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Discovery of bacteria linked to prostate cancer hailed as potential breakthrough

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.”

Over 5,500 New Viruses Identified in the Ocean — Including a Missing Link in Viral Evolution

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.

DNA Mutation Research Reveals Why Most Smokers Never Get Lung Cancer

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.

Dr. Andrew Adams, PhD — Lilly Institute for Genetic Medicine — Targeting Root Causes Of Diseases

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.

These novel approaches will also allow Lilly access to previously “undruggable” targets across the breath of therapeutic areas at Lilly, as well as potentially opening up novel avenues of clinical investigation.

In addition to these major roles, Dr. Adams over the recent years also took on scientific leadership of Lilly’s COVID-19 neutralizing antibody projects, as well as serving as Vice President for Lilly Genetic Medicine, and during his time at Lilly has served in roles across early discovery, external innovation, and as a leader of Lilly’s early trailblazer teams, championing new ways to bring Lilly science to patients with speed.

Genome editing for Duchenne muscular dystrophy: a glimpse of the future?

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.

YouthBio Therapeutics: New Epigenetic Rejuvenation Startup Emerges from Stealth

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.

Giving zebrafish psychotropic drugs to train AI algorithms

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.

Mystery of why humans die around 80 may finally be solved

Very good news, if unsurprising.

We already have multiple viable avenues of reducing — or eliminating altogether — this particularly pernicious form of remorseless biological entropy.

So good news… UNLESS you’re one of those people who think death is what MAKES life somehow MEANINGFUL, or that living for thousands of years or more would be BORING.

I — incase you haven’t noticed — am NOT one of those people! 😉👈


The mystery of why humans die at around 80, while other mammals live far shorter or longer lives, may finally have been solved by scientists.

Humans and animals die after amassing a similar number of genetic mutations, researchers have found, suggesting the speed of DNA errors is critical in determining the lifespan of a species.

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