Примери за използване на Vascular cells на Английски и техните преводи на Български
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Smoke(artificial thickeners and"liquid smoke" destroy the membranes of vascular cells).
Researchers were able to reprogram skin cells to become vascular cells in severely injured legs that lacked blood flow.
Using fluorescence microscopy and other analytical techniques,the team found that the Sakurajima Daikon radish induced more nitric oxide production in these vascular cells than a smaller Japanese radish.
Researchers were able to reprogram skin cells into vascular cells on a mouse that had a badly injured leg with no blood flow.
Nintedanib binds competitively to the adenosine triphosphate(ATP) binding pocket of these receptors and blocks the intracellular signalling which is crucial for the proliferation andsurvival of endothelial as well as perivascular cells(pericytes and vascular smooth muscle cells).
Therefore, blockade of the RAS not only in vascular cells but also in the bone marrow could be an important therapeutic approach to prevent atherosclerosis.
We reprogrammed their skin cells to become vascular cells," Sen said.
We then take the cells, the vascular cells, blood vessel cells, we perfuse the vascular tree with the patient's own cells. .
The technology works by converting normal skin cells into vascular cells, which helps heal wounds.
In addition, beer rejuvenates vascular cells due to acceleration of certain metabolic processes in the body, and also has a soothing and analgesic effect and contributes to the inhibition of growth and reproduction of bacteria.
In the study, researchers were able to reprogram skin cells to become vascular cells in badly injured legs that lacked blood flow.
Once they would grown,the scientists removed the cadaver's vascular cells, leaving a blood vessel made of proteins like collagen that surround and support the tissue's structure.
Accumulated is also significant amount of evidence that activators of PPAR-gamma have anti-inflammatory, antiproliferative andantioxidative effects on vascular cells, thus reducing the risk of developing atherosclerosis.
To overcome these obstacles,researchers at Humacyte wanted to use human vascular cells as a base to grow new blood vessels in the lab.
In general, inhibitors play a more important role, butangiogenesis activators promote the growth of vascular cells necessary for the formation of new blood vessels.
More often the inhibitors are more important, but then the activators of antiogenesis become necessary in order tostimulate the increased vascular cell growth for the formation of new blood vessels.
Typically, the inhibitors predominate, but it becomes necessary activators of angiogenesis andstimulate increased vascular cell growth for the formation of new blood vessels.
Usually the inhibitors are dominant but sometimes the activators of andangiogenesis are triggered which stimulate the vascular cell growth so new blood vessels could be formed.
By binding to α4β7 on certain lymphocytes,vedolizumab inhibits adhesion of these cells to mucosal addressin cell adhesion molecule-1(MAdCAM-1), but not to vascular cell adhesion molecule-1(VCAM-1).
Prostaglandins thus act on a variety of cells such as vascular smooth muscle cells causing constriction or dilation, on platelets causing aggregation or disaggregation and on spinal neurons causing pain.
In vitro, ixazomib affected cell types found in the bone marrow microenvironment including vascular endothelial cells, osteoclasts and osteoblasts.
This separated portion of cells is known as stromal vascular fraction cells(SVF).
Some researchers believe that atherosclerosis may be caused by an infection of the vascular smooth muscle cells.
You place the vascular blood vessel lining cells on the inside.
Ambrisentan blocks the ETA receptor subtype,localized predominantly on vascular smooth muscle cells and cardiac myocytes.
It also diffuses into the vascular smooth muscle cells adjacent to the endothelium where it binds to and activates guanylyl cyclase.
Although not studied directly with lenvatinib, the mechanism of action(MOA)for hypertension is postulated to be mediated by the inhibition of VEGFR2 in vascular endothelial cells.
They correct the underlying deficiency in millions of vascular wall cells thereby relaxing the blood vessel walls, increasing blood vessel diameter and helping to normalize high blood pressure.
These effects are mediated by endothelin binding to ETA andETB receptors located in the endothelium and vascular smooth muscle cells.
These effects are consistent with the vasodilatory effects of PDE5-inhibitors andare probably due to increased cGMP levels in vascular smooth muscle cells.