1.Antimicrobial Resistance of Acinetobacter baumannii and Clinical Strategies
Qunli DING ; Hualiang CHEN ; Zaichun DENG ; Lihua SHU ; Mingxia LANG ; Hongying MA ; Yiming YU
Chinese Journal of Nosocomiology 2009;0(19):-
OBJECTIVE To analyze the antimicrobial resistance of Acinetobacter baumannii.METHODS A.baumannii was collected in our hospital from Jan 2003 to Dec 2006.Antimicrobial susceptibility testing was performed by disk-diffusion method.RESULTS A total of 548 A.baumannii were collected during 4 years.Of these isolates,130(23.7%) strains were from intensive care unit(ICU),190 strains(34.7%)from surgical,and others from medical and emergency departments.Most of strains(78.5%) were isolated from sputum,next from wound.The prevalence of A.baumannii was increasing during last 4 years.Results of susceptibility test showed that imipenem was the most active antibiotic against A.baumannii.The resistance rates were high to most antibiotics.Most of the resistant strains was from the ICU and the general ward differentand had significant difference.More than 50% of isolates were resistant to all antimicrobial agents tested except imipenem and ciprofloxacin in ICU.CONCLUSIONS The prevalence of A.baumannii is increasing.A.baumannii isolates show high resistance to multiple antibiotics,especially in ICU.
2.Total saponins of Panax japonicus alleviates CCl4-induced acute liver injury in rats by regulating the PI3K/AktNF-κB signaling pathway
Guangyang WU ; Tianli SONG ; Lang TANG ; Yiming WANG ; Xu LIU ; Sheng HUANG
Journal of Southern Medical University 2024;44(2):244-251
Objective To investigate the protective effect of total saponins of Panax japonicus(TSPJ)against CCl4-induced acute liver injury(ALI)in rats and explore the underlying pharmacological mechanisms.Methods Male SD rat models of CCl4-induced ALI were given intraperitoneal injections of distilled water,100 mg/kg biphenyl bisabololol,or 50,100,and 200 mg/kg TSPJ during modeling(n=8).Liver functions(AST,ALT,TBil and ALP)of the rats were assessed and liver pathologies were observed with HE staining.Immunohistochemistry was used to detect the expressions of PI3K/Akt/NF-κB signaling pathway molecules in liver tissue;ELISA was used to determine the levels of T-SOD,GSH-Px,and MDA.Western blotting was performed to detect the expression levels of PI3K-Akt and SIRT6-NF-κB pathways in the liver tissue.Results Network pharmacological analysis indicated that the key pathways including PI3K/Akt mediated the therapeutic effect of TSPJ on ALI.In the rat models of ALI,treatments with biphenyl bisabololol and TSPJ significantly ameliorated CCl4-induced increase of serum levels AST,ALT,ALP,TBil and MDA and decrease of T-SOD and GSH-Px levels(all P<0.01).The rat models of ALI showed significantly increased expression of p-NF-κB(P<0.01),decreased expressions of PI3K,p-Akt and SIRT6 proteins,and elevated expression levels of p-NF-κB,TNF-α and IL-6 proteins in the liver,which were all significantly improved in the treatment groups(P<0.05 or 0.01).Conclusion TSPJ can effectively alleviate CCl4-induced ALI in rats by suppressing inflammatory responses and oxidative stress in the liver viaregulating the PI3K/Akt and SIRT6/NF-κB pathways.
3.Total saponins of Panax japonicus alleviates CCl4-induced acute liver injury in rats by regulating the PI3K/AktNF-κB signaling pathway
Guangyang WU ; Tianli SONG ; Lang TANG ; Yiming WANG ; Xu LIU ; Sheng HUANG
Journal of Southern Medical University 2024;44(2):244-251
Objective To investigate the protective effect of total saponins of Panax japonicus(TSPJ)against CCl4-induced acute liver injury(ALI)in rats and explore the underlying pharmacological mechanisms.Methods Male SD rat models of CCl4-induced ALI were given intraperitoneal injections of distilled water,100 mg/kg biphenyl bisabololol,or 50,100,and 200 mg/kg TSPJ during modeling(n=8).Liver functions(AST,ALT,TBil and ALP)of the rats were assessed and liver pathologies were observed with HE staining.Immunohistochemistry was used to detect the expressions of PI3K/Akt/NF-κB signaling pathway molecules in liver tissue;ELISA was used to determine the levels of T-SOD,GSH-Px,and MDA.Western blotting was performed to detect the expression levels of PI3K-Akt and SIRT6-NF-κB pathways in the liver tissue.Results Network pharmacological analysis indicated that the key pathways including PI3K/Akt mediated the therapeutic effect of TSPJ on ALI.In the rat models of ALI,treatments with biphenyl bisabololol and TSPJ significantly ameliorated CCl4-induced increase of serum levels AST,ALT,ALP,TBil and MDA and decrease of T-SOD and GSH-Px levels(all P<0.01).The rat models of ALI showed significantly increased expression of p-NF-κB(P<0.01),decreased expressions of PI3K,p-Akt and SIRT6 proteins,and elevated expression levels of p-NF-κB,TNF-α and IL-6 proteins in the liver,which were all significantly improved in the treatment groups(P<0.05 or 0.01).Conclusion TSPJ can effectively alleviate CCl4-induced ALI in rats by suppressing inflammatory responses and oxidative stress in the liver viaregulating the PI3K/Akt and SIRT6/NF-κB pathways.
4.Generation of a Cre recombinase knock-in mouse line labeling the mucous acinar cells of the sublingual gland
Yanli PENG ; Kecao SU ; Yiming LANG ; Zhongliang XIE ; Mingyue LI ; Xuetao ZHOU ; Qingye WANG ; Haizhen WANG ; Xiao YANG ; Guan YANG ; Yan TENG
Military Medical Sciences 2024;48(6):429-433
Objective To generate and identify the Itgbl1(integrin beta-like)promoter-driven Cre knock-in mouse line.Methods Itgbll-Cre knock-in mice were generated using clustered regularly interspaced short palindromic repeats(CRISPR)/CRISPR-associated protein 9(Cas9)gene editing.The Itgbl1-Cre mice were crossed with the Cre reporter ROSALSL-tdTomato)mice to detect the expression profile of Cre activity.The tdTomato expression pattern across tissues and cell-specific markers were used to identify the cell types of Itgbl1-expressing cells and their progeny.Results and Conclusion tdTomato was specifically expressed in mucous acinar cells of the sublingual gland,pancreatic islet cells,and gastric endocrine cells.In addition,tdTomato expression was also found in some of the neurons of the retina and brain,as well as in a few cells in the serosal layer of the intestine,articular cartilage,periosteum,and bone marrow.The first Itgbl1-Cre recombinase transgenic mouse line was established,which can specifically label the mucous acinar cells of the sublingual gland.
5.Spatial and temporal expression pattern of somatostatin receptor 2 in mouse.
Mingchuan TANG ; Chuan LIU ; Rongyu LI ; Huisang LIN ; Yanli PENG ; Yiming LANG ; Kecao SU ; Zhongliang XIE ; Mingyue LI ; Xiao YANG ; Guan YANG ; Xinjiong FAN ; Yan TENG
Chinese Journal of Biotechnology 2023;39(7):2656-2668
Somatostatin (SST) is an inhibitory polypeptide hormone that plays an important role in a variety of biological processes. Somatostatin receptor 2 (SSTR2) is the most widely expressed somatostatin receptor. However, the specific cell types expressing Sstr2 in the tissues have not been investigated. In this study, we detected the expression pattern of SSTR2 protein in mouse at different development stages, including the embryonic 15.5 days and the postnatal 1, 7, 15 days as well as 3 and 6 months, by multicolour immunofluorescence analyses. We found that Sstr2 was expressed in some specific cells types of several tissues, including the neuronal cells and astrocytes in the brain, the mesenchymal cells, the hematopoietic cells, the early hematopoietic stem cells, and the B cells in the bone marrow, the macrophages, the type Ⅱ alveolar epithelial cells, and the airway ciliated cells in the lung, the epithelial cells and the neuronal cells in the intestine, the hair follicle cells, the gastric epithelial cells, the hematopoietic stem cells and the nerve fibre in the spleen, and the tubular epithelial cells in the kidney. This study identified the specific cell types expressing Sstr2 in mouse at different developmental stages, providing new insights into the physiological function of SST and SSTR2 in several cell types.
Mice
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Animals
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Receptors, Somatostatin/metabolism*
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Hematopoietic Stem Cells/metabolism*
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Epithelial Cells