Electrocoagulation coupled with adsorption for effective removal of eosin yellow and nigrosin dyes in aqueous solution

This paper deals with the study of suitability and efficiency of electrocoagulation (EC) coupled with adsorption to remove dye from synthetic dye solution. The EC cell consisted of mild steel (MS)/copper plates as electrodes and dye solution as electrolyte. The effects of operating time, concentration, supporting electrolyte, current density and pH have been investigated to find out the optimum operating conditions for EC. The concentration of dye was successfully reduced (EY) ?50% and Nigrosin dye ?99% during EC under the optimum operating conditions of initial concentration 0.5ppm, 20ppm, current density 0.04 A/cm2, 0.015 A/cm2, supporting electrolyte 4g, 4g, electrolysis time 20min, 10min, Eosin Yellow and Nigrosin dye respectively, the removal efficiency of the dyes were found 46.69% and 99%, electrical conductivity were 125.0 S/m and 105.7 S/m and TDS left in the EC treated solution were 82.0 and 69.3 ppt. Further proceedings with solution for adsorption process help to improve the dye removal. Results of the studies are electrical conductivity 20 S/m and TDS 30 ppt for EY, for Nigrosin 64.2 S/m and 42.1 ppt

Association of IL-10 & IL-10RA polymorphisms with lymphatic filariasis in South Indian population

Aim: The filariasis infection is initiated by mosquito derived third stage larva (L3), which establishes itself in different immunocompetent niches by adopting different evasion and immunomodulatory mechanisms. Immunological and clinical outcomes can vary considerably at the individual and population levels during lymphatic filariasis infection. The protein product coded by the interleukin-10 (IL-10) gene has broad immunomodulatory function in filarial load and patency of the disease. The potential influence of altered IL-10 expression encoded by IL-10 promoter single nucleotide polymorphisms (SNPs) and IL-10RA signaling pathway, in pathogenesis and clinical outcome of filarial infection was established in the present study Study Design: Genetic association based on case-control study. Place and Duration of Study: Lymphatic filariasis cases referred to National Filariasis Control Program (NFCP), Siddipet, Medak, Andhra Pradesh, India between Feb 2006 to Dec 2009. Methodology: A total of 100 non-endemic, 50 endemic and 118 lymphatic filariasis patients were included in the present study based on clinical and diagnostic criteria. Genetic polymorphisms in the IL-10 promoter region (-1082G/A, -819C/T and -592 A/C) and IL-10 RA coding region S138G were screened following PCR-RFLP and ARMS-PCR technique respectively. Results: Patients with familial aggregation of lymphedema exhibited significant association with IL-10 -1082 ‘A’ allele (A vs G OR 2.68, CI - 1.12-6.37, P=0.02) coding for lower IL-10 levels. Similarly the G variant of IL-10RA S138G SNP revealed a significant association with lymphatic filariasis in the endemic population studied (GG vs AA OR 2.50 CI-1.22-5.13, P= 0.021). The Haplotype analysis also revealed the low signaling ATA is significantly associated with the disease in this cohort (P=0.03). The Multifactor Dimensionality Reduction Analysis (MDR) for IL-10 and IL-10RA SNPs interaction revealed the three locus model as the best model wherein the epistatic interactions of variant G allele of IL-10RA S138G, the A allele of the -1082G/A and the T allele of the - 819C/T SNPs in IL-10 were found to be a possible risk genotype for filarial infection. (TA = 0.5230, CV-10/10, P=0.001). Conclusion: IL-10 promoter haplotypes and IL-10 RA S138G polymorphisms are the possible genetic determinants of susceptibility to lymphatic filariasis. Further functional studies are warranted to validate these results.Yasmeen Sheik, Sameera Fatima Qureshi, Ananthapur Venkateshwari, Saeed Nourmohammadi, Basheeruddin Mohammad and Pratibha Nallar

MBOAT7-driven lysophosphatidylinositol acylation in adipocytes contributes to systemic glucose homeostasis

We previously demonstrated that antisense oligonucleotide-mediated knockdown of Mboat7, the gene encoding membrane bound O-acyltransferase 7, in the liver and adipose tissue of mice promoted high fat diet-induced hepatic steatosis, hyperinsulinemia, and systemic insulin resistance. Thereafter, other groups showed that hepatocyte-specific genetic deletion of Mboat7 promoted striking fatty liver and NAFLD progression in mice but does not alter insulin sensitivity, suggesting the potential for cell autonomous roles. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. We generated Mboat7 floxed mice and created hepatocyte- and adipocyte-specific Mboat7 knockout mice using Cre-recombinase mice under the control of the albumin and adiponectin promoter, respectively. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. The expression of Mboat7 in white adipose tissue closely correlates with diet-induced obesity across a panel of ∼100 inbred strains of mice fed a high fat/high sucrose diet. Moreover, we found that adipocyte-specific genetic deletion of Mboat7 is sufficient to promote hyperinsulinemia, systemic insulin resistance, and mild fatty liver. Unlike in the liver, where Mboat7 plays a relatively minor role in maintaining arachidonic acid-containing PI pools, Mboat7 is the major source of arachidonic acid-containing PI pools in adipose tissue. Our data demonstrate that MBOAT7 is a critical regulator of adipose tissue PI homeostasis, and adipocyte MBOAT7-driven PI biosynthesis is closely linked to hyperinsulinemia and insulin resistance in mice

Superoxide dismutase phenotypes in duodenal ulcers: A genetic marker?

Background:Cu-Zn superoxide dismutases are antioxidative defensive enzymes that catalyze the reduction of superoxide anions to hydrogen peroxide. Aim:The study focuses on the association of electromorph of superoxide dismutase with duodenal ulcers, which result due to an imbalance between aggressive and defensive factors. Materials and Methods:Endoscopically confirmed 210 duodenal ulcer patients and 185 healthy individuals for comparative analysis were considered for the present study. Phenotyping of superoxide dismutase was carried out by subjecting the RBC membranes to polyacrylamide gel electrophoresis, using appropriate staining protocols. Results:Statistical analysis of SOD phenotypes revealed a significant increase of SOD A*2 allele and Superoxide dismutases (SOD) 2-2 phenotype in duodenal ulcer group. Among these individuals, a predominance of Helicobacter pylori infection was observed. The increased preponderance of homozygotes can be explained on the basis of reduced and altered enzyme activity, which may lead to disturbance in homeostasis of antioxidant/oxidant culminating in high lipid peroxidative gastric mucosal tissue damage and ulceration. No variation in the distribution of SOD phenotypes with respect to Helicobacter pylori indicates the role of Mn-SOD rather than Cu-Zn SOD in the Helicobacter pylori infected cases as reported earlier. Conclusions:Superoxide dismutase as a genetic marker / gene modifier, encoding for an antioxidant enzyme in maintaining tissue homeostasis of the gastric mucosa is discussed

Helicobacter pylori infection in relation to gastric cancer progression

Gastric cancer is a major cause of cancer death worldwide, especially in developing countries. The incidence of gastric cancer varies from country to country, probably as a result of genetic, epigenetic, and environmental factors. H. pylori infection is considered as a major risk factor in the development of gastric cancer. However, the scenario varies in Asian countries, exhibiting a higher rate of H. pylori infection and low incidence of gastric cancer, which could be attributed to strain-specific virulence factors and host genetic makeup. In this review, we discuss the various virulence factors expressed by this bacterium and their interaction with the host factors, to influence pathogenesis

Helicobacter pylori infection in relation to gastric cancer progression

Gastric cancer is a major cause of cancer death worldwide, especially in developing countries. The incidence of gastric cancer varies from country to country, probably as a result of genetic, epigenetic, and environmental factors. H. pylori infection is considered as a major risk factor in the development of gastric cancer. However, the scenario varies in Asian countries, exhibiting a higher rate of H. pylori infection and low incidence of gastric cancer, which could be attributed to strain-specific virulence factors and host genetic makeup. In this review, we discuss the various virulence factors expressed by this bacterium and their interaction with the host factors, to influence pathogenesis

MMD collaborates with ACSL4 and MBOAT7 to promote polyunsaturated phosphatidylinositol remodeling and susceptibility to ferroptosis

Summary: Ferroptosis is a form of regulated cell death with roles in degenerative diseases and cancer. Excessive iron-catalyzed peroxidation of membrane phospholipids, especially those containing the polyunsaturated fatty acid arachidonic acid (AA), is central in driving ferroptosis. Here, we reveal that an understudied Golgi-resident scaffold protein, MMD, promotes susceptibility to ferroptosis in ovarian and renal carcinoma cells in an ACSL4- and MBOAT7-dependent manner. Mechanistically, MMD physically interacts with both ACSL4 and MBOAT7, two enzymes that catalyze sequential steps to incorporate AA in phosphatidylinositol (PI) lipids. Thus, MMD increases the flux of AA into PI, resulting in heightened cellular levels of AA-PI and other AA-containing phospholipid species. This molecular mechanism points to a pro-ferroptotic role for MBOAT7 and AA-PI, with potential therapeutic implications, and reveals that MMD is an important regulator of cellular lipid metabolism