Recent data about a person
Alexey Levin, Voice of America
Longevity genesAmerican scientists have identified 25 more genes that affect life expectancy.
This discovery was made by a team led by University of Washington staff Brian Kennedy and Matt Keberlein. It is of particular interest due to the fact that the newly discovered fragments of hereditary information belong to organisms that arose at very different stages of biological evolution.
They are found both in primitive unicellular yeast Saccharomyces cerevisiae, and in much more complex roundworms C.elegans, created by nature with an interval of one and a half billion years. Moreover, at least 60% of these genes have very close analogues in human cells. This suggests that the duration of the existence of a variety of organisms, from protozoa to mammals, is controlled by more or less identical genetic mechanisms.
Of course, so far this is only a hypothesis, but in principle it is verifiable. In any case, Kennedy and his colleagues have already started experiments that should find out whether the detected genes affect the longevity of mice. Whatever the result of these experiments, they will bring considerable benefits to science.
The island assesses the risksResearchers from the USA and Switzerland have identified a neurophysiological mechanism responsible for the incorrect assessment of financial and other risks.
As you know, it is natural for a person to plan his own behavior. Such planning is always based on the possible consequences of one's own actions, even if unconsciously. Often these actions are associated with certain risks that we calculate before making a decision. Mistakes in such estimates, as a rule, turn into unpleasant consequences. Underestimating the degree of risk contributes to adventurous behavior, while overestimation can cause a panic reaction and rejection of active behavior. In general, it is better to calculate the risks adequately, but in practice it is very difficult.
Scientists have long sought to understand exactly how the brain reacts to risky situations. Now this problem has become somewhat clearer thanks to a joint project of employees of the Federal Polytechnic School in Lausanne and the California Institute of Technology. They worked with a group of volunteers who were asked to solve test tasks that required them to quickly take into account constantly changing risks. During these experiments, they monitored the work of the subjects' brains with the help of functional tomography equipment.
This experiment gave the researchers very interesting information, which they presented in an article published in the Journal of Neuroscience. It turned out that one specific part of the brain, the anterior part of the insular lobe of the cerebral cortex, is directly involved in risk assessment. Scientists have also found that premature activation of this site leads to errors in risk assessment. This result is particularly noteworthy due to the fact that the anterior part of the insular lobe also plays an important role in managing emotions. So it follows from the new experiment that our brain is simply not programmed by nature to dispassionately assess risks. However, this is natural, because a person is not a robot.
Mitochondria under the gunHarvard University researchers have developed a package of analytical methods that allow us to study with unprecedented completeness the functioning of human mitochondria, organs of intracellular respiration.
These structures are often compared to power stations. Mitochondria actually generate most of the chemical energy needed by the cell for its normal operation. In animals, this proportion reaches 95%, in plants it is somewhat less. Mitochondria use their potential for the synthesis of ATP and adenosine triphosphate molecules, which, in turn, provide energy for almost all biochemical processes occurring in the cell.
It is now reliably known that many diseases are associated with malfunctions in the mitochondria. Thus, it has been proven that mitochondria work with reduced activity in the muscle cells of diabetics, as well as people prone to diabetes. There is reason to believe that mitochondrial disorders contribute to the development of neurodegenerative diseases and multiple sclerosis. Therefore, medicine is in dire need of tools that would make it possible to accurately identify such defects – figuratively speaking, to diagnose mitochondria.
The new methods, which Vamsi Muta and his colleagues reported in the journal Nature Biotechnology, just allow monitoring the main functions of mitochondria without disrupting the work of the cell. Scientists believe that with their help it will be possible to obtain the most valuable information that will be useful for the treatment of dozens of diseases.
Protein controllerDoctors from the University of Cincinnati have identified another molecular mechanism that directly affects the formation of fat reserves.
Suzanne Hofmann and her colleagues have experimentally proved that a significant role in this process belongs to the LPR1 protein. Its molecules are located on the outer membranes of adipocytes, specialized cells that serve as containers of fats and fat-like compounds. The researchers created a line of mice in which the gene storing information about the structure of this protein was disabled. It turned out that these mice gain much less weight than their normal relatives from the control group, who receive the same diets. Further studies have shown that the presence of LPR1 protein significantly increases the adipocyte fat capacity.
The LPR1 protein is expressed on the surface of not only adipocytes, but also a number of other cells. Scientists suggest that it performs many functions that have yet to be clarified. In particular, there are reasonable suspicions that this protein is somehow associated with the development of Alzheimer's disease.
It is still difficult to say whether the results of scientists from Cincinnati will help to create new ways to combat obesity and related diseases. However, practice shows that any new information about physiological processes has a lot of chances to eventually find application in practical medicine.
Capillaries grow differentlyBoston scientists have discovered a previously unknown molecular mechanism that triggers the growth of new blood vessels.
The process of such growth is called angiogenesis. It can start for many reasons, in particular, in cases when tissues lack oxygen, in scientific terminology hypoxia. At one time, it was proved that the mammalian body synthesizes special proteins of the HIF family, which work as indicators of oxygen content. When these substances register oxygen deficiency, they give the command to synthesize another specialized protein, which, in turn, stimulates angiogenesis.
Now it turned out that with oxygen starvation, new capillaries can arise without the participation of proteins from the HIF group. This is evidenced by the results of experiments on mice performed at the Dana and Farber Cancer Institute. Professor of cell biology Bruce Spigelman and his colleagues discovered that another protein PGC-1 alpha also monitors oxygen levels. When this protein feels a lack of oxygen, it also sends a signal to molecular transformations, which ultimately lead to the appearance of young capillaries.
Scientists had previously known that PGC-1 alpha plays an important role in metabolic processes, but until now there was no reason to believe that it takes part in triggering angiogenesis.
So far, information about the newly discovered functions of the PGC-1 alpha protein is of interest only to fundamental science, but it is unlikely to last long. The fact is that representatives of a number of biomedical specialties have long been trying to find ways to influence the processes of angiogenesis.
Oncologists would like to learn how to reliably block the proliferation of small blood vessels that deliver oxygen and nutrients to malignant neoplasms. Thus, they hope to put the tumor on a starvation regime, and also prevent the spread of its cells along with the blood flow throughout the body. On the other hand, cardiologists consider it possible to cure cardiovascular diseases by stimulating vascular growth with medications. Now there is reason to believe that angiogenesis can be controlled using the PGC-1 alpha protein. Therefore, it can be assumed that manipulating this protein will help practical medicine.
Portal "Eternal youth" www.vechnayamolodost.ru17.03.2008