Infuence of chemically synthesized copper nanoparticles and cupric ions on oxalate oxidation system in germinating Sorghum grain

58-63We have earlier reported the effects of chemically synthesized copper nanoparticles (CuNPs) on oxalate oxidase (OxOx) activity, extracted from the shoot tissue of germinating grain sorghum i.e. in vitro. Here, we tried to study this effect in vivo and compare it with those of Cu2+. We describe herein, characterization of CuNPs and their effects on oxalate oxidation system i.e. OxOx activity, total oxalate and H2O2 content in vivo i.e. in shoot tissues/leaves of germinating grain Sorghum (Sorghum vulgare L). To achieve it, grain sorghum seeds were grown up to 10 days in laboratory, irrigated with Hoagland’s solution containing either CuNPs (1.0 ppm) or Cu2+ (1.0 ppm) after 4 days of germination. Control were irrigated with Hoagland solution only. The shoot/leaves of the seedling plants were harvested at 4, 6, 8 and 10 day of germination and analysed quantitatively for OxOx activity, soluble protein, H2O2 and total oxalate. The growth of the Sorghum seedling plants supplemented with CuNPs and Cu2+ was decreased significantly (P 2+. CuNPs decreased the activity of OxOx but Cu2+ had no effect at day 10. Both CuNPs and Cu2+ decreased the specific activity of OxOx and H2O2 content but increased total oxalate content at day 10. The decrease in H2O2 content in both CuNPs and Cu2+ supplemented shoot tissues with concomitant increase in oxalate content confirmed the decreased activity of OxOx in CuNPs and Cu2+ supplemented seedling plants

Effect of alirocumab on mortality after acute coronary syndromes. An analysis of the ODYSSEY OUTCOMES randomized clinical trial

Background: Previous trials of PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibitors demonstrated reductions in major adverse cardiovascular events, but not death. We assessed the effects of alirocumab on death after index acute coronary syndrome. Methods: ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) was a double-blind, randomized comparison of alirocumab or placebo in 18 924 patients who had an ACS 1 to 12 months previously and elevated atherogenic lipoproteins despite intensive statin therapy. Alirocumab dose was blindly titrated to target achieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL. We examined the effects of treatment on all-cause death and its components, cardiovascular and noncardiovascular death, with log-rank testing. Joint semiparametric models tested associations between nonfatal cardiovascular events and cardiovascular or noncardiovascular death. Results: Median follow-up was 2.8 years. Death occurred in 334 (3.5%) and 392 (4.1%) patients, respectively, in the alirocumab and placebo groups (hazard ratio [HR], 0.85; 95% CI, 0.73 to 0.98; P=0.03, nominal P value). This resulted from nonsignificantly fewer cardiovascular (240 [2.5%] vs 271 [2.9%]; HR, 0.88; 95% CI, 0.74 to 1.05; P=0.15) and noncardiovascular (94 [1.0%] vs 121 [1.3%]; HR, 0.77; 95% CI, 0.59 to 1.01; P=0.06) deaths with alirocumab. In a prespecified analysis of 8242 patients eligible for ≥3 years follow-up, alirocumab reduced death (HR, 0.78; 95% CI, 0.65 to 0.94; P=0.01). Patients with nonfatal cardiovascular events were at increased risk for cardiovascular and noncardiovascular deaths (P<0.0001 for the associations). Alirocumab reduced total nonfatal cardiovascular events (P<0.001) and thereby may have attenuated the number of cardiovascular and noncardiovascular deaths. A post hoc analysis found that, compared to patients with lower LDL-C, patients with baseline LDL-C ≥100 mg/dL (2.59 mmol/L) had a greater absolute risk of death and a larger mortality benefit from alirocumab (HR, 0.71; 95% CI, 0.56 to 0.90; Pinteraction=0.007). In the alirocumab group, all-cause death declined wit h achieved LDL-C at 4 months of treatment, to a level of approximately 30 mg/dL (adjusted P=0.017 for linear trend). Conclusions: Alirocumab added to intensive statin therapy has the potential to reduce death after acute coronary syndrome, particularly if treatment is maintained for ≥3 years, if baseline LDL-C is ≥100 mg/dL, or if achieved LDL-C is low. Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01663402