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RISS 인기검색어
- 검색키워드
- 저자 : Qingmei Yang (검색결과 4 건)
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Yang Feng,Zhiming Fu,Yajun Luo,Wang Tan,Zilin Liu,Pengcheng Ye,Fei Lu,Wanping Xiang,Linghan Tang,Lin Yao,Mengyun Song,Qingmei Huang,Yilun Liu,Jiangwei Xiao 대한독성 유전단백체 학회 2019 Molecular & cellular toxicology Vol.15 No.3
Backgrounds: The role of long non-coding RNAs (lncRNA) in gastric cancer (GC) has been highlighted in studies conducted over the past decade. However, the potential clinical value and the mechanisms of action of RP11-6O2.4 in GC have not been thoroughly elucidated to date. The specific aim of the present study was to assess RP11-6O2.4 and to explore its role in human GC. Methods: Quantitative real-time polymerase chain reaction (qPCR) was performed to analyze the expression levels of RP11-6O2.4 in GC tissues, paired adjacent noncancerous tissues (ANTs) and GC cell lines. In addition, the correlation between RP11-6O2.4 expression and the clinical characteristics and prognosis of patients with GC was statistically analyzed. The effects of RP11- 6O2.4 on the GC cell cycle transformation through the p38-MAPK signaling pathway were explored by flow cytometry, qPCR and Western blot analysis after treatment with SB203580, a p38MAPK specific inhibitor, in vitro. Results: The expression levels of RP11-6O2.4 in GC tissues were significantly lower than the paired ANTs (P<0.05). In addition, RP11-6O2.4 expression was significantly lower in cases with older age, longer maximum tumor diameter, higher ASA grade and deeper invasive depth (P<0.05). RP11-6O2.4 expression was significantly higher in cases with well/middle differentiation than poor/no differentiation; higher in cases without lymph node metastasis than in lymph node metastasis; and higher in cases in stage Ⅰ/Ⅱ than in stage Ⅲ/Ⅳ. An in vitro assay showed that RP11-6O2.4 induced G0/ G1 phase cell cycle arrest, likely by regulating the p38- MAPK signaling pathway. Conclusion: The above mentioned data suggested that RP11-6O2.4 was a tumor-suppressor gene in GC. RP11- 6O2.4 might play an important role in the cell cycle transformation by regulating the p38-MAPK signaling pathway, thereby representing a specific biomarker and a potential molecular target for the treatment of GC.
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( Kai Yang ),( Yulong Tang ),( Yanyun Ma ),( Qingmei Liu ),( Yan Huang ),( Yuting Zhang ),( Xiangguang Shi ),( Li Zhang ),( Yue Zhang ),( Ji’an Wang ),( Yifei Zhu ),( Wei Liu ),( Yimei Tan ),( Jinran 대한피부과학회 2021 Annals of Dermatology Vol.33 No.6
Background: Androgenetic alopecia (AGA) leads to thinning of scalp hair and affects 60%~70% of the adult population worldwide. Developing more effective treatments and studying its mechanism are of great significance. Previous clinical studies have revealed that hair growth is stimulated by 650-nm red light. Objective: This study aimed to explore the effect and mechanism of 650-nm red light on the treatment of AGA by using ex vivo hair follicle culture. Methods: Human hair follicles were obtained from hair transplant patients with AGA. Hair follicles were cultured in Williams E medium and treated with or without 650-nm red light. Real-time RT-PCR and immunofluorescence staining were used to detect the expression level of genes and proteins in hair follicles, respectively. RNA-sequencing analysis was carried out to reveal the distinct gene signatures upon 650 nm treatment. Results: Low-level 650 nm red light promoted the proliferation of human hair follicles in the experimental cultured-tissue model. Consistently, 650 nm red light significantly delayed the transition of hair cycle from anagen to catagen in vitro. RNA-seq analysis and gene clustering for the differentially expressed genes suggests that leukocyte transendothelial migration, metabolism, adherens junction and other biological process maybe involved in stimulation of hair follicles by 650-nm red light treatment. Conclusion: The effect of 650-nm red light on ex vivo hair follicles and the transcriptome set which implicates the role of red light in promoting hair growth and reversing of miniaturization process of AGA were identified.
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Zhimin Ou,Qingmei Chen,Gensheng Yang,Li Xu 한국화학공학회 2011 Korean Journal of Chemical Engineering Vol.28 No.2
Ethyl (S)-3-hydroxy-3-phenylpropionate was synthesized by asymmetric reduction of 3-oxo-3-phenylpropionic acid ethyl ester with undifferentiated cells of white turnip in phosphate buffer/organic solvent. The conversion increased with the LogP_oct of organic solvent increase. The phosphate buffer (0.2 mol/L, pH 7.0)/dodecane was selected as optimum medium for reduction. The optimal content of dodecane in medium is 10% (v). The conversion decreased with initial substrate concentration increase. Addition of more biomass of plant cells and 10% ethanol as co-substrate can improve conversion. The plant cells can be reused well for three times. The enantiomeric excess of ethyl (S)-3-hydroxy-3-phenylpropionate reached 100% with 1% allyl bromide as inhibitor.
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Jing Xiao,Xiaoli Zhang,Chensheng Fu,Qingmei Yang,Ying Xie,Zhenxing Zhang,Zhibin Ye 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Hyperuricemia contributes to renal inflammation. We aimed to investigate the role of Na+–K+–ATPase (NKA) in hyperuricemiainduced renal tubular injury. Human primary proximal tubular epithelial cells (PTECs) were incubated with uric acid (UA) at increasing doses or for increasing lengths of time. PTECs were then stimulated by pre-incubation with an NKA α1 expression vector or small interfering RNA before UA (100 μg ml−1, 48 h) stimulation. Hyperuricemic rats were induced by gastric oxonic acid and treated with febuxostat (Feb). ATP levels, the activity of NKA and expression of its α1 subunit, Src, NOD-like receptor pyrin domain-containing protein 3 (NLRP3) and interleukin 1β (IL-1β) were measured both in vitro and in vivo. Beginning at concentrations of 100 μg ml−1, UA started to dose-dependently reduce NKA activity. UA at a concentration of 100 μg ml−1 time-dependently affected the NKA activity, with the maximal increased NKA activity at 24 h, but the activity started to decrease after 48 h. This inhibitory effect of UA on NKA activity at 48 h was in addition to a decrease in NKA α1 expression in the cell membrane, but an increase in lysosomes. This process also involved the subsequent activation of Src kinase and NLRP3, promoting IL-1β processing. In hyperuricemic rats, renal cortex NKA activity and its α1 expression were upregulated at the 7th week and both decreased at the 10th week, accompanied with increased renal cortex expression of Src, NLRP3 and IL-1β. The UA levels were reduced and renal tubular injuries in hyperuricemic rats were alleviated in the Feb group. Our data suggested that the impairment of NKA and its consequent regulation of Src, NLRP3 and IL-1β in the renal proximal tubule contributed to hyperuricemia-induced renal tubular injury.
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