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Effects of Chitosan on Body Weight Gain, Growth Hormone and Intestinal Morphology in Weaned Pigs
Xu, Yuanqing,Shi, Binlin,Yan, Sumei,Li, Tiyu,Guo, Yiwei,Li, Junliang Asian Australasian Association of Animal Productio 2013 Animal Bioscience Vol.26 No.10
The study was conducted to determine the effects of chitosan on the concentrations of GH and IGF-I in serum and small intestinal morphological structure of piglets, in order to evaluate the regulating action of chitosan on weaned pig growth through endocrine and intestinal morphological approaches. A total of 180 weaned pigs (35 d of age; $11.56{\pm}1.61kg$ of body weight) were selected and assigned randomly to 5 dietary treatments, including 1 basal diet (control) and 4 diets with chitosan supplementation (100, 500, 1,000 and 2,000 mg/kg, respectively). Each treatment contained six replicate pens with six pigs per pen. The experiment lasted for 28 d. The results showed that the average body weight gain (BWG) of pigs was improved quadratically by dietary chitosan during the former 14 d and the later 14 d after weaned (p<0.05). Furthermore, dietary supplementation of chitosan tended to quadratically increase the concentration of serum GH on d 14 (p = 0.082) and 28 (p = 0.087). Diets supplemented with increasing levels of chitosan increased quadratically the villus height of jejunum and ileum on d 14 (p = 0.089, p<0.01) and 28 (p = 0.074, p<0.01), meanwhile, chitosan increased quadratically the ratio of villus height to crypt depth in duodenum, jejunum and ileum on d 14 (p<0.05, p = 0.055, p<0.01) and 28 (p<0.01, p<0.01, p<0.01), however, it decreased quadratically crypt depth in ileum on d 14 (p<0.05) and that in duodenum, jejunum and ileum on d 28 (p<0.01, p<0.05, p<0.05). In conclusion, these results indicated that chitosan could quadratically improve growth in weaned pigs, and the underlying mechanism may due to the increase of the serum GH concentration and improvement of the small intestines morphological structure.
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Wenkai Zhang,Yanshan Zhan,Xiuxiu Gao,Runming Li,Weiwei Zhu,Hao Xu,Baoying Liu,Xiaomin Fang,Yuanqing Xu,Tao Ding 한국고분자학회 2018 Macromolecular Research Vol.26 No.1
Herein, we report the effect of oxygen functionalities of graphene oxide on thermal activated polymerization and thermal properties of reactive benzoxazine nanocomposites. The numbers of oxygen moieties of graphene oxide (GO) are controlled by hydrothermal reduction. The polymerization behavior of benzoxazine monomer (BA-a) is studied by Fourier transform infrared spectroscopy, differential scanning calorimetry and rheological analysis. It is hypothesized that the GO not only exhibits accelerated effect on the polymerization of the BA-a, but also the oxygen moieties such as carboxyl groups of GO interact with the benzoxazine polymers, leading to several orders of magnitude increase in the chemoviscosity and modulus of composite system. Thermal conductivity of poly(BA-a)/GO composite increases from an initial value of ∼0.27 W/mK to 0.47 W/mK as the loading increases from 1 wt% to 6 wt% (enhancement factor up to 176%). Moreover, the nanocomposites display enhanced initial decomposition temperature and char yields as the degree of GO reduction increases.
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A brain somatic RHEB doublet mutation causes focal cortical dysplasia type II
Shanshan Zhao,Zhenghui Li,Muxian Zhang,Lingliang Zhang,Honghua Zheng,Jinhuan Ning,Yanyan Wang,Feng-Peng Wang,Xiaobin Zhang,Hexia Gan,Yuanqing Wang,Xian Zhang,Hong Luo,Guojun Bu,Huaxi Xu,Yi Yao,Yun-wu 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Focal cortical dysplasia type II (FCDII) is a cerebral cortex malformation characterized by local cortical structure disorganization, neuronal dysmorphology, and refractory epilepsy. Brain somatic mutations in several genes involved in the PI3K/AKT/mTOR pathway are associated with FCDII, but they are only found in a proportion of patients with FCDII. The genetic causes underlying the development FCDII in other patients remain unclear. Here, we carried out whole exome sequencing and targeted sequencing in paired brain–blood DNA from patients with FCDII and identified a brain somatic doublet mutation c.(A104T, C105A) in the Ras homolog, mTORC1 binding (RHEB) gene, which led to the RHEB p.Y35L mutation in one patient with FCDII. This RHEB mutation carrier had a dramatic increase of ribosomal protein S6 phosphorylation, indicating mTOR activation in the region of the brain lesion. The RHEB p.Y35L mutant protein had increased GTPλS-binding activity compared with wild-type RHEB. Overexpression of the RHEB p. Y35L variant in cultured cells also resulted in elevated S6 phosphorylation compared to wild-type RHEB. Importantly, in utero electroporation of the RHEB p.Y35L variant in mice induced S6 phosphorylation, cytomegalic neurons, dysregulated neuron migration, abnormal electroencephalogram, and seizures, all of which are found in patients with FCDII. Rapamycin treatment rescued abnormal electroencephalograms and alleviated seizures in these mice. These results demonstrate that brain somatic mutations in RHEB are also responsible for the pathogenesis of FCDII, indicating that aberrant activation of mTOR signaling is a primary driver and potential drug target for FCDII.
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