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To date, genetic engineering of agricultural plants is developing mainly in line with classical selection. The main effo...
02/09/2021

To date, genetic engineering of agricultural plants is developing mainly in line with classical selection. The main efforts of scientists are focused on protecting plants from adverse (biotic and abiotic) factors, improving quality and reducing losses during storage of crop products. In particular, it is increasing resistance to diseases, pests, frosts, soil salinity, etc., removing unwanted components from vegetable oils, changing the properties of protein and starch in wheat flour, improving the shelf life and taste of vegetables and others.Compared to traditional selection, the main tools of which are crossbreeding and selection, genetic engineering makes it possible to use fundamentally new genes that determine agronomically important traits, and new molecular genetic methods of monitoring transgenes (molecular gene markers), which many times accelerate the process of transgenic plants.Breeders are attracted by the possibility of purposeful genetic "repair" of plants. An important area is the creation of genetically modified plants (GMP) with a sign of male sterility. In addition, due to genetic modification, plants can perform a function not previously characteristic of them. Examples are sugar beet roots, which accumulate low-molecular-weight fruits instead of sucrose, and bananas, which are used as an edible vaccine.Due to the introduction of bacterial genes, higher plants acquire the ability to destroy foreign organic compounds (xenobiotics) that pollute the environment. Growing GMRs resistant to a wide range of diseases and insect pests can significantly reduce and further minimize the pesticide load on the environment.

American scientists have pointed to the role of resistance of pulmonary macrophages to apoptosis in the development of p...
31/08/2021

American scientists have pointed to the role of resistance of pulmonary macrophages to apoptosis in the development of pulmonary fibrosis. As a result, they were able to rid laboratory mice of pulmonary fibrosis with an anti-leukemia drug that initiates apoptosis in cells. The results suggest a new target for the development of drugs against idiopathic pulmonary fibrosis. They were published in the journal Cell Death & Differentiation. Pulmonary fibrosis is a chronic disease that involves the gradual replacement of a patient's lung tissue with scar tissue. The first manifestations of the disease may be shortness of breath during exercise, cough and fatigue. But as lung fibrosis progresses, serious complications can occur, such as heart failure, which greatly increases the risk of premature death. More often the exact cause of the disease can not be found, and then the diagnosis is referred to as idiopathic pulmonary fibrosis.There are currently no effective drugs that can cure the disease, and drugs to slow its development are often of limited effectiveness. Because of this, patients with idiopathic pulmonary fibrosis live an average of only three years after diagnosis. This is largely due to an incomplete understanding of the mechanisms of the disease. Previous studies have shown that it may be related to the resistance of macrophage immune cells in the lungs to apoptosis - programmed cell death. And scientists at the University of Alabama have decided to study this cell resistance in more detail.
The authors decided to test what happens to mice that have been modified so that their lung macrophages do not produce Bcl-2 protein. And it turned out that these animals are resistant to the development of pulmonary fibrosis caused by chemicals or asbestos. This has led scientists to believe that the available drug ABT-199, which is effective in treating leukemia and skin fibrosis, may also help with idiopathic pulmonary fibrosis, as it blocks the activity of Bcl-2. So they started giving it to healthy mice and mice with chemically induced pulmonary fibrosis, and three weeks later the animals were examined.In healthy mice, ABT-199 did not cause changes in lung tissue, but in animals with scarring fibrosis, the lungs were able to be removed and returned to normal. The main findings of their work are the demonstration of the role of macrophages in the development of pulmonary fibrosis and stabilization of Bcl-2 in their mitochondria to return cells to sensitivity to apoptosis. The results may be useful in subsequent drug searches for idiopathic pulmonary fibrosis.

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