Lifeboat Foundation

Scientists at Hollings Cancer Center at the Medical University of South Carolina have found that human lung cancer cells resist dying by controlling parts of the aging process, in results published online May 10th in the Journal of Biological Chemistry. The discovery could help us better understand aging and eventually could lead to new treatments for cancer.

Cancer becomes more common as people get older, but scientists are still searching for answers about why this happens. At Hollings Cancer Center, research into the connections between aging and cancer is led by Besim Ogretmen, Ph.D., SmartState Endowed Chair in Lipidomics and Drug Discovery. Ogretmen’s team found that cancer cells have specific ways to resist dying the way normal cells do. They do so by protecting the tips of their chromosomes, which hold our DNA, from age-related damage.

Ogretmen studies how cancer cells are different than normal cells to understand how cancer grows and spreads in the body. His work is part of an $8.9 million program project grant to research how alterations of lipid metabolism affect cancer therapy. The grant is helping fund a clinical trial of an anticancer medicine to inhibit cellular signaling that helps cancer survive. The drug was found to be useful against cancer in the research reported in the group’s new paper.

“I am extremely excited about the research involved in the current Scientific Reports article,” said Joseph I. Shapiro, M.D., senior author and dean of the Joan C. Edwards School of Medicine. “I believe that our team has not only implicated the NAKL discovered by our colleague, Dr. Zijian Xie, in the aging process but identified a novel therapeutic target as well as a specific pharmacological strategy to actually slow the aging process. Although it will be some time before we can test these concepts in human subjects, I am cautiously optimistic that clinical therapeutics will ultimately result.”

The team’s extensive year-long study first focused on aging mice who were given a western diet to stimulate oxidant stress to antagonize the NAKL. The western diet increased the functional and structural evidence for aging; however, the introduction of pNaKtide slowed these changes in the mice. The same results were then replicated when human dermal fibroblasts were exposed to different types of oxidant stress in vitro by stimulating the NAKL, increasing expression of senescence markers, and causing cell injury. With pNaKtide treatment, the researchers demonstrated that the negative attributes associated with aging were significantly dampened.

“Our data clearly suggest that the Na/K-ATPase oxidant amplification loop is intimately involved in the aging process and, if confirmed in human studies, might ultimately serve as a therapeutic target,” said first author Komal Sodhi, M.D., an associate professor of surgery and biomedical sciences at the Joan C. Edwards School of Medicine. “If the pNaKtide can be safely used in humans, it might be possible to study the applicability of that specific agent to the problem of clinical aging.”

A remarkable new study has successfully used the CRISPR-Cas9 gene editing technique to edit a specific gene in mice engineered to have fragile X syndrome (FXS), a single-gene disorder often related to autism. The single gene edit in the live mice resulted in significant improvements in repetitive and obsessive behaviors, making this the first time gene editing has been used to effectively target behavioral symptoms related to autism spectrum disorder (ASD).

FXS is a genetic disorder associated with intellectual disability, seizures and exaggerated repetitive behavior. Previous studies have shown that the repetitive behaviors associated with FXS are related to a specific excitatory receptor in the brain that, when dysregulated, causes exaggerated signaling between cells.

The CRISPR technique homes in on the gene that controls that excitatory receptor, the metabotropic glutamate receptor 5 (mGluR5), and essentially disables it, dampening the excessive signaling the corresponds with repetitive behaviors. In mice treated with the new system, obsessive digging behavior was reduced by 30 percent and repetitive leaping actions dropped by 70 percent.

Chemical innovation plays a key role in developing cutting-edge technologies for the military. Research chemists design and synthesize new molecules that could enable a slew of next-generation military products, such as novel propellants for spacecraft engines; new pharmaceuticals and medicines for troops in the field; lighter and longer-lasting batteries and fuel cells; advanced adhesives, coatings and paints; and less expensive explosives that are safer to handle. The problem, however, is that existing molecule design and production methods rely primarily on experts’ intuition in a laborious, trial-and-error research process.

DARPA’s Make-It program, currently in year three of a four-year effort, is developing software tools based on machine learning and expert-encoded rules to recommend synthetic routes (i.e., the “recipe” to make a particular molecule) optimized for factors such as cost, time, safety, or waste reduction. The program seeks to free chemists so that they may focus their energy on chemical innovation, rather than testing various molecular synthesis pathways. The program also is developing automated devices that uniformly and reproducibly create the desired chemical based on the software-generated recipe – this one-device, many-molecules concept is a departure from the traditional dedicated reactors in chemical production. Make-It research teams have recently demonstrated significant progress toward fully automated rapid molecule production, which could speed the pace of chemical discovery for a range of defense products and applications.

“A seasoned research chemist may spend dozens of hours designing synthetic routes to a new molecule and months implementing and optimizing the synthesis in a lab,” said Anne Fischer, program manager in DARPA’s Defense Sciences Office. “Make-It is not only freeing chemists to expend brain power in other areas such as molecular discovery and innovation, it is opening chemical synthesis and discovery to a much broader community of scientific researchers who will benefit from faster development of new molecules.”

Today, we have part one of a two-part interview with Dr. Michael Fossel, the driving force behind Telocyte, a new company focused on telomerase therapy for various diseases, and a strong advocate of telomerase therapy to treat human disease over the past three decades.

I interviewed Dr. Fossel as an individual thought leader in this field and not in his role representing Telocyte, so the opinions stated here are purely his own.

Born in 1950, Michael Fossel grew up in New York and lived in London, Palo Alto, San Francisco, Portland, and Denver. He graduated cum laude from Phillips Exeter Academy, received a joint B.A. and M.A. in psychology in four years from Wesleyan University in Connecticut, and, after completing a Ph.D. in neurobiology at Stanford University in 1978, went on to finish his M.D. at Stanford Medical School in two and a half years. He was awarded a National Science Foundation Fellowship and taught at Stanford University, where he began studying aging with an emphasis on premature aging syndromes. Dr. Fossel was a Clinical Professor of Medicine at Michigan State University for almost three decades and taught the Biology of Aging at Grand Valley State University.

At MBC Biolabs, an incubator for biotech startups in San Francisco’s Dogpatch neighborhood, a team of scientists and interns working for the small startup Prellis Biologics have just taken a big step on the path toward developing viable 3D-printed organs for humans.

The company, which was founded in 2016 by research scientists Melanie Matheu and Noelle Mullin, staked its future (and a small $3 million investment) on a new technology to manufacture capillaries, the one-cell-thick blood vessels that are the pathways which oxygen and nutrients move through to nourish tissues in the body.

Continue reading “Implantable 3D-printed organs could be coming sooner than you think” »

Research team successfully administers insulin to rats in capsule form, raising hopes that a version for humans could be developed.

Nicola Davis

Engineered strains of E. coli and other microbes are being tested in humans to combat a slew of illnesses.

TRX-1 inhibitor TXNIP might be implicated in increased oxidative stress as we age.

According to scientists at the German Cancer Research Center (Deutsches Krebsforschungszentrum, or DKFZ), the enzyme TXNIP, which inhibits the enzyme TRX-1, might be a regulator of aging and might be a viable candidate for future interventions against age-related diseases [1].

Study summary

Continue reading “Antioxidant inhibitor might be a regulator of aging” »