In this study, the potential effects of a novel alkali-soluble polysaccharide (ASPP) from purple sweet potato on colonic histopathology, inflammation and microbiota composition in dextran sulfate sodium (DSS)-induced colitis mice were evaluated. The results indicated that ASPP restored the immune organ indices, increased colon length, improved colonic histopathology in colitis mice as well as inhibited the levels of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) in colonic tissue and serum. Moreover, 16S rRNA phylogenetic sequencing revealed that ASPP ameliorated the compositions and functions of gut microbiota in DSS-induced colitis mice. It was found that Parasutterella, Desulfovibrio, Lachnospiraceae, Lactobacillus, Erysipelotrichaceae, Bacteroidetes were the key bacteria associated with ulcerative colitis (UC). Taken together, ASPP alleviated colonic inflammation via blocking pro-inflammatory cytokines; meanwhile ASPP could modulate the structure of gut microbiota in DSS-induced colitis mice. V.Multifunctional chitosan/magnetite (CS/Fe3O4) and graphene/chitosan/magnetite (Gr/CS/Fe3O4) nanocomposites (NCs) were synthesized using a simple hydrothermal method. The NCs were subsequently evaluated as magnetic photocatalysts towards the photodegradation of dye molecules that are detrimental to the environment. In the present study, sphere shaped Fe3O4 nanoparticles (NPs) were found to uniformly decorate CS and Gr surfaces. The synthesized Fe3O4 NPs, CS/Fe3O4 and Gr/CS/Fe3O4 NCs were characterized by powder X-ray diffraction, Fourier-transform infrared and Raman spectroscopy, thermogravimetric analysis, UV-visible diffuse reflectance and photoluminescence spectroscopy, and field emission scanning electron microscopy coupled with energy dispersive X-ray spectroscopy. The Gr/CS/Fe3O4 NCs showed 100% photocatalytic efficiency against rhodamine B (40 min), bromothymol blue (60 min), methylene blue (80 min) and methyl orange (100 min) compared to Fe3O4 NPs (100 min for Rh-B, 120 min for BTB, 160 min for MB and 180 min for MO) and CS/Fe3O4 NCs (90 min for Rh-B, 100 min for BTB, 140 min for MB and 150 min for MO). The photocatalytic irradiation efficiency of Fe3O4 NPs, CS/Fe3O4 and Gr/CS/Fe3O4 NCs, evaluated against visible light, was found to be significantly higher for Rh-B (100% within 40 min) compared to the other tested dyes. V.Notch-1 intervenes in the reparative processes of mucosa by controlling cell proliferation, differentiation and stem cell maintenance. Cigarette smoke alters airway epithelial homeostasis. The present study explored whether Smokers showed altered Notch-1 expression; and whether in bronchial epithelial cells (16HBE) a) cigarette smoke extracts (CSE) altered the expression of Notch-1, of its ligand Jagged-1 (Jag-1) and the nuclear translocation of Notch-1; b) Notch-1 signaling activation as well as CSE modified Ki67, PCNA, p21, IL-33 expression, cell proliferation and repair processes. Notch-1 expression was assessed in the epithelium from large airway surgical samples from non-smoker and smoker subjects by immunohistochemistry.16HBE were cultured with/without CSE and Jag-1. A Notch-1 inhibitor (DAPT) was used as control. The expression of Notch-1, Jag-1, Ki67, PCNA, p21, IL-33 and cell proliferation (by CFSE) were all assessed by flow cytometry. Notch-1 nuclear expression was evaluated by immunofluorescence and western blot analysis. Repair processes were assessed by wound assay. Smokers had cytoplasmic but not nuclear Notch-1 expression. Although CSE increased Notch-1 expression, it counteracted Notch-1 signaling activation since it reduced Jag-1 expression and Notch-1 nuclear translocation. Notch-1 signaling activation by Jag-1 increased Ki67, PCNA and repair processes but reduced intracellular IL-33 and p21 expression without affecting cell proliferation. DAPT counteracted the effects of Notch-1 activation on PCNA and IL-33. CSE increased Ki67, PCNA, p21 and IL-33 expression but reduced cell proliferation and repair processes. In conclusion, cigarette smoke exposure, limiting Notch-1 signaling activation and hindering repair processes, amplifies injury processes in bronchial epithelial cells. Angiotensin (Ang) A differs from Ang II in a single N-terminal alanine residue. The aim of this study was to investigate whether the effects of Ang A on postischemic cardiac injury and hemodynamics differ from Ang II. After euthanizing Sprague-Dawley rats, hearts were perfused with Krebs-Henseleit buffer for a 20 min preischemic period with or without Ang A or Ang II, followed by 20 min global ischemia and 50 min reperfusion. Capmatinib cost The blood pressure was measured in anesthetized rats. Ang A (0.1, 1.0, 10 μg/kg) deteriorated the postischemic left ventricular hemodynamics in a dose-dependent manner, which was similar to that by Ang II. Ang A (10 μg/kg) increased the infarct size and the lactate dehydrogenase level, and decreased the coronary flow, which were attenuated by the pretreatment with Ang type 1 receptor (AT1R) antagonist (losartan) but not by AT2R antagonist (PD123319). Ang A increased the expression of apoptotic proteins and decreased the expression of antioxidative proteins. Interestingly, Ang A increased the atrial natriuretic peptide (ANP) level in coronary effluent and in atrial perfusate but Ang II did not increase it. Ang A increased mean arterial blood pressure, which was less potent than Ang II. These results suggest that Ang A has a similar effect on postischemic injury via AT1R and less potent vasopressor effect but opposite effect on ANP secretion as compared to Ang II. The relationship between microRNA (miR) and immune activity in allergic rhinitis (AR) remains unclear. 37 children with AR and 30 healthy children were enrolled to study the correlation of miR-223 and IL-35. There was a significant inverse correlation between plasma levels of IL-35 and serum eosinophil cationic protein (ECP) levels and eosinophils counts, while there was a positive correlation between serum miR-223 level and ECP levels and eosinophils counts. Besides, the serum levels of IL-35 or miR-223 were found to be negatively or positively correlated with TNSS respectively. The serum level of miR-223 was increased, while IL-35 level was decreased. Moreover, the expression of miRNA-223 was inversely correlated with expression of IL-35. Finally, the levels of miR-223 and IL-35 were related to Th1/Th2 cytokines, eosinophils count as well as the clinical severity. Our study suggests the potential of miR-223 and IL-35 as a molecular target for the treatment of AR.