A team of scientists from the Wellcome Sanger Institute, the Francis Crick Institute, and EMBL-EBI has created a comprehensive structural variation atlas for a geographically diverse set of human genomes and recovered sequences missing from the human reference sequence. Among the 126,018 structural variations discovered by the team were medically-important genes in Oceanian populations that were inherited from Denisovans, a sister group to Neanderthals.
Researchers have discovered a new set of signals that cells send and receive to prompt one type of fat cell to convert fat into heat. The signaling pathway, discovered in mice, has potential implications for activating this same type of thermogenic fat in humans.
Thermogenic fat cells, also called beige fat or beige adipocytes, have gained attention in recent years for their potential to curb obesity and other metabolic disorders, due to their ability to burn energy stored as fat. But scientists have yet to translate this potential into effective therapies.
The challenge of activating beige fat in humans arises, in part, because this process is regulated through so-called adrenergic signaling, which uses the hormone catecholamine to instruct beige fat cells to start burning energy. But adrenergic signaling also controls other important biological functions, including blood pressure and heartbeat regulation, so activating it in humans with agonists has potentially dangerous side effects.
The ability to restore sight to the blind is one of the most profound acts of healing medicine can achieve, in terms of the impact on the affected patient’s life — and one of the most difficult for modern medicine to achieve. We can restore vision in a limited number of scenarios and there are some early bionic eyes on the market that can restore limited vision in very specific scenarios. Researchers may have taken a dramatic step towards changing that in the future, with the results of a new experiment to design a bionic retina.
The research team in question has published a paper in Nature detailing the construction of a hemispherical retina built out of high-density nanowires. The spherical shape of the retina has historically been a major challenge for biomimetic devices.
Good talk, not just about NAD. Q&A just before 35 minutes. A lot of epigenetics here.
David A. Sinclair, Ph.D., A.O. is a Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School. He is best known for his work on understanding why we age and how to slow its effects. He obtained his Ph.D. in Molecular Genetics at the University of New South Wales, Sydney in 1995. He worked as a postdoctoral researcher at M.I.T. with Dr. Leonard Guarente where he co discovered a cause of aging for yeast as well as the role of Sir2 in epigenetic changes driven by genome instability. In 1999 he was recruited to Harvard Medical School where he has been teaching aging biology and translational medicine for aging for the past 16 years. His research has been primarily focused on the sirtuins, protein-modifying enzymes that respond to changing NAD+ levels and to caloric restriction (CR) with associated interests in chromatin, energy metabolism, mitochondria, learning and memory, neurodegeneration, and cancer. The Sinclair lab was the first one to identify a role for NAD+ biosynthesis in regulation of lifespan and first showed that sirtuins are involved in CR in mammals. They first identified small molecules that activate SIRT1 such as resveratrol and studied how they improve metabolic function using a combination of genetic, enzymological, biophysical and pharmacological approaches. They recently showed that natural and synthetic activators require SIRT1 to mediate the in vivo effects in muscle and identified a structured activation domain. They demonstrated that miscommunication between the mitochondrial and nuclear genomes is a cause of age-related physiological decline and that relocalization of chromatin factors in response to DNA breaks may be a cause of aging.
Data governs our lives more than ever. But when it comes to disease and death, every data point is a person, someone who became sick and needed treatment.
Recent studies have revealed that people suffering from the same disease category may have different manifestations. As doctors and scientists better understand the reasons underlying this variability, they can develop novel preventive, diagnostic and therapeutic approaches and provide optimal, personalized care for every patient.
To accomplish this goal often requires broadscale collaborations between physicians, basic researchers, theoreticians, experimentalists, computational biologists, computer scientists and data scientists, engineers, statisticians, epidemiologists and others. They must work together to integrate scientific and medical knowledge, theory, analysis of medical big data and extensive experimental work.
This year, the Israel Precision Medicine Partnership (IPMP) selected 16 research projects to receive NIS 60 million in grants with the goal of advancing the implementation of personalized healthcare approaches – providing the right treatment to the right patient at the right time. All the research projects pull data from Israel’s unique and vast medical databases.
“Now, nearly 2,000 people in and around Leticia are sick with COVID-19. About 70 have died. That might not sound like a colossal death toll at first. But because the surrounding state of Amazonas is sparsely populated, this amounts to the highest per-capita death rate in all of Colombia, according to figures from Colombia’s Health Ministry.”
The governor of Amazonas, Colombia, says it was impossible to cut the area off from Brazil, even as the virus spiked. Now the Colombian border town of Leticia is a coronavirus hot spot.
J&J Chief Scientific Officer Dr. Paul Stoffels says the vaccine being produced needs a minimum 70% efficacy to be considered successful.
Scientists in Europe have created embryo-like structures that mimic a crucial yet enigmatic stage of human development.
The structures, created from stem cells and called gastruloids, are the first to form a 3D assembly that lays out how the body will take shape. The gastruloids developed rudimentary components of a heart and nervous system, but lacked the components to form a brain and other cell types that would make them capable of becoming a viable fetus.
Researchers are creating ever more sophisticated artificial structures to study embryo development in the lab. The latest method for making these structures, published in Nature today1, could shed light on the causes of pregnancy loss and early developmental disorders, such as congenital heart conditions and spina bifida.
BioMed Realty, a real estate development firm that specializes in life-sciences and biotech space, is taking over development of a multi-acre site in Somerville’s Assembly Square to create a “best-in-class life science office park.”
BioMed has agreed to acquire an existing office at 5 Middlesex Ave. in Somerville, as well as 7.5 acres of land for future development, from a joint venture of Novaya Real Estate Ventures and Cresset Development. The firms did not disclose terms of the agreement.
BioMed, which investment giant Blackstone acquired in 2016, has a local portfolio spanning 3.5 million square feet, including a number of properties in Cambridge, as well as facilities in Watertown and Boston’s Longwood Medical Area. Its most recent project proposal in Cambridge is for a 16-story office and lab at 585 Third St.
