5 research outputs found
Stereo-Selectivity of Human Serum Albumin to Enantiomeric and Isoelectronic Pollutants Dissected by Spectroscopy, Calorimetry and Bioinformatics
1–naphthol (1N), 2–naphthol (2N) and 8–quinolinol (8H) are general water pollutants. 1N and 2N are the configurational enantiomers and 8H is isoelectronic to 1N and 2N. These pollutants when ingested are transported in the blood by proteins like human serum albumin (HSA). Binding of these pollutants to HSA has been explored to elucidate the specific selectivity of molecular recognition by this multiligand binding protein. The association constants (Kb) of these pollutants to HSA were moderate (104–105 M−1). The proximity of the ligands to HSA is also revealed by their average binding distance, r, which is estimated to be in the range of 4.39–5.37 nm. The binding free energy (ΔG) in each case remains effectively the same for each site because of enthalpy–entropy compensation (EEC). The difference observed between ΔCpexp and ΔCpcalc are suggested to be caused by binding–induced flexibility changes in the HSA. Efforts are also made to elaborate the differences observed in binding isotherms obtained through multiple approaches of calorimetry, spectroscopy and bioinformatics. We suggest that difference in dissociation constants of pollutants by calorimetry, spectroscopic and computational approaches could correspond to occurrence of different set of populations of pollutants having different molecular characteristics in ground state and excited state. Furthermore, our observation of enhanced binding of pollutants (2N and 8H) in the presence of hemin signifies that ligands like hemin may enhance the storage period of these pollutants in blood that may even facilitate the ill effects of these pollutants
Transformations of ortho- and pyrophosphates with or without zinc in chemical solutions and major Indian soils
Transformation of pWWO in Rhizobium leguminosarum DPT to Engineer Toluene Degrading Ability for Rhizoremediation
Vascular Stenosis: An Introduction
International audienceAn arterial stenosis is a narrowing of the lumen that disturbs the local blood flow and precludes the adequate irrigation of perfused organs. A vascular stenosis can be extrinsic, which is caused by external compression (e.g., aneurysms and tumors), or intrinsic, currently related to atherosclerosis.Atherosclerosis is defined by an intramural retention of lipids coupled to inflammation and dyslipidemia. Atherosclerosis scatters throughout large and medium thick-walled systemic arteries, especially near and in branching regions. (Pulmonary arterial stenosis is a congenital defect.)Atherosclerosis is characterized by migration from the media, proliferation, and dedifferentiation of vascular smooth myocytes in the subendothelial layer, in addition to monocyte diapedesis and differentiation into macrophages. Both smooth myocytes and macrophages scavenge accumulated oxidized low-density lipoproteins (oxLDL) and transform into foam cells. Atherosclerosis produces symptoms when the arterial lumen is severely narrowed.Advanced atherosclerotic plaques can be destabilized, thereby being a source of clotting and subsequent emboli. Emboli block tissue perfusion in a smaller downstream artery, thereby causing ischemia and infarction.The treatment of stenotic arterial segments relies on surgical grafting or medical minimally invasive procedures such as stenting. However, both methods often lead to intimal hyperplasia resulting from uncontrolled proliferation of vascular smooth myocytes. Whereas atheroma evolves during a time magnitude order of 10 years, posttherapeutic intimal hyperplasia develops in a period of order 1 month.Successful stenting can be assumed as a procedure without strong endothelial injury. In other words, both delayed thrombosis and intimal hyperplasia result from stent deployment that more or less severely damages the vascular endothelium. To eliminate these complications, drug-eluting stents have been designed and fabricated. However, the antiproliferative drug not only blocks vascular smooth myocyte division but also precludes endothelium healing. In the absence of proper endothelial interface between blood and arterial wall, that is, when the local controller of blood coagulation and cell proliferation is missing, thrombosis and restenosis occur.Arterial stenoses have stimulated biomechanicians and applied mathematicians. They carried out flow visualization and pressure and velocity measurements in experimental models of stenoses with idealized, symmetrical or not, geometry. In parallel to technological improvements of medical imaging techniques, computational fluid dynamics, due to new numerical schemes and high-performance computing, enables to perform numerical tests on subject-specific compartments of the blood circulation, after 3D reconstruction, rather than focusing on more or less short arterial, branched or not, segments. In addition, the drug release from drug-eluting stents is investigated using mathematical models