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Increasing crystallize size or aluminum content in MFI-type zeolites independently enhances the propagation of the aromatics-based methylation/dealkylation cycle relative to that of the olefins-based methylation/cracking cycle in methanol-to-hydrocarbons (MTH) conversion and consequentially results in higher ethene selectivity. Ethene selectivity increases monotonically with increasing aluminum content for HZSM-5 samples with nearly identical crystallite size consequent to an increase in the intracrystalline contact time analogous to our recent report detailing the effects of crystallite size (Khare et al., 2015) on MTH selectivity. The confected effects of crystallite size and site density on MTH selectivity can therefore, be correlated using a descriptor that represents the average number of acid sites that an olefin-precursor will interact with before elution. [ABSTRACT FROM AUTHOR]

Background High mobility group box-1 (HMGB1) acts as an inflammatory mediator and has been implicated in pathophysiological damage of vascular inflammatory diseases. Ketamine, an anesthetic agent with sedative and analgesic properties, has been shown to have potent anti-inflammatory effects in a variety of models of systemic inflammation. However, the effects of ketamine on HMGB1-mediated proinflammatory responses have not been fully investigated. In the present study, we investigated the effects of ketamine on HMGB1-activated endothelial cells and explored the underlying mechanisms. Methods Human endothelial cells were incubated with or without HMGB1 (1 μg/mL) in the presence or absence of ketamine, an nuclear factor (NF)-κB inhibitor (PDTC), anti–toll-like receptor (TLR)2/4 antibody, or small interfering RNA (siRNA). The anti-inflammatory activities of ketamine were determined by measuring solute flux, leukocyte adhesion and migration, and activation of proinflammatory proteins in HMGB1-activated endothelial cells. The effect of ketamine on TLR-2/4 and NF-κB activation was evaluated using enzyme-linked immunosorbent assays and immunofluorescence confocal microscopy assay. Results We found that ketamine inhibited the HMGB1-mediated barrier disruption, neutrophil adhesion and migration, and expression of cell adhesion molecules in a dose-dependent manner. Furthermore, ketamine downregulated the TLR-2 and -4, expression in HMGB1-activated endothelial cells. Treatment with ketamine also significantly inhibited the activation of TLR2/4 and the nuclear translocation of NF-κB p50/p65. Furthermore, our study shows that the HMGB1-induced release of inflammatory mediators was suppressed by PDTC, anti-TLR2/4 antibody, and siRNA. Conclusions Our study has demonstrated that ketamine exerts anti-inflammatory effects in HMGB1-mediated proinflammatory responses in a dose-dependent manner. The mechanism responsible for these effects involves the TLR2/4 and NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

The high prevalence and serious long-term sequelae of Trichomonas vaginalis (TV) infection worldwide is of a particular concern; however, data regarding the differences in the composition of the vaginal microbiome in cases of single TV infection or mixed infections (i.e., presence of TV and bacterial vaginosis) are scarce. We employed metagenomic sequencing analyses to study gene expression in the vaginal microbiota of women with single TV infection and mixed infection. Women infected with only TV had significantly higher abundance of Mycoplasma, Prevotella , and Streptococcus compared to women without vaginal infection (control). Women infected with mixed infections had a significantly higher abundance of Mycoplasma , Prevotella , Streptococcus , Anaerococcus , Dialister , Peptostreptococcus , Peptoniphilus and a significantly lower abundance of Lactobacillus than TV alone. Mixed infections had a significantly higher abundance of Prevotella , Anaerococcus and Dialister. Our findings suggest that the bacterial community composition varies among healthy women, women with TV alone, and those with mixed infection, and we hypothesize that these bacterial vaginosis (BV)-associated bacterium may play a role in the pathogenesis and recurrence of TV. Probiotic pessaries may necessarily be the answer because shifting the vaginal microbiome and host responses is probably a complex undertaking. • Vaginal microbiome of Chinese women with Trichomonas vaginalis and mixed infection. • Bacterial vaginosis (BV)-associated bacterium and TV. • Vaginal Lactobacillus and TV. [ABSTRACT FROM AUTHOR]

Vulvovaginal candidiasis (VVC) affects approximately 75% of all women of during their reproductive years. Previously, we reported that recombinant human IFN α-2b (rhIFNα-2b) protects vaginal epithelial cells from candidal injury in vitro. In the current study, we examined the effects of rhIFNα-2b (1.25 mg/mL, 10% inhibition concentration) on fungal clearance, immunocompetent cytokine responses, non-B IgG production, and tissue repair in a rat model of VVC. Following rhIFNα-2b treatment, the negative pathogen conversion rate reached 50.0% (3/6). Although rhIFNα-2b exhibited a limited ability to decrease inflammation and injury progression (P > 0.05), the Flameng mitochondrial injury scores were significantly reduced (P < 0.001) compared with those of the Model rats. After rhIFNα-2b treatment, the levels of IFN-γ and epithelial-derived IgG (tested by RP215) in vaginal tissues were significantly increased with those in the Control and Model groups (both P < 0.001), while there were no significant differences in the levels of IL-4 and IL-17 (P > 0.05). This is the first study to address the efficacy of rhIFNα-2b in treating VVC in a rat model, providing a theoretical basis for development of this promising treatment for clinical use. • RhIFNα-2b administration protects host response against yeast via stimulating immune protection and reduces the vaginal epithelial damage.. • RhIFNα-2b administration increases the expression of vaginal epithelial-derived IgG and regulates antibody-mediated protection. • RhIFNα-2b administration reduces the damage to the vaginal epithelium. [ABSTRACT FROM AUTHOR]

Abstract Recently, several long non-coding RNAs (lncRNAs) have been revealed to play crucial roles in tumorigenesis and progression of many cancers. Nevertheless, more than 50,000 lncRNAs were identified in human cells and the roles of majority of these lncRNAs in non-small cell lung cancer (NSCLC) are unknown. In this study, using public NSCLC microarray data we identified a novel lncRNA BRE antisense RNA 1 (BRE-AS1). BRE-AS1 is significantly down-regulated in NSCLC tissues and cell lines. Gain-of-function and loss-of-function assays showed that BRE-AS1 reduces NSCLC cell viability, represses NSCLC cell proliferation, and induces NSCLC cell apoptosis in vitro , and represses NSCLC tumor growth in vivo. Mechanistic investigation revealed that BRE-AS1 physically binds STAT3, reduces the binding of STAT3 to the promoter of NR4A3 , relieves the repression of NR4A3 caused by STAT3, and up-regulates NR4A3 expression. Consistently, NR4A3 is significantly down-regulated in NSCLC tissues and the expression of NR4A3 is positively correlated with the expression of BRE-AS1 in NSCLC tissues. In addition, depletion of NR4A3 attenuates the tumor suppressive roles of BRE-AS1 in NSCLC. Collectively, our data demonstrate that BRE-AS1 represses NSCLC cell growth and survival via up-regulating NR4A3 and suggest that enhancing BRE-AS1 may be potential therapeutic strategy for NSCLC. [ABSTRACT FROM AUTHOR]

Diabetes mellitus type 2 (DM2) results in bone abnormalities that manifest as increased bone fragility. Bone consists of two phases, the mineral phase and the matrix phase, and disorders in both are seen in DM2. However, the phase in which DM2 mediated bone fragility is initiated is still unknown. In this study, a male Zucker diabetic fatty (fa/fa) (ZDF) rat model was used to investigate the underlying mechanism initiating DM2 mediated bone fragility. The fracture surface morphology, pre- and post-yield bone mechanical behavior, insoluble collagen volume, lysyl oxidase family (LOX) enzyme levels and correlation analysis was performed to determine the relationship between insoluble collagen and post-yield behavior. Four weeks after the induction of diabetes, insoluble collagen was decreased in only the matrix phase in diabetic rats. Consistently, mechanical testing of the bone showed changes only in post-yield behavior. Diabetic rats also had decreased levels of enzymes involved in insoluble collagen formation (LOX and LOXL1 families). Correlation analysis demonstrated that insoluble collagen was a positive regressor of post-yield displacement (R = 0.894, P < 0.001) and post-yield energy (R = 0.918, P < 0.001). Together, these findings suggest that bone fragility in DM2 is initiated in the matrix phase and that the LOX family may play a critical part in the pathogenesis of DM2 mediated bone fragility. [ABSTRACT FROM AUTHOR]

The ascomycete Pyrenophora tritici-repentis ( Ptr ) is an important fungal pathogen worldwide that causes tan spot of wheat. The fungus is self-fertile because each isolate contains both mating type ( MAT ) idiomorphs. In this work, we developed knockouts of the MAT genes in Ptr and tested fertility of the knockout strains and outcrossing between the knockout strains carrying the opposite mating type. The fungal strains with deletions of either MAT1-1 - 1 or MAT1-2 - 1 did not form mature pseudothecia making them functionally heterothallic. The cross between the heterothallic strains of the same isolate (86–124) was fully fertile with the only difference compared to the homothallic wild type strain being the slightly lower percentage of pseudothecium formation. However, the cross between 86–124 (race 2, ToxA -containing isolate) and DW5 (race 5, ToxB -containing isolate) was partially fertile and had fewer mature pseudothecia. Furthermore, most mature asci produced only two or four instead of eight functional ascospores. A collection of ascospores from this cross was obtained and genotyped for the presence of the ToxA , ToxB and MAT genes as well as simple sequence repeat markers. The segregation of these genes and markers and recombination of different allele types at these loci was observed. This work clearly demonstrates that the fungus requires both MAT genes for sexual production and can undergo outcrossing and sexual recombination. It also establishes a new and practical way for further characterizing fungal virulence in Ptr through the development of segregating fungal populations and subsequent genetic analysis. [ABSTRACT FROM AUTHOR]

Culture filtrates (CFs) of the fungal wheat pathogen Zymoseptoria tritici were assayed for necrosis-inducing activity after infiltration in leaves of various wheat cultivars. Active fractions were partially purified and characterized. The necrosis-inducing factors in CFs are proteinaceous, heat stable and their necrosis-inducing activity is temperature and light dependent. The in planta activity of CFs was tested by a time series of proteinase K (PK) co-infiltrations, which was unable to affect activity 30 min after CF infiltrations. This suggests that the necrosis inducing proteins (NIPs) are either absent from the apoplast and likely actively transported into mesophyll cells or protected from the protease by association with a receptor. Alternatively, plant cell death signaling pathways might be fully engaged during the first 30 min and cannot be reversed even after PK treatment. Further fractionation of the CFs with the highest necrosis-inducing activity involved fast performance liquid chromatography, SDS–PAGE and mass spectrometry. This revealed that most of the proteins present in the fractions have not been described before. The two most prominent ZtNIP encoding candidates were heterologously expressed in Pichia pastoris and subsequent infiltration assays showed their differential activity in a range of wheat cultivars. [ABSTRACT FROM AUTHOR]

• The first genetic linkage map was developed in P. tritici-repentis. • ToxA and mating type genes mapped to the expected chromosomal locations. • A high-quality genome sequence was developed for a new race of P. tritici-repentis. • Our work provides valuable tools for gene cloning and comparative genomics in P. tritici-repentis. Pyrenophora tritici-repentis is an ascomycete fungus that causes tan spot of wheat. The disease has a worldwide distribution and can cause significant yield and quality losses in wheat production. The fungal pathogen is homothallic in nature, which means it can undergo sexual reproduction by selfing to produce pseudothecia on wheat stubble for seasonal survival. Since homothallism precludes the development of bi-parental fungal populations, no genetic linkage map has been developed for P. tritici-repentis for mapping and map-based cloning of fungal virulence genes. In this work, we created two heterothallic strains by deleting one of the mating type genes in each of two parental isolates 86–124 (race 2) and AR CrossB10 (a new race) and developed a bi-parental fungal population between them. The draft genome sequences of the two parental isolates were aligned to the Pt-1C-BFP reference sequence to mine single nucleotide polymorphisms (SNPs). A total of 225 SNP markers were developed for genotyping the entire population. Additionally, 75 simple sequence repeat, and two gene markers were also developed and used in the genotyping. The resulting linkage map consisted of 13 linkage groups spanning 5,075.83 cM in genetic distance. Because the parental isolate AR CrossB10 is a new race and produces Ptr ToxC, it was sequenced using long-read sequencing platforms and de novo assembled into contigs. The majority of the contigs were further anchored into chromosomes with the aid of the linkage maps. The whole genome comparison of AR CrossB10 to the reference genome of M4 revealed a few chromosomal rearrangements. The genetic linkage map and the new AR CrossB10 genome sequence are valuable tools for gene cloning in P. tritici-repentis. [ABSTRACT FROM AUTHOR]