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At the more advanced end of things, genetic modifications and advanced medical procedures might be available in the future that can restore muscle tissue, bone density, and organ health. If such treatments are available down the road, periodic visits to the doctor could allow Loonies to live happy and healthy lives in lower gravity.

In so many ways, a permanent human presence on the Moon could open the door to the entire Solar System. With the ability to refuel and resupply missions from a lunar site, space agencies could shave billions off the cost of deep-space missions. It would also facilitate missions to Mars, Venus, the Asteroid Belt, and beyond.

Cellular senescence, a state of permanent growth arrest, has emerged as a hallmark and fundamental driver of organismal aging. It is regulated by both genetic and epigenetic factors. Despite a few previously reported aging-associated genes, the identity and roles of additional genes involved in the regulation of human cellular aging remain to be elucidated. Yet, there is a lack of systematic investigation on the intervention of these genes to treat aging and aging-related diseases.

How many aging-promoting are there in the ? What are the molecular mechanisms by which these genes regulate aging? Can gene therapy alleviate individual aging? Recently, researchers from the Chinese Academy of Sciences have shed new light on the regulation of aging.

Recently, researchers from the Institute of Zoology of the Chinese Academy of Sciences (CAS), Peking University, and Beijing Institute of Genomics of CAS have collaborated to identify new human senescence-promoting genes by using a genome-wide CRISPR/Cas9 screening system and provide a new therapeutic approach for treating aging and aging-related pathologies.

Gene-editing method shows promise for premature aging syndrome.

Scientists have fixed a genetic mutation in mice with progeria, a rapid aging disease. The treatment could one day be used in humans who would otherwise die in childhood.

Approximately 1 in 4 million children are diagnosed with progeria within the first two years of birth, and virtually all of these children develop health issues in childhood and adolescence that are normally associated with old age – including cardiovascular disease (heart attacks and strokes), hair loss, skeletal problems, subcutaneous fat loss and hardened skin.

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Two or three meters of DNA are packed into each of your cells, but that careful arrangement gets muddled over time, which is one reason we grow old.

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Larson K, Yan SJ, Tsurumi A, Liu J, Zhou J, Gaur K, Guo D, Eickbush TH, Li WX. (2012) Heterochromatin formation promotes longevity and represses ribosomal RNA synthesis. PLoS Genet. 8:e1002473.

Oberdoerffer P, Sinclair DA. (2007) The role of nuclear architecture in genomic instability and ageing. Nat Rev Mol Cell Biol. 8:692–702.

Pegoraro G, Kubben N, Wickert U, Gohler H, Hoffmann K, Misteli T. (2009) Ageing-related chromatin defects through loss of the NURD complex. Nat Cell Biol. 11:1261–1267.

Pollina EA, Brunet A. (2011) Epigenetic regulation of aging stem cells. Oncogene 30:3105–3126.

One mouse is hunched over, graying, and barely moves at 7 months old. Others, at 11 months, have sleek black coats and run around. The videos and other results from a new study have inspired hope for treating children born with progeria, a rare, fatal, genetic disease that causes symptoms much like early aging. In mice with a progeria-causing mutation, a cousin of the celebrated genome editor known as CRISPR corrected the DNA mistake, preventing the heart damage typical of the disease, a research team reports today in. Treated mice lived about 500 days, more than twice as long as untreated animals.

“The outcome is incredible,” says gene-therapy researcher Guangping Gao of the University of Massachusetts, who was not involved with the study.

Although the developers of the progeria therapy aim to improve it, they are also taking steps toward testing the current version in affected children, and some other scientists endorse a rush. The mouse results are “beyond anyone’s wildest expectations,” says Fyodor Urnov, a gene-editing researcher at the University of California, Berkeley. “The new data are an imperative to treat a child with progeria … and do so in the next 3 years.”

Biochemists use protein engineering to transfer photocaging groups to DNA.

DNA (deoxyribonucleic acid) is the basis of life on earth. The function of DNA is to store all the genetic information, which an organism needs to develop, function and reproduce. It is essentially a biological instruction manual found in every cell.

Biochemists at the University of Münster have now developed a strategy for controlling the biological functions of DNA with the aid of light. This enables researchers to better understand and control the different processes which take place in the cell – for example epigenetics, the key chemical change and regulatory lever in DNA.

Ralph Baric, PhD, is the William R. Kenan, Jr. Distinguished Professor in the Department of Epidemiology and Professor in the Department of Microbiology and Immunology. He is a Harvey Weaver Scholar from the National Multiple Sclerosis Society and an Established Investigator Awardee from the American Heart Association. In addition, he is a World Technology Award Finalist and a fellow of the American Association for Microbiology. He has spent the past three decades as a world leader in the study of coronaviruses and is responsible for UNC-Chapel Hill’s world leadership in coronavirus research. For these past three decades, Dr. Baric has warned that the emerging coronaviruses represent a significant and ongoing global health threat, particularly because they can jump, without warning, from animals into the human population, and they tend to spread rapidly.

The Baric Lab uses coronaviruses as models to study the genetics of RNA virus transcription, replication, persistence, pathogenesis, genetics and cross-species transmission. He has used alphavirus vaccine vectors to develop novel candidate vaccines. Dr. Baric has led the world in recognizing the importance of zoonotic viruses as a potentially rich source of new emerging pathogens in humans, with detailed studies of the molecular, genetic and evolutionary mechanisms that regulate the establishment and dissemination of such a virus within a newly adopted host. Specifically, he works to decipher the complex interactions between the virion and cell surface molecules that function in the entry and cross-species transmission of positive-strand RNA viruses.

In 20172018 and 2019, Dr. Baric was named to Clarivate Analytics’ Highly Cited Researchers list, which recognizes researchers from around the world who published the most widely-cited papers in their field. Also in 2017, he was awarded a grant for more than $6 million from the National Institute of Allergy and Infectious Diseases (NIAID) to accelerate the development of a promising new drug in the fight against deadly coronaviruses, which is currently in clinical trials to reverse COVID-19 disease in humans. In this collaboration, he continued his partnership between the Gillings School and Gilead Sciences Inc. to focus on an experimental antiviral treatment that he had previously shown to prevent the development of severe acute respiratory syndrome coronavirus (SARS-CoV) in mice. The drug also was shown to inhibit MERS-CoV and multiple other coronaviruses (CoV), suggesting that it may actually inhibit all CoV. He continues to work with this drug.

Lots of good telomere info but one small problem with Mr Andrews here. He states that he agrees with the FDA that you can’t target aging as a disease since it is not measurable. Well i think this has been shown to be false as a result of epigenetic clocks.

I posted a question under the comments on the matter,(Lord Mon) we’ll see if we get a response.

Andres de Tenyi.

· 1tShponsShrorehd ·


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A piece of high school genetics, relied on for many sorts of genetic testing, has been found to have exceptions. Although mitochondrial DNA (mtDNA) is normally received from the mother, three families have been identified where people received some of their mtDNA, three-quarters in the most extreme case, from their father. The finding may change the way we treat mitochondrial diseases and brings genetic testing for maternal ancestry into question.

MtDNA exists separately from the rest of our DNA, inside the thousands of mitochondria within each cell, rather than the cell nucleus. It is so widely accepted as being from the mother’s side it is sometimes known as the Eve Gene, the idea being that it can be traced back to some primeval mother of all living humans. Testing of mtDNA is used to identify maternal ancestry.

However, all that will have to change after Dr Shiyu Luo of the Cincinnati Children’s Hospital Medical Center published a paper in the Proceedings of the National Academy of Sciences.

I have to admit, they really sound “alien-like” if you ask me. 😃


Just when we thought octopuses couldn’t be any weirder, it turns out that they and their cephalopod brethren evolve differently from nearly every other organism on the planet.

In a surprising twist, in April 2017 scientists discovered that octopuses, along with some squid and cuttlefish species, routinely edit their RNA (ribonucleic acid) sequences to adapt to their environment.

This is weird because that’s really not how adaptations usually happen in multicellular animals. When an organism changes in some fundamental way, it typically starts with a genetic mutation — a change to the DNA.