Lifeboat Foundation

Summary: Researchers have identified 2,000 genes in humans linked to longevity. The genes are associated with biological mechanisms that drive the prolongation of life in mammals, including DNA repair, coagulation, and immune response.

Source: UPF Barcelona.

What determines the life expectancy of each species? This is a fundamental and highly complex question that has intrigued the field of research throughout history. From the evolutionary point of view, the major cause of these differences between species lies in their ecological adaptations. For example, life expectancy is longer in species adapted to living in trees, underground, or with large body mass, since all these adaptations reduce mortality by predation.

Youthereum talking about rejuvenation, funding, there is a history lesson here but the modern look starts at 38:01.

My overview of the history of partial reprogramming — a novel approach to epigenetic rejuvenation that uses short bursts of Yamanaka factors expression to periodically roll back the epigenetic state of cells to a younger pattern.

A newly discovered antibody was able to neutralize not only all strains of COVID-19, but other coronaviruses known to cause respiratory infections in humans — a potential silver bullet for a whole class of deadly, flu-like viruses.

Mutant viruses: As viruses spread, they undergo tiny genetic mutations, and when we find a unique version of the virus, we call it a new strain.

Occasionally, new strains appear that can spread more easily, evade the immune system, or cause more severe disease.

The groups also explained why in previous studies by other scientists, the chromatin appeared to fill the cell nuclei. “When scientists plate cells on a glass slide in order to study them under a microscope, they change their volume and physically flatten them. This may perturb some of the forces governing chromatin arrangement and reduce the distance between the upper part of the nucleus to its base,” Safran explains.

If you open a biology textbook and run through the images depicting how DNA is organized in the cell’s nucleus, chances are you’ll start feeling hungry; the chains of DNA would seem like a bowl of ramen: long strings floating in liquid. However, according to two new studies—one experimental and the other theoretical—that are the outcome of the collaboration between the groups of Prof. Talila Volk of the Molecular Genetics Department and Prof. Sam Safran of the Chemical and Biological Physics Department at the Weizmann Institute of Science, this image should be reconsidered. Clarifying it is essential since DNA’s spatial arrangement in the nucleus can affect the expression of genes contained within the DNA molecule, and hence the proteins found in the cell.

This story began when Volk was studying how mechanical forces influence cell nuclei in the muscle and found evidence that muscle contractions had an immediate effect on gene expression patterns. “We couldn’t explore this further because existing methods relied on imaging of chemically preserved cells, so they failed to capture what happens in the cell nuclei of an actual working muscle,” she says.

Continue reading “Novel imaging method reveals a surprising arrangement of DNA in the cell’s nucleus” »

A genomic analysis of lung cancer in people with no history of smoking has found that a majority of these tumors arise from the accumulation of mutations caused by natural processes in the body. This study was conducted by an international team led by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), and describes for the first time three molecular subtypes of lung cancer in people who have never smoked.

These insights will help unlock the mystery of how lung cancer arises in people who have no history of smoking and may guide the development of more precise clinical treatments. The findings were published September 6 2021, in Nature Genetics.

“What we’re seeing is that there are different subtypes of lung cancer in never smokers that have distinct molecular characteristics and evolutionary processes,” said epidemiologist Maria Teresa Landi, M.D., Ph.D., of the Integrative Tumor Epidemiology Branch in NCI’s Division of Cancer Epidemiology and Genetics, who led the study, which was done in collaboration with researchers at the National Institute of Environmental Health Sciences, another part of NIH, and other institutions. “In the future we may be able to have different treatments based on these subtypes.”

To Sheng-Ying Pao, the power of reframing CRISPR lies in what is absolutely ordinary: paper. In CRISPaper, Pao revisited a cultural past in the ancient art of papermaking.

Over thousands of years, farmers painstakingly converted the wild rice plant into a staple crop. Today, researchers are using CRISPR to change genes to optimize grain yield. However, rice is more than food. In ancient China, it was used to make paper.

Continue reading “CRISPaper: Understanding CRISPR Gene-Editing through Art” »

Learn More.

Ian Bremmer.

If you could cure genetic diseases by editing DNA sequences, would you?

Continue reading “CRISPR gene editing and the human race” »

International research team isolates DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

The cumulative effect of reduced PTPN2 activity on both mechanisms was an elevated fluid loss. The researchers proved this defect could be reversed by treating cells lacking PTPN2 with recombinant -; or synthetic -; matriptase.

A team of researchers led by a biomedical scientist at the University of California, Riverside, has identified a novel mechanism by which loss-of-function mutations in the gene PTPN2, found in many patients with inflammatory bowel disease, or IBD, affect how intestinal epithelial cells maintain a barrier.

The intestinal epithelium, a single layer of cells, plays a critical role in human health by providing a barrier while also allowing nutrient and water absorption. Intestinal epithelial cells are needed for regulating immune function, communicating with the intestinal microbiota, and protecting the gut from pathogen infection -; all of which critically depend on an intact epithelial barrier.

Continue reading “Scientists identify novel mechanism that links genetic defect in IBD patients to gut leakiness” »