Background Trastuzumab is used widely for the treatment of early and advanced breast ***,concerns have arisen regarding its cardiac *** did a systematic review and meta-analysis of published randomized controlled tria...
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Background Trastuzumab is used widely for the treatment of early and advanced breast ***,concerns have arisen regarding its cardiac *** did a systematic review and meta-analysis of published randomized controlled trials(RCTs) to assess the overall risk of cardiac dysfunction associated with trastuzumab treatment. Methods We searched PubMed and Web of Science(January 1966 to July 2009) and American Society of Clinical Oncology conferences held(January 2000 to July 2009) for relevant articles and *** incidence rates,relative risks(RRs),and 95%confident intervals(CIs) were calculated using a fixed-effects or random-effects model. Results 11,892 patients from 10 RCTs were included for *** incidences of LVEF decrease and congested heart failure(CHF) were 7.5%(95%CI 4.2-13.1) and 1.9%(95%CI 1.0-3.8) among patients receiving *** significantly increased the risk of LVEF decrease(RR=1.75,95%CI,1.16-2.64;p=0.007).In addition,it significantly increased the risk of CHF(RR=4.23,95%CI, 2.76-6.48;p<0.001).The increased risk of CHF was observed in patients with early stage(RR=4.39,95%CI,2.54-7.60;p<0.001) as well as metastatic disease(RR=4.94, 95%CI,2.0-12.19;p=0.005).Furthermore,trastuzumab significantly increased the risk of CHF(RR=4.27;95%CI:2.75-6.61,p<0.001) in patients receiving anthracycline-based chemotherapy,but not in patients receiving non-anthracycline chemotherapy(RR= 2.42;95%CI:0.36-16.19,p=0.36). Conclusion The addition of trastuzumab to anthracycline-based chemotherapy may significantly increase the risk of cardiac dysfunction in breast cancer *** studies are recommended for non-anthracycline chemotherapy.
Objective:Impaired emigration of dendritic cells（DCs） has recently been considered to play important role in atherosclerosis（AS）,yet risk factors and mechanism for regulating the emigration function of DCs during ...
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Objective:Impaired emigration of dendritic cells（DCs） has recently been considered to play important role in atherosclerosis（AS）,yet risk factors and mechanism for regulating the emigration function of DCs during AS is unclear. Psychosocial factors are independent predictors of atherosclerosis and epinephrine（EPI） is the major neurotransmitter of chronic *** sought to study the effects of EPI on emigration function and chemokine receptor expression of DCs and its molecule mechanism. Methods:Monocytes were purified by CD14 immunomagnetic micro beads, and were induced into *** stimulated with LPS with or without EPI, emigration function of DCs towards MIP-3 was tested by Transwell assay, expression of CCR7 was measured by FACS and PCR,and secretion cytokines were measured by *** also study the role of MARK and BAR using different signal inhabitor and receptor blocker. Results:Exposure of DCs to EPI neither induces apoptosis nor alters maturation,in vitro,EPI impairs the migration of human monocyte-derived DCs toward MIP-3 after LPS-stimulated DC *** can significantly inhibit LPS-triggered upregulation of CCR7 expression in DC and increases IL-10 *** of BAR blocker reverses the effects of EPI on chemokine receptor expression and DC migration.P38-MAPK and NF-κB inhibitor significantly inhibited the migration of mature *** inhabited the phosphorylation of p38 MAPK and the phosphorylation of NF-κB in LPS-treated DCs. Conclusion:EPI inhibits the migration function of DCs through the down-regulation of CCR7,while NF-B and p38-MAPK pathway may be involved in EPI-mediated effects on *** of DCs migration due to regulation of chemokine receptor expression by EPI may contribute,in part,to chronic stress induced AS.
Background—In China,the occurrence rule,mechanisms and prevention measures of diseases under extreme weather are few reported,and which only focused on pathophysiological manifestation rather than molecular mechanism...
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Background—In China,the occurrence rule,mechanisms and prevention measures of diseases under extreme weather are few reported,and which only focused on pathophysiological manifestation rather than molecular mechanism *** further study in this work will be carried out from molecular cytological *** study explored the effect of hyperthermia on ventricular cardiomyocytes and the participative roles of classic MAPK—ERK5 pathways on hyperthermia induced cardiomyocytes damage. Materials and methods—Neonatal rat ventricular cardiac myocytes(NRVM) were isolated from the hearts of 1- to 3-day-old Sprague Dawley *** were exposed to hyperthermia(42℃,60 min) *** degree of cell damage was observed at 0,4,8,12,16,and 24 hours after *** effects of hyperthermia on myocardial cells were probed by evaluating lactate dehydrogenase(LDH) release, cells beating rate and rhythm and viability(assessed by MTS assay).Apoptosis was detected using an annexin V-FITC/propidium iodide(PI) staining binding assay. Using western blot semi-quantitating Bim and extracellular signal-related kinase (ERK5) / phosphorylated extracellular signal-related kinase(p-ERK).Using PD98059 as inhibitor of MAPK pathways,semi-quantitating Bim by western blot. RESULTS—(1) the beating rate of myocardial cells was slightly decreased immediately after temperature recovery,gradually decreased with time prolonged,and the cell viability was decreased(P<0.05);the activity of lactate dehydrogenase was increased(P<0.05).(2) Based on western blot analysis,the elevation of Bim protein expression occurred at recovery time(8h) and peaked at 12h then went down slowly at 24h after hyperthermia(P<0.05);ERK5 pathway responding to hyperthermia treatment(P<0.05).(3) Levels of Bim slightly decreased at PD98059 group compared with hyperthermia group(P<0.05) CONCLUSION—Hyperthermia induces myocardial cells damage with apoptosis as main ***5 participated the injure process of *** play
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