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Mao, Juan,Won, Sung Wook,Yun, Yeoung-Sang American Chemical Society 2013 INDUSTRIAL & ENGINEERING CHEMISTRY RESEARCH - Vol.52 No.19
<P>Anionic polymer, poly(acrylic acid) (PAA), was chemically attached onto the surface of Corynebacterium glutamicum biomass in order to introduce plenty of binding sites for cationic metals. In addition, to reinforce the mechanical strength of PAA-modified biomass (PAAB), it was cross-linked with glutaraldehyde (GA), referred as PAAB-G. Cd(II) was chosen as a model cationic pollutant in this work. FTIR and SEM were used to characterize PAAB-G. pH edge experiments revealed that Cd(II) biosorption was favored at pH 6. According to the Langmuir model, PAAB-G recorded the maximum Cd(II) uptake of 139.8 mg g<SUP>–1</SUP>, with 3.2 times enhancement comparing that for raw biomass. Kinetic experiments showed that equilibrium was quickly obtained within 10 and 30 min for the raw biomass and PAAB-G, respectively. Desorption studies indicated that Cd-loaded PAAB-G could be easily eluted by adjusting water solution to pH 2.0. Therefore, this simple and cost-effective method for surface modification can be considered as a promising design tool for developing a high-performance biosorbent for removal of cationic metals from aqueous solution.</P>
Keratin 1 maintains the intestinal barrier in ulcerative colitis
Jing Wu,Junkun Niu,Maojuan Li,Yinglei Miao 한국유전학회 2021 Genes & Genomics Vol.43 No.12
Background The intestinal mechanical barrier plays a key role in the pathogenesis of ulcerative colitis (UC). Our previous study showed keratin 1 (KRT1) was downregulated in UC, but the mechanism by which KRT1 afects the intestinal barrier remains unknown. Objectives To explore the mechanism of KRT1 in the intestinal barrier in UC. Methods Colonic tissues were collected from 20 UC patients before and after mucosal healing (MH) and 15 healthy controls. The expression of KRT1 was measured by PCR, western blotting and immunohistochemistry (IHC). A dextran sulfate sodium (DSS)-induced colitis model was established in krt1 transgenic (TG) mice, and the mice were treated with methylprednisolone (MP) to explore the role of KRT1 in the intestinal barrier. Infammation was evaluated through the DAI score, colon, spleen and H&E. The expression of KRT1 and tight junction (TJ) proteins in mouse was analysed by the same methods. Results The transcription and expression of KRT1 in UC was decreased and recovered after MH but did not reach the level of the healthy controls. Similar to the clinical results, the expression of krt1 was decreased in DSS-induced colitis and upregulated after MP. Moreover, the krt1 TG group exhibited less infammation than wild-type (WT) group. The expression of Occludin and ZO-1 decreased after DSS induction, the decreases in Occludin and ZO-1 in the krt1 TG group were lower than WT group, which was signifcantly increased after MP, while the expression of Claudin-2 exhibited the opposite efect. Conclusions Keratin 1 maintains the intestinal barrier by upregulating TJ proteins in UC.
Malnutrition worsens fluorosis-induced damage in hypothalamic-pituitary-ovarian axis of rats
Yongmei Liu,Ling Li,Jingfeng Xu,Siwen Yu,Shijun Wang,Maojuan Yu,Wenbing Zou,Mingliang Cheng,Shuhua Xia 대한독성 유전단백체 학회 2019 Molecular & cellular toxicology Vol.15 No.2
Backgrounds: This study aimed to evaluate the effects of malnutrition on the hypothalamic-pituitary-ovarian axis (HPOA) sex hormones in female rats with coal burning-type fluorosis. Methods: Female rats were divided into four groups: control, malnutrition, fluorosis, and fluorosis with malnutrition. Rats in the control and malnutrition groups were fed pollution-free corn with either regular or low protein content. Rats in the fluorosis and fluorosis with malnutrition groups were fed corn roasted with coals from the fluorosis endemic areas of Zhijin, China,with either regular or low protein content. Results: Results revealed that the body weight of rats with protein malnutrition was significantly reduced compared with that of the control and fluorosis rats. Urinary fluoride was significantly decreased and bone fluoride was significantly increased in the fluorosis with malnutrition group compared to the fluorosis group. Moreover, protein malnutrition significantly enhanced the effect of fluoride on gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone, and testosterone. Histological and ultrastructural analyses revealed that protein malnutrition intensified fluoride-induced ovary damage. Conclusion: Malnourishment could promote the abnormal secretion of HPOA sex hormones in females with fluorosis.