Lifeboat Foundation

Scientists have recovered DNA from a well-preserved horned lark found in Siberian permafrost. The results can contribute to explaining the evolution of sub species, as well as how the mammoth steppe transformed into tundra, forest and steppe biomes at the end of the last Ice Age.

In 2018, a well-preserved frozen bird was found in the ground in the Belaya Gora area of north-eastern Siberia. Researchers at the Centre for Palaeogenetics, a new research center at Stockholm University and the Swedish Museum of Natural History, haves studied the bird and the results are now published in the scientific journal Communications Biology. The analyses reveals that the bird is a 46,000-year-old female horned lark.

“Not only can we identify the bird as a horned lark. The genetic analysis also suggests that the bird belonged to a population that was a joint ancestor of two sub species of horned lark living today, one in Siberia, and one in the steppe in Mongolia. This helps us understand how the diversity of sub species evolves,” says Nicolas Dussex, researcher at the Department of Zoology at Stockholm University.

Cellular reprogramming can reverse the aging that leads to a decline in the activities and functions of mesenchymal stem/stromal cells (MSCs). This is something that scientists have known for a while. But what they had not figured out is which molecular mechanisms are responsible for this reversal. A study released today in STEM CELLS appears to have solved this mystery. It not only enhances the knowledge of MSC aging and associated diseases, but also provides insight into developing pharmacological strategies to reduce or reverse the aging process.

The research team, made up of scientists at the University of Wisconsin-Madison, relied on cellular reprogramming — a commonly used approach to reverse cell aging — to establish a genetically identical young and old cell model for this study. “While agreeing with previous findings in MSC rejuvenation by cellular reprogramming, our study goes further to provide insight into how reprogrammed MSCs are regulated molecularly to ameliorate the cellular hallmarks of aging,” explained lead investigator, Wan-Ju Li, Ph.D., a faculty member in the Department of Orthopedics and Rehabilitation and the Department of Biomedical Engineering.

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Continue reading “David Sinclair — Aging Can Be Cured” »

Methylation definition at 5:05, 27:20 a lil about reprogramming, 32:00 q&a, 47:44 Aubrey chimes in, 57:00 Keith Comito(and other throughout)

Zoom transcription: https://otter.ai/u/AIIhn4i_p4DIXHAJx0ZaG0HUnAU

Continue reading “Underlying Features of Epigenetic Aging Clocks | Morgan Levine, Yale University” »

AI, Genetics, and Health-Tech / Wearables — 21st Century Technologies For Healthy Companion Animals.

Ira Pastor ideaXme life sciences ambassador interviews Dr. Angela Hughes, the Global Scientific Advocacy Relations Senior Manager and Veterinary Geneticist at Mars Petcare.

Continue reading “Mars Personalised Petcare: High Tech, Genetics and Wearables” »

These findings […] strongly suggest that high levels of iron in the blood reduces our healthy years of life, and keeping these levels in check could prevent age-related damage.

Genes linked to ageing that could help explain why some people age at different rates to others have been identified by scientists.

The international study using genetic data from more than a million people suggests that maintaining healthy levels of iron in the blood could be a key to ageing better and living longer.

Continue reading “Blood iron levels could be key to slowing ageing, gene study shows” »

RNA-binding proteins (RBPs) are critical effectors of gene expression, and as such their malfunction underlies the origin of many diseases. RBPs can recognize hundreds of transcripts and form extensive regulatory networks that help to maintain cell homeostasis. System-wide unbiased identification of RBPs has increased the number of recognized RBPs into the four-digit range and revealed new paradigms: from the prevalence of structurally disordered RNA-binding regions with roles in the formation of membraneless organelles to unsuspected and potentially pervasive connections between intermediary metabolism and RNA regulation. Together with an increasingly detailed understanding of molecular mechanisms of RBP function, these insights are facilitating the development of new therapies to treat malignancies. Here, we provide an overview of RBPs involved in human genetic disorders, both Mendelian and somatic, and discuss emerging aspects in the field with emphasis on molecular mechanisms of disease and therapeutic interventions.

Researchers at Lund University in Sweden have discovered a new method to treat human herpes viruses. The new broad-spectrum method targets physical properties in the genome of the virus rather than viral proteins, which have previously been targeted. The treatment consists of new molecules that penetrate the protein shell of the virus and prevent genes from leaving the virus to infect the cell. It does not lead to resistance and acts independently of mutations in the genome of the virus. The results are published in the journal PLOS Pathogens.

Herpes virus infections are lifelong, with latency periods between recurring reactivations, making treatment difficult. The major challenge lies in the fact that all existing antiviral drugs to treat herpes viruses lead to rapid development of resistance in patients with compromised immune systems where the need for herpes treatment is the greatest (e.g. newborn children, patients with HIV, cancer or who have undergone organ transplantation). Both the molecular and physical properties of a virus determine the course of infection. However, the physical properties have so far received little attention, according to researcher Alex Evilevitch.

“We have a new and unique approach to studying viruses based on their specific physical properties. Our discovery marks a breakthrough in the development of antiviral drugs as it does not target specific viral proteins that can rapidly mutate, causing the development of drug resistance — something that remains unresolved by current antiviral drugs against herpes and other viruses. We hope that our research will contribute to the fight against viral infections that have so far been incurable,” says Alex Evilevitch, Associate Professor and senior lecturer at Lund University who, together with his research team, Virus Biophysics, has published the new findings.

Although Drosophila is an insect whose genome has only about 14,000 genes, roughly half the human count, a remarkable number of these have very close counterparts in humans; some even occur in the same order in the fly’s DNA as in our own. This, plus the organism’s more than 100-year history in the lab, makes it one of the most important models for studying basic biology and disease.

To take full advantage of the opportunities offered by Drosophila, researchers need improved tools to manipulate the fly’s genes with precision, allowing them to introduce mutations to break genes, control their activity, label their protein products, or introduce other inherited genetic changes.

“We now have the genome sequences of lots of different animals — worms, flies, fish, mice, chimps, humans,” says Roger Hoskins of Berkeley Lab’s Life Sciences Division. “Now we want improved technologies for introducing precise changes into the genomes of lab animals; we want efficient genome engineering. Methods for doing this are very advanced in bacteria and yeast. Good methods for worms, flies, and mice have also been around for a long time, and improvements have come along fairly regularly. But with whole genome sequences in hand, the goals are becoming more ambitious.”