Lifeboat Foundation

Both shocking and intriguing for the possibilities of gynogenesis reproduction in which sperm is used from one creature to fertilize an egg, but its DNA is ignored.

A team of researchers working at Hungary’s National Agricultural Research and Innovation Centre, Research Institute for Fisheries and Aquaculture, has accidentally bred a new kind of fish—dubbed the sturddlefish by some observers, it is a cross between an American Paddlefish and a Russian Sturgeon. In their paper published in the journal Genes, the group describes accidentally breeding the fish and what they learned by doing so.

In the past, scientists and others have bred animals from different species for various reasons, from research to utility—mules (crossed between donkeys and horses) are considered to have beneficial traits from both animals, and ligers (a cross between lions and tigers) have helped researchers understand their respective genetic backgrounds. In this new effort, the researchers claim that they were not trying to create a new type of fish, they were instead attempting to apply gynogenesis (a type of reproduction in which sperm is used from one creature to fertilize an egg, but its DNA is ignored) using American paddlefish and Russian sturgeon. To their surprise, the eggs produced fish that grew to adults.

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Abbott’s BinaxNOW COVID-19 test will cost $5 and take 15 minutes to run. It looks for the protein on the surface of the coronavirus, instead of the genetic sequence of the virus, and doesn’t take any lab equipment. People who test negative can display that result on an app.

An international, first-of-its-kind cardiology trial used personalized genetic testing to reduce by 34 percent the number of serious adverse events following balloon angioplasty, a treatment for the most common form of heart disease.

For patients undergoing percutaneous coronary intervention (PCI)—a non-surgical procedure where physicians inflate a balloon and place a metal stent in narrowed heart arteries to improve blood flow to the heart —the choice of antiplatelet therapy can be critical to post-treatment success, and to minimize the chance of heart attack or stroke.

The TAILOR-PCI trial, co-led by principal investigators Dr. Michael Farkouh, cardiologist and Multinational Clinical Trials Chair at the Peter Munk Cardiac Centre and Dr. Naveen Pereira, Professor of Medicine and cardiologist at Mayo Clinic, studied the effectiveness of genetic-guided therapy in patients that have had PCIs when compared to conventional therapy.

Obesity is the main cause of type 2 diabetes and related chronic illnesses that together will kill more people around the globe this year than the COVID-19 coronavirus. Scientists at Joslin Diabetes Center have delivered a proof of concept for a novel cell-based therapy against this dangerous condition.

The potential therapy for obesity would transplant HUMBLE (human brown-like) fat cells, human white fat cells that have been genetically modified to become similar to heat-generating brown fat cells, says Yu-Hua Tseng, Ph.D., a Senior Investigator in Joslin’s Section on Integrative Physiology and Metabolism.

Brown fat cells burn energy instead of storing energy as white fat cells do, says Tseng, senior author on a paper about the work in Science Translational Medicine. In the process, brown fat can lower excessive levels of glucose and lipids in the blood that are linked to metabolic diseases such as diabetes.

Research looking at a possible new therapeutic approach for Alzheimer’s disease was recently published in the Journal of Neuroinflammation. The paper out of the University of Kentucky’s Sanders-Brown Center on Aging (SBCoA) is titled “Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition”. The work looked at targeting inflammation by using an antibody. Alzheimer’s disease and related dementias have no disease-modifying treatments at this time and represent a looming public health crisis given the continually growing aging population.

The paper explains that current therapeutic approaches to the treatment of Alzheimer’s disease focus on the major pathological hallmarks of the disease which are amyloid plaques and neurofibrillary tangles. They are the requirements for a diagnosis of Alzheimer’s disease. However, the authors say there has been an explosion of genetic data suggesting the risk for sporadic Alzheimer’s disease is driven by several other factors including neuroinflammation, membrane turnover and storage, and lipid metabolism.

In this study the researchers focused on triggering receptor expressed on myeloid cell-2 (TREM2). “TREM2 was identified several years ago as a gene that, when there’s a mutation, significantly increases risk of Alzheimer’s disease. The field thinks that this mutation reduces the function of the receptor, so we hypothesized that targeting TREM2 to increase its function might be a valid treatment for Alzheimer’s,” explained Donna Wilcock, SBCoA associate director.

White fat cells can be turned into energy-burning brown fat using CRISPR gene-editing technology. These engineered cells have helped mice avoid weight gain and diabetes when on a high-fat diet, and could eventually be used to treat obesity-related disorders, say the researchers behind the work.

Human adults have plenty of white fat, the cells filled with lipid that make up fatty deposits. But we have much smaller reserves of brown fat cells, which burn energy as well as storing it. People typically lose brown fat as they age or put on weight. While brown fat seems to be stimulated when we are exposed to cold temperatures, there are no established methods of building up brown fat in the body.

Researchers at the Fred Hutchinson Cancer Research Center in Seattle, USA, have used gene editing to remove latent herpes simplex virus 1 (HSV-1), also known as oral herpes.

In mice, the technique showed a 92% decrease in the latent virus – enough to keep the infection from coming back, according to the scientists. The study used two sets of “genetic scissors” to damage the virus’s DNA, fine-tune a delivery vehicle to the infected cells, and target the nerve pathways connecting the neck with the face, reaching the tissue where the virus lies dormant. The findings are published in Nature Communications.

“This is the first time that scientists have been able to go in and actually eliminate most of the herpes in a body,” said senior author Dr. Keith Jerome, Professor in the Vaccine and Infectious Disease Division at Fred Hutch. “We are targeting the root cause of the infection: the infected cells where the virus lies dormant and are the seeds that give rise to repeat infections.”

Bits of DNA known as gene drives that force themselves through a population could be use maliciously, but thankfully there is a way to detect them before they spread.

Biologists often speak of switching genes on and off to give microbes new abilities–like producing biofuels or drugs, or gobbling up environmental toxins. For the most part, though, it’s nearly impossible to turn off a gene without deleting it (which means you can’t turn it on again). This limits biologists’ ability to control how much of a particular protein a microbe produces. It also restricts bioengineers’ ability to design new microbes.

Now researchers at Boston University, led by biomedical engineering professor James Collins, have developed a highly tunable genetic “switch” that offers a greater degree of control over microbes. It makes it possible to stop the production of a protein and restart it again. The switch, which could be used to control any gene, can also act as a “dimmer switch” to finely tune how much protein a microbe would produce over time.

The researchers made a highly effective microbe “kill switch” to demonstrate the precision of the approach. For years, researchers have been trying to develop these self-destruction mechanisms to allay concerns that genetically engineered microbes might prove impossible to eradicate once they’ve outlived their usefulness. But previous kill switches haven’t offered tight enough control to pass governmental regulatory muster because it was difficult to make it turn on in all the cells in a population at the same time.