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Background and Aims. Abnormal expression of lncRNAs is relevant to the occurrence and development of gastric cancer (GC), but the significance remains inconclusive. We performed a diagnostic meta-bioinformatics analysis to elucidate the association between lncRNA expression and GC risk. Methods. Published datasets were selected from PubMed, Embase, CNKI, and Web of Science, up to 1st December 2021. The pooled sensitivity (SEN), specificity (SPE), positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and area under the curve (AUC) were calculated to evaluate the diagnostic value. RNA sequencing data were downloaded for validation. Results. 54 studies with 4671 patients and 4652 matched controls were included in the meta-analysis. The pooled SEN, SPE, PLR, NLR, DOR, and AUC were 0.71, 0.76, 2.9, 0.39, 8, and 0.79, respectively. Subgroup analyses showed that the DOR and AUC of intergenic lncRNAs, circulating lncRNAs, larger sample size (>200), and high-quality ( NOS score ≥ 7 ) groups were superior to antisense lncRNAs, tissue lncRNAs, smaller sample size (≤200), and low-quality ( NOS score < 7 ) groups, respectively. However, only circulating lncRNAs had significantly higher diagnostic utility than that tissue lncRNAs. Nine differentially expressed lncRNAs in the meta-analysis were verified in TCGA-STAD. PVT1 was the most effective single lncRNA, with AUC of 0.949, SEN of 0.808, and SPE of 0.969, while PVT1 and C5orf66-AS1 were the most effective combination, with AUC of 0.972, SEN of 0.941, and SPE of 0.937. Conclusion. Abnormally expressed lncRNAs, especially circulating lncRNAs, might be potential diagnostic biomarkers for GC risk. A novel combined model of lncRNAs might achieve better GC diagnosis performance.

Aim Post-stroke depression (PSD) is one of the most frequent neuropsychiatric disorders associated with stroke characterized by depression. The neuroplasticity hypothesis postulates that loss of brain-derived neurotrophic factor (BDNF) plays a major role in pathophysiology of PSD, and restoration of it may represent a critical mechanism underlying antidepressant efficacy. Methods In previous studies, we designed a new fusion gene, HA2TAT-BDNF, and cloned it into adenovirus associated virus (AAV) to construct the BDNF-HA2TAT/AAV for the delivery of BDNF to central nervous system (CNS) via nose-brain pathway. In this study, we used it to explore the antidepressant effects on PSD rats through behavioral and various histological methods, and try to find out its specific mechanism. Results Compared with the control group, the PSD+AAV group showed decreased sucrose consumption percentage in the sucrose preference test (SPT) (P 0.05, P >0.05), showing an adequate antidepressant effect. Compared with the control group, the concentrations of BDNF mRNA and protein in the hippocampus (P 0.05, P < 0.05), without notable change in the hippocampus (P < 0.05, P < 0.001) of PSD+BDNF rats. Conclusion These results suggest that BDNF reductions in the prefrontal cortex and hippocampus are associated with the development of post-stroke depression, and that increased levels of BDNF in the prefrontal cortex could be used as a therapeutic target to treat PSD. However, the exact mechanism of BDNF action remains unclear in this regard, hindering the wider application of our method. We expect that our research could facilitate the exploration of pathogenesis and the new treatment method of PSD.

Hafnium(IV) triflate (Hf(OTf)

This paper is concerned with the problem of finite-time stabilization for a class of high-order nonlinear systems with zero dynamic. As a significant feature, the systems considered suffer from both the unmeasurable dynamic uncertainties and inherent nonlinearities, including high-order and low-order nonlinear growth rates. On the basis of integral Lyapunov functions equipped with sign functions and the notion of input-to-state stability, a partial state feedback stabilizer is proposed to provide a faster finite-time state convergence compared to traditional finite-time one. The novelty of this paper lies in a distinct perspective to applying the concept of fast finite-time stability developed recently in partial state feedback control design, which has been previously regarded as a rather difficult problem.

Due to missing values, incomplete dataset is ubiquitous in multimodal scene. Complete data is a prerequisite of the most existing multimodality data fusion methods. For incomplete multimodal high-dimensional data, we propose a feature selection and classification method. Our method mainly focuses on extracting the most relevant features from the high-dimensional features and then improving the classification accuracy. The experimental results show that our method produces considerably better performance on incomplete multimodal data such as ADNI dataset and Office dataset, compared to the case of complete data.

Depression is a disturbing psychiatric disease with unsatisfied therapy. Not all patients are sensitive to anti-depressants currently in use, side-effects are unavoidable during therapy and the cases with effectiveness are always accompanied with delayed onset of clinical efficacy. Delivering brain-derived neurotrophic factor (BDNF) to brain seems to be a promising therapy. However, a better approach to delivery is still rudimentary. The purpose of our present work is to look for a rapid-onset and long-lasting therapeutic strategy for major depressive disorder (MDD) by effectively delivering BDNF to brain. BDNF, fused with cell-penetrating peptides (TAT and HA2), was packaged in adenovirus associated virus (AAV) to construct the BDNF-HA2TAT/AAV for intranasally delivering BDNF to central nervous system (CNS) via nose-brain pathway. Intranasal administration of BDNF-HA2TAT/AAV to normal mice displayed anti-depression effect in forced swimming test when the delivery lasted relatively longer. The AAV applied to mice subjected to chronic mild stress (CMS) through intranasal administration for 10 days also alleviated depression-like behaviors. Western-blotting analysis revealed that BDNF-HA2TAT/AAV nasal administration enhanced hippocampal BDNF content. These results indicate intranasal administration of constructed BDNF-HA2TAT/AAV exerts anti-depression effect in CMS mice by increasing hippocampal BDNF, suggesting that this strategy holds a promising therapeutic potential for MDD.

Emerging evidence indicates that obesity impairs granulosa cell (GC) function, but the underlying mechanisms remain unclear. Gene expression profiles in GC of non-polycystic ovary syndrome (PCOS) obese (NPO), PCOS obese (PO), PCOS normal weight (PN) and non-PCOS normal weight (NPN) patients were analysed by microarray analysis. Compared with the NPN group, there were 16, 545 and 416 differently expressed genes in the NPO, PO and PN groups respectively. CD36 was the only intersecting gene, with greater than two fold changes in expression between the NPO versus NPN and PO versus NPN comparisons, and was not present in the PN versus NPN comparison. In addition, levels of CD36 protein were higher in GC from obese than normal weight patients. Furthermore, CD36 overexpression in a GC line inhibited cell proliferation, as determined by the cell counting kit-8 (CCK8) test, promoted cell apoptosis, as determined by flow cytometry, and inhibited the secretion of oestradiol by depositing triglyceride in cells and increasing cellular lipid peroxide levels. These adverse effects were reduced by sulfo-N-succinimidyloleate, a specific inhibitor of CD36. Together, the findings of this study suggest that obesity with and without PCOS should be regarded as separate entities, and that CD36 overexpression in GC of obese patients is one of the mechanisms by which obesity impairs GC function.

Candida utilis often encounters an acid stress environment when hexose and pentose are metabolized to produce acidic bio-based materials. In order to reveal the physiological role of glutathione (GSH) in the response of cells of this industrial yeast to acid stress, an efficient GSH-producing strain of C. utilis CCTCC M 209298 and its mutants deficient in GSH biosynthesis, C. utilis Δgsh1 and Δgsh2, were used in this study. A long-term mild acid challenge (pH 3.5 for 6 h) and a short-term severe acid challenge (pH 1.5 for 2 h) were conducted at 18 h during batch culture of the yeast to generate acid stress conditions. Differences in the physiological performances among the three strains under acid stress were analyzed in terms of GSH biosynthesis and distribution; intracellular pH; activities of γ-glutamylcysteine synthetase, catalase, and superoxide dismutase; intracellular ATP level; and ATP/ADP ratio. The intracellular GSH content of the yeast was found to be correlated with changes in physiological data, and a higher intracellular GSH content led to greater relief of cells to the acid stress, suggesting that GSH may be involved in protecting C. utilis against acid stress. Results presented in this manuscript not only increase our understanding of the impact of GSH on the physiology of C. utilis but also help us to comprehend the mechanism underlying the response to acid stress of eukaryotic microorganisms.

The complete organic molecule in the title dihydrate, C(20)H(22)N(4)O(4), is generated by crystallographic twofold symmetry, with two C atoms lying on the rotation axis. The symmetry unique pyridine ring forms a dihedral angle of 83.16 (8)° with the central benzene ring. In the crystal, inter-molecular N-H⋯O, O-H⋯N and O-H⋯O hydrogen bonds connect the components into a two-dimensional network lying parallel to (101).

Different interacting signaling modules involving Ca(2+)/calmodulin-dependent myosin light chain kinase, Ca(2+)-independent regulatory light chain phosphorylation, myosin phosphatase inhibition, and actin filament-based proteins are proposed as specific cellular mechanisms involved in the regulation of smooth muscle contraction. However, the relative importance of specific modules is not well defined. By using tamoxifen-activated and smooth muscle-specific knock-out of myosin light chain kinase in mice, we analyzed its role in tonic airway smooth muscle contraction. Knock-out of the kinase in both tracheal and bronchial smooth muscle significantly reduced contraction and myosin phosphorylation responses to K(+)-depolarization and acetylcholine. Kinase-deficient mice lacked bronchial constrictions in normal and asthmatic airways, whereas the asthmatic inflammation response was not affected. These results indicate that myosin light chain kinase acts as a central participant in the contractile signaling module of tonic smooth muscle. Importantly, contractile airway smooth muscles are necessary for physiological and asthmatic airway resistance.

The cardiac venous system possesses up to 30% of total coronary vascular resistance and the effect of hypoxia-reoxygenation (H-R) and St Thomas (ST) cardioplegic solution on the vein is unknown. We investigated the effects of H-R, with or without ST, on endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in porcine cardiac microveins under clinically relevant temperatures.The microveins (diameter 200 to 450 microM) mounted in a myograph were subjected to hypoxia (Po25 mm Hg) for 30 minutes in Krebs solution (n = 8) or for 60 minutes in Krebs (n = 8) or in ST at 37 degrees C (n = 8) or 4 degrees C (n = 8), followed by 30-minute reoxygenation. The microvein was precontracted with thromboxane A2 mimetic U46619 (-7 log M) and the EDHF-mediated relaxation was induced by bradykinin (-10 to -6 log M) in the presence of indomethacin, NG-nitro-L-arginine, and oxyhemoglobin before and after H-R.The maximal EDHF-mediated relaxation was significantly reduced after 30-minute hypoxia (38.7 +/- 2.0% vs 61.1 +/- 2.3%, n = 8, p0.001) or 60-minute hypoxia in either Krebs or ST at 37 degrees C (Krebs: 27.8 +/- 1.2% vs 56.6 +/- 2.5%, n = 8, p0.001; ST: 23.8 +/- 4.1% vs 57.1 +/- 1.5%, n = 8, p0.001). The relaxation was significantly less after prolonged H-R in Krebs (p0.001). Incubation in Krebs or ST at 4 degrees C also reduced the EDHF-mediated relaxation (Krebs: 25.3 +/- 3.3%, n = 8, p0.001; ST: 29.1 +/- 4.4%, n = 8, p0.001) and there were no significant differences between Krebs and ST regarding the relaxation at either 37 degrees C or 4 degrees C (p0.05).We conclude that (1) H-R impairs EDHF-mediated relaxation in the coronary microveins with more severe injury during prolonged H-R and (2) ST does not provide protection to the EDHF-mediated relaxation impaired by H-R at either 37 degrees C or 4 degrees C.

We investigated effects of hypoxia-reoxygenation (H-R) with and without St. Thomas solution under clinically relevant temperatures and effects of nicorandil on endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in porcine coronary microarteries.In a myograph, rings of porcine microarteries (diameter 200 to 450 microm) were subjected to hypoxia (PO25 mm Hg) for 30 minutes in Krebs at 37 degrees C, or for 60 minutes in Krebs and St. Thomas solution with or without nicorandil (0.1 microM) at 37 degrees C or 4 degrees C, followed by 30-minute reoxygenation. The EDHF-mediated relaxation by bradykinin (-10 to approximately -6 logM) with inhibitors of nitric oxide and prostacyclin was studied.The maximal EDHF-mediated relaxation was reduced after hypoxia for 30 minutes (59.9%% +/- 1.6% versus 81.2%% +/- 3.5%, p0.05) or 60 minutes (44.4% +/- 6.0% versus 82.7% +/- 7.4%, p0.001) in Krebs or St. Thomas (28.9% +/- 1.8% versus 78.1% +/- 3.0%, p0.001) at 37 degrees C and at 4 degrees C (Krebs: 49.3% +/- 3.0%, p0.001; ST: 43.1% +/- 2.6%, p0.001) and it was less in St. Thomas solution at 37 degrees C than at 4 degrees C (p0.001). The reduced relaxation was recovered by nicorandil (Krebs at 37 degrees C: 81.7% +/- 3.4%, p0.001; St. Thomas at 37 degrees C: 71.0% +/- 7.9%, p0.001; St. Thomas at 4 degrees C: 85.3% +/- 3.3%, p0.001).We conclude that (1) H-R impairs EDHF-mediated relaxation in the coronary microarteries with more injury during prolonged H-R, and this can be partially eliminated by St. Thomas at 4 degrees C but not at 37 degrees C; and (2) as an additive, nicorandil may fully restore EDHF-mediated endothelial function after prolonged H-R.

The complete organic molecule in the title dihydrate, C20H22N4O4, is generated by crystallographic twofold symmetry, with two C atoms lying on the rotation axis. The symmetry unique pyridine ring forms a dihedral angle of 83.16 (8)° with the central benzene ring. In the crystal, intermolecular N—H...O, O—H...N and O—H...O hydrogen bonds connect the components into a two-dimensional network lying parallel to (101).