanned by magnetic resonance imaging (MRI). The technique could have applications ranging from studying and treating cancer to tracking live-cell medical treatments, such as stem cell therapies.

A Bristol academic has achieved a milestone in statistical/mathematical physics by solving a 100-year-old physics problem – the discrete diffusion equation in finite space.

The long-sought-after solution could be used to accurately predict encounter and transmission probability between individuals in a closed environment, without the need for time-consuming computer simulations.

In his paper, published in Physical Review X, Dr. Luca Giuggioli from the Department of Engineering Mathematics at the University of Bristol describes how to analytically calculate the probability of occupation (in discrete time and discrete space) of a diffusing particle or entity in a confined space – something that until now was only possible computationally.

GUANGZHOU/TOKYO — Tech startups in Shenzhen, known as China’s Silicon Valley, are set to experience a range of outcomes as the novel coronavirus pandemic appears to near its end, with some seeing their businesses thrive while others face headwinds following significantly reduced investment.


AI and robot companies feel positive impact, while some face harsh climate.

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.

ROME (Reuters) — The new coronavirus is losing its potency and has become much less lethal, a senior Italian doctor said on Sunday.

“In reality, the virus clinically no longer exists in Italy,” said Alberto Zangrillo, the head of the San Raffaele Hospital in Milan in the northern region of Lombardy, which has borne the brunt of Italy’s coronavirus contagion.

“The swabs that were performed over the last 10 days showed a viral load in quantitative terms that was absolutely infinitesimal compared to the ones carried out a month or two months ago,” he told RAI television.

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.