Clinical Effects and Safety of Tongxieyaofang on Diarrhea Predominant Irritable Bowel Syndrome: A Meta-Analysis of Randomized Trails

Background. Tongxieyaofang (TXYF), a prescription originated from traditional Chinese medicine (TCM), has been widely used on treating Diarrhea Predominant Irritable Bowel Syndrome (IBS-D). The purpose of this meta-analysis was to investigate whether TXYF was effective and safe for IBS-D. Methods. We searched seven electronic databases including CENTRAL, MEDLINE, PubMed, CNKI, VIP, CBM, and Wanfang Data up to 26 July 2017. Randomized controlled trails (RCTs) were eligible, regardless of blinding. Risk of bias of included trials was evaluated according to the Cochrane Handbook. Results. The total number of participants analyzed in the meta-analysis was 3062, of which 1556 received TXYF, while 1506 received ordinary treatment. The primary outcome was clinical effective rate. Compared with conventional medication which included probiotics, pinaverium bromide, trimebutine, and Oryzanol, TXYF significantly improved the clinical effective rate (n=37, OR: 4.61; 95% CI: 3.67–5.78; P < 0.00001) and decreased the adverse events (n=10, OR: 0.26; 95% CI: 0.08–0.86; P = 0.03). There was not significant association with the score of abdominal pain, defecating frequency, fecal property, and total symptom. Conclusions. We suggested a moderate recommendation for TXYF on IBS-D, due to the fact that the risk of bias of the finally included trails was not high. Considering that all identified studies were not of high qualities and large samples, further rigorously designed and large scale RCTs were necessary to improve the applicability of our study results

Formation Of Bimetallic Dumbbell Shaped Particles With A Hollow Junction During Galvanic Replacement Reaction

The galvanic replacement reaction (GRR) has been shown to be an effective method to fine tune the structure of monometallic nanoparticles by controlling the precursor concentration and surface ligands. However, the structural evolution of nanoparticles is not well understood in multimetallic systems, where along with oxidation, dealloying and diffusion occur simultaneously. Here, we demonstrate that by controlling the rate of GRR in AuCu alloy nanorods, they can be transformed into either AuCu hollow rods or AuCu@Au core-shell spheroids. Interestingly, the transformation of rods into spheroids involved a critical intermediate state with a hollow junction and dumbbell shape. The formation of a hollow junction region was attributed to preferential diffusion of Cu atoms to the tips caused by the polycrystallinity and high curvature of the tips of the initial template. This structural transformation was also monitored in situ by single particle scattering spectroscopy. The coupling between the two ends of the dumbbell-shaped intermediate connected with a hollow metallic junction gives rise to additional plasmonic features compared with regular rods. Electrodynamic simulations showed that varying the dimensions of the hollow part by even one nanometer altered the plasmon resonance wavelength and lineshape drastically. This study shows that single particle plasmon resonance can be used as an exquisite tool to probe the internal structure of the nanoscale junctions

Structural Defect Induced Peak Splitting In Gold-Copper Bimetallic Nanorods During Growth By Single Particle Spectroscopy

A single particle level study of bimetallic nanoparticle growth provides valuable information that is usually hidden in ensemble measurements, helping to improve the understanding of a reaction mechanism and overcome the synthetic challenges. In this study, we use single particle spectroscopy to monitor the changes in the scattering spectra of Au-Cu alloy nanorods during growth. We found that the unique features of the single particle scattering spectra were due to atomic level geometric defects in the nanorods. Electrodynamics simulations have demonstrated that small structural defects of a few atomic layers split the scattering peaks, giving rise to higher order modes, which do not exist in defect-free rods of similar geometry. The study shows that single particle scattering technique is as sensitive as high-resolution electron microscopy in revealing atomic level structural defects

Juvenile hormone promotes paracellular transport of yolk proteins via remodeling zonula adherens at tricellular junctions in the follicular epithelium.

Juvenile hormone (JH) acts as a gonadotrophic hormone stimulating insect vitellogenesis and oogenesis. Paracellular transport of yolk proteins through intercellular channels (patency) in the follicular epithelium is a developmentally regulated and evolutionarily conserved process during vitellogenesis. However, the mechanisms underlying patency opening are poorly understood. Using the migratory locust Locusta migratoria as a model system, we report here that JH-regulated remodeling of zonula adherens (ZA), the belt-like adherens junction maintaining physical linking between follicle cells controlled the opening of patency. JH triggered phosphorylation of Partitioning defective protein 3 (Par3) via a signaling cascade including G protein-coupled receptor (GPCR), small GTPase Cell division cycle 42 (Cdc42) and atypical Protein kinase C (aPKC). Par3 phosphorylation resulted in its disassociation from β-Catenin, the cytoplasmic partner of ZA core component E-Cadherin. Release of Par3 from the β-Catenin/E-Cadherin complex caused ZA disassembly at tricellular contacts, consequently leading to patency enlargement. This study provides new insight into how JH stimulates insect vitellogenesis and egg production via inducing the opening of paracellular route for vitellogenin transport crossing the follicular epithelium barrier

Masculinizer and Doublesex as Key Factors Regulate Sexual Dimorphism in Ostrinia furnacalis

Sex determination is an important and traditional biological process. In Lepidoptera, Masculinizer (Masc) and doublesex (dsx) are the essential genes for sex determination and play critical roles in sexual differentiation and development. The functions of Masc and dsx have been characterized in several model insect species. However, the molecular mechanism and sex determination functions of Masc and dsx in Ostrinia furnacalis, an agricultural pest, are still unknown. Here, we successfully used the CRISPR/Cas9 genome editing system to knock out OfMasc and Ofdsx. Mutation of OfMasc induced male external genital defects and sterility. Disruptions of the Ofdsx common region caused sex-specific defects in the external genitals and adult sterility. In addition, we found that OfMasc and Ofdsx can regulate the pigmentation genes that control wing pigmentation patterns. These results demonstrate that OfMasc and Ofdsx play key roles in the sex determination of O. furnacalis, and suggest novel genetic control approaches for the management of pests, including O. furnacalis

Ligand specificity and developmental expression of RXR and ecdysone receptor in the migratory locust

The ecdysone receptor 1, which is a heterodimer of EcR and the retinoic acid receptor (RXR) homolog, Ultraspiracle (USP), has been well studied in the evolutionarily advanced and derived insects, the flies and moths. It is less well characterized in mor

NPAS3 is a trachealess homolog critical for lung development and homeostasis

Trachealess (Trh) is a PAS domain transcription factor regulating Drosophila tracheogenesis. No other Trh homolog has been associated with a respiratory phenotype. Seeking homolog(s) regulating lung development, we screened murine genomic DNA using trh oligonucleotides, identifying only Npas3. Npas3 mRNA peaks in lung from E10.5 to E13.5, verified by sequencing, with immunostaining in airway epithelial cells. Npas3-null mice have reduced lung branching morphogenesis but are viable prenatally. Npas3-null newborns die in respiratory distress, with diminished alveolarization, decreased Shh, Fgf9, Fgf10, and Bmp4 mRNAs, and increased Spry2, consistent with reduced FGF signaling. Exogenous FGF10 rescues branching morphogenesis in Npas3-null lungs. In promoter reporter assays, NPAS3 directly upregulates Shh and represses Spry2. Npas3+/− mice have a milder lung phenotype, surviving postnatally, but develop emphysema and airways hyperreactivity. Therefore, absence of a developmentally expressed transcription factor can alter downstream gene expression and multiple signaling pathways in organogenesis. NPAS3 haploinsufficiency may also lead to emphysema and asthma

Gastrin-releasing peptide blockade as a broad-spectrum anti-inflammatory therapy for asthma

Gastrin-releasing peptide (GRP) is synthesized by pulmonary neuroendocrine cells in inflammatory lung diseases, such as bronchopulmonary dysplasia (BPD). Many BPD infants develop asthma, a serious disorder of intermittent airway obstruction. Despite extensive research, early mechanisms of asthma remain controversial. The incidence of asthma is growing, now affecting >300 million people worldwide. To test the hypothesis that GRP mediates asthma, we used two murine models: ozone exposure for air pollution-induced airway hyperreactivity (AHR), and ovalbumin (OVA)-induced allergic airway disease. BALB/c mice were given small molecule GRP blocking agent 77427, or GRP blocking antibody 2A11, before exposure to ozone or OVA challenge. In both models, GRP blockade abrogated AHR and bronchoalveolar lavage (BAL) macrophages and granulocytes, and decreased BAL cytokines implicated in asthma, including those typically derived from Th1 (e.g., IL-2, TNFα), Th2 (e.g., IL-5, IL-13), Th17 (IL-17), macrophages (e.g., MCP-1, IL-1), and neutrophils (KC = IL-8). Dexamethasone generally had smaller effects on all parameters. Macrophages, T cells, and neutrophils express GRP receptor (GRPR). GRP blockade diminished serine phosphorylation of GRPR with ozone or OVA. Thus, GRP mediates AHR and airway inflammation in mice, suggesting that GRP blockade is promising as a broad-spectrum therapeutic approach to treat and/or prevent asthma in humans