This video explains the structural forms of DNA, why DNA have different forms and what are the differences present between each form.
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In a study of gorilla skeletons collected in the wild, Johns Hopkins Medicine researchers and their international collaborators report that aging female gorillas do not experience the accelerated bone loss associated with the bone-weakening condition called osteoporosis, as their human counterparts often do. The findings, they say, could offer clues as to how humans evolved with age-related diseases.
The study was published on Sept. 21, 2020, in Philosophical Translations of the Royal Society B.
“Osteoporosis in humans is a really interesting mechanical problem,” says Christopher Ruff, Ph.D., professor at the Center for Functional Anatomy and Evolution at the Johns Hopkins University School of Medicine. “In terms of natural selection, there is no evolutionary advantage in developing bone loss with aging to the point of a potential fracture. By looking at close relatives of humans on the evolutionary tree, we can infer more about the origins of this condition.”
Some people are at higher risk of developing obesity because they possess genetic variants that affect how the brain processes sensory information and regulates feeding and behavior. The findings from scientists at the University of Copenhagen support a growing body of evidence that obesity is a disease whose roots are in the brain.
Over the past decade, scientists have identified hundreds of different genetic variants that increase a person’s risk of developing obesity. But a lot of work remains to understand how these variants translate into obesity. Now scientists at the University of Copenhagen have identified populations of cells in the body that play a role in the development of the disease—and they are all in the brain.
“Our results provide evidence that biological processes outside the traditional organs investigated in obesity research, such as fat cells, play a key role in human obesity,” says Associate Professor Tune H Pers from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR), at the University of Copenhagen, who published his team’s findings in the internationally-recognized journal eLife.
Two active genetics strategies help address concerns about gene-drive releases into the wild.
In the past decade, researchers have engineered an array of new tools that control the balance of genetic inheritance. Based on CRISPR technology, such gene drives are poised to move from the laboratory into the wild where they are being engineered to suppress devastating diseases such as mosquito-borne malaria, dengue, Zika, chikungunya, yellow fever and West Nile. Gene drives carry the power to immunize mosquitoes against malarial parasites, or act as genetic insecticides that reduce mosquito populations.
Although the newest gene drives have been proven to spread efficiently as designed in laboratory settings, concerns have been raised regarding the safety of releasing such systems into wild populations. Questions have emerged about the predictability and controllability of gene drives and whether, once let loose, they can be recalled in the field if they spread beyond their intended application region.
For the first time, Senckenberg scientist Mónica Solórzano-Kraemer, together with lead authors David Peris and Kathrin Janssen of the University of Bonn and additional colleagues from Spain and Norway, successfully extracted genetic material from insects that were embedded in six- and two-year-old resin samples. DNA—in particular, DNA from extinct animals—is an important tool in the identification of species. In the future, the researchers plan to use their new methods on older resin inclusions, as well. The study was published today in the scientific journal PLOS ONE.
The idea of extracting DNA from resin-embedded organisms inevitably invokes memories of the blockbuster “Jurassic Park.”
“However, we have no intention of raising dinosaurs,” says Dr. Mónica Solórzano-Kraemer of the Senckenberg Research Institute and Natural History Museum. “Rather, our current study is a structured attempt to determine how long the DNA of insects enclosed in resinous materials can be preserved.”
Quantum computers, which harness the strange probabilities of quantum mechanics, may prove revolutionary. They have the potential to achieve an exponential speedup over their classical counterparts, at least when it comes to solving some problems. But for now, these computers are still in their infancy, useful for only a few applications, just as the first digital computers were in the 1940s. So isn’t a book about the communications network that will link quantum computers — the quantum internet — more than a little ahead of itself?
Surprisingly, no. As theoretical physicist Jonathan Dowling makes clear in Schrödinger’s Web, early versions of the quantum internet are here already — for example, quantum communication has been taking place between Beijing and Shanghai via fiber-optic cables since 2016 — and more are coming fast. So now is the perfect time to read up.
Dowling, who helped found the U.S. government’s quantum computing program in the 1990s, is the perfect guide. Armed with a seemingly endless supply of outrageous anecdotes, memorable analogies, puns and quips, he makes the thorny theoretical details of the quantum internet both entertaining and accessible.
Continue reading “‘Schrödinger’s Web’ offers a sneak peek at the quantum internet” »
Not too much here, but longevity research fans might like.
Time may be our worst enemy, and aging its most powerful weapon. Our hair turns gray, our strength wanes, and a slew of age-related diseases represent what is happening at the cellular and molecular levels. Aging affects all the cells in our body’s different tissues, and understanding its impact would be of great value in fighting this eternal enemy of all ephemeral life forms.
The key is to first observe and measure. In a paper published in Cell Reports, scientists led by Johan Auwerx at EPFL started by asking a simple question: how do the tissues of aging mice differ from those of mice that are mere adults?
Continue reading “Understanding the effect of aging on the genome” »
Stopping the cannibalistic behavior of a well-studied enzyme could be the key to new drugs to fight age-related diseases, according to a new study published online in Nature Cell Biology. For the first time, researchers in the Perelman School of Medicine at the University of Pennsylvania show how the self-eating cellular process known as autophagy is causing the SIRT1 enzyme, long known to play a role in longevity, to degrade over time in cells and tissue in mice. Identifying an enzymatic target is an important step that may lead to new or modified existing therapeutics.
“Blocking this pathway could be another potential approach to restore the level of SIRT1 in patients to help treat or prevent age-related organ and immune system decline,” said first author Lu Wang, Ph.D., a postdoctoral researcher in the lab of Shelly Berger, Ph.D., a professor of Cell and Developmental Biology in the Perelman School of Medicine and a professor of Biology in the School of Arts and Sciences at Penn. Berger also serves as senior author on the paper.
“The findings may be of most interest to the immune aging field, as autophagy’s role in SIRT1 in immune cells is a concept that hasn’t been shown before,” Wang added. “Exploiting this mechanism presents us with a new possibility of restoring immune function.”
A newly identified genetic factor allows adult skin to repair itself like the skin of a newborn babe. The discovery by Washington State University researchers has implications for better skin wound treatment as well as preventing some of the aging process in skin.
In a study, published in the journal eLife on Sept. 29, the researchers identified a factor that acts like a molecular switch in the skin of baby mice that controls the formation of hair follicles as they develop during the first week of life. The switch is mostly turned off after skin forms and remains off in adult tissue. When it was activated in specialized cells in adult mice, their skin was able to heal wounds without scarring. The reformed skin even included fur and could make goose bumps, an ability that is lost in adult human scars.
“We were able to take the innate ability of young, neonatal skin to regenerate and transfer that ability to old skin,” said Driskell, an assistant professor in WSU’s School of Molecular Biosciences. “We have shown in principle that this kind of regeneration is possible.”
Additionally, some reports have suggested that then-President Woodrow Wilson downplayed the virus, but that is a “wrong and a false trope of popular history,” Markel said. Wilson, who would later contract the virus, was organizing and commanding the U.S. effort in World War I and once the war ended, he sailed for Paris, where he stayed until April of 1919 organizing a peace treaty and the League of Nations, Markel said.
“The federal government played a very small role in American public health during that era. It was primarily a city and state role and those agencies were hardly downplaying it,” he said.
Unlike today, there was no CDC or national public health department. The Food and Drug Administration existed but consisted of a very small group of men. Additionally, there were no antibiotics, intensive care units, ventilators, IV fluids or vaccines. “You got a bed or maybe nursing care,” Markel said.
