Toggle light / dark theme

Dr. Mike Chan, Stellar Biomolecular Reserch, chats with James Strole, Director of the Coalition for Radical Life Extension, about what he’s bringing to RAADfest 2019: age reversal of organs using cell and stem cell therapies.


For more info and to register: http://www.raadfest.com/

Organized by the Coalition for Radical Life Extension, RAADfest is the largest event in the world where practical and cutting-edge methods to reverse aging are presented for all interest levels, from beginner to expert. An interactive, inclusive event featuring dozens of top presenters in life extension, regenerative medicine, super longevity, lifestyle, genetics, life hacking, finances, and more. RAADfest will also feature activists and advocate entertainers, celebrations, RAADcity the Expo and RAADclinic.

Scientists have produced and tested, in mice, a vaccine that protects against a worrisome superbug: a hypervirulent form of the bacteria Klebsiella pneumoniae. And they’ve done so by genetically manipulating a harmless form of E. coli, report researchers at Washington University School of Medicine in St. Louis and VaxNewMo, a St. Louis-based startup.

Klebsiella pneumoniae causes a variety of infections including rare but life-threatening liver, respiratory tract, bloodstream and other infections. Little is known about how exactly people become infected, and the bacteria are unusually adept at acquiring resistance to antibiotics. The prototype , details of which are published online Aug. 27 in Proceedings of the National Academy of Sciences, may offer a way to protect people against a lethal infection that is hard to prevent and treat.

“For a long time, Klebsiella was primarily an issue in the hospital setting, so even though was a real problem in treating these infections, the impact on the public was limited,” said co-author David A. Rosen, MD, Ph.D., an assistant professor of pediatrics and of molecular microbiology at Washington University. “But now we’re seeing Klebsiella strains that are virulent enough to cause death or severe disease in healthy people in the community. And in the past five years, the really resistant bugs and the really virulent bugs have begun to merge so we’re beginning to see drug-resistant, hypervirulent strains. And that’s very scary.”

Researchers have launched a new database dedicated to mapping and understanding the complexity of cellular senescence in a bid to help us fully understand this age-related phenomenon.

Introducing the CellAge database

The Human Ageing Genomic Resources ( HAGR ) is a series of databases and tools that have been developed to aid researchers on aging and help them study the genetic elements of human aging. The databases utilize modern techniques, such as functional genomics, network analyses, systems biology, and evolutionary analyses, to build what is one of the most valuable resources available today.

SAN ANTONIO — Sleep-disordered breathing (SDB), and the disruption in nightly sleep it causes, speeds up the aging process, according to preliminary research.

SDB is a common disorder that results in oxidative stress and inflammation and is associated with several age-related health disorders. However, it hasn’t been well studied with respect to epigenetic aging.

“To our knowledge, this study is the first empirical study that has linked sleep-disordered breathing with epigenetic age acceleration,” Xiaoyu Li, ScD, of Brigham and Women’s Hospital and Harvard Medical School in Boston, Massachusetts, told Medscape Medical News.

An international group of scientists studied the effects of 17 different lifespan-extending interventions on gene activity in mice and discovered genetic biomarkers of longevity. The results of their study were published in the journal Cell Metabolism.

Nowadays, dozens of interventions are known that extend the lifespan of various living organisms ranging from yeast to mammals. They include chemical compounds (e.g. rapamycin), genetic interventions (e.g. mutations associated with disruption of growth hormone synthesis), and diets (e.g. caloric restriction). Some targets of these interventions have been discovered. However, there is still no clear understanding of the systemic molecular mechanisms leading to lifespan extension.

A group of scientists from Skoltech, Moscow State University and Harvard University decided to fill this gap and identify crucial molecular processes associated with longevity. To do so, they looked at the effects of various lifespan-extending interventions on the activity of genes in a mouse, a commonly used model organism closely related to humans.

Chemotherapy works off of a basic premise: kill all rapidly-growing cells in an effort to wipe out tumor cells. The tactic, while generally effective, has quite a few off-target casualties, including cells that produce hair and cells that line the stomach.

Scientists have tried to skirt the problem by creating missile-like drugs that zero in on cancer cells specifically, sparing healthy cells.

These missile-like drugs, known as antibody-drug conjugates (ADCs), have been in the works for decades, but only in recent years have they made it to clinical trials, Kimberly Tsui, a genetics graduate student, told me.

Today, thanks to remarkable advances in antiretroviral drugs, most people with the human immunodeficiency virus (HIV) can expect to live an almost normal lifespan. But that means staying on medications for life. If those are stopped, HIV comes roaring back in just weeks. Finding a permanent cure for HIV infection, where the virus is completely and permanently eliminated from the body, has proven much tougher. So, I’m encouraged by recent work that shows it may be possible to eliminate HIV in a mouse model, and perhaps—with continued progress—someday we will actually cure HIV in humans.

This innovative approach relies on a one-two punch: drugs and genetic editing. First, HIV-infected mice received an experimental, long-acting form of antiretroviral therapy (ART) that suppresses viral replication. This step cleared the active HIV infection. But more was needed because HIV can “hide” by inserting its DNA into its host’s chromosomes—lying dormant until conditions are right for viral replication. To get at this infectious reservoir, researchers infused the mice with a gene-editing system designed to snip out any HIV DNA still lurking in the genomes of their spleen, bone marrow, lymph nodes, and other cells. The result? Researchers detected no signs of HIV in more than one-third of mice that received the combination treatment.

The new study in Nature Communications is the product of a collaboration between the NIH-funded labs of Howard Gendelman, University of Nebraska Medical Center, Omaha, and Kamel Khalili, Temple University, Philadelphia [1]. A virologist by training, Khalili years ago realized that HIV’s ability to integrate into the genomes of its host’s cells meant that the disease couldn’t be thought of only as a typical viral infection. It had a genetic component too, suggesting that an HIV cure might require a genetic answer.

An international group of scientists studied the effects of 17 lifespan-extending interventions on gene activity in mice and discovered genetic biomarkers of longevity. The results of their study were published in the journal Cell Metabolism.

Nowadays, dozens of interventions are known that extend the lifespan of various living organisms ranging from yeast to mammals. They include chemical compounds (e.g. rapamycin), genetic interventions (e.g. mutations associated with disruption of growth hormone synthesis), and diets (e.g. caloric restriction). Some targets of these interventions have been discovered. However, there is still no clear understanding of the systemic molecular mechanisms leading to lifespan extension.

A group of scientists from Skoltech, Moscow State University and Harvard University decided to fill this gap and identify crucial molecular processes associated with longevity. To do so, they looked at the effects of various lifespan-extending interventions on the activity of in a mouse, a commonly used model organism closely related to humans.

Scientists have identified a class of drugs that may have potential to treat a rare and deadly form of brain cancer that affects young children.

The research team, led by Ranjit Bindra, MD, PhD, and colleagues at the Yale Cancer Center, also included co-senior authors Charles Brenner, PhD, professor and DEO of biochemistry at the University of Iowa Carver College of Medicine, and Michael E. Berens, PhD, from the Translational Genomics Research Institute in Phoenix.

The findings, published Aug. 22 in Nature Communications, focus on Diffuse Intrinsic Pontine Glioma (DIPG), a rare, incurable cancer that affects the brainstem in children under age 10. Previous work had identified mutations in a gene called PPM1D as a cause of this cancer.

First it was human embryos. Now scientists are trying to develop another way to modify human DNA that can be passed on to future generations, NPR has learned.

Reproductive biologists at Weill Cornell Medicine in New York City are attempting to use the powerful gene-editing technique called CRISPR to alter genes in human sperm. NPR got exclusive access to watch the controversial experiments underway.

The research is aimed at finding new ways to prevent disorders caused by genetic mutations that are passed down from men — including some forms of male infertility. The team is starting with a gene that can increase the risk for breast, ovarian, prostate and other cancers.