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5% vs. 47.2%, P < 0.001), and drug use (76.2% vs. 59.8%, P < 0.001). Mortality was comparable (8.1% vs. 10.6%, aRR = 1.03, 95% CI 0.71-1.48). Compared to patients delivering without IE, IE complicating delivery was associated with worse maternal and fetal outcomes, including maternal mortality (17.2% vs. <0.01%, aRR = 323.32, 95% CI 127.74-818.37) and preterm birth (55.7% vs. 10.1%, aRR = 3.61, 95% CI 2.58-5.08).

Maternity-associated IE does not appear to confer additional risk for adverse outcome over non-maternity-associated infection. Patients delivering with IE have worse maternal and fetal outcomes than those whose deliveries are not complicated by IE.

Maternity-associated IE does not appear to confer additional risk for adverse outcome over non-maternity-associated infection. Patients delivering with IE have worse maternal and fetal outcomes than those whose deliveries are not complicated by IE.

The aim of the current study was to identify the long noncoding RNAs (lncRNAs) ANRIL function and molecular pathways underlying hepatocellular carcinoma progression.

ANRIL knockdown with specific siRNA, and transfected into HepG2 cells according to the protocol of Lipofectamine 2000. Cell proliferation, apoptosis, migration and metastasis were assessed with MTT assay, flow cytometry and wound healing assay, respectively. Moreover, the expression level of ANRIL, apoptosis-related genes, and the Wnt pathway-associated genes were assessed by real time-PCR and Western blot assay.

Knocking down of ANRIL led to alleviated cell growth and increased cell apoptosis of HepG2 cells through markedly increased expression levels of Bax and Bad. In contrast, dramatically diminished the expressions of anti-apoptotic factors including Bid and Bcl-2 in comparison to the scrambled control group (si-NC). Furthermore, ANRIL silencing resulted in an inactivated Wnt/β-catenin pathway by suppressing key genes associated with this pathway.

Taken together, these findings imply new insights into the regulatory network of the Wnt pathway through lncRNA ANRIL that indicate ANRIL may be a therapeutic factor potential for hepatocellular carcinoma.

Taken together, these findings imply new insights into the regulatory network of the Wnt pathway through lncRNA ANRIL that indicate ANRIL may be a therapeutic factor potential for hepatocellular carcinoma.

The programmed softening occurring during fruit development requires scission of cell-wall polysaccharides, especially pectin. Proposed mechanisms include the action of wall enzymes or hydroxyl radicals. 1-Thioglycerol Enzyme activities found in fruit extracts include pectate lyase (PL) and endo-polygalacturonase (EPG), which, in vitro, cleave de-esterified homogalacturonan in mid-chain by β-elimination and hydrolysis respectively. However, the important biological question of whether PL exhibits action in vivo had not been tested.

We developed a method for specifically and sensitively detecting in-vivo PL products, based on Driselase digestion of cell-wall polysaccharides and detection of the characteristic unsaturated product of PL action.

In model in-vitro experiments, pectic homogalacturonan that had been partially cleaved by commercial PL was digested to completion with Driselase, releasing an unsaturated disaccharide ('ΔUA-GalA'), taken as diagnostic of PL action. ΔUA-GalA was separated from saturated oligogalacibute to fruit softening.

The results provide the first demonstration that PL, previously known from studies of fruit gene expression, proteomic studies and in-vitro enzyme activity, exhibits enzyme action in the walls of soft fruits and may thus be proposed to contribute to fruit softening.The world of long non-coding RNAs (lncRNAs) has opened up massive new prospects in understanding the regulation of gene expression. Not only are there seemingly almost infinite numbers of lncRNAs in the mammalian cell, but they have highly diverse mechanisms of action. In the nucleus, some are chromatin-associated, transcribed from transcriptional enhancers (eRNAs) and/or direct changes in the epigenetic landscape with profound effects on gene expression. The pituitary gonadotrope is responsible for activation of reproduction through production and secretion of appropriate levels of the gonadotropic hormones. As such, it exemplifies a cell whose function is defined through changes in developmental and temporal patterns of gene expression, including those that are hormonally induced. Roles for diverse distal regulatory elements and eRNAs in gonadotrope biology have only just begun to emerge. Here, we will present an overview of the different kinds of lncRNAs that alter gene expression, and what is known about their roles in regulating some of the key gonadotrope genes. We will also review various screens that have detected differentially expressed pituitary lncRNAs associated with changes in reproductive state and those whose expression is found to play a role in gonadotrope-derived nonfunctioning pituitary adenomas. We hope to shed light on this exciting new field, emphasize the open questions, and encourage research to illuminate the roles of lncRNAs in various endocrine systems.

Using a patient simulator, dental professionals were tested to determine their ability to light-polymerize simulated restorations in their dental practice. After receiving specific instructions and training using the simulator, their ability to deliver sufficient light to polymerize restorations was significantly and substantially improved.

Objectives To determine the ability of dental professionals to deliver a radiant exposure of at least six J/cm2 in 10 seconds to simulated restorations.Methods and Materials The study initially examined 113 light-emitting-diode (LED) light polymerization units (LPUs) used in dental offices to determine if they could deliver at least 6 J/cm2 radiant exposure (RE) in 10s. This assessment was completed by using a laboratory-grade light measuring device (checkMARC, BlueLight Analytics, Halifax, NS, Canada). The participating dental professionals whose LPUs could deliver 6 J/cm2 then used their own LPU to light-cure simulated anterior and posterior restorations in the MARC posterior restorations by 22.5% and 30%, respectively.Conclusion This study revealed that at the baseline, 44.7% of participating dental professionals failed to deliver 6 J/cm2 in 10s to the posterior simulated restoration when using their own LPU.Patients with acute myeloid leukemia (AML) have conventionally received more "intense" therapy than patients with myelodysplastic syndromes (MDS). Although less intense therapies are being used more often in AML, the AML-MDS dichotomy remains, with the presence of ≥ 20% myeloblasts in marrow or peripheral blood generally regarded as defining AML. Consequently, patients with 19% blasts are typically ineligible for AML studies, with patients with 21% blasts ineligible for MDS studies. Here we cite biologic and clinical data to question this practice. Biologically, abnormalities in chromosome 3q26,and mutations in NPM1, and FLT3, regarded as AML-associated, also occur in MDS. The genetic signatures of MDS, particularly cases with 10-19% blasts (MDS-EB2), resemble those of AML following a preceding MDS ("secondary AML"). Mutationally, secondary AML appears at least as similar to MDS-EB2 as to de novo AML. Patients presenting with de novo AML but with secondary-type AML mutations, appear to have the same poor prognoses associated with clinically defined secondary AML. Seattle data indicate that after accounting for European LeukemiaNet (ELN) 2017 risk, age, performance status, clinically secondary AML, and treatment including allogeneic transplant, patients with WHO-defined AML (n=769) have similar rates of OS, EFS and CR/CRi as patients with MDS-EB2 (n=202). We suggest defining patients with 10-30% blasts ("AML/MDS") as eligible for either AML or MDS studies. This would permit empirical testing of the independent effect of blast percentage on outcome, allow patients access to more therapies, and potentially simplify the regulatory approval process.

There is no standardized aerosol exposure apparatus to deliver heated tobacco products (HTPs) for in vivo experiments. Therefore, we developed a novel HTPs aerosol exposure apparatus for mice and demonstrated that nicotine and other chemicals in HTPs aerosol generated by the apparatus can be delivered to mice which replicate human smoke.

The amounts of nicotine, tar, and carbon monoxide (CO) in IQOS (Marlboro Regular HeatSticks™) aerosol generated by two types of apparatuses were determined. C57BL/6N mice were exposed to IQOS aerosol, followed by determination of the urinary nicotine metabolites. Further, the skin surface temperature of mice was monitored to confirm the vasoconstriction action of nicotine.

The amounts of chemicals in IQOS aerosol by the novel air push-in inhalation apparatus for HTPs (APIA) was equivalent to that of the analytical vaping machine (LM4E) [1.60 ± 0.08 (APIA) vs 1.46 ± 0.07mg/stick (LM4E) in nicotine and 0.55 ± 0.04 (APIA) vs 0.45 ± 0.01mg/stick (LM4E) in CO]. After mice were exposed to IQOS aerosol by APIA, the urinary nicotine metabolites levels were determined; peak values in cotinine and 3-hydroxycotinine were 6.82 μg/mg creatinine at 1h after exposure and 32.9 μg/mg creatinine at 2h after exposure, respectively. The skin surface temperature decreased and was lower (33.5°C ± 0.5°C) at 30min than before exposure (37.6°C ± 0.8°C).

The new apparatus for HTPs aerosol exposure to mice showed good performances in terms of both chemical analysis of collected aerosol and fluctuations in the urinary nicotine metabolites.

The new apparatus for HTPs aerosol exposure to mice showed good performances in terms of both chemical analysis of collected aerosol and fluctuations in the urinary nicotine metabolites.Complex signalling pathways are involved in plant protection against single and combined stresses. Plants are able to coordinate genome-wide transcriptional reprogramming and display a unique program of transcript responses to a combination of stresses which differ from single stresses. However, a significant overlap between pathways and some defence genes in the form of shared and general stress-responsive genes appears to be commonly involved in responses to multiple biotic and abiotic stresses. Reactive oxygen and nitrogen species (ROS/RNS), as well as redox signals, are key molecules involved at the crossroads of perceptions of different stress factors and regulation of both specific and general plant responses to biotic and abiotic stress. In this review, we focus on crosstalk between plant responses to biotic and abiotic stresses, in addition to possible plant protection against pathogens caused by previous abiotic stress. Bioinformatic analyses of transcriptome data from Cd- and fungal pathogen-treated plants focusing on redox gene ontology (GO) categories were carried out to gain a better understanding of common plant responses to abiotic and biotic stresses. The role of ROS and RNS in the complex network involved in plant responses to changes in their environment is also discussed.The cumulative impact of chronic inflammation in patients with inflammatory bowel diseases predisposes to the development of inflammatory bowel disease-associated colorectal cancer (IBD-CRC). Inflammation can induce mutagenesis and the relapsing-remitting nature of this inflammation, together with epithelial regeneration, may exert selective pressure accelerating carcinogenesis. The molecular pathogenesis of IBD-CRC, termed the 'inflammation-dysplasia-carcinoma' sequence, is well described. However, the immunopathogenesis of IBD-CRC is less well understood. The impact of novel immunosuppressive therapies, which aim to achieve deep remission, is mostly unknown. Therefore, this timely review summarises the clinical context of IBD-CRC, outlines the molecular and immunological basis of disease pathogenesis and considers the impact of novel biologic therapies.