Space travel has been one of the greatest achievements of the last century. Indeed, putting humans in space took a lot of time, effort, dedication, and planning. However, there is still a lot to learn. Recently, scientists have gained a better understanding of how space travel specifically affects the body at the molecular level, providing insight into the potential long-term effects it will have on an individual’s health. According to a recent NASA statement, scientists are now starting to understand that “a possible underlying factor of these impacts [is] the powerhouse of the cell, called the mitochondria, [which] undergoes changes in activity during space flights. This full view of the International Space Station was photographed from Space Shuttle Discovery … [+] during the STS-114 return flight mission, following the undocking of the two spacecraft. getty The statement says this preliminary belief stems from decades of research conducted on the International Space Station and samples from around 59 astronauts. The findings are based on a larger compendium of research by several principal investigators, studies and scientific efforts that take a closer look at how space affects human health. Afshin Beheshti, who is one of the key scientists, says, “We have found a universal mechanism that explains the types of changes we are seeing in the body in space, and in a place that we did not expect. […] Everything is turned upside down and it all starts with the mitochondria. Beheshti continues: “When we started to compare the tissues of mice transported on separate space missions, we noticed that mitochondrial dysfunction continued to emerge. […] Whether we were looking at eye or liver problems, the same mitochondrial pathways were causing the problem. CAP CANAVERAL, FL – NOVEMBER 15: NASA astronauts, vehicle pilot Victor Glover (front L), commander … [+] Mike Hopkins (front R), mission specialist Shannon Walker (rear L) and Japan Aerospace Exploration Agency (JAXA) mission specialist, astronaut Soichi Noguchi (rear R) exit the operations building and aircraft en route to the SpaceX Falcon 9 rocket with the Crew Dragon spacecraft on Launch Pad 39A at the Kennedy Space Center November 15, 2020 in Cape Canaveral, Florida. This will mark the second astronaut launch from American soil by NASA and SpaceX and the first operational mission named Crew-1 to the International Space Station. (Photo by Red Huber / Getty Images) Getty Images The press release further states that “NASA data on humans has confirmed this hypothesis. The changes identified in the immune system of astronaut Scott Kelly during his year in space from 2015 can also be explained by the changes observed in the activity of his mitochondria. Blood and urine samples from dozens of other astronauts have shown additional evidence that in various cell types being in space results in altered mitochondrial activity. Evagelia C. Laiakis, PhD, associate professor of oncology at Georgetown said that “although we have each studied different tissues, we have all come to the same conclusion: that mitochondrial function has been adversely affected by travel in l ‘space.” Regardless, the disease related to mitochondrial dysfunction is a broad area of study, which has some level of understanding in both physiological and pathological contexts. So, Beheshti states that perhaps “We can look at the countermeasures and drugs that we are already using to treat mitochondrial disorders on Earth to see how they might work in space, to begin with. Indeed, this crucial finding reaffirms that more research needs to be done in this area to continue examining the short and long term health effects of space travel on humans. Only then can humanity truly unlock and explore the full potential that space has to offer. .
New research has identified specific brain cells that control how much sugar you eat and how hungry you are for sweet foods.
Most people enjoy sweets from time to time. However, unchecked “sweets” can lead to excessive consumption of sugary foods and chronic health problems such as obesity and type 2 diabetes. Understanding the biological mechanisms that control sugar intake and preference for sweetness may have important implications for controlling and preventing these health problems.
The new research is led by Dr. Matthew Potthoff, associate professor of neuroscience and pharmacology at Carver University in Iowa, and Dr. Matthew Gillum at Copenhagen University in Denmark. The research focuses on the action of a hormone called fibroblast growth. Factor 21 (FGF21). This hormone is known to play a role in energy balance, weight control and insulin sensitivity.
This is the first study to truly identify where this hormone works in the brain, and provides very cool insights into how to regulate sugar intake. “
Matthew Potthoff, a member of the Eagle Diabetes Brotherhood Research Center at UI and the Iowa Neuroscience Institute
Potthoff and his colleagues previously discovered that FGF21 is made in the liver in response to elevated sugar levels and plays a role in the brain to suppress sugar intake and preference for sweetness.
Based on this discovery, the team now shows for the first time which brain cells respond to FGF21 signaling and how this interaction helps regulate sugar intake and sweetness preferences. The study was published in the journal Cell metabolism, Also revealed how hormones mediate their effects.
Although FGF21 is known to function in the brain, because hormone receptors are expressed at very low levels, it is difficult to “see”, so determining the exact cellular target becomes complicated. Using various techniques, the researchers were able to accurately identify which cells express the FGF21 receptor. By studying these cells, studies have shown that FGF21 targets glutamatergic neurons in the brain to reduce sugar intake and sweet taste preference. The researchers also showed that the effect of FGF21 on specific neurons in the hypothalamus of the peritoneum reduces sugar intake by enhancing the sensitivity of neurons to glucose.
Several drugs based on modified forms of FGF21 have been tested as treatments for obesity and diabetes. The new discovery may cause the new drug to more precisely target the different behaviors controlled by FGF21, which may help control how much sugar a person eats.
University of Wisconsin-Madison researchers have developed safer and more effective way to deliver promising new treatment for cancer and liver diseases and for vaccination, including COVID-19 vaccine from modern therapy, which was published in clinical trials with people.
The technology is based on the introduction in cells pieces of carefully designed RNA (mRNA), a strip of genetic material of human cells usually decode human DNA, to make beneficial proteins and to go about their business. Problems delivering RNAi safely and undamaged without breaking the immune system inhibit mRNA therapy, but UW-Madison researchers make little balls of minerals that seems to do the trick on mice.
These microparticles have pores on their surface, which are in the nanometer scale that will allow them to lift and carry molecules, such as proteins or RNA. They mimic something seen often in archaeology, when we find intact protein or DNA in the sample is bone or eggshell from thousands of years ago. The mineral components help to stabilize these molecules for all this time.”
William Murphy, Professor of biomedical engineering and Orthopaedics, UW-Madison
Murphy and UW-Madison collaborators used mineral-coated microparticles (ILMC), which in the diameter from 5 to 10 µm, the size of a man … in a series of experiments to deliver RNA into cells around the wound in diabetic mice. Wounds healed faster in MCM-treated mice, and cells in adjacent experiments have shown a much more efficient pickup of mRNA molecules are compared with other delivery methods.
The researchers described their findings today in the journal Science Progress.
In a healthy cell, DNA is transcribed into mRNA and the mRNA serves as the instructions the cell uses to produce proteins. Strip mRNA created in the laboratory can be replaced in the process to tell the cell to do something new. If something is of a certain type of antigen molecule that alerts the immune system to the presence potentially dangerous virus mRNA did the work of the vaccine.
At UW-Madison researchers encoded an mRNA with instructions directing the cells ribosomes to pump out the growth factor, a protein that encourages the healing process, which otherwise is slow to unfold or absent in diabetic mice (and many serious patients with diabetes).
mRNA short-lived, although in the body, so to deliver enough cells usually means of the introduction of large and frequent doses, in which mRNA strands is carried out containers made of molecules called cationic polymers.
“Often the cationic component is non-toxic. The more mRNA you put, the more therapeutic benefit you will receive, but the greater the likelihood that you’re going to see a toxic effect. So, it is a compromise,” says Murphy. What we found when we ship out of the ILMC, we do not see toxicity. And because the supply mkm protects mRNA from degradation, you can get more mRNA where you want it, to reduce toxic effects.”
The new study also paired mRNA with the immune system inhibiting protein, to make sure that the target cell did not take mRNA as foreign bodies and destroy or remove it.
Successful delivery of mRNA, as a rule, keeps the cells working on new instructions for about 24 hours, and molecules that they produce to disperse throughout the body. This is sufficient for vaccines and antigens they produce. To maintain the long processes of growing replacement tissue to repair the skin or organs, proteins and growth factors produced by cells want to hang around here much longer.
“What we saw with mcms is once the cells absorb the mRNA and start to take protein is that the protein will bind right back to MICRON particles,” says Murphy. “Then he was released within weeks. We basically take something that would normally last maybe hours or even a day, and we do it in the past for a long time.”
Because MCMS are large enough that they do not get into the bloodstream and disappear, they stay where they need to keep releasing useful therapy. In mice that therapeutic activity to continue for more than 20 days.
“They are made of minerals similar to tooth enamel and bone, but designed to be absorbed into the body when they are not useful anymore,” says Murphy, whose work is supported by the Agency for environmental protection, the National institutes of health and the national science Foundation, and donations from University of Wisconsin-Madison alum Michael and Mary sue Shannon.
“We can control their lives, adjusting as they are made so they dissolve harmlessly, when we want.”
The technology underlying the microparticles were patented by research Fund of the graduates of the University of Wisconsin and is licensed to Dianomi therapy in the company Murphy co-founder.
The researchers are now working on growing bone and cartilage tissue and restore injury to the spinal cord with the mRNA made by the ILMC.