The maximum lifespan for humans is between 120 and 150, according to a longitudinal analysis of blood markers, published in Nature.
Category: biotech/medical – Page 1,537
This in turn led the team to an FDA-approved drug called Sirturo, which is used to treat tuberculosis and works by targeting this process in bacteria. In vivo animal experiments showed that the drug could target the fuel supply of these ultra-fit cancer cells and selectively create a “power failure” in them, while leaving healthy cells unharmed. This blocked 85 percent of metastasis in the animal experiments.
Leveraging a newfound ability to identify the “fittest” metastatic cancer cells, scientists at the UK’s University of Salford have discovered that an already approved drug can be deployed to cut off their fuel supply, while leaving normal healthy cells unharmed.
Metastatic cancer cells are dangerous, fast-moving cells cancer cells that have spread away from the primary site to other parts of the body where they can give rise to new tumors. These cells have often already survived chemotherapy and radiation treatments which makes tackling them difficult, though scientists continue to learn more about their behavior and how they might be targeted for better outcomes.
Research has shown that part of the reason these cells are able to resist treatments and spread throughout the body is because they are the fittest cancer cells, and therefore require relatively large amounts of energy. Building on this, the University of Salford scientists used an advanced biosensor to measure energy-carrying molecules in cells called ATP which, for the first time, enabled them to identify which of these cells are the “fittest.”
The team says that the technique could be used to develop new vaccines against antibiotic-resistant bacteria, and potentially even wipe out some dangerous strains in a similar way to how smallpox was eradicated.
Pathogens like bacteria and viruses are extremely good at evolving in response to drugs, which can render vaccines ineffective. But now, researchers at ETH Zurich have found a way to weaponize that ability against them, forcing the bugs down harmless evolutionary dead ends.
Microbes are living examples of evolution in action. Darwin’s classic theory says that when lifeforms are exposed to pressures from their environment, some of them will develop new genetic mutations that help them cope better. Since other individuals will be at a disadvantage, the mutations will eventually become the norm throughout a population.
In the world of bacteria and viruses, drugs and vaccines are the environmental pressures that they must overcome. And they do it with frustrating ease, quickly finding ways around the attacks and then swapping those genes like trading cards. The end result is the constant looming threat of antibiotic-resistant “superbugs” that render our best drugs ineffective.
The published results indicate several possible methods of preventing metastasis: immunotherapy based on interleukin-15, which increases the number of natural killer cells in the tissue; interferon gamma therapy, which maintains the dormant state of the cancer cells; and inhibitors of the mechanism through which the hepatic stellate cells paralyze the natural killer cells. Appropriate therapies already exist for all these approaches, but they still need to be clinically tested.
Metastases can develop in the body even years after apparently successful cancer treatment. They originate from cancer cells that migrated from the original tumor to other organs, and which can lie there inactive for a considerable time. Researchers have now discovered how these “sleeping cells” are kept dormant and how they wake up and form fatal metastases. They have reported their findings in the journal Nature.
A tumor can leave behind an ominous legacy in the body: cancer cells can migrate from the tumor to other tissues in the body, where they survive after treatment in a kind of hibernation called dormancy. Currently, cancer medicine relies on monitoring cancer patients after their initial treatment in order to detect the awakening of these cells to form metastases. One of the biggest questions in cancer research is what exactly causes this transition.
“This dormancy period offers an important therapeutic window in which the number of cancer cells and their heterogeneity are still manageable,” says Professor Mohamed Bentires-Alj, group leader at the Department of Biomedicine at the University of Basel and University Hospital Basel. “Understanding the cellular and molecular mechanisms underlying tumor dormancy is therefore crucial to preventing the recurrence of cancer.” His team has made an important step in this direction.
New research in Nano Energy introduces revolutionary scalable material that senses and powers itself.
From the biggest bridges to the smallest medical implants, sensors are everywhere, and for good reason: The ability to sense and monitor changes before they become problems can be both cost-saving and life-saving.
To better address these potential threats, the Intelligent Structural Monitoring and Response Testing (iSMaRT) Lab at the University of Pittsburgh Swanson School of Engineering has designed a new class of materials that are both sensing mediums and nanogenerators, and are poised to revolutionize the multifunctional material technology big and small.
Inspired by the mantis shrimp visual system, researchers have built a camera that helps cancer surgeons see the unseen.
Circa 2015
Monkey and rat limbs are being grown in the lab by teams hoping to one day grow human organs and limbs for use as transplants.
Circa 2017
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Aging is associated with an overall decline in health and increased frailty, and is a major risk factor for multiple chronic diseases. Frailty syndrome, characterized by weakness, fatigue and low physical activity, affects more than 30% of the elderly population. Increasing our understanding of the mechanisms underlying the aging process is a top priority to facilitate the development of interventions that will lead to the preservation of health and improvements on survival and lifespan.
Cumulative evidence suggests that diet and metabolism are key targetable regulators of healthy lifespan. Prof. Haim Cohen, Director of the Sagol Healthy Human Longevity Center at Bar-Ilan University, focuses much of his research on the SIRT6 protein that is involved in regulating many biological processes, such as aging, obesity, and insulin resistance.
In a study just published in the journal Nature Communications, an international team led by Cohen and his Ph.D. student Asael Roichman—together with Prof. Rafael de Cabo, of the National Institute on Aging at the National Institutes of Health, Prof. Manuel Serrani, of the Institute for Research in Biomedicine in Barcelona, and Prof. Eyal Gottlieb from the Technion—report that transgenic mice express high levels of the SIRT6 gene, and show that their life expectancy can be increased by an average of 30% in both males and females. Translated into human terms this means that a 90-year-old could live until nearly 120!
CRISPR-based technologies offer enormous potential to benefit human health and safety, from disease eradication to fortified food supplies. As one example, CRISPR-based gene drives, which are engineered to spread specific traits through targeted populations, are being developed to stop the transmission of devastating diseases such as malaria and dengue fever.
But many scientists and ethicists have raised concerns over the unchecked spread of gene drives. Once deployed in the wild, how can scientists prevent gene drives from uncontrollably spreading across populations like wildfire?
Now, scientists at the University of California San Diego and their colleagues have developed a gene drive with a built-in genetic barrier that is designed to keep the drive under control. Led by molecular geneticist Omar Akbari’s lab, the researchers engineered synthetic fly species that, upon release in sufficient numbers, act as gene drives that can spread locally and be reversed if desired.