Growth, Characterization, Vortex Pinning and Vortex Flow Properties of Single Crystals of Iron Chalcogenide Superconductor FeCr0.02_{0.02}Se

We report the growth and characterization of single crystals of iron chalcogenide superconductor FeCr$_{0.02}$Se. There is an enhancement of the superconducting transition temperature (T$_{\rm c}$) as compared to the T$_{\rm c}$ of the single crystals of the parent compound Fe$_{1+x}$Se by about 25%. The superconducting parameters such as the critical fields, coherence length, penetration depth and the Ginzburg-Landau parameter have been estimated for these single crystals. Analysis of the critical current data suggests a fluctuation in electronic mean free path induced ($\delta l$) pinning mechanism in this material. Thermally activated transport across the superconducting transition in the presence of external magnetic fields suggests a crossover from a single vortex pinning regime at low fields to a collective flux creep regime at higher magnetic fields. The nature of charge carriers in the normal state estimated from the Hall effect and thermal transport measurements could provide crucial information on the mechanism of superconductivity in Fe-based materials.Comment: 2 additional figures, additional discussion on nature of charge carrier

Evolocumab: rising momentum as novel antidyslipidemic drug

Increased levels of low density lipoprotein cholesterol are responsible for the major cardiovascular events. Low density lipoprotein cholesterol reduction has proved to be highly effective in reducing the risk of major cardiovascular (CV) events in various trials. ACC/AHA guidelines recommend lipid-lowering therapy for patients with known cardiovascular diseases (CVD). Statins are the gold standard treatment for all types hypercholeterolemia but still there is need of some other lipid-lowering therapies especially in patients with statin intolerance and in patients responding inadequately to statins. Proprotein convertase subtilisin/kexin type 9 (PCSK9) was discovered in 2003 and subsequently emerged as a novel target for LDLC-lowering therapy. Evolocumab is a fully human monoclonal immunoglobulin G2 (IgG2) directed against human PCSK9. Evolocumab binds to PCSK9 enzyme rendering it unable to bind to the LDLR. More LDLR are available to bind to LDLC. Evolocumab increase the density of LDLR on the surface of hepatocytes, thereby increasing the uptake of LDL particles and decreasing the LDLC in the blood. Evolocumab has proved its efficacy with LDLC reduction from 53% to 75% and associated with minor side effects. Evolocumab has corroborated its effectiveness in reduction in the levels of LDLC. This drug has shown efficacy in heterozygous and homozygous subtypes of familial hypercholesterolemia. Statin intolerance seen in about 15% of all patients restricts the use of first line drug for dyslipidemia. Evolocumab can be a useful option in statin intolerant patients and in patients responding inadequately to statins

Antioxidant activity of Peanut (Arachis Hypogaea L.) Skin Extract: Application in Soybean and Mustard Oil

Total phenolics of peanut skin obtained by different methods were estimated; the effect of different solvents on extractability of total phenolic compounds has also been evaluated. The effect of peanut skin extract, possessing highest phenolics and DPPH radical scavenging activity, was evaluated by schaal oven test in the soybean oil, while oxidative stability of mustard oil was evaluated by Rancimat method. Total phenolics were obtained highest (76.0 ± 2.12 to 101.7 ± 5.54 mg/g GAE dw) in the roasted samples, followed by the dry samples (54.7 ± 1.78 to 89.1 ± 3.78 mg/g GAE dw), and lowest (14.5 ± 0.95 to 21.6 ± 1.02 mg/g GAE dw) in the blanched samples; 80% methanol extraction provided better extractability of phenolic compounds than the aqueous and 80% ethanol extraction method. The peroxide value and induction period of different oils was also evaluated in the present study, which clearly showed that peanut skin extract offered significantly (P < 0.05) better or at least similar protection against oxidation in the oils; than the synthetic antioxidant (BHT). Thus, peanut skin may be a good source of natural antioxidants for stabilization of various vegetable oils, during harsh processing and unavoidable storage conditions

AR-A 014418 Used against GSK3beta Downregulates Expression of hnRNPA1 and SF2/ASF Splicing Factors

Glioblastoma is one of the most aggressive forms of primary brain tumors of glial cells, including aberrant regulation of glycogen synthase kinase 3β (GSK3β) and splicing factors deregulation. Here, we investigate the role of small molecule AR-A014418 and Manzamine A against GSK3 kinase with factual control on splicing regulators. AR-A 014418, 48 hrs posttreatment, caused dose (25–100 μM) dependent inhibition in U373 and U87 cell viability with also inhibition in activating tyrosine phosphorylation of GSK3alpha (Tyr 279) and beta (Tyr 216). Furthermore, inhibition of GSK3 kinase resulted in significant downregulation of splicing factors (SRSF1, SRSF5, PTPB1, and hnRNP) in U87 cells with downregulation of antiapoptotic genes such as BCL2, BCL-xL, Survivin, MCL1, and BMI1. Similarly, downregulation of splicing factors was also observed in U373 glioma cell after using SiRNA against AKT and GSK3beta kinase. In addition, potential roles of AR-A014418 in downregulation of splicing factors were reflected with decrease in Anxa7 (VA) variant and increase in Anxa7 WT tumor suppressor transcript and protein. The above results suggest that inhibition of GSK3beta kinase activation could be the beneficial strategy to inhibit the occurrence of alternative cancer escape pathway via downregulating the expression of splicing regulators as well as apoptosis

AR-A 014418 Used against GSK3beta Downregulates Expression of hnRNPA1 and SF2/ASF Splicing Factors

Glioblastoma is one of the most aggressive forms of primary brain tumors of glial cells, including aberrant regulation of glycogen synthase kinase 3 (GSK3 ) and splicing factors deregulation. Here, we investigate the role of small molecule AR-A014418 and Manzamine A against GSK3 kinase with factual control on splicing regulators. AR-A 014418, 48 hrs posttreatment, caused dose (25-100 M) dependent inhibition in U373 and U87 cell viability with also inhibition in activating tyrosine phosphorylation of GSK3alpha (Tyr 279) and beta (Tyr 216). Furthermore, inhibition of GSK3 kinase resulted in significant downregulation of splicing factors (SRSF1, SRSF5, PTPB1, and hnRNP) in U87 cells with downregulation of antiapoptotic genes such as BCL2, BCL-xL, Survivin, MCL1, and BMI1. Similarly, downregulation of splicing factors was also observed in U373 glioma cell after using SiRNA against AKT and GSK3beta kinase. In addition, potential roles of AR-A014418 in downregulation of splicing factors were reflected with decrease in Anxa7 (VA) variant and increase in Anxa7 WT tumor suppressor transcript and protein. The above results suggest that inhibition of GSK3beta kinase activation could be the beneficial strategy to inhibit the occurrence of alternative cancer escape pathway via downregulating the expression of splicing regulators as well as apoptosis