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991.
Ruilong Zhang Zhiping Zhou Yi Wang Xiaohui Dai Li Chen Jiangdong Dai 《仿生工程学报(英文版)》2021,18(3):559-573
Mimicry of nature drives the development of bionic materials.Bionic superhydrophobic materials are a kind of high-efficiency materials to handle oil spills and ... 相似文献
992.
Liang Ji Zhi-hong Wang Yu-hua Zhang Yi Zhou De-sheng Tang Chang-sheng Yan Jia-min Ma Kun Fang Lei Gao Nian-sheng Ren Long Cheng Xiao-yu Guo Bei Sun Gang Wang 《Cell death & disease》2022,13(3)
The present study was performed to explore whether and how impaired autophagy could modulate calcium/calmodulin-dependent protein kinase II (CAMKII)-regulated necrosis in the pathogenesis of acute pancreatitis (AP). Wistar rats and AR42J cells were used for AP modeling. When indicated, genetic regulation of CAMKII or ATG7 was performed prior to AP induction. AP-related necrotic injury was positively regulated by the incubation level of CAMKII. ATG7 positively modulated the level of CAMKII and necrosis following AP induction, indicating that there might be a connection between impaired autophagy and CAMKII-regulated necrosis in the pathogenesis of AP. microRNA (miR)-30b-5p was predicted and then verified as the upstream regulator of CAMKII mRNA in our setting of AP. Given that the level of miR-30b-5p was negatively correlated with the incubation levels of ATG7 after AP induction, a rescue experiment was performed and indicated that the miR-30b-5p mimic compromised ATG7 overexpression-induced upregulation of CAMKII-regulated necrosis after AP induction. In conclusion, our results indicate that ATG7-enhanced impaired autophagy exacerbates AP by promoting regulated necrosis via the miR-30b-5p/CAMKII pathway.Subject terms: Cytokines, Acute inflammation 相似文献
993.
994.
Longjia Yan Qin Wang Li Liu Yi Le 《Journal of enzyme inhibition and medicinal chemistry》2022,37(1):832
This paper described our efforts to develop dianilinopyrimidines as novel EGFR inhibitors. All the target compounds were tested for inhibitory effects against wild type EGFR (EGFRwt) and three tumour cells, including A549, PC-3, and HepG2. Some of the compounds performed well in antitumor activities. Especially, compound 4c 2-((2-((4-(3-fluorobenzamido)phenyl)amino)-5-(trifluoromethyl) pyrimidin-4-yl)amino)-N-methylthiophene-3-carboxamide showed higher anti-tumour activities than Gefitinib. The IC50 values of compound 4c against A549, PC-3, and HepG2. reached 0.56 μM, 2.46 μM, and 2.21 μM, respectively. In addition, further studies indicated that compound 4c could induce apoptosis against A549 cells and arrest A549 cells in the G2/M phase. Molecular docking studies showed that compound 4c could closely interact with EGFR. Generally, compound 4c was the potential for developing into an anti-tumour drug. 相似文献
995.
Yi Xiao Fang Liu Qinghong Kong Xinting Zhu Haijuan Wang Sanhua Li Nian Jiang Changyan Yu Liu Yun 《Aging cell》2022,21(3)
Metformin, a widely prescribed first‐line drug for the treatment of type II diabetes mellitus, has been shown to extend lifespan and delay the onset of age‐related diseases. The precisely mechanisms by which these effects are realized remain elusive. We find that metformin exposure is restricted to adults, which is sufficient to extend lifespan. However, limiting metformin exposure to the larvae has no significant effect on Caenorhabditis elegans longevity. Here, we show that after metformin treatment, the level of S‐adenosylmethionine (SAM) is reduced in adults but not in the larvae. Potential mechanisms by which reduced SAM might increase lifespan include altering the histone methylation. However, the molecular connections between metformin, SAM limitation, methyltransferases, and healthspan‐associated phenotypes are unclear. Through genetic screening of C. elegans, we find that metformin promotes the healthspan through an H3K4 methyltransferase/demethylase complex to downregulate the targets, including mTOR and S6 kinase. Thus, our studies provide molecular links between meformin, SAM limitation, histone methylation, and healthspan and elucidate the mode action of metformin‐regulated healthspan extension will boost its therapeutic application in the treatment of human aging and age‐related diseases. 相似文献
996.
Xinyi Sun Yi Zhang Fang Shen Yang Liu George
Qiaoqi Chen Min Zhao Qi Chen 《Bioscience reports》2022,42(3)
The latest evidence suggests that type 2 endometrial cancer may not be completely oestrogen-independent, indicating that the status of hormonal change may not be associated with the traditional classification of endometrial cancer, including the histological subtypes. However, this has not been investigated. Menopause is commonly considered a state of hormonal change in women. In the present study, we investigated the association of menopause with the histological types of endometrial cancer. Data on the histological type, menopause status at diagnosis, age at diagnosis, parity, body mass index (BMI), and overall survival rate from 2122 cases were collected. The difference in risk in developing type 1 or type 2 endometrial cancer between premenopausal and postmenopausal patients was 5.457%. A statistical difference in the association of menopause with the histological types between the two groups was seen in endometrioid and serous carcinoma, with a risk difference of 5.6 or 3.8%. A statistical difference in the association of menopause with parity between the groups was only seen in endometrioid and adenosquamous carcinoma, with a risk difference of 7.1 or 3.7%. However, BMI was not associated with histological type and the overall survival rate was not associated with menopause (P=0.764). We reported a relatively small difference in the association of menopause with type 1 or type 2, or the histological types of endometrial cancer. The survival rate was not associated with menopause. Our study suggests that menopause status at diagnosis was not strongly associated with the histological subtypes of endometrial cancer. 相似文献
997.
998.
通过生物信息学的方法对双峰驼凝乳酶原基因及相应的氨基酸序列的同源性、理化性质、保守结构域、亚细胞定位、信号肽、跨膜结构域、亲水性/疏水性、二级结构进行预测分析.结果表明,双峰驼凝乳酶原基因开放阅读框全长1 146 bp,编码381个氨基酸,属于胃蛋白酶A超家族,预测定位于内质网(膜)的稳定亲水性蛋白,具有一个16个氨基酸的信号肽,其不含跨膜结构域.无规卷曲是其二级结构中最大量的结构元件,α螺旋和延抻链分散于整个蛋白质中,活性位点的分析表明,编码蛋白有6类活性位点.分析双峰驼凝乳酶原基因及其编码蛋白质的特征,能够为深入开展双峰驼凝乳酶的表达和凝乳特性研究提供理论依据. 相似文献
999.
应用生物信息学方法分析肝移植临床耐受患者PBMC基因表达特征,筛选临床耐受关键基因。从GEO数据库获取19个肝移植临床耐受病例及22个非临床耐受病例基因表达谱数据。应用DAVID网络软件进行差异基因功能注释与聚类分析;通过Cytoscape软件的MiMI插件构建蛋白质相互作用网络(PPIN)筛选肝移植临床耐受关键基因。差异基因涉及蛋白质及RNA代谢、免疫应答、膜结构调节等复杂生物过程。PPIN网络分析获得10个临床耐受核心基因。我们的研究表明:肝移植临床耐受涉及外周血免疫细胞复杂的基因表达调控机制及蛋白质间相互作用;RNA的转录后加工及蛋白质降解在免疫耐受的形成中发挥了重要作用;RBM8A、DHX9、CBL、IKBKB、CSNK2A1、HSPA8等核心基因发挥重要的免疫调节功能。 相似文献
1000.
分析黑龙江省气象因素与猩红热发病的关系,建立时间序列模型,为今后制定更科学有效的猩红热防控策略提供参考依据。收集黑龙江省2010~2020年猩红热月发病数据以及同期气温、气压等气象资料,应用广义相加模型分析气象因素与猩红热发病之间的关联程度和形式。结果发现: 猩红热全年均有发病而且呈现出较为典型的双峰型特征,在春季的4~5月份和冬季的11~12月份发病数达到高峰;月平均气压、月平均相对湿度、月日照时数和月平均风速的P值均小于0.05,表明具有统计学意义。同时,RR(相对危险度Risk Ratio)值均小于1,即猩红热发病与四个气象因素呈负相关。黑龙江省猩红热发病每年存在两个流行高峰,主要以冬季为主,发病数随着月平均相对湿度、月日照时数、月平均风速与月平均气压的升高而降低。 相似文献