NF-kappaB p65-Dependent Transactivation of miRNA Genes following Cryptosporidium parvum Infection Stimulates Epithelial Cell Immune Responses

Cryptosporidium parvum is a protozoan parasite that infects the gastrointestinal epithelium and causes diarrheal disease worldwide. Innate epithelial immune responses are key mediators of the host's defense to C. parvum. MicroRNAs (miRNAs) regulate gene expression at the posttranscriptional level and are involved in regulation of both innate and adaptive immune responses. Using an in vitro model of human cryptosporidiosis, we analyzed C. parvum-induced miRNA expression in biliary epithelial cells (i.e., cholangiocytes). Our results demonstrated differential alterations in the mature miRNA expression profile in cholangiocytes following C. parvum infection or lipopolysaccharide stimulation. Database analysis of C. parvum-upregulated miRNAs revealed potential NF-κB binding sites in the promoter elements of a subset of miRNA genes. We demonstrated that mir-125b-1, mir-21, mir-30b, and mir-23b-27b-24-1 cluster genes were transactivated through promoter binding of the NF-κB p65 subunit following C. parvum infection. In contrast, C. parvum transactivated mir-30c and mir-16 genes in cholangiocytes in a p65-independent manner. Importantly, functional inhibition of selected p65-dependent miRNAs in cholangiocytes increased C. parvum burden. Thus, we have identified a panel of miRNAs regulated through promoter binding of the NF-κB p65 subunit in human cholangiocytes in response to C. parvum infection, a process that may be relevant to the regulation of epithelial anti-microbial defense in general

Synthesis and Application of Carbon–Iron Oxide Microspheres’ Black Pigments in Electrophoretic Displays

Carbon–iron oxide microspheres’ black pigments (CIOMBs) had been prepared via ultrasonic spray pyrolysis of aqueous solutions containing ferrous chloride and glucose. Due to the presence of carbon, CIOMBs not only exhibited remarkably acid resistance, but also could be well dispersed in both polar solvents and nonpolar solvent. Finally, dispersions of hollow CIOMBs in tetrachloroethylene had successfully been applied in electrophoretic displays

Evaluation of the association between the common E469K polymorphism in the ICAM-1 gene and diabetic nephropathy among type 1 diabetic patients in GoKinD population

<p>Abstract</p> <p>Background</p> <p>The ICAM-1 gene is a strong positional and biological candidate for susceptibility to the development of T1D and DN. We have recently demonstrated that SNP rs5498(E469K) confers susceptibility to the development of T1D and might be associated with DN in Swedish Caucasians. The present study aimed to further evaluate the association between the ICAM-1 genetic polymorphisms and DN.</p> <p>Methods</p> <p>Two common non-synonymous SNPs, including rs5498(E469K) and rs1799969(R241G), in the ICAM-1 gene were genotyped in 662 (312 female/350 male) T1D patients with DN and 620 (369/251) without DN. All patients were selected from the GoKinD study.</p> <p>Results</p> <p>Genotype distributions of both SNPs were in Hardy-Weinberg equilibrium but SNP rs5498(E469K) had high heterozygous index. In this SNP, the heterozygosity and positivity for the allele G were found to be significantly associated with DN in female T1D patients (P = 0.010, OR = 0.633, CI 95% 0.447–0.895 and P = 0.026, OR = 0.692, CI 95% 0.500–0.958). Furthermore, the female patients without DN carrying three genotypes A/A, A/G and G/G had different cystatin levels (0.79 ± 0.17, 0.81 ± 0.14 and 0.75 ± 0.12 mg/L, P = 0.021). No significant association of SNP rs1799969 (R241G) with DN was found.</p> <p>Conclusion</p> <p>The present study provides further evidence that SNP rs5498(E469K) in the ICAM-1 gene presents a high heterozygous index and the allele G of this polymorphism may confers the decreased risk susceptibility to the development of DN in female T1D patients among the GoKinD population.</p

Superhydrophobic Surface Based on a Coral-Like Hierarchical Structure of ZnO

Background: Fabrication of superhydrophobic surfaces has attracted much interest in the past decade. The fabrication methods that have been studied are chemical vapour deposition, the sol-gel method, etching technique, electrochemical deposition, the layer-by-layer deposition, and so on. Simple and inexpensive methods for manufacturing environmentally stable superhydrophobic surfaces have also been proposed lately. However, work referring to the influence of special structures on the wettability, such as hierarchical ZnO nanostructures, is rare. Methodology: This study presents a simple and reproducible method to fabricate a superhydrophobic surface with microscale roughness based on zinc oxide (ZnO) hierarchical structure, which is grown by the hydrothermal method with an alkaline aqueous solution. Coral-like structures of ZnO were fabricated on a glass substrate with a micro-scale roughness, while the antennas of the coral formed the nano-scale roughness. The fresh ZnO films exhibited excellent superhydrophilicity (the apparent contact angle for water droplet was about 0u), while the ability to be wet could be changed to superhydrophobicity after spin-coating Teflon (the apparent contact angle greater than 168u). The procedure reported here can be applied to substrates consisting of other materials and having various shapes. Results: The new process is convenient and environmentally friendly compared to conventional methods. Furthermore, the hierarchical structure generates the extraordinary solid/gas/liquid three-phase contact interface, which is the essentia

Synthesis of Aqueous CdTe/CdS/ZnS Core/shell/shell Quantum Dots by a Chemical Aerosol Flow Method

This work described a continuous method to synthesize CdTe/CdS/ZnS core/shell/shell quantum dots. In an integrated system by flawlessly combining the chemical aerosol flow system working at high temperature (200–300°C) to generate CdTe/CdS intermediate products and an additional heat-up setup at relatively low temperature to overcoat the ZnS shells, the CdTe/CdS/ZnS multishell structures were realized. The as-synthesized CdTe/CdS/ZnS core/shell/shell quantum dots are characterized by photoluminescence spectra, X-ray diffraction (XRD), energy-dispersive X-ray spectra (EDS), transmission electron microscopy (TEM), and high-resolution transmission electron microscopy (HRTEM). Fluorescence and XRD results confirm that the obtained quantum dots have a core/shell/shell structure. It shows the highest quantum yield above 45% when compared to the rhodamine 6G. The core/shell/shell QDs were more stable via the oxidation experiment by H2O2

Potential new genes for resistance to Mycosphaerella graminicola identified in Triticum aestivum x Lophopyrum elongatum disomic substitution lines.

Lophopyrum species carry many desirable agronomic traits, including disease resistance, which can be transferred towheat by interspecific hybridization. To identify potentially new genes for disease and insect resistance carried by individual Lophopyrum chromosomes, 19 of 21 possible wheat cultivar Chinese Spring 9 Lophopyrum elongatum disomic substitution lines were tested for resistance to barley yellow dwarf virus (BYDV), cereal yellow dwarf virus (CYDV), the Hessian fly Mayetiola destructor, and the fungal pathogens Blumeria graminis and Mycosphaerella graminicola (asexual stage: Septoria tritici). Low resistance to BYDV occurred in some of the disomic substitution lines, but viral titers were significantly higher than those of two Lophopyrum species tested. This suggested that genes on more than one Lophopyrum chromosome are required for complete resistance to this virus. A potentially new gene for resistance to CYDV was detected on wheatgrass chromosome 3E. All of the substitution lines were susceptible to Mayetiola destructor and one strain of B. graminis. Disomic substitution lines containing wheatgrass chromosomes 1E and 6E were significantly more resistant to M. graminicola compared to Chinese Spring. Although neither chromosome by itself conferred resistance as high as that in the wheatgrass parent, they do appear to contain potentially new genes for resistance against this pathogen that could be useful for future plant-improvement programs

Methylenetetrahydrofolate reductase C677T polymorphism in patients with lung cancer in a Korean population

<p>Abstract</p> <p>Background</p> <p>This study was designed to investigate an association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and the risk of lung cancer in a Korean population.</p> <p>Methods</p> <p>We conducted a large-scale, case-control study involving 3938 patients with newly diagnosed lung cancer and 1700 healthy controls. Genotyping was performed with peripheral blood DNA for MTHFR C677T polymorphisms. Statistical significance was estimated by logistic regression analysis.</p> <p>Results</p> <p>The MTHFR C677T frequencies of CC, CT, and TT genotypes were 34.5%, 48.5%, and 17% among lung cancer patients, and 31.8%, 50.7%, and 17.5% in the controls, respectively. The MTHFR 677CT and TT genotype showed a weak protection against lung cancer compared with the homozygous CC genotype, although the results did not reach statistical significance. The age- and gender-adjusted odds ratio (OR) of overall lung cancer was 0.90 (95% confidence interval (CI), 0.77-1.04) for MTHFR 677 CT and 0.88 (95% CI, 0.71-1.07) for MTHFR 677TT. However, after stratification analysis by histological type, the MTHFR 677CT genotype showed a significantly decreased risk for squamous cell carcinoma (age- and gender-adjusted OR, 0.78; 95% CI, 0.64-0.96). The combination of 677 TT homozygous with 677 CT heterozygous also appeared to have a protection effect on the risk of squamous cell carcinoma. We observed no significant interaction between the MTHFR C677T polymorphism and age and gender or smoking habit.</p> <p>Conclusions</p> <p>This is the first reported study focusing on the association between MTHFR C677T polymorphisms and the risk of lung cancer in a Korean population. The T allele was found to provide a weak protective association with lung squamous cell carcinoma.</p

Association between HLA-DRB1 alleles polymorphism and hepatocellular carcinoma: a meta-analysis

<p>Abstract</p> <p>Background</p> <p>HLA-DRB1 allele polymorphisms have been reported to be associated with hepatocellular carcinoma susceptibility, but the results of these previous studies have been inconsistent. The purpose of the present study was to explore whether specific HLA-DRB1 alleles (DRB1*07, DRB1*12, DRB1*15) confer susceptibility to hepatocellular carcinoma.</p> <p>Methods</p> <p>Case-control studies on HLA-DRB1 alleles association with HCC were searched up to January 2010 through a systematic review of the literature. The odds ratios (ORs) of HLA-DRB1 allele distributions in patients with hepatocellular carcinoma were analyzed against healthy controls. The meta-analysis software REVMAN 5.0 was applied for investigating heterogeneity among individual studies and for summarizing all the studies. Meta-analysis was performed using fixed-effect or random-effect methods, depending on absence or presence of significant heterogeneity.</p> <p>Results</p> <p>Eight case-control studies were included in the final analysis. Among the 3 HLA-DRB1 alleles studied, DRB1*07 and DRB1*12 were significantly associated with the risk of HCC in the whole populations (OR = 1.65, 95% CI: 1.08-2.51, P = 0.02 and OR = 1.59, 95% CI: 1.09-2.32, P = 0.02, respectively). No significant association was established for DRB1*15 allele with HCC in the whole populations. Subgroup analysis by ethnicity showed that DRB1*07, DRB1*12 and DRB1*15 alleles significantly increased the risk of hepatocellular carcinoma in Asians (OR = 2.10, 95% CI: 1.06-4.14, P = 0.03; OR = 1.73, 95% CI: 1.17-2.57, P = 0.006 and <b><it>OR </it></b>= 2.88, <it><b>95%CI: 1</b></it>.77-4.69, P <<it><b>0.001</b></it>, respectively).</p> <p>Conclusion</p> <p>These results support the hypothesis that specific HLA-DRB1 alleles might influence the susceptibility of hepatocellular carcinoma. Large, multi-ethnic confirmatory and well designed studies are needed to determine the host genetic determinants of hepatocellular carcinoma.</p