Origin and tectonic evolution of the Qilian Precambrian basement on NW China were investigated using zircon U-Pb ages with collaborating stratigraphic and paleontological evidence. Zircon grains were separated from two schists, two granitic gneisses and one mylonized gneiss and dated with SHRIMP. Seventy percent of sixty-one detrital zircon ages from two schists ranges from 0.88 Ga to 3.09 Ga, mostly within 1.0 Ga to 1.8 Ga with a peak at 1.6 Ga to 1.8 Ga, and twenty percent varies from 2.0 Ga to 2.5 Ga. A few falls in the Archean and Neoproterozoic periods. The two granitic gneisses were dated 930±8 Ma and 918±14 Ma, whereas the mylonized granitic gneiss was dated 790±12 Ma. These ages represent two periods of magmatisms, which can be correlated with the early and late stages of magmatisms associated with the Jinningian movement on the Yangtze Blocks.The results from this and previous studies indicate that the ages of the Precambrian detrital zircons from the Qilian Block are widely distributed in the Proterozoic era, distinct from the North China Block which was stable in the Neo-Mesoproterozoic era. By contrast, the age histograms of the detrital zircons from the Qilian Block is similar to those from Precambrian basement of the Yangtze Craton. Therefore, it is suggested that the Qilian Block had a strong affinity toward the Yangtze Craton and might belong to the supercontinent Gondwana in the Neoproterozoic time. This inference is supported by Nd model age (T DM ), stratigraphic, and paleontological evidence. It is further considered that the Qilian Block was rifted from the supercontinent Gondwana during late Sinian to form an isolated continent in the Proto-Tethyan Ocean, moving towards the Alaxa Block in the North China Craton. The part of Proto-Tethyan Ocean between the Qilian and Alaxa Blocks should correspond to the so-called Paleo-Qilian Ocean. Following the closure of the Paleo-Qilian Ocean in the early Paleozoic, the Qilian Block collided with the Alaxa Block to form the North Qilian Orogenic Belt. Based on this tectonic explanation, the North Qilian ophiolites should represent parts of lithosphere from the Proto-Tethyan Ocean. Lithological and geochronological evidence also indicates that the Qilian Block underwent continental reactivation possibly induced by the deep northward subduction of the North Qaidam Block in early Paleozoic time.
BackgroundH. pylori infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways.ResultsChallenge with H. pylori increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after H. pylori infection in a dose-dependent manner. A higher dose (MOI 100) of L. acidophilus pre-treatment attenuated the H. pylori-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. L. acidophilus also inhibited H. pylori-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. L. acidophilus pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting.ConclusionsH. pylori infection induces Smad7, NFκB, IL-8, and TNF-α production in vitro. Higher doses of L. acidophilus pre-treatment reduce H. pylori-induced inflammation through the inactivation of the Smad7 and NFκB pathways.
The most critical factor for fracture union is the blood supply to the fracture site, which is usually impaired in patients with diabetes. Recently, mesenchymal stem cells-derived conditioned medium (MSC-CM) has shown significantly higher levels of angiogenic factors, such as VEGF and IL-6. We demonstrate in this report that MSC-CM delivered in gelatin sponges stimulates angiogenesis and promotes fracture healing in a diabetic rat model. Subcutaneous implantation of gelatin sponges soaked in MSC-CM demonstrated better tissue ingrowth and higher capillary densities at 2 and 3 weeks than gelatin sponges in minimal essential medium (MEM) or 293 cell-derived conditioned medium (293-CM). Implantation of fibular defects with gelatin sponges soaked in MSC-CM enhanced bone ingrowth and fracture healing rates compared to 293-CM and MEM groups at 8 weeks. Micro-computed tomography analysis further indicated a higher new bone volume in the MSC-CM group compared to the other diabetic groups. Histological analysis with CD31 immunostaining also revealed that MSC-CM increased endothelial cell counts compared to the other groups. Together, these results indicated that gelatin sponges used to deliver MSC-CM promote angiogenesis and fracture healing in a diabetic model and may be an alternative strategy for treating fracture non-union in patients with diabetes.
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