Search

Late Carboniferous–Early Permian granitoids are widespread in the Tianshan area and their tectonic setting is controversially discussed. Our research presents fresh whole-rock geochemical and Pb isotopic data, along with zircon U-Pb ages and Hf isotopic data for representative monzonitic and granitic intrusions in the Kumishi area. The aim is to decipher their magma sources and illuminate their geodynamic evolution. Zircon U-Pb dating results reveal that biotite monzonites in the Central Tianshan Belt were emplaced at 312.7 ± 2.9 Ma, while the quartz-monzonites and syenogranites in the South Tianshan Belt were formed at 284.5 ± 2.4 Ma and 283.4 ± 3.9 Ma, respectively. The biotite monzonites generally exhibit metaluminous and high-K calc-alkaline characteristics. They have a positive εHf(t) value (+4.9–+14.1), and are enriched in LREEs and LILEs but depleted in HREEs and HFSEs. These characteristics indicate that they were derived from a mixed magma source of the lower crust and the input of components derived from the mantle wedge above the subduction zone. The quartz-monzonites and syenogranites are high-K calc-alkaline to shoshonitic I-type granites, with εHf(t) values of +14.9–+15.5 and +6.6–+14.9, respectively. They are enriched in LREEs but depleted in HFSEs (e.g., Nb, Ta, and Ti), displaying relatively flat HREE patterns and negative Eu anomalies. The genesis of these rocks is attributed to a partial melting of the lower crust in which mantle-derived magmas participated, which was triggered by an upwelling asthenosphere in a post-collisional extensional geodynamic setting. These granitoids, together with regional analysis of other magmatism in the study area, suggest that the Kumishi area has experienced an evolution from subduction to post-collision from the Late Carboniferous to the Early Permian, which constrains the local closure of the Paleo-Asian Ocean. [ABSTRACT FROM AUTHOR]

BackgroundCeliac disease (CD) is an immune-mediated disorder induced by the ingestion of gluten in genetically susceptible persons. The prevalence of CD in Malaysia is unknown. We aim to determine the seroprevalence of CD antibodies and also investigate the correlation between H. pylori infection and CD in the young and healthy multiracial Malaysian population.MethodsHealthy young adult volunteers between the ages of 18-30 years were consecutively recruited from June 2012 to May 2014 at the University of Malaya Medical Centre (UMMC), Kuala Lumpur. Serum samples from all the participants were tested for anti-gliadin antibody immunoglobulin A/immunoglobulin G (IgA/IgG) and anti-tissue transglutaminase antibody (tTG) IgA/IgG. Samples positive for both anti-gliadin and anti-tTG were further validated for anti-human endomysial IgA antibodies (EmA). Serological diagnosis of CD was made when anti-gliadin, anti-tTG and anti-EmA were positive.Results562 qualified participants with mean age 24 ± 2.4 years old were recruited into our study. CD was found in 7 participants where most of them were asymptomatic and unaware of their CD status. The median of anti-gliadin and anti-tTG IgA/IgG value was 38.2 U/ml (interquartile range, 28.3-60.4 U/ml) and 49.2 U/ml (interquartile range, 41.1-65.9 U/ml), respectively. Seroprevalence of CD antibodies was 1.9% (6 out of 324) in female while only 0.4% (1 out of 238) in male. Seroprevalence among Malay was 0.8% (2 of 236), Chinese was 1.7% (3 of 177) and Indian was 1.3% (2 of 149). Overall, seroprevalence of CD antibodies in healthy asymptomatic adults in the Malaysian population was 1.25% (95% CI, 0.78%-1.72%). No significant relationship was discovered between CD and H. pylori infection.ConclusionsThe seroprevalence of CD antibodies in healthy young adults in the Malaysian population was 1.25% (1 in 100). CD is underdiagnosed and it could be a much greater problem in Malaysia than previously thought.

How T cells differentiate in the neonate may critically determine the ability of the infant to cope with infections, respond to vaccines and avert allergies. Previously, we found that naïve cord blood CD4+ T cells differentiated toward an IL-4-expressing phenotype when activated in the presence of TGF-β and monocyte-derived inflammatory cytokines, the latter are more highly secreted by infants who developed food allergy. Here, we show that in the absence of IL-2 or IL-12, naïve cord blood CD8+ T cells have a natural propensity to differentiate into IL-4-producing non-classic TC2 cells when they are activated alone, or in the presence of TGF-β and/or inflammatory cytokines. Mechanistically, non-classic TC2 development is associated with decreased expression of IL-2 receptor alpha (CD25) and glycolysis, and increased fatty acid metabolism and caspase-dependent cell death. Consequently, the short chain fatty acid, sodium propionate (NaPo), enhanced IL-4 expression, but exogenous IL-2 or pan-caspase inhibition prevented IL-4 expression. In children with endoscopically and histologically confirmed non-inflammatory bowel disease and non-infectious pediatric idiopathic colitis, the presence of TGF-β, NaPo, and IL-1β or TNF-α promoted TC2 differentiation in vitro. In vivo, colonic mucosa of children with colitis had significantly increased expression of IL-4 in CD8+ T cells compared with controls. In addition, activated caspase-3 and IL-4 were co-expressed in CD8+ T cells in the colonic mucosa of children with colitis. Thus, in the context of colonic inflammation and limited IL-2 signaling, CD8+ T cells differentiate into non-classic TC2 that may contribute to the pathology of inflammatory/allergic diseases in children. [ABSTRACT FROM AUTHOR]