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Category: biotech/medical – Page 1939

Every year, we’re reminded to return to the pharmacy for a flu shot. Why can’t we have a flu vaccine that offers long-term protection, like those for measles or polio? That’s because the influenza virus continuously evolves, so the immune response we build up one year might not work the next year—or even on the version of the flu you catch the same year. As a result, the virus remains dangerous: last year, it caused more than 60,000 deaths in the United States alone.

New findings, published in Cell, reveal why making a general-purpose vaccine that guards against all versions of the flu is so hard: Instead of improving its memory of the previous version of virus, the develops its response to the new virus variant from scratch, mostly using that have no memory of the virus.

“If we can figure out how to help the immune system to keep building on what it has already learned, we could develop better vaccines for highly evolving viruses like the flu, or HIV, or Hepatitis C,” says Gabriel D. Victora, assistant professor at Rockefeller.

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P53 is the most famous cancer gene, not least because it’s involved in causing over 50% of all cancers. When a cell loses its p53 gene—when the gene becomes mutated—it unleashes many processes that lead to the uncontrolled cell growth and refusal to die, which are hallmarks of cancer growth. But there are some cancers, like kidney cancer, that that had few p53 mutations. In order to understand whether the inactivation of the p53 pathway might contribute to kidney cancer development, Haifang Yang, Ph.D., a researcher with the Sidney Kimmel Cancer Center—Jefferson Health probed kidney cancer’s genes for interactions with p53.

Earlier work found that PBRM1—the second most mutated gene in —could interact with p53. However, other researchers were unable to definitively show that it was truly an important mechanism in kidney cancer.

Rather than looking at the p53 protein itself, first author Weijia Cai a postdoc in Dr. Yang’s lab and other collaborators looked at an activated version of p53, one that is studded with an additional chemical marker—an —at many specific spots.

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Anxious Astronaut has suffered an anxiety attack in space. It could be debilitating, they’re not sure. And unlike, say, a broken arm, it is not immediately visible to Anxious’ co-workers. Anxious Astronaut is good at hiding their problem, which is how they got through the screening process on Earth. But Anxious Astronaut needs to be operating at peak functionality, which Anxious Astronaut knows, which is making them more stressed, and they haven’t even acknowledged to themselves that they’re undergoing a silent crisis. Stress is tough.

Anxious Astronaut does not want to give up their duties, so they’re not taking time to self-evaluate. And besides, any human diagnosis is millions of miles of way, considering Anxious Astronaut and their team are halfway to Mars. So how can Anxious Astronaut’s team figure out what’s wrong? A biosensor. A small, nearly invisible biosensor placed on Anxious Astronaut’s forehead has detected unusually high cortisol, which the body releases when stressed. The data is shared with the medical staff on the mission, and Anxious is able to have their workloads reduced until they’re feeling up to snuff.

Thanks to developments in biosensors that NASA and outside group NextFlex are working on today, Anxious or Unhealthy Astronaut might be able to figure out what’s ailing them at speeds unimaginable today.

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Ultraprecise 3D printing technology is a key enabler for manufacturing precision biomedical and photonic devices. However, the existing printing technology is limited by its low efficiency and high cost. Professor Shih-Chi Chen and his team from the Department of Mechanical and Automation Engineering, The Chinese University of Hong Kong (CUHK), collaborated with the Lawrence Livermore National Laboratory to develop the Femtosecond Projection Two-photon Lithography (FP-TPL) printing technology.

By controlling the spectrum via temporal focusing, the laser 3D printing process is performed in a parallel layer-by-layer fashion instead of point-by-point writing. This new technique substantially increases the printing speed by 1,000—10,000 times, and reduces the cost by 98 percent. The achievement has recently been published in Science, affirming its technological breakthrough that leads nanoscale 3D printing into a new era.

The conventional nanoscale 3D , i.e., two-photon polymerization (TPP), operates in a point-by-point scanning fashion. As such, even a centimeter-sized object can take several days to weeks to fabricate (build rate ~ 0.1 mm3/hour). The process is time-consuming and expensive, which prevents practical and industrial applications. To increase speed, the resolution of the finished product is often sacrificed. Professor Chen and his team have overcome the challenging problem by exploiting the concept of temporal focusing, where a programmable femtosecond light sheet is formed at the focal plane for parallel nanowriting; this is equivalent to simultaneously projecting millions of laser foci at the , replacing the traditional method of focusing and scanning laser at one point only. In other words, the FP-TPL technology can fabricate a whole plane within the time that the point-scanning system fabricates a point.

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From the beginning of time, humankind has searched for the secret to a long life. Now science may have found an answer, in the form of molecular augury. The pattern of chemical chains that attach to the DNA in your cells—on-off switches known as epigenetic markers—can reveal how swiftly you are aging, and perhaps even how much longer you will live. While genetic testing might tell you where you came from, epigenetics promises a glimpse into the future. Now, a handful of companies are offering commercial blood or saliva tests based on the science of epigenetics—a chance to find out how old you truly are.

Companies claim they can now easily calculate your biological age. Should you take them up on it?

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To that end, Fields decided to ask a Florida judge to grant him a warrant that would override the new policy, allowing him to search GEDmatch’s entire database, including users who hadn’t opted in — and Judge Patricia Strowbridge did just that, the detective announced at a recent police convention, according to the NYT.

Legal experts told the NYT that this appears to be the first time a judge has approved a DNA website warrant this broad, with New York University law professor Erin Murphy calling it “a huge game-changer.”

“The company made a decision to keep law enforcement out, and that’s been overridden by a court,” Murphy told the newspaper. “It’s a signal that no genetic information can be safe.”

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Objective Failing to properly repair damaged DNA drives the ageing process. Furthermore, age-related inflammation contributes to the manifestation of ageing. Recently, we demonstrated that the efficiency of repair of diethylnitrosamine (DEN)-induced double-strand breaks (DSBs) rapidly declines with age. We therefore hypothesised that with age, the decline in DNA damage repair stems from age-related inflammation.

Design We used DEN-induced DNA damage in mouse livers and compared the efficiency of their resolution in different ages and following various permutations aimed at manipulating the liver age-related inflammation.

Results We found that age-related deregulation of innate immunity was linked to altered gut microbiota. Consequently, antibiotic treatment, MyD88 ablation or germ-free mice had reduced cytokine expression and improved DSBs rejoining in 6-month-old mice. In contrast, feeding young mice with a high-fat diet enhanced inflammation and facilitated the decline in DSBs repair. This latter effect was reversed by antibiotic treatment. Kupffer cell replenishment or their inactivation with gadolinium chloride reduced proinflammatory cytokine expression and reversed the decline in DSBs repair. The addition of proinflammatory cytokines ablated DSBs rejoining mediated by macrophage-derived heparin-binding epidermal growth factor-like growth factor.

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Rejuvenation Roundup November 2019

Quite a number of readily understandable reviews were published this month, along with an X10 episode on epigenetic alterations; if you’re new to the biology of aging or want to introduce someone else to the topic with new material, this is a great time to start.

LEAF News

We will be returning to New York in 2020 for our third conference focused on aging research, investment, and biotech business. Judy Campisi, Aubrey de Grey, Hanadie Yousef, Steve Horvath, Andrei Gudkov, and Polina Mamoshina are among the speakers confirmed so far. Join the conference mailing list to stay informed as more details are announced.

Continue reading “Rejuvenation Roundup December 2019” | >