Obesity promotes the onset of high blood pressure and hypertension and a team of researchers from the School of Medicine at the University of Virginia seems to have discovered the trigger.
As Swapnil K. Sonkusare of the Department of Molecular Physiology and Biological Physics of UVA explains, there are cellular mechanisms that cause blood pressure in obese people to increase.
This means that if appropriate compounds are designed to target these mechanisms, it may be possible to treat and eliminate hypertension in obese patients.
Obesity is a global problem: the number of obese people has almost tripled since 1975 (especially in Western countries) and with it the risk of diseases such as cardiovascular disease, hypertension and strokes has also increased.
Scientists have already concluded in the past that hypertension in obese passers-by is related to problems in the behaviour of endothelial cells lining the arteries, but the reasons have been unclear.
The Sonkusare research team discovered the existence of a protein called TRPV4 on the membranes surrounding endothelial cells. These proteins allow calcium to enter the cells while maintaining stable blood pressure levels.
Obesity affects this very protein and makes it defective, as Sonkusare himself explains: “Under healthy conditions, TRPV4 in these tiny microdomains helps maintain normal blood pressure. For the first time, we show the sequence of events leading to a microenvironment that is harmful to calcium intake through TRPV4. I think the concept of pathological microdomain will be very important not only for studies on obesity, but also for studies on other cardiovascular disorders”.
The same researchers have also found that obesity increases the levels of enzymes that produce peroxynitrites in microdomains containing TRPV4. So targeting peroxynitrite or enzymes directly could become an effective way to prevent or treat high blood pressure from obesity without the side effects that would result from directly targeting the TRPV4 protein.
TRPV4 protein is present in many other tissues, from the brain to the bladder, so if you target it with a drug you would get desired side effects.
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There might actually be ice on Mercury, the closest planet to the Sun in our solar system. Although it’s hard to believe that ice could be present on a planet that exceeds 400 °C in surface temperatures, a new study shows that ice could exist thanks to the same heat as the planet.
On Mercury, in fact, there are small areas in craters at the poles that basically never see sunlight. Ice can form in these areas, as scientists at the Georgia Institute of Technology explain.
The model developed by the researchers sees first of all the extreme heat of the planet releasing the so-called hydroxyl groups, minerals present in the surface soil of the planet. This process leads to the production of water and hydrogen molecules that rise up as they move around the planet.
Most water molecules are decomposed by sunlight or rise far above the surface of the planet itself. However, some of these molecules end up landing in the above areas near the poles, areas in permanent shade due to the crater formation.
Since there is no atmosphere on Mercury, there is not even a transmission of air that can conduct heat. This means that these water molecules that go to rest inside these shaded craters freeze permanently.
“It’s a bit like the Hotel California song. Water molecules can get into the shadows but they can never leave,” explains Thomas Orlando, the studio’s lead author.
This process would form up to 10 percent of the total ice on the planet and could form up to 1013 kilograms of ice in 3 million years.
On the other hand, already in 2011, NASA’s MESSENGER space probe had identified the presence of typical signs of ice around the poles, signs that indicated the presence of “dirty” ice hiding in the permanent shadow in the polar craters, craters naturally formed by the impact of asteroids and meteorites in the planet’s past.
Plants also have hormones and even these living creatures need to signal to the various parts of the plant a possible danger, whether it is an insect attack or a particular hot or cold state.
A team of researchers, who have published a study on Nature Plants, is focusing on one of these hormones, probably one of the most important in terms of danger warnings, called jasmonic acid or Jasmonate.
The study confirms the existence of what can be considered as a complex network of communication within plants, a knowledge that could prove useful to develop a more resistant crop able to resist insect attack as well as cold and heat.
Joseph Ecker, corresponding author of the study and researcher at the Howard Hughes Medical Institute, states that this study describes in great detail this hormone, its functioning and the fact that it acts at different levels.
The researchers focused mainly on Arabidopsis thaliana, a small plant of the mustard family. It is a plant whose genome has already been extensively described.
“Jasmonic acid is particularly important for a plant’s defense response against fungi and insects,” explains author Mark Zander, researcher in Ecker’s laboratory and other author of the study. “We wanted to understand exactly what happens after jasmonic acid is perceived by the plant. Which genes are activated and deactivated, which proteins are produced and which factors are in control of these well orchestrated cellular processes?”
The researchers identified two important genes, called MYC2 and MYC3, which encode the proteins that act as transcription factors, which means that they regulate the activity of many genes, probably thousands.
“Deciphering all these genetic networks and subnets helps us understand the architecture of the entire system,” Zander explains. “We now have a very complete picture of which genes are activated and deactivated during a plant’s defense response. With the availability of gene modification via CRISPR, this type of detail can be useful for crops that are better able to resist pest attacks.
A team of researchers from the University of Bern has discovered particular cells responsible for the regeneration of zebrafish heart muscle. These animals, in fact, can regenerate their heart in an extremely flexible way following an injury, unlike most mammals, including humans, for whom the heart muscles heal in a limited way following an injury.
In humans, for example, when there is damage to the heart, millions of muscle cells called cardiomyocytes die and are replaced by a scar. In some fish, especially in the zebra fish, a regeneration takes place in a way that interests scientists very much because perhaps it could be possible to establish the same process also in future humans.
Among other things, zebrafish are animals already known in medical research and used in a myriad of studies and experiments because they share many of their genes with humans.
Following a cardiac trauma, the cardiomyocytes of the zebrafish do not die but divide and generate a new heart muscle. However, researchers from the Swiss institute have noted that not all cardiomyocytes of this fish contribute to muscle regeneration; some of them seem to have an enhanced regeneration ability.
As explained in the study published in Cell Reports, these special cells differ in gene expression from other cardiomyocytes. This indicates that they are part of another different subset of cells. By eliminating this subset of cells, heart regeneration itself was severely impaired in fish, indicating their primary role in the heart regeneration process.
Now the researchers want to understand if the discovery related to the special role of these “super cells” in terms of regeneration of the heart tissue can be useful for those mammals in which the heart does not regenerate instead very efficiently, as in humans.