Buggemackay1800

in the arylselanyl moiety. The tested compounds presented significant antioxidant potential in the tests of inhibition of DPPH, ABTS+ and NO radicals, as well as in the FRAP and superoxide dismutase-like activity assays (SOD-Like). Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.OBJECTIVE This study aims to synthesize and characterize 2,4-thiazolidinediones and evaluate their antitumor activity. METHOD TZDs were synthesized from three components 2,4-thiazolidinedione, arene-aldehydes, and aryl chlorides. The reactions were carried out inside a microwave and monitored using thin-layer chromatography (TLC). Compounds were identified and characterized using gas chromatography coupled to mass spectrometry (CG-MS) and hydrogen (1 H-NMR) and carbon nuclear magnetic resonance spectroscopy (13C-NMR). The antitumor activity was analyzed using the 3-(4,5-dimethyl)-2,5- diphenyltetrazolium bromide (MTT) reduction test, in which cell viability was verified in the primary cultures of astrocytes and in rat and mouse glioblastoma cells exposed to the synthesized compounds. The cytotoxicity of all derivatives was analyzed at the 100 μM concentration, both in astrocytes and in the mouse and rat glioblastoma cell lines. The compounds that showed the best results, 4CI and 4DI, were also tested at concentrations 25, 50, 100, 175, and 250 μM to obtain the IC50. RESULTS Seventeen TZD derivatives were easily obtained through one-pot reactions in 40 minutes with yields ranging from 12% to 49%. All compounds were cytotoxic to both glioblastoma cell lines without being toxic to the astrocyte primary cell line at 100 μM, thus demonstrating a selective activity. Compounds 4CI and 4DI showed the best results in the C6 cells IC50 of 28.51 μM and 54.26 μM, respectively. CONCLUSION The compounds were not cytotoxic in astrocyte culture, demonstrating selectivity for malignant cells. Changes in both rings are important for antiglioma activity in the cell lines tested. TZD 4CI had the best antiglioma activity. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND The 26kDa glutathione transferase (GST, EC 2.5.1.18) from Schistosoma japonicum (SjGST) is recognized as the major detoxification enzyme of S. japonicum, a pathogenic helminth causing schistosomiasis. OBJECTIVE In the present study, the interaction of the chlorotriazine dye Cibacron blue 3GA (CB3GA) and its structural analogues with SjGST was investigated. The work aimed to shine light on the non-substrate ligand-binding properties of the enzyme. METHODS Kinetic inhibition analysis, affinity labelling experiments and molecular modelling studies were employed. RESULTS The results showed that CB3GA is a potent inhibitor (IC50 0.057 ± 0.003μM) towards SjGST. The enzyme was specifically and irreversibly inactivated by the dichlorotriazine-analogue of CB3GA (IC50 0.190 ± 0.024 μM), following a biphasic pseudo-first-order saturation kinetics with approximately 1 mol of inhibitor per mol of dimeric enzyme being incorporated. All other monochlorotriazine analogues behave as reversible inhibitors with lower inhibition potency (IC50 5.2-82.3 μM). Kinetic inhibition studies together with molecular modelling and molecular dynamics simulations established that the CB3GA binding site overlaps both the G- and H-sites. Both hydrophobic/polar interactions as well as steric effects have decisive roles in determining the inhibitory strength of CB3GA and its analogues. CONCLUSION The results of the present study might be useful in future drug design and development efforts towards SjGST. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.The association between presence of coronary artery calcium (CAC) and risk of coronary artery disease (CAD) has been appreciated for decades. In this review, we critically appraise the role of CAC based on computerized tomography in contemporary risk stratification. check details Available evidence suggests that measurement of CAC is a useful modality in many patients for more precise risk stratification and prognostic determination. Whether newer CAC score incorporating extra coronary calcification, will add incremental value, especially for stroke and other non-coronary vascular outcomes needs prospective study. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Among patients with end-stage kidney disease (ESKD), arterial stiffness is considered as a powerful predictor of cardiovascular (CV) morbidity and mortality. However, the relevance of aortic pulse wave velocity (PWV) as a prognostic biomarker for CV risk estimation is not yet fully clear. METHODS We performed a systematic search of Medline/PubMed database from inception through August 21, 2019 to identify observational cohort studies conducted in ESKD patients and exploring the association of PWV with CV events and mortality. RESULTS Whereas "historical" cohort studies showed aortic PWV to be associated with higher risk of CV and all-cause mortality, recent studies failed to reproduce the independent predictive value of aortic PWV in older ESKD patients. Studies using state-of-the-art prognostic tests showed that the addition of aortic PWV to standard clinical risk scores could only modestly improve CV risk reclassification. Studies associating improvement in PWV in response to blood pressure (BP)-lowering with improvement in survival cannot demonstrate direct cause-and-effect associations due to their observational design and absence of accurate methodology to assess the BP burden. CONCLUSION Despite the strong pathophysiological relevance of arterial stiffness as a mediator of CV disease in ESKD, the assessment of aortic PWV for CV risk stratification in this population appears to be of limited value. Whether aortic PWV assessment is valuable in guiding CV risk factor management and whether such a therapeutic approach is translated into improvement in clinical outcomes is an issue of clinical relevance that warrants investigation in properly-designed randomized trials. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.