Thursday, April 30, 2020

NASA’s Mars Helicopter - UNIVERSE



This summer, NASA plans to launch its next Mars rover, Perseverance, which will carry with it the first aircraft to ever fly on another planet, the Mars Helicopter. As the first of its kind, the Mars Helicopter will carry no instruments and collect no data — NASA describes merely flying it all as “high-risk, high-reward” research.


The Mars Helicopter will hitch a ride on the Perseverance rover’s belly, covered by a shield to protect it during the descent and landing. Once at a suitable spot on Mars, the shield covering beneath the rover will drop. Then, the team will release the Helicopter in several steps to get it safely onto the surface.






Syphilis eludes immune attack by altering a single gene



The bacterium that causes syphilis, Treponema pallidum, likely uses a single gene to escape the immune system, research from UW Medicine in Seattle suggests.

The finding may help explain how syphilis can hide in the body for decades, thereby frustrating the immune system’s attempts to eradicate it. It might also account for the bacterium’s ability to re-infect people who had been previously been infected and should have acquired some immunity to it.

Although syphilis remains easily treated with penicillin, infection rates in the United States have increased steadily over the past two decades. The count rose to more than 115,000 new U.S. cases of the infection in 2018.

Worldwide there are an estimated 6 million new cases of syphilis among adults. The infection is responsible for an estimated 300,000 fetal and neonatal deaths annually.

However, despite its importance as a cause of disease, relatively little is known about the biology of Treponema pallidum.

One reason for this is that until recently it was impossible to grow it in a laboratory dish. As a consequence, many of the laboratory tools used to study other bacteria had not been developed for syphilis specifically.

In a new study, researchers compared the genomes of syphilis bacteria collected from a man who had been infected four times. He was enrolled in a UW Medicine study of spinal fluid abnormalities in individuals with syphilis conducted by Dr. Christina Marra, professor of neurolgy.

The samples were derived from his blood during two infections that occurred six years apart. Between those infections he had been infected and treated two additional times.

The researchers wanted to see if there were differences between the genomes of bacteria from the first and last infection. This differences might reveal how the genes of the bacteria had changed and how those changes might have enabled the bacteria to infect a person whose immune system had already seen and mounted an immune response to several different strains of syphilis.

Surprisingly, the researchers found that there were very few changes between the genomes from the two different samples — except for one gene.

“Across the about 1.1 million bases that make up the bacteria’s genome there were about 20 changes total. That’s very low,” said Dr. Alex Greninger, assistant professor of laboratory medicine at the UW School of Medicine, who led the research project. “But on this one gene, we saw hundreds of changes.”


That gene, called Treponema pallidum repeat gene K (tprK), provides the instructions for the synthesis of a protein found on the surface of the bacterium. Proteins on the surface of a bacterium are typically more easily seen by immune cells and so are often prime targets for immune attack.


The study builds on decades of work from Drs. Sheila Lukehart and Arturo Centurion-Lara in the Department of Medicine at the University of Washington School of Medicine.

They first showed that TprK generated considerable diversity across seven discrete regions in which DNA sequences from elsewhere in the bacterium’s genome could be swapped in and out. This process is called gene conversion.

Work in their lab demonstrated that bacterial cells with new tprK variants can evade the immune response to cause a persistent infection that can lead to the later stages of syphilis.

Amin Addetia, a research scientist in Greninger’s lab and lead author on the study, said it was as though the bacterium has a deck of cards in its genome from which it can draw and deal to these variable regions, essentially changing the protein’s “hand.” These substitutions change the protein’s appearance on the surface to allow it to elude the immune system.

“I’ve looked at a lot of bacterial genomes,” Addetia said, “and they’re a lot more interesting than the Treponema’s, except for this one gene.It can generate an astounding number of diverse sequences within these variable regions without impairing the protein’s ability to function.”

Although bacteria, viruses and parasites may have many proteins on their surfaces that the immune system could detect and attack, in many cases only one protein seems to attract most of the attention. Such proteins are called immunodominant.

They may protect the bacterium by catching the immune system’s attention, Greninger said. “The protein acts like a distraction that draws the immune system away from proteins that might be the bacterium’s Achilles heel. More work will be required to determine if this is the case in TprK.”

Greninger said he hoped the findings might help researchers develop vaccines that allow the immune system either to attack TprK more effectively or to ignore TprK and target other, less variable syphilis proteins.



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Wednesday, April 29, 2020

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Link between obesity and sleep loss



Can staying up late make you fat? A growing body of research has suggested that poor sleep quality is linked to an increased risk of obesity by deregulating appetite, which in turn leads to more calorie consumption.

But a new study published this week in PLOS Biology found that the direction of this reaction might actually be flipped: It’s not the sleep loss that leads to obesity, but rather that excess weight can cause poor sleep, according to researchers from the University of Pennsylvania’s Perelman School of Medicine and the University of Nevada, Reno, who discovered their findings in the microscopic worm Caenorhabditis elegans (C. elegans).


“We think that sleep is a function of the body trying to conserve energy in a setting where energetic levels are going down. Our findings suggest that if you were to fast for a day, we would predict you might get sleepy because your energetic stores would be depleted,” said study co-author David Raizen, MD, PhD, an associate professor of Neurology and member of the Chronobiology and Sleep Institute at Penn.

Raizen emphasized that while these findings in worms may not translate directly to humans, C. elegans offer a surprisingly good model for studying mammalian slumber. Like all other animals that have nervous systems, they need sleep. But unlike humans, who have complex neural circuitry and are difficult to study, a C. elegans has only 302 neurons — one of which scientists know for certain is a sleep regulator.


In humans, acute sleep disruption can result in increased appetite and insulin resistance, and people who chronically get fewer than six hours of sleep per night are more likely be obese and diabetic. Moreover, starvation in humans, rats, fruit flies, and worms has been shown to affect sleep, indicating that it is regulated, at least in part, by nutrient availability. However, the ways in which sleeping and eating work in tandem has remained unclear.

“We wanted to know, what is sleep actually doing? Short sleep and other chronic conditions, like diabetes, are linked, but it’s just an association. It’s not clear if short sleep is causing the propensity for obesity, or that the obesity, perhaps, causes the propensity for short sleep,” said study co-author Alexander van der Linden, PhD, an associate professor of Biology at the University of Nevada, Reno.

To study the association between metabolism and sleep, the researchers genetically modified C. elegans to “turn off” a neuron that controls sleep. These worms could still eat, breathe, and reproduce, but they lost their ability to sleep. With this neuron turned off, the researchers saw a severe drop in adenosine triphosphate (ATP) levels, which is the body’s energy currency.


“That suggests that sleep is an attempt to conserve energy; it’s not actually causing the loss of energy,” Raizen explained.

In previous research, the van der Linden lab studied a gene in C. elegans called KIN-29. This gene is homologous to the Salt-Inducible Kinase (SIK-3) gene in humans, which was already known to signal sleep pressure. Surprisingly, when the researchers knocked out the KIN-29 gene to create sleepless worms, the mutant C. elegans accumulated excess fat — resembling the human obesity condition — even though their ATP levels lowered.


The researchers hypothesized that the release of fat stores is a mechanism for which sleep is promoted, and that the reason KIN-29 mutants did not sleep is because they were unable to liberate their fat. To test this hypothesis, the researchers again manipulated the KIN-29 mutant worms, this time expressing an enzyme that “freed” their fat. With that manipulation, the worms were again able to sleep.

Raizen said this could explain one reason why people with obesity may experience sleep problems. “There could be a signaling problem between the fat stores and the brain cells that control sleep,” he said.

While there is still much to unravel about sleep, Raizen said that this paper takes the research community one step closer to understanding one of its core functions — and how to treat common sleep disorders.

“There is a common, over-arching sentiment in the sleep field that sleep is all about the brain, or the nerve cells, and our work suggests that this isn’t necessarily true,” he said. “There is some complex interaction between the brain and the rest of the body that connects to sleep regulation.”


Source: https://myfusimotors.com/2020/04/25/link-between-obesity-and-sleep-loss/

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