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Category: genetics – Page 222

The pancreas is a key metabolic regulator. When pancreatic beta cells cease producing enough insulin, blood sugar levels rise dangerously — a phenomenon known as hyperglycemia — thus triggering diabetes. After discovering that other mature pancreatic cells can adapt and partly compensate for the lack of insulin, a team from the University of Geneva (UNIGE) demonstrates that the stem cells from which beta cells are derived are only present during embryonic development. This discovery puts an end to a long-standing controversy about the hypothetical existence of adult pancreatic stem cells that would give rise to newly differentiated hormone-producing cells after birth. The scientists also succeeded in precisely defining the ‘identity card’ of pancreatic endocrine cells, which is a promising tool for the production of replacement insulin-secreting cells. These results can be read in Cell Reports and Nature Communications.

Diabetes is a common metabolic disease. It is characterised by a persistent hyperglycemia that occurs when pancreatic cells responsible for the production of insulin — the beta cells — are destroyed or are no longer able to produce this regulatory hormone in sufficient quantities. Since 2010, studies performed by the team of Pedro Herrera, a professor in the Department of Genetic Medicine and Development and in the Diabetes Centre at the UNIGE Faculty of Medicine, as well as at the Geneva Institute of Genetics and Genomics (iGE3), reveal that the other pancreatic endocrine cells — namely alpha, delta and gamma cells, which produce other hormones useful for the metabolic balance — can “learn” to produce insulin when beta cells are absent or defective. This phenomenon, observed in mice and humans, demonstrates the plasticity of pancreatic cells and paves the way to new therapeutic strategies.

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And if bacteria causes one kind, whos to say it doesnt cause every other kind.

Genetic information on the microbes has already allowed the scientists to piece together how they may behave in the body, including what toxins and other substances they might release. This has led them to develop half a dozen hypotheses around how the bugs could cause prostate cancer.

“We currently have no way of reliably identifying aggressive prostate cancers, and this research could help make sure men get the right treatment for them,” Luxton added.

“If the team can demonstrate that these newly identified bacteria can not only predict, but actually cause aggressive prostate cancer, for the first time we may actually be able to prevent prostate cancer occurring. This would be a huge breakthrough that could save thousands of lives each year.”

Continue reading “Discovery of bacteria linked to prostate cancer hailed as potential breakthrough” | >

An analysis of the genetic material in the ocean has identified thousands of previously unknown RNA viruses and doubled the number of phyla, or biological groups, of viruses thought to exist, according to a new study our team of researchers has published in the journal Science.

RNA viruses are best known for the diseases they cause in people, ranging from the common cold to COVID-19. They also infect plants and animals important to people.

These viruses carry their genetic information in RNA, rather than DNA. RNA viruses evolve at much quicker rates than DNA viruses do. While scientists have cataloged hundreds of thousands of DNA viruses in their natural ecosystems, RNA viruses have been relatively unstudied.

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Cigarette smoking is overwhelmingly the main cause of lung cancer, yet only a minority of smokers develop the disease. A study led by scientists at Albert Einstein College of Medicine and published online on April 11, 2022, in Nature Genetics suggests that some smokers may have robust mechanisms that protect them from lung cancer by limiting mutations. The findings could help identify those smokers who face an increased risk for the disease and therefore warrant especially close monitoring.

“This may prove to be an important step toward the prevention and early detection of lung cancer risk and away from the current herculean efforts needed to battle late-stage disease, where the majority of health expenditures and misery occur,” said Simon Spivack, M.D., M.P.H., a co-senior author of the study, professor of medicine, of epidemiology & population health, and of genetics at Einstein, and a pulmonologist at Montefiore Health System.

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Targeting Root Causes Of Diseases And Aging — Dr. Andrew Adams, Ph.D., Vice President, Neurodegeneration Research; Co-Director, Lilly Institute for Genetic Medicine, Eli Lilly.

Dr. Andrew Adams, Ph.D. is Vice President of Neurodegeneration Research at Eli Lilly (https://www.lilly.com/) and Co-Director of their new Lilly Institute for Genetic Medicine (https://lilly.mediaroom.com/2022-02-22-Lilly-Announc…ort-Site), a $700 million initiative to establish an institute for researching and developing genetic medicines, specifically acting at the nucleic acid level, to advance an entirely new drug class that target the root cause of diseases, an approach that is fundamentally different than medicines available today.

In this role, Dr. Adams will be responsible for leading the discovery of various new types of therapies, via both internal research, and robust collaborations with external partners.

Continue reading “Dr. Andrew Adams, PhD — Lilly Institute for Genetic Medicine — Targeting Root Causes Of Diseases” | >

Circa 2021

As described above, molecular therapeutics enabling expression of a truncated dystrophin have been far developed. However, an unprecedented opportunity to correct the disease-causing mutation has arisen with the advent of Crispr-Cas9 technology (Fig. 1).

Since the generation of a Cas9-transgenic mouse [28], which allowed for pinpoint gene alterations specifically in organs targeted by AAVs encoding for the corresponding guide RNAs (gRNAs), it became clear that the inevitable course of inherited diseases might be altered by Cas9-mediated correction. Although certain limitations were unmasked early on, such as the preference of non-homologous end-joining (NHEJ) over homology-directed repair (HDR) upon enzymatic cleavage of the double stranded DNA by Cas9, or the packaging capacity of AAVs, muscular dystrophies seemed an ideal target for genome editing. DMD mutations inducing Duchenne muscular dystrophy (DMD) seemed particularly well suited, since internal truncations of the protein may lead to a shortened but stable protein with partial functional restitution and a milder disease progression, as seen in the allelic Becker muscular dystrophy (BMD).

The group of E. Olson was first in showing that correction of the loss-of-function mutation on exon 23 in mdx mouse zygotes is possible [29]. Notably, Cas9 combined with a single gRNA was used to inflict a cut in the vicinity of the mutation, accompanied by a single-stranded oligodeoxynucleotide, was efficient in providing HDR in 7 and NHEJ in 4 of the 11 reported corrected mdx mice. Whereas HDR correction of 41% of genomes in the mosaic mice sufficed for a full restoration of dystrophin expression in the muscles examined, a 17% HDR correction level yielded a 47–60% of muscle fibers expressing dystrophin, indicating a selection advantage of the corrected muscle and satellite cells. Moving DMD correction into the postnatal arena, the same group [30] and others [31,32,33] demonstrated feasibility of an AAV-based systemic Cas9 treatment, albeit in different flavors.

Continue reading “Genome editing for Duchenne muscular dystrophy: a glimpse of the future?” | >

Seattle-based longevity biotech YouthBio Therapeutics has emerged from stealth mode, revealing it is working on the development of “gene therapies aimed at epigenetic rejuvenation, particularly with the help of partial reprogramming by Yamanaka factors.” The company boasts some top longevity science talent, with Dr João Pedro de Magalhães serving as its chief scientific officer and Dr Alejandro Ocampo as lead research collaborator.

Longevity. Technology: Cellular reprogramming is hot, hot hot! YouthBio joins a growing list of companies, including Altos Labs, Shift Bioscience and Turn Bio, among others, all aiming to change the course of human health through this exciting, yet early stage, science. Like everyone else, we’ll be watching all the players very closely – where will the first major breakthrough come from?

Cellular reprogramming is the process by which aged cells can be returned to a pluripotent (embryonic-like) state. This process, which can be achieved using Yamanaka factors, also improves the cells’ aging hallmarks. Partial reprogramming means that Yamanaka factors are induced only for short periods, which is not enough to fully change cells beyond a point of no return but is enough to induce rejuvenation.

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Neuroscientists from St. Petersburg University, led by Professor Allan V. Kalueff, in collaboration with an international team of IT specialists, have become the first in the world to apply the artificial intelligence (AI) algorithms to phenotype zebrafish psychoactive drug responses. They managed to train AI to determine—by fish response—which psychotropic agents were used in the experiment.

The research findings are published in the journal Progress in Neuro-Psychopharmacology and Biological Psychiatry.

The zebrafish (Danio rerio) is a freshwater bony fish that is presently the second-most (after mice) used model organism in biomedical research. The advantages for utilizing zebrafish as a model biological system are numerous, including low maintenance costs and high genetic and physiological similarity to humans. Zebrafish share 70% of genes with us. Furthermore, the simplicity of the zebrafish nervous system enables researchers to achieve more explicit and accurate results, as compared to studies with more complex organisms.

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