Wuhan, China

Hubei University of Technology ; simplified Chinese: 湖北工业大学; traditional Chinese: 湖北工業大學; pinyin: Húběi gōngyè dàxué; Specializing in engineering,is founded in 1952, located in Wuhan, Hubei, China. It's a public key multi-discipline university of Hubei Province. Wikipedia.


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Wang Z.,Hubei Engineering University | Kang Y.,Hubei University of Technology | Wang Z.,Hubei University of Technology
Journal of Polymer Engineering | Year: 2017

Crumb rubber (CR), as a final product from end-of-life tires through size reduction process, has proved an appropriate end product for accumulated discard waste tires all around the world. Unlike pre-existing pulverization methods, such as ambient or cryogenic grinding and solid-state shear extrusion, an entire cool pulverization process utilizing ultra-high pressure water jet (UHPWJ) was proposed in this paper. Pulverization experiments under various processing parameters were designed and conducted. The particle size distributions of produced CR were obtained using laser particle analyzer. Microscopic morphologies of CR and rubber fracture surface were observed under scanning electron microscopy. The crosslink density and gel fraction of produced CR were experimentally determined. Influence of four main processing parameters as pump pressure, transverse velocity, standoff distance and impacting angle was discussed in detail, and the most suitable processing parameters were recommended. The results show that the particle size distribution of produced CR with UHPWJ is between 45 μm and 200 μm, and the surface of CR is coarse and porous. High compressive shear effect and erosion are the main mechanisms in UHPWJ pulverization. Besides, the produced CR has already been partly devulcanized after UHPWJ pulverization, and polymer degradation occurred in the meanwhile. © 2017 Walter de Gruyter GmbH, Berlin/Boston.


PubMed | Tongji University, The Innovation Group, Hubei University of Technology, Membrane Protein Disease Research Group and 2 more.
Type: Journal Article | Journal: Journal of the American Society of Nephrology : JASN | Year: 2016

Autosomal dominant polycystic kidney disease pathogenesis can be recapitulated in animal models by gene mutations in or dosage alterations of polycystic kidney disease 1 (PKD1) or PKD2, demonstrating that too much and too little PKD1/PKD2 are both pathogenic. Gene dosage manipulation has become an appealing approach by which to compensate for loss or gain of gene function, but the mechanisms controlling PKD2 expression remain incompletely characterized. In this study, using cultured mammalian cells and dual-luciferase assays, we found that the 3 untranslated region (3UTR) of PKD2 mRNA inhibits luciferase protein expression. We then identified nucleotides 691-1044, which we called 3FI, as the 3UTR fragment necessary for repressing the expression of luciferase or PKD2 in this system. Using a pull-down assay and mass spectrometry we identified far upstream element-binding protein 1 (FUBP1) as a 3FI-binding protein. In vitro overexpression of FUBP1 inhibited the expression of PKD2 protein but not mRNA. In embryonic zebrafish, FUBP1 knockdown (KD) by morpholino injection increased PKD2 expression and alleviated fish tail curling caused by morpholino-mediated KD of PKD2. Conversely, FUBP1 overexpression by mRNA injection significantly increased pronephric cyst occurrence and tail curling in zebrafish embryos. Furthermore, FUBP1 binds directly to eukaryotic translation initiation factor 4E-binding protein 1, indicating a link to the translation initiation complex. These results show that FUBP1 binds 3FI in the PKD2 3UTR to inhibit PKD2 translation, regulating zebrafish disease phenotypes associated with PKD2 KD.


PubMed | University of Alberta, Texas A&M University, University of Washington, Hubei University of Technology and University of Louisville
Type: | Journal: Gastroenterology research and practice | Year: 2016

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world, and it comprises a spectrum of hepatic abnormalities from simple hepatic steatosis to steatohepatitis, fibrosis, cirrhosis, and liver cancer. While the pathogenesis of NAFLD remains incompletely understood, a multihit model has been proposed that accommodates causal factors from a variety of sources, including intestinal and adipose proinflammatory stimuli acting on the liver simultaneously. Prior cellular and molecular studies of patient and animal models have characterized several common pathogenic mechanisms of NAFLD, including proinflammation cytokines, lipotoxicity, oxidative stress, and endoplasmic reticulum stress. In recent years, gut microbiota has gained much attention, and dysbiosis is recognized as a crucial factor in NAFLD. Moreover, several genetic variants have been identified through genome-wide association studies, particularly rs738409 (Ile748Met) in PNPLA3 and rs58542926 (Glu167Lys) in TM6SF2, which are critical risk alleles of the disease. Although a high-fat diet and inactive lifestyles are typical risk factors for NAFLD, the interplay between diet, gut microbiota, and genetic background is believed to be more important in the development and progression of NAFLD. This review summarizes the common pathogenic mechanisms, the gut microbiota relevant mechanisms, and the major genetic variants leading to NAFLD and its progression.

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