Ginsenoside Rh1 attenuates ovalbumin-induced asthma by regulating Th1/Th2 cytokines balance.

Ginsenoside Rh1 (Rh1) has anti-inflammatory effects in asthma mice, but the underlying mechanism remains unclear. BALB/c mice were sensitized and challenged with ovalbumin (OVA) to construct asthma model. Mice received Rh1 or tiotropium bromide 0.5 h before OVA challenge. Airway morphology and airway remodeling were assessed by HE staining and Masson's trichrome staining, respectively. Th1/Th2 cytokines in serum or broncho alveolar lavage fluid (BALF) were measured by ELISA kits. Rh1 significantly alleviated the lung resistance and airway resistance, and reduced the number of total inflammation cells, eosinophils, neutrophils, and lymphocytes in BALF of the asthmatic mice. The morphological changes and collagen deposition of airway were also reduced by Rh1 in asthmatic mice. The increase of Eotaxin, IL-4, IL-5, IL-13, and IL-33 and the decrease of IL-12 and IFN-γ in both BALF and serum of OVA exposed mice were reversed by Rh1. Rh1 attenuates OVA-induced asthma in the mice model by regulating Th1/Th2 cytokines balance.

SNHG12 inhibits oxygen­glucose deprivation­induced neuronal apoptosis via the miR­181a­5p/NEGR1 axis.

Emerging evidence has indicated that long non­coding RNAs (lncRNAs) are closely associated with the pathogenesis of ischemic stroke. It has been reported that small nucleolar RNA host gene 12 (SNHG12) serves a critical role in ischemic stroke by acting as a competitive endogenous RNA (ceRNA). SNHG12 competes with various microRNAs (miRs) to regulate RNA transcription of specific targets. However, the effect of SNHG12 on oxygen­glucose deprivation (OGD)­induced neuronal apoptosis has rarely been reported. The present study demonstrated that SNHG12 expression was downregulated in OGD­injured SH­SY5Y cells. Furthermore, miR­181a­5p was reported as a target of SNHG12 and was negatively regulated by SNHG12. Moreover, NEGR1 was a target of miR­181a­5p, which functions as a negative regulator of NEGR1 in OGD­induced neuronal apoptosis. In summary, the results strongly confirmed the hypothesis that SNHG12 functions as a ceRNA for miR­181a­5p and regulates the expression of NEGR1 thus inhibiting OGD­induced apoptosis of SH­SY5Y cells. Neuronal apoptosis aggravates brain damage during ischemic stroke, indicating that the activation of SNHG12 and NEGR1 expression and inhibition of miR­181a­5p may be a novel strategy for the clinical treatment of ischemic stroke.

Correlation Between SIRT2 3'UTR Gene Polymorphism and the Susceptibility to Alzheimer's Disease.

The purpose of this study is to investigate the correlation between single-nucleotide polymorphism (SNP) at the 3' end of the untranslated region (UTR) of Sirtuin 2 (SIRT2) gene and the risk of developing Alzheimer's disease (AD), and to explore its underlying mechanisms. In total, 260 patients with AD and 260 healthy controls were recruited in this study. The genotype of rs2015 and rs2241703 loci of the SIRT2 gene was analyzed by Sanger sequencing for all participants. Quantitative real-time Polymerase chain reaction (qRT-PCR) was used to analyze microRNAs (miRNAs) and SIRT2 mRNA levels. Western blotting was used to analyze the expression level of SIRT2 protein. The dual luciferase reporter gene assay and cell transfection were performed to examine the role of miRNAs in regulating SIRT2 expression. Carriers of the SIRT2 gene rs2015 locus A allele were 0.69 times less likely to develop AD than the carriers of the C allele (95% confidence interval (CI): 0.59-0.80, p < 0.01). The carriers of the SIRT2 gene rs2241703 locus A allele were 1.43 times more likely to develop AD than the carriers of the G allele (95% CI: 1.23-1.61, p < 0.01). The rs2015 locus single-nucleotide polymorphism (SNP) affected the binding efficiency between miR-376a-5p and miR-8061 and the 3'UTR of the SIRT2 gene, and miR-376a-5p and miR-8061 bound to SIRT2 rs2015 A allele to down-regulate the expression of the SIRT2 protein. The rs2241703 SNP affected the binding efficiency between miR-486-3p and the 3'UTR of SIRT2 gene, and miR-486-3p bound to SIRT2 rs2241703 A allele to down-regulate SIRT2 protein expression. The SIRT2 gene rs2015 and rs2241703 loci SNPs are associated with the risk of AD. The rs2015 locus SNP affects regulation of miR-376a-5p and miR-8061 in SIRT2 expression and the rs2241703 locus SNP affects regulation of miR-486-3p in SIRT2, but further studies are needed to verify this mechanism.

Bio-Capture of Solid Pollutants by Vegetation Canopy Cave in Shallow Water Flow.

Vegetation has already been acknowledged to have the ability to remove fine solid pollutants by retention and absorption, and is widely used in the biorestoration engineering of natural shallow water flow. Vegetation usually takes a long time to obtain the expected removal rate. Therefore, vegetation is not applicable for some urgent or pressing situations. In addition, in traditional biorestoration engineering, solid pollutants usually deposit in the soil of flow bed, which infiltrates into the far-field and accumulates in crops to threaten human health. Herein, we propose a new biotechnique of foliage capture by designing a cave on the top of a vegetation canopy, which is aimed to enhance the removal efficiency (i.e., achieve quick removal) and avoid the soil deposition of pollutants. The effectiveness and efficiency of this new design were validated by a set of indoor water flume experiments, with one flat canopy top configuration serving as the model of a traditional bioretention system and three cave configurations of differing aspect ratios. The results showed that compared with that of the flat canopy top, the total amount of foliage-captured solid particles for the three caved canopies increased by 3.8, 7.3, and 12.2 times. Further, we found that the foliage-capture efficiency depended on the aspect ratio of the canopy cave. The results revealed that the effectiveness of foliage capture and the enhanced efficiency were mainly from three hydrodynamic mechanisms: (i) as flow penetrated the cave boundary from the above-canopy region to the within-canopy region, it entrained solid pollutants to collide with the foliage and increased their fate of capture; (ii) the large eddy vortices of turbulence broke due to the increasing canopy resistance, which resulted in enhanced mixing dynamics for fine, suspended, solid pollutants to collide into foliage; and (iii) the flow shear along the cave boundary decreased, which provided a reduced lift force for solid pollutants to suspend or resuspend. Comparisons between the flat canopy and caved canopies of three aspect ratios showed that the design of the canopy cave is highly significant for capture efficiency.

Experimental study on bed pressure around geotextile mattress with sloping plate.

A geotextile mattress with sloping curtain is a newly proposed countermeasure against river and estuarine scour. In previous laboratory experiments, a geotextile mattress with sloping curtain was capable of protecting the bed downstream from scour and stimulating sediment deposition on both sides. However, the seepage scour under its geotextile mattress is inadequately researched at present. In this study, the Geotextile Mattress with Sloping Plate (GMSP) is proposed based on the simplification of the geotextile mattress with sloping curtain with the construction feasibility considered. A series of experiments was conducted to investigate the pressure distribution around the GMSP and the averaged seepage hydraulic gradient beneath its mattress. The results indicate remarkable pressure difference on two sides of the GMSP. The minimum bed pressure appears about 1.3 times the plate height downstream to the GMSP. The averaged seepage hydraulic gradient beneath the mattress increases with the sloping angle increasing from 35° to 60° in general. The averaged hydraulic gradient also ascends as the relative plate height increases, but reduces as the opening ratio increases at opening ratios greater than 0.143. The safety boundary for the averaged hydraulic gradient under the geotextile mattress of the GMSP could get much smaller than the critical hydraulic gradient of piping and can easily be overwhelmed. This phenomenon can mainly be attributed to the discontinuous contact between the mattress and the seabed. A suggestion for the parametric design of the GMSP is to extend the width of the mattress to reduce the risk of seepage failure.