Control of Cluster Structures in Catalyst Inks by a Dispersion Medium.

The cluster structure in the catalyst ink of a proton exchange membrane fuel cell determines its performance. The interaction among solvent, ionomer, and catalyst in ink determines the cluster structure and affects the microstructure and surface morphology of the catalyst layer, which is of great significance to improve the conductivity of the catalyst layer to protons, electrons, and water. First, the dissolved state of the main chain and the side chain of the ionomer in solvent was characterized. The results of relative viscosity, ζ-potential, effective proton fraction, and nuclear magnetic resonance (NMR) showed that the alcohol aqueous solution promoted the stretching electrolysis of the main chain and the side chain of the ionomer more than the pure aqueous solvent, making the ionomer clusters smaller. The rheological test of the ink shows that the pure water solvent ink has the largest cluster and the strongest network structure. Under the test conditions, the clusters in the ink can be reconstructed quickly after breakage through viscous shearing. The addition of alcohols will make the clusters in the ink smaller and the network structure brittle. After the clusters and the network structure are damaged, they will slowly recombine and the viscosity in the ink will gradually recover. Ethanol will minimize the clusters in the ink, and the network structure in the ink is the weakest. The effect of the network strength on the cluster structure is weakened by reducing the solid content in the ink. The amplitude scanning test shows that the network structure in the slurry is almost eliminated after reducing the solid content, the storage modulus of ink with water, 50 wt % isopropyl alcohol (IPA), 50 wt % n-propanol (NPA), and 50 wt % ethanol (ET) decreases in turn, as well as the liquid viscosity behavior increases and the cluster particle size in the ink decreases. In conclusion, more dispersed ionomers and alcohol molecules with smaller molecular structures are more conducive to the dispersion of clusters in the ink.

Effectiveness of digestive endoscopy and surgery in the treatment of necrotizing pancreatitis: a meta-analysis and systematic review.

BACKGROUND: Digestive endoscopy and surgery are the primary invasive methods for the clinical treatment of necrotizing pancreatitis. However, there are relatively few studies evaluating the effectiveness and safety of these two methods. METHODS: Randomized controlled trials (RCTs) on endoscopic and surgical treatment of necrotizing pancreatitis published from January 2000 to December 2020 were searched in the PubMed, Medline, Embase, China Biology Medicine Disc (CBM), and WanFang databases. The Cochrane System Review Manual was adopted to evaluate the quality of the included literature, and Review Manager 5.3 was used for data analysis. RESULTS: Ten articles were included in this meta-analysis, involving a total of 401 patients, including 188 in the endoscopy group and 213 in the surgery group. Meta-analysis results revealed that the clinical remission rate (CRR) [odds ratio (OR) =1.30, 95% confidence interval (CI): 0.58-2.92, P=0.52], new organ failure rate (OFR) (OR =0.53, 95% CI: 0.26-1.09, P=0.08), abdominal bleeding rate (ABR) (OR =0.62, 95% CI: 0.33-1.15, P=0.13), and intensive care unit (ICU) stay time (IST) [mean deviation (MD) =-7.33, 95% CI: -16.76 to 2.11, P=0.13] were not significantly different between the endoscopy and surgery groups. In the endoscopy group, the mortality rate (OR =0.56, 95% CI: 0.31-1.02, P=0.05), intestinal fistula rate (IFR) or gastrointestinal perforation rate (GPR) (OR =0.50, 95% CI: 0.26-0.99, P=0.05), and pancreatic fistula rate (PFR) (OR =0.09, 95% CI: 0.04-0.23, P<0.00001) were markedly lower compared to the surgery group. DISCUSSION: There was no obvious difference in the clinical efficacy of endoscopic and surgical treatment of necrotizing pancreatitis. However, endoscopy can greatly reduce the incidence of postoperative death and major complications in patients.

Dexmedetomidine Suppressed the Biological Behavior of HK-2 Cells Treated with LPS by Down-Regulating ALKBH5.

Dexmedetomidine inhibits the release of inflammatory cytokines and exerts a systemic anti-inflammatory effect and has potential protective effects on vital organs such as lung, heart, and kidneys. The aim of this study was to investigate the effect of dexmedetomidine on LPS-treated HK-2 cells in vitro and explore the potential mechanisms. The HK-2 cells were pretreated with dexmedetomidine before LPS induction. CCK-8, flow cytometry, ELISA, or qRT-PCR was performed to detect cell proliferation, apoptosis, and proinflammatory cytokine expression. The levels of MALAT1 in HK-2 cells under different stimulation were measured by qRT-PCR. Then, m6A RNA immunoprecipitation was performed to detect methylated MALAT1 in HK-2 cells. The results showed dexmedetomidine suppressed cell viability, induced cell apoptosis, and reduced inflammation cytokine production of LPS-treated HK-2 cells. Besides, dexmedetomidine reduced the expression of MALAT1 in HK-2 cells under LPS stimulation. In addition, ALKBH5 could up-regulate MALAT1 expression by demethylation. Furthermore, dexmedetomidine inhibited the expression of ALKBH5 in LPS-treated HK-2 cells. ALKBH5 knockdown inhibited cell viability, induced cell apoptosis, and decreased inflammation cytokine production of LPS-treated HK-2 cells. In short, dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which may provide potential targets for the prevention and treatment of sepsis-induced kidney injury.

Relevance of methylenetetrahydrofolate reductase gene variants C677T and A1298C with response to fluoropyrimidine-based chemotherapy in colorectal cancer: a systematic review and meta-analysis.

Methylenetetrahydrofolate reductase (MTHFR) is a critical enzyme influencing the metabolism of fluoropyrimidines. The relevance of MTHFR polymorphisms with the clinical response to fluoropyrimidine-based chemotherapy has been explored, but the results remain controversial. Thus, a meta-analysis was performed to provide a comprehensive estimate in this account. Relevant studies were identified through PubMed, Embase and Web of Science databases from inception up to May 2017. Odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were applied to assess the strength of association. A total of 2118 colorectal cancer patients from 21 studies were included in the meta-analysis. Overall, there was no significant association between MTHFR C677T (rs1801133) or A1298C (rs1801131) polymorphisms and the clinical response to fluoropyrimidine-based chemotherapy under all of the three genetic models (allele model, dominant model, and recessive model) and stratification analysis, except for the retrospective study subgroup in the dominant model of MTHFR C677T and the "5-Fu + FA" treatment group in the allele contrast of MTHFR A1298C. No or moderate heterogeneity was observed in all genetic models. This meta-analysis suggested that MTHFR polymorphisms could not be considered as reliable factors for predicting the clinical response to fluoropyrimidine-based chemotherapy in colorectal cancer patients.

Continuous electrochemical oxidation of methyl orange waste water using a three-dimensional electrode reactor.

The removal of methyl orange wastewater was experimentally investigated using a three-dimensional electrode reactor with granular activated carbon and titanium filter electrodes arrays. The effects of the electric current, the residence time and the initial dye concentration on the methyl orange removal were evaluated. For the initial concentration of 1150 mg/L, the COD removal was obtained as 90% under the conditions of electric current 2 A, residence time 40 min. The effluent path of the electrochemical cell was optimized, using the anode effluent instead of the top effluent, where the COD removal was increased to 93% and the corresponding energy consumption was decreased from 15.5 to 14.6 kW-hr/kg COD.

Investigation of variants in the promoter region of PIK3C3 in schizophrenia.

The PIK3C3 gene has been implicated as a candidate gene for schizophrenia by functional evidence and genetic association studies. A series of previous studies have found susceptibility SNPs in promoter region. To further verify its susceptibility to schizophrenia in the Chinese population and the function of the polymorphisms, we performed a case control study in 556 unrelated schizophrenia patients and 563 normal controls as well as an in vitro functional analysis. In our association analysis of-432C-/T, we discovered obvious differences in allele frequency between patients and controls (P=0.017). A T/C haplotype constructed by -432C-/T and -86insC, which are tightly linked with each other (r(2)=1) can significantly weaken promoter's transcriptional activity by 20% (p=0.002 by t-test). Though we cannot exclude the possibility that susceptibility of -432C-/T is caused by its linkage disequilibrium with other causal variants, our results do support PIK3C3 play a significant role in the etiology of schizophrenia.

A case-control association study between the GRID1 gene and schizophrenia in the Chinese Northern Han population.

The glutamatergic dysfunction hypothesis of schizophrenia implicates the genes involved in glutamatergic transmission as strong candidates for schizophrenia-susceptibility. Recent linkage and association studies have identified the glutamate receptor, ionotropic, delta 1 gene GRID1 on 10q22 as a strong candidate for schizophrenia. In this current association study, we genotyped five genetic variants within the GRID1 gene in 567 Chinese Han subjects recruited from Northeast of China (260 schizophrenics and 307 normal controls). Four SNPs, rs1902666 (P=0.024), rs2814351 (P=0.027), rs11591408 (P=0.0000107) and rs999383 (P=0.000093) were found to be significantly associated with schizophrenia. Haplotype analysis also revealed significance with global P values of 0.0081 and 0.00076 for SNPs 1-2 and SNPs 3-4-5 haplotypes, respectively. Our results strongly support previously reported association studies, implicating GRID1 in the etiology of schizophrenia.

A novel Ir-hexaaluminate catalyst for N(2)O as a propellant.

Aiming for designing a novel catalyst for N(2)O as a green propellant, Ir-substituted hexaaluminate, which can initiate N(2)O decomposition at 623 K and can sustain the stability at 1473 K, has been developed for the first time.

Brain-derived neurotrophic factor and risk of schizophrenia: an association study and meta-analysis.

Brain-derived neurotrophic factor (BDNF) is the most widely distributed neurotrophin in the central nervous system (CNS), and performs many biological functions such as neural survival, differentiation, and plasticity. Previous studies have suggested that variants in the BDNF gene increase the risk of schizophrenia. In this study, we genotyped one (GT)n dinucleotide repeat and three SNPs (rs6265, rs2030324, and rs2883187) in a Chinese sample (617 cases and 672 controls). In addition, we performed an updated meta-analysis based on 16 population-based case-control studies examining association between rs6265 and schizophrenia. In single-locus analysis, no significant association was found between BDNF polymorphisms and schizophrenia in our subjects. The meta-analysis based on Asian and Caucasian subjects did not give positive result that rs6265 is associated with schizophrenia. However, haplotype analysis found a common four-locus haplotype is protective against schizophrenia (Case 3.1% vs Control 7%, p=0.0011). Our data provides evidence that BDNF is a susceptibility gene for schizophrenia in Chinese subjects.

Functional variants in the promoter region of Chitinase 3-like 1 (CHI3L1) and susceptibility to schizophrenia.

The chitinase 3-like 1 gene (CHI3L1) is abnormally expressed in the hippocampus of subjects with schizophrenia and may be involved in the cellular response to various environmental events that are reported to increase the risk of schizophrenia. Here, we provide evidence that the functional variants at the CHI3L1 locus influence the genetic risk of schizophrenia. First, using case-control and transmission/disequilibrium-test (TDT) methodologies, we detected a significant association between schizophrenia and haplotypes within the promoter region of CHI3L1 in two independent cohorts of Chinese individuals. Second, the at-risk CCC haplotype (P=.00058 and .0018 in case-control and TDT studies, respectively) revealed lower transcriptional activity (P=2.2 x 10(-7)) and was associated with lower expression (P=3.1 x 10(-5)) compared with neutral and protective haplotypes. Third, we found that an allele of SNP4 (rs4950928), the tagging SNP of CCC, impaired the MYC/MAX-regulated transcriptional activation of CHI3L1 by altering the transcriptional-factor consensus sequences, and this may be responsible for the decreased expression of the CCC haplotype. In contrast, the protective TTG haplotype was associated with a high level of CHI3L1 expression. Our findings identify CHI3L1 as a potential schizophrenia-susceptibility gene and suggest that the genes involved in the biological response to adverse environmental conditions are likely to play roles in the predisposition to schizophrenia.

An investigation of the dihydropyrimidinase-like 2 (DPYSL2) gene in schizophrenia: genetic association study and expression analysis.

Several linkage studies support a susceptibility locus for schizophrenia on chromosome 8p21-22. In this study, we investigated a gene mapping to 8p21, dihydropyrimidinase-like 2 (DPYSL2). DPYSL2 plays an important role in axonal formation and dysfunction of DPYSL2 may result in neurodevelopmental abnormalities. In previous studies, the expression of the gene has been shown to display alteration in the brain of schizophrenia patients compared with those of healthy controls. Recently, Nakata and colleagues found polymorphisms in the 3'-end of DPYSL2 to be associated with schizophrenia, especially the paranoid type, in a Japanese population. In this study, we genotyped four SNPs in DPYSL2 in 2552 Chinese Han specimens. Case-control and TDT analyses were performed to detect association of DPYSL2 with schizophrenia. However, no allele, genotype or haplotype association was found. We investigated the expression of DPYSL2 in 29 schizophrenia patients and 54 healthy controls using quantitative real-time PCR and no difference was found between the two groups. In a comparative allele-specific expression test, we used two SNPs as markers. Only a small proportion of heterozygotes revealed a significant difference (>20%) in allele representation. The results indicated the mRNA level did not contribute mainly in the altered expression of the gene in schizophrenia patients. Although our results provided no evidence for DPYSL2 itself as a susceptibility gene for schizophrenia, recent findings have indicated that DPYSL2 may interact with other candidate genes for schizophrenia and be worthy of further studies.

Polymorphisms of myelin-associated glycoprotein gene are associated with schizophrenia in the Chinese Han population.

Results of gene expression microarray and quantitative PCR studies have suggested abnormalities in the expression of myelin-related genes including myelin-associated glycoprotein (MAG) in schizophrenic patients. Research provides strong evidence for oligodendrocyte dysfunction in schizophrenics. In order to further assess the role of MAG in schizophrenia, we examined four single nucleotide polymorphisms (SNPs), namely rs2301600, rs3746248, rs720309 and rs720308, of this gene in Chinese schizophrenic patients (n=470) and healthy controls (n=470). The distribution of rs720309 T/A genotypes showed a strong association with schizophrenia (chi(2)=14.58, d.f.=2, P=0.0008). A haplotype constructed of rs720309-rs720308 also revealed a significant association with schizophrenia (chi(2)=11.914, d.f.=3, P=0.0084). Our findings of a significant associations between schizophrenia and the MAG gene suggest that this gene may be involved in susceptibility to schizophrenia in the Chinese Han population.

Positive association of the human GABA-A-receptor beta 2 subunit gene haplotype with schizophrenia in the Chinese Han population.

A converging body of evidence implicates the gamma-amino butyric acid neurotransmitter system in the pathogenesis of schizophrenia. Recently, Lo et al. reported strong positive association between schizophrenia and GABRB2, demonstrated by single markers and haplotypes of five markers in introns of GABRB2, rs6556547, rs1816071, rs194072, rs252944, and rs187269. To validate this linkage disequilibrium report, we genotyped these five SNPs and additional rs1816072 in 352 Chinese Han family trios. Though we failed to detect any positive results in single markers, we did find a significant haplotypic association (global p = 0.00157-0.00588) which had not been identified in Lo's study. Our data indicated that the haplotype 'GACTCT' (p = 0.00215, frequency = 53.6%) was overtransmitted which suggests that GABRB2 is in linkage disequilibrium with schizophrenia in the Chinese Han population. The difference between the two studies may be due to the respective analytic power of the two designs. These two independent studies highlighting linkage disequilibrium support the potential involvement of GABRB2 or a nearby gene in the genetic etiology of schizophrenia.

SNPs and haplotypes in the S100B gene reveal association with schizophrenia.

The S100B gene locates in 21q22.3 and produces neurotrophin mainly in astrocytes of CNS which can act as an extensive marker of glial cell integrity. The synaptic destabilization hypothesis (GGF/SD) suggests that the functional deficiency of growth factors like S100B is involved in the etiology of schizophrenia and the S100B serum concentration is reported to be significantly increased in patients with acute schizophrenia and decreased in chronic schizophrenia patients. To validate the association between S100B and schizophrenia, 384 cases and 401 controls, all Chinese Han subjects, were recruited. Four SNPs V1 (-960C>G), V2 (-111C>T), V3 (2757C>G, rs1051169), and V4 (5748C>T, rs9722) were studied. And haplotype V3-V4 (G-C) showed a significant association with schizophrenia. Our study showed an association between schizophrenia and a possible susceptible haplotype V3-V4 (G-C) which possesses a genetic tendency for increased S100B expression. Our results suggest that S100B could be a susceptible gene for schizophrenia and provide indirect evidence for the GGF/SD hypothesis.

No genetic association between polymorphisms in the AMPA receptor subunit GluR4 gene (GRIA4) and schizophrenia in the Chinese population.

The glutamatergic dysfunction hypothesis of schizophrenia suggests genes involved in glutamatergic transmission as candidates for schizophrenia-susceptibility genes. It has recently been reported that some haplotypes in the AMPA receptor subunit GluR4 Gene (GRIA4), which is located on chromosome 11q22, are positively associated with schizophrenia in the Japanese population. In order to assess the role of GRIA4 in schizophrenia, we examined three reported positive SNPs (single nucleotide polymorphisms): rs609239, rs641574 and rs659840 at the GRIA4 locus in schizophrenic cases (n = 372) and controls (n = 392) of the Chinese population. Although we had observed similar allele and genotype frequencies compared with that in the Japanese population, no evidence was found for association with the disease in the analysis of either single nucleotide polymorphisms (all P-values > 0.300) or haplotype relative risk (all P-values > 0.088). Our results suggest that the three SNPs of GRIA4 are unlikely to play a major role in the susceptibility to schizophrenia in the Chinese population.

Genetic structure adds power to detect schizophrenia susceptibility at SLIT3 in the Chinese Han population.

The Chinese Han population, the largest population in the world, has traditionally been geographically divided into two parts, the Southern Han and Northern Han. In practice, however, these commonly used ethnic labels are both insufficient and inaccurate as descriptors of inferred genetic clustering, and can lead to the observation of "spurious association" as well as the concealment of real association. In this study, we attempted to address this problem by using 14 microsatellite markers to reconstruct the population genetic structure in 768 Han Chinese samples, including 384 Southern Han and 384 Northern Han, and in samples from Chinese minorities including 48 Yao and 48 BouYei subjects. Furthermore, with a dense set of markers around the region 5q34-35, we built fine-scale haplotype networks for each population/subpopulation and tested for association to schizophrenia susceptibility. We found that more variants in SLIT3 tend to associate with schizophrenia susceptibility in the genetically structured samples, compared to geographically structured samples and samples without identified population substructure. Our results imply that identifying the hidden genetic substructure adds power when detecting association, and suggest that SLIT3 or a nearby gene is associated with schizophrenia.

[Transmission disequilibrium test of polymorphisms of serotonin transporter gene and schizophrenia based on family trios].

OBJECTIVE: To investigate the relationship between two polymorphisms (Intronic VNTR and 5-HTTLPR) of the serotonin transporter gene and schizophrenia. METHODS: A set of 314 schizophrenic trio samples collected from Shanghai, Xi'an and Jilin regions of China independently was subjected to analysis of the polymorphisms by transmission/disequilibrium test(TDT). RESULTS: No significantly preferential transmission of any allele was detected from both polymorphisms investigated. CONCLUSION: The results suggest that the serotonin transporter gene is unlikely to have a major contribution to susceptibility to schizophrenia in Han Chinese population.