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Irritable bowel syndrome with predominant diarrhea (IBS-D) is characterized by increased intestinal permeability. Previous studies have shown that the microRNA-29 gene is involved in the regulation of intestinal permeability in patients with IBS-D. NF-κB was proved to play a key role in inflammatory response of intestine and resultant disruption of tight junction integrity, whose activity could be inhibited by TNF Receptor-Associated Factor 3 (TRAF3). However, the exact mechanism that induces increased intestinal permeability in IBS-D patients has not been clarified. In this study, we found that microRNA-29b‑3p (miR-29b-3p) was significantly upregulated, while TRAF3 was decreased and the NF-κB-MLCK pathway was activated within the colonic tissue of IBS-D patients. Subsequently, we confirmed the targeting relationship between miR-29b-3p and TRAF3 through a double-luciferase reporter assay. Lentivirus transfection of NCM460 cells with miR-29b-3p-overexpressing and -silencing vectors demonstrated that the expression of TRAF3 was negatively correlated with the level of miR-29b-3p. The NF-κB/MLCK pathway was activated in the miR-29b-3p-overexpressing group and inhibited to some extent in the miR-29b-3p-silencing group. Results in WT and miR-29 knockout mice showed that miR-29b-3p levels were increased, TRAF3 levels were decreased, and the NF-κB/MLCK signaling was activated in the WT IBS-D group as compared with the WT control group. The protein levels of TRAF3 and TJs in the miR-29b-/- IBS-D group were partially recovered and NF-κB/MLCK pathway indicators were, to a certain extent, decreased as compared with the WT IBS-D group. These results suggested that miR-29b-3p deletion enhances the TRAF3 level in IBS-D mice and alleviates the high intestinal permeability. In brief, through the analysis of intestinal tissue samples from IBS-D patients and miR-29b-/- IBS-D mice, we showed that miR-29b-3p is involved in the pathogenesis of intestinal hyperpermeability in IBS-D via targeting TRAF3 to regulate the NF-κB-MLCK signaling pathway. [ABSTRACT FROM AUTHOR]

In this paper, we are concerned with the continuation criteria to the 3D isentropic compressible Navier–Stokes equations in Lorentz spaces. We prove that there exists a positive constant ε$$ \varepsilon $$ such that no blowup occurs at time T$$ T $$ in this system provided that the supernorm of the density is bounded and the space‐time Lorentz spaces norm ‖ρu‖Lp,∞(0,T;Lq,∞)$$ {\left\Vert \sqrt{\rho }u\right\Vert}_{L&amp;#x0005E;{p,\infty}\left(0,T;{L}&amp;#x0005E;{q,\infty}\right)} $$ with 2/p+3/q=1$$ 2/p&amp;#x0002B;3/q&amp;#x0003D;1 $$(3≤q<∞)$$ \left(3\le q&lt;\infty \right) $$ is small. As a direct application, we established some Serrin's blow‐up criteria in the Lorentz spaces. [ABSTRACT FROM AUTHOR]

The proficient control algorithms for the air-feed system of proton exchange membrane fuel cell can significantly improve the output net power and prevent the polymeric membranes deterioration. To this end, a novel adaptive high-order sliding mode (HOSM) control method for air feed system is proposed in this paper. There are several meaningful contributions. Firstly, in order to reduce the number of redundant sensors and overall cost, the high-gain observer is implemented to estimate unmeasured tracking error derivatives. Secondly, without the priori knowledge of accurate dynamic model and parameters, the proposed adaptive HOSM controller ensures a real sliding mode established in finite time and a continuous control input signal to the motor. Thirdly, based on the estimated tracking error derivatives, the developed adaptive schemes guarantee the control gain would not be overestimated without the information about the bounds of the uncertainties/perturbations, which significantly suppresses the formidable chattering caused by high frequency switching of the control signal. Finally, the robustness and effectiveness of the adaptive HOSM controller are indicated by numerical simulations and hardware-in-loop experiments. [ABSTRACT FROM AUTHOR]

Background: Powdery mildew caused by Blumeria graminis f. sp. tritici (Bgt) is prevalent in the main wheat-producing regions of China, resulting in severe yield losses in recent years. Mining and utilization of resistant genes from wild relatives of wheat is the most environmentally sound measure to control disease. Aegilops geniculata Roth (2n = 2x = 28, UgUgMgMg) is an essential and valuable disease-resistance gene donor for wheat improvement as a close relative species. Results: In this study, to validate powdery mildew resistance locus on chromosome 7Mg, two genetic populations were constructed and through crossing wheat – Ae. geniculata 7Mg disomic addition line NA0973-5-4-1-2-9-1 and 7Mg (7 A) alien disomic substitution line W16998 with susceptible Yuanfeng175 (YF175, authorized varieties from Shaanxi province in 2005), respectively. Cytological examination, in situ hybridization (ISH), and functional molecular markers analysis revealed that the plants carrying chromosome 7Mg showed high resistance to powdery mildew in both F1 and F2 generation at the seedling stage. Besides, 84 specific markers were developed to identify the plants carrying chromosome 7Mg resistance based on the specific-locus amplified fragment sequencing (SLAF-seq) technique. Among them, four markers were selected randomly to check the reliability in F2 segregating populations derived from YF175/NA0973-5-4-1-2-9-1 and YF175/W16998. In summary, the above analysis confirmed that a dominant high powdery mildew resistance gene was located on chromosome 7Mg of Ae. geniculata. Conclusion: The results provide a basis for mapping the powdery mildew resistance gene mapping on chromosome 7Mg and specific markers for their utilization in the future. [ABSTRACT FROM AUTHOR]