Helicobacter pylori and its virulence factors’ effect on serum oxidative DNA damages in adults with dyspepsia

Helicobacter Pylori infection is a common gastrointestinal infection that can cause pathological effects, increase oxidative stress and induce an inflammatory response in gastric mucosa. Inflammatory aspects may prompt the production of radical oxygen substance (ROS) which may damage cells and release 8-hydroxydyoxyguanosine (8-OHdG) to serum. In this study, we evaluate the prevalence of H. pylori virulence factors and the association between serum level of 8-OHdG, H. pylori infection, and its various virulence factors. The presence of H. pylori and prevalence of cagA, babA and oipA genes in samples were determined by rapid urease test (RUT), histopathological exam (HE) and polymerase chain reaction (PCR) and oxidative DNA damage situation were assessed by using serum level of 8-OHdG. There was not any direct relation between H. pylori negative and H. pylori oipA+specimens by 8-OHdG serum level (P>0.05). In all clinical observations, the presence of cagA and oipA genes was common. There was a statistical relationship between the presence of cagA, babA factors, and high serum level of 8-OHdG (P<0.05). The presence of cagA and babA virulence factors may be associated with increased serum 8-OHdG in dyspeptic patients and may induce the damage to gastric cells. © 2016 Tehran University of Medical Sciences. All rights reserved

Relationship between helicobacter pylori CagA+ infection and iron deficiency anemia in children under 5 years of age

Background and purpose: Iron anemia deficiency and helicobacter pylori infection are common diseases throughout the world. The aim of this study was to evaluate the association between iron deficiency anemia (IDA) and H. pylori CagA+ infection among children under 5 years of age. Materials and methods: An analytical-descriptive study was performed in Hajar and Kashani hospitals in Shahrekord, Iran, 2014. We investigated the seropositive prevalence of H. pylori CagA+ infection in 59 children with IDA and compared the results with that of 69 sex- and age-matched non-anemic children using SPSS V.20. Results: The mean age of participants in case and control groups was 42±3 and 40±2 months, respectively. The controls and cases included 30 boys and 29 girls and 30 boys and 39 girls, respectively. In anemic children 50% were found to be positive for IgG anti-CagA while in non-anemic group 8% were detected. The results showed significant relationship between the two groups (P< 0.01). Conclusion: Helicobacter pylori infection may induce iron deficiency anemia and CagA virulence factor may play a role in the severity of anemia

Study of association between helicobacter pylori infection and microalbuminuria in type-2 diabetic patients

BACKGROUND/AIMS: As default, Helicobacter pylori infection may cause systemic inflammation and vascular endothelial damage. Therefore, it can be assumed that the glomerular damage as a result may lead to an increase in urinary albumin excretion. In this study, this hypothesis was set, and the relationship between Helicobacter pylori infection and microalbuminuria was examined. METHODS: Ninety-three patients with type 2 diabetes were included in the study. These patients were divided into two groups as Helicobacter pylori infection-positive (Group 1) or -negative (Group 2). In all infected and non-infected patients, urinary albumin excretion and other parameters were compared. RESULTS: The presence of Helicobacter pylori infection was detected in 53 of 93 diabetic patients (56.98%). Diabetic patients infected by Helicobacter pylori (Group 1; 186.7±24.2 mg/24 h) showed significantly higher microalbuminuria than non-infected patients (Group 2; 131.2±11.6 mg/24 h) (p=0.012). Diabetics infected with Helicobacter pylori had significantly higher inflammation marker levels than non-infected patients (p<0.05). It has been concluded that the relation between microalbuminuria level and Helicobacter pylori infection in diabetics is independent from other study variables. CONCLUSIONS: Helicobacter pylori infection, because of the systemic inflammatory response, may play an important role in the progression of diabetic nephropathy or its development. In this study, demonstrating the relationship between Helicobacter pylori infection with diabetic microalbuminuria, due to the small number of patients, is inadequate. Therefore, clinical and molecular studies involving more patients should be supported

High-throughput bioaccumulation, biotransformation, and production of silver and selenium nanoparticles using genetically engineered Pichia pastoris

A genetically modified Pichia pastoris strain overexpressing a metal-resistant variant of cytochrome b5 reductase enzyme was developed for silver and selenium biosorption and for nanoparticle production. The maximum recombinant enzyme expression level was approximately 31 IU/ml in the intercellular fluid after 24 h of incubation, and the capacity of the recombinant biomass for the biosorption of silver and selenium in aqueous batch models were measured as 163.90 and 63.71 mg/g, respectively. The ions were reduced in the presence of enzyme, leading to the formation of stable 70–180 nm metal nanoparticles. Various instrumental analyses confirmed the well-dispersed and crystalline nature of the spherical nanometals. The purified silver and selenium nanoparticles exhibited at least 10-fold less cytotoxicity toward HDF, EPG85–257, and T47D cells than silver nitrate and selenium dioxide. These results revealed that the engineered Pichia strain is an eco-friendly, rapid, high-throughput, and versatile reduction system for nanometal production

Conjunctival Reconstruction with Progenitor Cell-Derived Autologous Epidermal Sheets in Rhesus Monkey

Severe ocular surface diseases are some of the most challenging problems that the clinician faces today. Conventional management is generally unsatisfactory, and the long-term ocular consequences of these conditions are devastating. It is significantly important to find a substitute for conjunctival epithelial cells. This study was to explore the possibility of progenitor cell-derived epidermal sheets on denuded amniotic membrane to reconstruct ocular surface of conjunctiva damaged monkeys. We isolated epidermal progenitor cells of rhesus monkeys by type IV collagen adhesion, and then expanded progenitor cell-derived epidermal sheets on denuded amniotic membrane ex vivo. At 3 weeks after the conjunctiva injury, the damaged ocular surface of four monkeys was surgically reconstructed by transplanting the autologous cultivated epidermal progenitor cells. At 2 weeks after surgery, transplants were removed and examined with Hematoxylin-eosin staining, Periodic acid Schiff staining, immunofluorescent staining, scanning and transmission electron microscopy. Histological examination of transplanted sheets revealed that the cell sheets were healthy alive, adhered well to the denuded amniotic membrane, and had several layers of epithelial cells. Electron microscopy showed that the epithelial cells were very similar in appearance to those of normal conjunctival epithelium, even without goblet cell detected. Epithelial cells of transplants had numerous desmosomal junctions and were attached to the amniotic membrane with hemidesmosomes. Immunohistochemistry confirmed the presence of the conjunctival specific markers, mucin 4 and keratin 4, in the transplanted epidermal progenitor cells. In conclusion, our present study successfully reconstructed conjunctiva with autologous transplantation of progenitor cell-derived epidermal sheets on denuded AM in conjunctival damaged monkeys, which is the first step toward assessing the use of autologous transplantation of progenitor cells of nonocular surface origin. Epidermal progenitor cells could be provided as a new substitute for conjunctival epithelial cells to overcome the problems of autologous conjunctiva shortage

Association of plasma homocysteine, folic acid levels, and C677T polymorphism in methylene tetra hydrofolate reductase with risk of preeclampsia: a case-control study in Iranian women

Introduction: Preeclampsia is the most dangerous hypertension with unknown etiology. Preeclampsia is a kind of pregnancy-specific syndrome. Objective: The aim of this study was to evaluate the correlation between C677T polymorphism of MTHFR gene, folic acid, and homocysteine serum levels in Iranian pregnant women with preeclampsia. Materials and Methods: This study was performed in 129 pre-eclamptic pregnant women and 125 control individuals and MTHFR gene (C677T polymorphism) was determined by PCRRFLP method, and the plasma levels of the homocysteine and acid folic was measured by ELISA method. Result: The CC, CT, and TT genotypes were not significantly different in patients compared to control (p = 0.614). Low mean levels of homocysteine and folic acid in the preeclamptic cases were observed compared to control group. The levels of BMI, gestational age, and neonatal weight were statistically different in two groups and other variables revealed no significant difference between these groups. Conclusion: These findings showed that there was no correlation between the C677T polymorphism of MTHFR gene and preeclampsia but the TT genotype of C677T polymorphism seems to be a protective factor for preeclampsia. It is also concluded that in this study, homocysteine and folic acid serum levels and BMI are significantly affected in patients with preeclampsia compared to controls and can increase the risk of developing sever side effect to mothers and neonates

Increased risk of polycystic ovary syndrome (PCOS) associated with CC genotype of miR-146a gene variation

Polycystic ovary syndrome (PCOS) is an endocrinopathy in reproductive-age women believed to be affected by several genetics and environmental factors or both. Different miRNAs are one of such genetic factors that their associations with PCOS have been implicated. For instance, miR-146a that is well known for strongly regulating the immune response and inflammation was upregulated in serum plasma, follicular fluid and granulosa cells of PCOS patients. Different studies have shown that genetic changes in pre-miRNA can cause change in the expression or biological function of mature miRNA. Therefore, the main aim of this study was to investigate the association of miR-146a gene variation (rs2910164) with the susceptibility to PCOS. This study consists of 180 patients with PCOS and 192 healthy women matched by age and geographical region. Genotyping were determined by using PCR-RFLP in all subjects. The genotype frequency and allele distributions of all subjects were evaluated using Fisher’s exact test directed by SPSS v.20. The genotype and allele frequencies of the miR-146a polymorphism (rs2910164) significantly differ between PCOS and healthy controls. The frequencies of CC genotype (p = .054) and ‘C’ allele (p = .0001) of the miR-146a variant indicated a significant incidence in cases compared to controls. Such association was obtained in co-dominant (OR = 3.16) and dominant (OR = 2.29) models. Result of this study can be proposed that women with miR-146a variation are at a higher risk for developing PCOS, which can be due to up-regulation of miR-146a. © 2018 Informa UK Limited, trading as Taylor & Francis Grou