为探究重庆某大鲵养殖基地大鲵死亡的原因,对从死亡大鲵的肾脏分离得到的菌株进行形态学观察,生物学特性分析,鲫鱼致病性试验,16S r DNA PCR鉴定,药敏试验和中药试验。结果显示,一株命名为KN-4株基因序列与恶臭假单胞菌(Pseudomonas put...为探究重庆某大鲵养殖基地大鲵死亡的原因,对从死亡大鲵的肾脏分离得到的菌株进行形态学观察,生物学特性分析,鲫鱼致病性试验,16S r DNA PCR鉴定,药敏试验和中药试验。结果显示,一株命名为KN-4株基因序列与恶臭假单胞菌(Pseudomonas putida)的同源性为98.9%,对鲫鱼有较强致病性。药物敏感性试验结果显示,KN-4菌株对头孢他啶、丁胺卡那霉素、新霉素、头孢曲松、多黏菌素B均敏感。中药试验结果表明,连翘、苦参、甘草、鱼腥草、黄连、黄芩、老鹤草对分离株KN-4有较强抑菌活性,而板蓝根、蒲公英等7种中药对其无抑菌作用。展开更多
Potassium-calcium activates channel subfamily N member 3(KCNN3/SK3/KCa2.3)is involved in regulating cellular calcium signaling,muscle contraction and neurotransmitter release.Dysregulation of the KCNN3 channel is asso...Potassium-calcium activates channel subfamily N member 3(KCNN3/SK3/KCa2.3)is involved in regulating cellular calcium signaling,muscle contraction and neurotransmitter release.Dysregulation of the KCNN3 channel is associated with the development of various tumors.We use bioinformatics analysis to identify whether KCNN3 regulates the occurrence and development of stomach adenocarcinoma(STAD)as a prognostic target.By analyzing the Human Protein Atlas(HPA)database and The Cancer Genome Atlas(TCGA)database,we found that the protein and mRNA levels of KCNN3 were dramatically reduced in STAD,and TCGA database showed that KCNN3 significantly correlated with the prognosis and clinical features of STAD.In addition,we found that high expression of KCNN3 in STAD reduced the IC 50 of several drugs in STAD cells,suggesting that high expression of KCNN3 correlated with the drug sensitivity of STAD.To investigate the underlying biological mechanism,we identified a potential KCNN3 interaction factor,tumor necrosis factor receptor superfamily member 7(CD27/TNFRSF7),which is expressed at low levels in STAD.RT-qPCR and Western blotting confirmed that KCNN3 and CD27 positively correlated with each other at protein and mRNA levels,and co-immunoprecipitation and immunofluorescence experiments confirmed that the two proteins interact and colocalize in the cytoplasm.Moreover,we confirmed the inhibitory effect of KCNN3 on the proliferation,migration and invasion of human STAD cells in vitro and in vivo through subcutaneous tumorigenesis and cellular experiments.Furthermore,GO/KEGG enrichment analysis showed that KCNN3 was enriched in signaling pathways regulating the immune response and calcium or metal ion transport.Lastly,we verified through cell co-culture,RT-qPCR and CCK8 assays that high expression of KCNN3 can promote the increase of T cell activating factor and the killing effect of T cells on STAD cells.Therefore,our results suggest that KCNN3 is a potential inhibitory factor affecting the occurrence and progression of STAD.展开更多
文摘为探究重庆某大鲵养殖基地大鲵死亡的原因,对从死亡大鲵的肾脏分离得到的菌株进行形态学观察,生物学特性分析,鲫鱼致病性试验,16S r DNA PCR鉴定,药敏试验和中药试验。结果显示,一株命名为KN-4株基因序列与恶臭假单胞菌(Pseudomonas putida)的同源性为98.9%,对鲫鱼有较强致病性。药物敏感性试验结果显示,KN-4菌株对头孢他啶、丁胺卡那霉素、新霉素、头孢曲松、多黏菌素B均敏感。中药试验结果表明,连翘、苦参、甘草、鱼腥草、黄连、黄芩、老鹤草对分离株KN-4有较强抑菌活性,而板蓝根、蒲公英等7种中药对其无抑菌作用。
文摘Potassium-calcium activates channel subfamily N member 3(KCNN3/SK3/KCa2.3)is involved in regulating cellular calcium signaling,muscle contraction and neurotransmitter release.Dysregulation of the KCNN3 channel is associated with the development of various tumors.We use bioinformatics analysis to identify whether KCNN3 regulates the occurrence and development of stomach adenocarcinoma(STAD)as a prognostic target.By analyzing the Human Protein Atlas(HPA)database and The Cancer Genome Atlas(TCGA)database,we found that the protein and mRNA levels of KCNN3 were dramatically reduced in STAD,and TCGA database showed that KCNN3 significantly correlated with the prognosis and clinical features of STAD.In addition,we found that high expression of KCNN3 in STAD reduced the IC 50 of several drugs in STAD cells,suggesting that high expression of KCNN3 correlated with the drug sensitivity of STAD.To investigate the underlying biological mechanism,we identified a potential KCNN3 interaction factor,tumor necrosis factor receptor superfamily member 7(CD27/TNFRSF7),which is expressed at low levels in STAD.RT-qPCR and Western blotting confirmed that KCNN3 and CD27 positively correlated with each other at protein and mRNA levels,and co-immunoprecipitation and immunofluorescence experiments confirmed that the two proteins interact and colocalize in the cytoplasm.Moreover,we confirmed the inhibitory effect of KCNN3 on the proliferation,migration and invasion of human STAD cells in vitro and in vivo through subcutaneous tumorigenesis and cellular experiments.Furthermore,GO/KEGG enrichment analysis showed that KCNN3 was enriched in signaling pathways regulating the immune response and calcium or metal ion transport.Lastly,we verified through cell co-culture,RT-qPCR and CCK8 assays that high expression of KCNN3 can promote the increase of T cell activating factor and the killing effect of T cells on STAD cells.Therefore,our results suggest that KCNN3 is a potential inhibitory factor affecting the occurrence and progression of STAD.
