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Molecular interaction of some cardiovascular drugs with human serum albumin at physiological‐like conditions: A new approach
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In the present study, the interaction of human serum albumin (HSA) with some cardiovascular drugs (CARs) under physiological conditions was investigated via the fluorescence spectroscopic and Fourier transform infrared spectroscopy. The CAR included Captopril, Timolol, Propranolol, Atenolol, and Amiodarone. Cardiovascular drugs can effectively quench the endogenous fluorescence of HSA by static quenching mechanism. The fluorescence quenching of HSA is mainly caused by complex formation of HSA with CAR. The binding reaction of CAR with HSA can be concluded that hydrophobic and electrostatic interactions are the main binding forces in the CAR‐HSA system. The results showed that CAR strongly quenched the intrinsic fluorescence of HSA through a static quenching procedure, and nonradiation energy transfer happened within molecules. Fourier transform infrared spectroscopy absorption studies showed that the secondary structure was changed according to the interaction of HSA and CAR. The binding reaction of CAR with HSA can be concluded that hydrophobic and electrostatic interactions are the main binding forces in the CAR‐HSA system. The results obtained herein will be of biological significance in pharmacology and clinical medicines. 相似文献
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Navid Madani Amy M. Princiotto David Easterhoff Todd Bradley Kan Luo Wilton B. Williams Hua-Xin Liao M. Anthony Moody Ganesh E. Phad Néstor Vázquez Bernat Bruno Melillo Sampa Santra Amos B. Smith III Gunilla B. Karlsson Hedestam Barton Haynes Joseph Sodroski 《Journal of virology》2016,90(10):5031-5046
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Maryam?Shahbazi Masoud?Haghkhah Mohammad?Reza?Rahbar Navid?Nezafat Younes?GhasemiEmail author 《International journal of peptide research and therapeutics》2016,22(1):101-117
Staphylococcus aureus is responsible for significant and increasing number of hospital-and community-acquired infections worldwide. A pool of pathogenesis factors helps the bacterium to cause the range of mild to severe infections leading the high mortality and morbidity. Staphylococcus aureus and Candida albicans can be co-isolated from all human mucosal sites and are responsible for diverse infections. Vaccine design for related polymicrobial infections should consider the consortia of microorganisms responsible for the disease. In this study we considered biofilm mode of growth and polymicrobial nature of the infections caused by S. aureus. In the first phase of study the prediction of putative antigenic targets of S. aureus and C. albicans was conducted based on data mining and bioinformatic characterization of their proteins. Various properties of proteins were evaluated such as subcellular localization, hydrophilicity, repeat containing modules, beta turns, surface accessibility and number of antigenic determinants. The second phase includes various immunoinformatics analyses on six proteins include ALS, ClfA, FtmB, SdrE, Spa and Bap leading to design a novel sub-unit hexavalent vaccine. Several potential T cell and B-cell epitopes are present in our vaccine. Also the vaccine is expected to strongly induce IFN-gamma production. The amino acid sequence introduced here is expected to enhance cell-mediated and humoral responses against S. aureus biofilm-related infections to clear biofilm communities of S. aureus and intracellular colonies of pathogen as well as planktonic cells and thus reduces colonization and persistence. 相似文献
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Navid Sahebekhtiari Michelle M. Thomsen Jens J. Sloth Vibeke Stenbroen Massimo Zeviani Niels Gregersen Carlo Viscomi Johan Palmfeldt 《Proteomics》2016,16(7):1166-1176
Deficiency of mitochondrial sulfur dioxygenase (ETHE1) causes the severe metabolic disorder ethylmalonic encephalopathy, which is characterized by early‐onset encephalopathy and defective cytochrome C oxidase because of hydrogen sulfide accumulation. Although the severe systemic consequences of the disorder are becoming clear, the molecular effects are not well defined. Therefore, for further elucidating the effects of ETHE1‐deficiency, we performed a large scale quantitative proteomics study on liver tissue from ETHE1‐deficient mice. Our results demonstrated a clear link between ETHE1‐deficiency and redox active proteins, as reflected by downregulation of several proteins related to oxidation‐reduction, such as different dehydrogenases and cytochrome P450 (CYP450) members. Furthermore, the protein data indicated impact of the ETHE1‐deficiency on metabolic reprogramming through upregulation of glycolytic enzymes and by altering several heterogeneous ribonucleoproteins, indicating novel link between ETHE1 and gene expression regulation. We also found increase in total protein acetylation level, pointing out the link between ETHE1 and acetylation, which is likely controlled by both redox state and cellular metabolites. These findings are relevant for understanding the complexity of the disease and may shed light on important functions influenced by ETHE1 deficiency and by the concomitant increase in the gaseous mediator hydrogen sulfide. All MS data have been deposited in the ProteomeXchange with the dataset identifiers PXD002741 ( http://proteomecentral.proteomexchange.org/dataset/PXD002741 ) and PXD002742 ( http://proteomecentral.proteomexchange.org/dataset/PXD002741 ). 相似文献
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Genetica - This study aimed to investigate the effects of incidence rate, heritability, and polygenic variance on the statistical power of genome-wide association studies (GWAS) for threshold... 相似文献
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We have developed a microfluidic platform modeled after the physiologic microcirculation for multiplexed tissue-like culture and high-throughput analysis. Each microfabricated culture unit consisted of three functional components: a 50 microm wide cell culture pocket, an artificial endothelial barrier with 2 microm pores, and a nutrient transport channel. This configuration enabled a high density of cancer cells to be maintained for over 1 week in a solid tumor-like morphology when fed with continuous flow. The microfluidic chip contained 16 parallel units for "flow cell" based experiments where live cells were exposed to a soluble factor and analyzed via fluorescence microscopy or flow-through biochemistry. Each fluidically independent tissue unit contained approximately 500 cells fed with a continuous flow of 10 nL/min. As a demonstration, the toxicity profile of the anti-cancer drug paclitaxel was collected on HeLa cells cultured in the microfluidic format and compared with a 384-well dish for up to 5 days of continuous drug exposure. 相似文献
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Schön A Madani N Klein JC Hubicki A Ng D Yang X Smith AB Sodroski J Freire E 《Biochemistry》2006,45(36):10973-10980
NBD-556 and the chemically and structurally similar NBD-557 are two low-molecular weight compounds that reportedly block the interaction between the HIV-1 envelope glycoprotein gp120 and its receptor, CD4. NBD-556 binds to gp120 with a binding affinity of 2.7 x 10(5) M(-1) (K(d) = 3.7 muM) in a process characterized by a large favorable change in enthalpy partially compensated by a large unfavorable entropy change, a thermodynamic signature similar to that observed for binding of sCD4 to gp120. NBD-556 binding is associated with a large structuring of the gp120 molecule, as also demonstrated by CD spectroscopy. NBD-556, like CD4, activates the binding of gp120 to the HIV-1 coreceptor, CCR5, and to the 17b monoclonal antibody, which recognizes the coreceptor binding site of gp120. NBD-556 stimulates HIV-1 infection of CD4-negative, CCR5-expressing cells. The thermodynamic signature of the binding of NBD-556 to gp120 is very different from that of another viral entry inhibitor, BMS-378806. Whereas NBD-556 binds gp120 with a large favorable enthalpy and compensating unfavorable entropy changes, BMS-378806 does so with a small binding enthalpy change in a mostly entropy-driven process. NBD-556 is a competitive inhibitor of sCD4 and elicits a similar structuring of the coreceptor binding site, whereas BMS-378806 does not compete with sCD4 and does not induce coreceptor binding. These studies demonstrate that low-molecular-weight compounds can induce conformational changes in the HIV-1 gp120 glycoprotein similar to those observed upon CD4 binding, revealing distinct strategies for inhibiting the function of the HIV-1 gp120 envelope glycoprotein. Furthermore, competitive and noncompetitive compounds have characteristic thermodynamic signatures that can be used to guide the design of more potent and effective viral entry inhibitors. 相似文献