Lifeboat Foundation

A new statistical tool developed by researchers at the University of Chicago improves the ability to find genetic variants that cause disease. The tool, described in a new paper published January 26, 2024, in Nature Genetics, combines data from genome-wide association studies (GWAS) and predictions of genetic expression to limit the number of false positives and more accurately identify causal genes and variants for a disease.

GWAS is a commonly used approach to identify genes associated with a range of human traits, including most common diseases. Researchers compare genome sequences of a large group of people with a specific disease, for example, with another set of sequences from healthy individuals. The differences identified in the disease group could point to genetic variants that increase risk for that disease and warrant further study.

Most human diseases are not caused by a single genetic variation, however. Instead, they are the result of a complex interaction of multiple genes, environmental factors, and host of other variables. As a result, GWAS often identifies many variants across many regions in the genome that are associated with a disease.

According to a paper submitted for peer review on January 4th, 2024, Lethal Infection of Human ACE2-Transgenic Mice Caused by SARS-CoV-2-related Pangolin Coronavirus GX_P2V(short_3UTR), a new lab-created coronavirus has the potential to kill 100% of those infected with the virus within 8 days of infection.

The mice were genetically modified to express the human ACE2 receptor. This is the receptor responsible for allowing coronavirus to gain cellular entry. The lab infected mice with a coronavirus engineered from a strain found in pangolins. Pangolins are medium-sized animals growing to 12 — 30 inches in length and have the appearance of a scale-plated anteater.

Researchers monitored the mice for signs of infection by recording body weight, taking tissue samples, and monitoring for other symptoms. By the third day post-infection, tissue samples from the infected mice had a significant amount of viral RNA in the brain, eye, lung, and nasal tissue.

“If we give it to aged mice, they rejuvenate. If we give it to young mice, they age slower. No other therapy right now can do this.”

The fountain of youth has eluded explorers for ages. It turns out the magic anti-aging elixir might have been inside us all along.

Cold Spring Harbor Laboratory (CSHL) Assistant Professor Corina Amor Vegas and colleagues have discovered that T cells can be reprogrammed to fight aging, so to speak. Given the right set of genetic modifications, these white blood cells can attack another group of cells known as senescent cells. These cells are thought to be responsible for many of the diseases we grapple with later in life.

Continue reading “The fountain of youth is … a T cell?” »

His father’s voice, the sounds of passing cars and scissors clipping his hair: An 11-year-old boy is hearing for the first time in his life after receiving a breakthrough gene therapy.

The Children’s Hospital of Philadelphia (CHOP) which carried out the treatment – a first in the United States – said in a statement Tuesday the milestone represents hope for patients around the world with hearing loss caused by genetic mutations.

Aissam Dam was born “profoundly deaf” because of a highly rare abnormality in a single gene.

The fountain of youth has eluded explorers for ages.

Summary: Researchers found that T cells can be genetically reprogrammed to target and eliminate senescent cells, which contribute to aging-related diseases. By using CAR (chimeric antigen receptor) T cells in mice, they achieved significant health improvements including lower body weight, enhanced metabolism, and increased physical activity.

This groundbreaking approach, offering long-term effects from a single treatment, could revolutionize treatments for age-related conditions like obesity and diabetes, transcending the potential of CAR T cells beyond their current use in cancer therapy.

A review discusses the current state of CRISPR-mediated genetic manipulation in human cells, animals, and plants and considers its future potential.

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhDDiscount Links: Telomere, Epigenetic Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7x…

Aging is a common phenomenon among organisms, however, lifespan tends to vary across different species to a significant extent among vertebrates themselves. Aging occurs due to the gradual increase in DNA damage, disruption of cellular organelles, deregulation of protein function, disrupted metabolism and oxidative stress [1].

Longevity. Technology: The differences in lifespan are driven by trade-offs and evolutionary trajectories in the genomes of organisms. Age-specific selection also impacts allele (variations of a gene) frequencies in a population. This in turn impacts environment-specific mortality risk and disease susceptibility. Moreover, mutational processes are influenced by life history and age in both somatic and germline cells.

Now, a new review published in Trends in Genetics discusses recent advances in the evolution of aging at population, organismal and cellular scales.

Biomedical engineers at Duke University have demonstrated that one of the most dangerous mutations found in skin cancers might moonlight as a pathway to mending a broken heart.

The genetic mutation in the protein BRAF, a part of the MAPK signaling pathway that can promote cell division, is one of the most common and most aggressive found in melanoma patients. In a new study, researchers show that introducing this mutation to rat heart tissue grown in a laboratory can induce growth.

Repairing cardiac muscle after a heart attack is the “holy grail” of heart research, complicated by the fact that heart tissue does not regenerate on its own. One potential strategy would be to persuade heart muscle cells to divide by safely delivering a therapeutic gene to patients and fully controlling its activity in the heart.