ABSTRACT
Objective To investigate the effect of remote medical information platform on efficiency of chest pain diagnosis and treatment and on clinical decision analyses in chest pain center.Methods A total of 537 chest pain patients who met the inclusion and exclusion criteria were consecutively enrolled and divided into two groups.The group without the chest pain platform(before setting up the platform)was 251 cases,and the group with chest pain platform(after setting up the platform)was 286 cases.The constituent ratio of acute coronary syndrome (ACS),the numbers of cases of both emergency thrombolysis and emergency percutaneous coronary intervention(PCI),the mean transfer treatment time,the first time medical contact to balloon catheter technique(FMC-to-B) and the door-to-balloon(D-to-B) time were compared between the two groups.The important multivariate factors affecting the D-to-B time were analyzed.Results The group with versus without chest pain platform showed the statistically significant improvements in the parameters as follows:(1)getting long range treatment (249 cases or 87.1％ vs.92 cases or 36.7 ％,x2 =146.56,P ＜0.05),(2) receiving thrombolysis(64 cases or 22.4％ vs.15 cases or 6.0％,x2 =28.61,P＜0.05),(3)average transfer treatment time(TTT) (176.3 ± 86.1 min vs.360.7 ± 107.4 min,t =11.53,P ＜0.05),(4)FMC-to-B(203.8±65.9 min vs.583.4±125.1 min,t =8.41,P＜0.05)and (5)D-to-B time(86.5±30.6 min vs.148.2 ± 41.7 min,t =4.49,P ＜ 0.05).Especially,patients after setting up the chest pain platform reached the standard of D-to-B time less than 90 min.According to whether reaching the standard of D-to-B time or not,clinical decision-making model analysis showed that the average Gini coefficient achieving the millennium development goal(MDG) was highest in the hospital referral,followed by the average transfer treatment time and emergency thrombolysis.Conclusions Reducing average transfer treatment time,improving the efficiency of hospital referral,and refining the remote terminal information platform for chest pain diagnosis and treatment are important for chest pain center by analyzing clinical data of chest pain patients.
ABSTRACT
Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.
Subject(s)
Animals , Male , Rats , Aging , Metabolism , Physiology , Galactose , Metabolism , Hippocampus , Metabolism , Physiology , Mitochondria , Metabolism , Physiology , NADPH Oxidases , Metabolism , Oxidative Stress , Physiology , Rats, Sprague-DawleyABSTRACT
Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.