OBJECTIVE: To observe the localization of adrenomedullin (AM) in rat kidney tissue and its inhibitory effect on the growth of cultured rat mesangial cells (MsC). METHODS: A monoclonal antibody against AM developed by ...OBJECTIVE: To observe the localization of adrenomedullin (AM) in rat kidney tissue and its inhibitory effect on the growth of cultured rat mesangial cells (MsC). METHODS: A monoclonal antibody against AM developed by our laboratory was used to detect the localization of AM protein in rat kidney tissue by avidin-biotin complex immunohistochemistry. The expressions of AM and its receptor CRLR mRNA on cultured glomerular epithelial cells (GEC) and MsC were investigated by Northern blot assay, and the possible effect of AM secreted by GEC on MsC proliferation was observed using [3H]thymidine incorporation as an index. RESULTS: A specific monoclonal antibody against AM was succesfully developed. AM was immunohistochemically localized mainly in glomeruli (GEC and endothelial cells), some cortical proximal tubules, medullary collecting duct cells, interstitial cells, vascular smooth muscle cells and endothelial cells. Northern blot assay showed that AM mRNA was expressed only on cultured GEC, but not on MsC, however, AM receptor CRLR mRNA was only expressed on MsC. GEC conditioned medium containing AM can inhibit MsC growth and AM receptor blocker CGRP8-37 may partially decreased this inhibitory effect. CONCLUSION: AM produced by GEC inhibits the proliferation of MsC, which suggests that AM as an important regulator is involved in glomerular normal physiological functions and pathologic processes.展开更多
Background No-reflow is associated with an adverse outcome and higher mortality in patients with ST-segment elevation acute myocardial infarction （STEMI） who undergo percutaneous coronary intervention （PCI） and is...Background No-reflow is associated with an adverse outcome and higher mortality in patients with ST-segment elevation acute myocardial infarction （STEMI） who undergo percutaneous coronary intervention （PCI） and is considered a dynamic process characterized by multiple pathogenetic components. The aim of this study was to investigate the effectiveness of a combination therapy for the prevention of no-reflow in patient with acute myocardial infarction （AMI） undergoing primary PCI. Methods A total of 621 patients with STEMI who underwent emergency primary PCI were enrolled in this study. Patients with high risk of no-reflow （no-flow score 〉 10, by using a no-flow risk prediction model, n = 216） were randomly divided into a controlled group （n = 108） and a combination therapy group （n = 108）. Patients in the controlled group received conventional treatment, while patients in combination therapy group received high-dose （80 mg） atorvastatin pre-treatment, intracoronary administration of adenosine （140 ~tg/min per kilogram） during PCI procedure, platelet membrane glycoprotein lib/Ilia receptor antagonist （tirofiban, 101.tg/kg bolus followed by 0.15 ~tg/kg per minute） and thrombus aspiration. Myocardial contrast echocardiography was performed to assess the myocardial perfusion 72 h after PCI. Major adverse cardiac events （MACE） were followed up for six months. Results Incidence of no-reflow in combination therapy group was 2.8%, which was similar to that in low risk group 2.7% and was significantly lower than that in control group （35.2%, P 〈 0.01）. The myocardial perfusion （A= 13） values were higher in combination therapy group than that in control group 72 h after PCI. After 6 months, there were six （6.3%） MACE events （one death, two non-fatal MIs and three revasculafizations） in combination therapy group and 12 （13.2%） （four deaths, three non-fatal MIs and five revascularizations, P 〈 0.05） in control group. Conclusions Combination of thrombus aspiration, high-dose statin pre-treatment, intmcoronary administration of adenosine during PCI procedure and platelet membrane glycoprotein Ⅱ b/Ⅲa receptor antagonist reduces the incidence of no-reflow after primary PCI in patients with acute myocardial infarction who are at high risk of no-reflow.展开更多
Objective: To study the effects of hyperbaric air exposure on the functions of peritoneal macrophages of mice. Methods: Forty-eight mice were equally randomized to 6 groups: (1) normal air group (NA); (2) hyperbaric a...Objective: To study the effects of hyperbaric air exposure on the functions of peritoneal macrophages of mice. Methods: Forty-eight mice were equally randomized to 6 groups: (1) normal air group (NA); (2) hyperbaric air group 1 (HA1); (3) hyperbaric air group 2 (HA2); (4) hyperbaric air group 3 (HA3); (5) hyperbaric oxygen group (HO);(6) hyperbaric nitrogen group (HN). Every group was exposed to corresponding pressure for 60 min, twice a day for 3 d. Peritoneal macrophages were obtained at the corresponding time to observe the changes of phagocytosis, acid phos-phatase, antigen presentation function and the produce of NO and TNF-α. Results: Compared with those in NA group, the activity of phagocytosis, acid phosphatase, antigen presentation function and the produce of NO and TNF-a were markedly inhibited in hyperbaric oxygen group and hyperbaric air group 1 ( P < 0.05, P < 0.01) and they changed little in HN group. These changes could disappear in 3 - 5 d. Conclusion: The functions of mice peritoneal macrophages were obviously inhibited in simulated air diving environment and hyperoxia may play an important role in it.展开更多
文摘OBJECTIVE: To observe the localization of adrenomedullin (AM) in rat kidney tissue and its inhibitory effect on the growth of cultured rat mesangial cells (MsC). METHODS: A monoclonal antibody against AM developed by our laboratory was used to detect the localization of AM protein in rat kidney tissue by avidin-biotin complex immunohistochemistry. The expressions of AM and its receptor CRLR mRNA on cultured glomerular epithelial cells (GEC) and MsC were investigated by Northern blot assay, and the possible effect of AM secreted by GEC on MsC proliferation was observed using [3H]thymidine incorporation as an index. RESULTS: A specific monoclonal antibody against AM was succesfully developed. AM was immunohistochemically localized mainly in glomeruli (GEC and endothelial cells), some cortical proximal tubules, medullary collecting duct cells, interstitial cells, vascular smooth muscle cells and endothelial cells. Northern blot assay showed that AM mRNA was expressed only on cultured GEC, but not on MsC, however, AM receptor CRLR mRNA was only expressed on MsC. GEC conditioned medium containing AM can inhibit MsC growth and AM receptor blocker CGRP8-37 may partially decreased this inhibitory effect. CONCLUSION: AM produced by GEC inhibits the proliferation of MsC, which suggests that AM as an important regulator is involved in glomerular normal physiological functions and pathologic processes.
文摘Background No-reflow is associated with an adverse outcome and higher mortality in patients with ST-segment elevation acute myocardial infarction （STEMI） who undergo percutaneous coronary intervention （PCI） and is considered a dynamic process characterized by multiple pathogenetic components. The aim of this study was to investigate the effectiveness of a combination therapy for the prevention of no-reflow in patient with acute myocardial infarction （AMI） undergoing primary PCI. Methods A total of 621 patients with STEMI who underwent emergency primary PCI were enrolled in this study. Patients with high risk of no-reflow （no-flow score 〉 10, by using a no-flow risk prediction model, n = 216） were randomly divided into a controlled group （n = 108） and a combination therapy group （n = 108）. Patients in the controlled group received conventional treatment, while patients in combination therapy group received high-dose （80 mg） atorvastatin pre-treatment, intracoronary administration of adenosine （140 ~tg/min per kilogram） during PCI procedure, platelet membrane glycoprotein lib/Ilia receptor antagonist （tirofiban, 101.tg/kg bolus followed by 0.15 ~tg/kg per minute） and thrombus aspiration. Myocardial contrast echocardiography was performed to assess the myocardial perfusion 72 h after PCI. Major adverse cardiac events （MACE） were followed up for six months. Results Incidence of no-reflow in combination therapy group was 2.8%, which was similar to that in low risk group 2.7% and was significantly lower than that in control group （35.2%, P 〈 0.01）. The myocardial perfusion （A= 13） values were higher in combination therapy group than that in control group 72 h after PCI. After 6 months, there were six （6.3%） MACE events （one death, two non-fatal MIs and three revasculafizations） in combination therapy group and 12 （13.2%） （four deaths, three non-fatal MIs and five revascularizations, P 〈 0.05） in control group. Conclusions Combination of thrombus aspiration, high-dose statin pre-treatment, intmcoronary administration of adenosine during PCI procedure and platelet membrane glycoprotein Ⅱ b/Ⅲa receptor antagonist reduces the incidence of no-reflow after primary PCI in patients with acute myocardial infarction who are at high risk of no-reflow.
文摘Objective: To study the effects of hyperbaric air exposure on the functions of peritoneal macrophages of mice. Methods: Forty-eight mice were equally randomized to 6 groups: (1) normal air group (NA); (2) hyperbaric air group 1 (HA1); (3) hyperbaric air group 2 (HA2); (4) hyperbaric air group 3 (HA3); (5) hyperbaric oxygen group (HO);(6) hyperbaric nitrogen group (HN). Every group was exposed to corresponding pressure for 60 min, twice a day for 3 d. Peritoneal macrophages were obtained at the corresponding time to observe the changes of phagocytosis, acid phos-phatase, antigen presentation function and the produce of NO and TNF-α. Results: Compared with those in NA group, the activity of phagocytosis, acid phosphatase, antigen presentation function and the produce of NO and TNF-a were markedly inhibited in hyperbaric oxygen group and hyperbaric air group 1 ( P < 0.05, P < 0.01) and they changed little in HN group. These changes could disappear in 3 - 5 d. Conclusion: The functions of mice peritoneal macrophages were obviously inhibited in simulated air diving environment and hyperoxia may play an important role in it.
