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Myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) is characterized by clinical evidence of myocardial infarction with nonobstructive coronary stenosis on angiography (stenosis 50%). Studies on the effect that exercise-based cardiac rehabilitation (CR) has on outcomes in MINOCA patients are lacking. Therefore, the purpose of this study was to determine the effect of exercise-based CR on clinical outcomes in patients with MINOCA.A total of 524 participants with MINOCA were recruited in this prospective cohort study from August 2014 to October 2016 and followed for three years. We randomly divided 524 patients into an exercise-based cardiac rehabilitation group (CR+) and a control group (CR-). The CR+ group followed a home-based exercise-training program three times a week during the three years of moderate continuous training (MCT; 65%-75% of peak heart rate) on a bicycle or treadmill.After one year of follow-up, the Short Form 36 (SF-36) survey showed apparent improvement in the mean physical health score in the CR+ group compared with the CR- group (P 0.01). During the three-year follow-up, all-cause mortality occurred in 60 individuals, and major adverse cardiovascular events (MACE) happened in 136 individuals. Kaplan-Meier curves indicated a significant reduction in all-cause mortality (log-rank P 0.05) and MACE (log-rank P 0.01) in the CR+ group. A multivariate Cox regression analysis indicated that exercise-based CR was associated with a significant reduction in all-cause mortality (hazard ratio [HR] = 0.483; 95% confidence interval [CI], 0.279-0.818; P 0.01) and MACE (HR = 0.574; 95% CI, 0.403-0.827; P 0.001).A long-term exercise-based CR program was associated with superior physical health and a significant reduction in all-cause mortality and MACE in patients with MINOCA.

Background and Aims: Myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) occurs in 5–10% of all patients with acute myocardial infarction. Obstructive sleep apnea-hypopnea syndrome (OSAHS) is linked to increased cardiovascular morbidity and mortality, but the relationship of OSAHS and outcomes in patients with MINOCA remains unknown. We aimed to evaluate the association between OSAHS and clinical outcomes in patients with MINOCA.Methods: Between January 2015 and December 2016, we carried out a consecutive cohort study of 583 patients with MINOCA and followed them up for 3 years. An apnea-hypopnea index of ≥ 15 events per hour recorded by polysomnography was defined as the diagnostic criterion for OSAHS. The primary end point was all-cause mortality, and the second end point was major adverse cardiovascular or cerebrovascular events (MACCE), a composite of cardiac death, non-fatal myocardial infarction, heart failure, cardiovascular-related rehospitalization, and stroke.Results: All-cause mortality happened in 69 patients and MACCE occurred in 113 patients during the 3-year follow-up. Kaplan–Meier survival curves indicated the significant relationship of OSAHS with all-cause mortality (log-rank P = 0.012) and MACCE (log-rank P = 0.002). Multivariate Cox regression analysis indicated OSAHS as an independent predictor of all-cause mortality and MACCE [adjusted hazard ratio: 1.706; 95% confidence interval (CI): 1.286–2.423; P = 0.008; and adjusted hazard ratio: 1.733; 95% CI: 1.201–2.389; P < 0.001; respectively], independent of age, sex, cardiovascular risk factors and discharge medications.Conclusions: OSAHS is independently associated with increased risk of all-cause mortality and MACCE in patients with MINOCA. Intervention and treatment should be considered to alleviate OSAHS-associated risk.

To determine the diagnostic accuracy, validity, current limitations of, and possible solutions to, fetal RhD genotyping from maternal blood based on existing studies written in English.A literature search was conducted that described fetal RhD determination from maternal blood. The number of samples tested, fetal RhD genotype, the source of cell-free fetal DNA, gestational age and fetal Rh type were examined in each study to calculate the accuracy, sensitivity and specificity of fetal RhD genotyping.Forty-one publications, which included 11,129 samples with non-invasive Rh genotyping of cell-free fetal DNA from maternal blood, were selected. After the exclusion of 352 inconclusive samples, the overall diagnostic accuracy was 98.5% (10,611/10,777), and sensitivity and specificity were 99% and 98%, respectively. First trimester diagnosis showed an accuracy of 99%, higher than second and third trimester diagnosis. Thirty studies reported a 100% diagnostic accuracy of fetal RhD genotyping.Non-invasive fetal RhD genotyping from maternal blood has high accuracy, sensitivity and specificity. METHODS reducing false results have been explored and applied in research. These achievements indicate that this technique will be widely used in routine clinical care.

This paper proposes a method based on extended reachability matrix combined with component design for the AGENT to build the model of aircraft systems in maintenance simulation process. It can not only solve the problem of expression of logic relationship between the LRUs, but also can provide the system with redundancy. The method can describe the component's work logic in the system and the effect of component state change on the system. The logic of aircraft system can be abstracted and transformed into the effable object of computer with this method. Through the analysis of the reachable matrix, The behavior of the signal transmission and the behavior of the service can be defined. At Last, the feasibility of the method is verified by constructing an automatic flight system (AFS).

Cyclophosphamide has a role of decreasing high-sensitivity C-reactive protein in the treatment of autoimmune disorders. The effect of cyclophosphasmide on high-sensitivity C-reactive protein was investigated in myocardial ischemia/reperfusion rat.Open-chest rats were submitted to 30 minutes of ischemia and followed for 3, 12, or 24 hours of reperfusion. All 72 rats survived and were divided into sham, ischemia/reperfusion (I/R) and cyclophosphamide groups, and each group included 3 time-point subgroups (3, 12, and 24 hours; n = 8 for each subgroup). Cyclophosphamide (0.75 g/m(2)) or saline was intraperitoneally administrated in the cyclophosphamide or I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure, left ventricular end-diastolic pressure, and maximum rate of rise or fall of left ventricular pressure. In the end, blood was collected for detection of high-sensitivity C-reactive protein, and hearts were harvested for histopathologic assessment and infarct size determination.Compared with the I/R group, rats treated with cyclophosphamide showed a significant recovery in myocardial function with improved left ventricular systolic pressure (88.27 +/- 3.78 vs 68.62 +/- 3.78 mm Hg at 3 hours, 92.04 +/- 3.77 vs 63.74 +/- 4.87 mm Hg at 12 hours, and 90.41 +/- 3.98 vs 64.21 +/- 4.88 mm Hg at 24 hours; P.05, respectively). Left ventricular end-diastolic pressure and maximum rate of rise or fall of left ventricular pressure also had similar trends. Infarct size was reduced (26.1% +/- 0.4% vs 40.4% +/- 0.4% at 3 hours, 21.6% +/- 0.4% vs 49.9% +/- 0.4% at 12 hours, and 21.6% +/- 0.4% vs 40.0% +/- 0.4% at 24 hours; P.01, respectively). Histopathologic damage score was attenuated (1.83 +/- 0.14 vs 2.17 +/- 0.14 at 3 hours, 2.33 +/- 0.14 vs 3.17 +/- 0.14 at 12 hours, and 2.83 +/- 0.14 vs 3.83 +/- 0.14 at 24 hours; P.01, respectively). Plasma high-sensitivity C-reactive protein concentration was significantly reduced (29.28 +/- 0.51 vs 32.26 +/- 0.51 ng/mL at 3 hours, 29.06 +/- 0.50 vs 31.8 +/- 0.51 ng/mL at 12 hours, and 28.61 +/- 0.51 vs 31.86 +/- 0.51 ng/mL at 24 h; P.01, respectively).Cyclophosphamide protects myocardial ischemia/reperfusion injury in the rat with a decrease in plasma concentration of high-sensitivity C-reactive protein.

Objectives:The effect of low dose of cyclophosphamide (CP)protecting cardiacfunction from ischemia-reperfusioninjury was studied on rats. The premise is that CP inhibits immune and inflammatory process, thereby limits I/R injury and improves myocardial function. Methods: Open chest rats were submitted to 30 min of ischemia followed by 3 h, 12 h or 24 h of reperfusion. Rats were divided into sham group, I/R group and CP group, and each group included 3 time-point subgroups (3 h, 12 h and 24 h; n = 8 for each subgroup). A total of 750 mg/m 2 cyclophosphamide was intraperitoneally administrated in CP group and saline was given to I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure (LVSP) and dp/dtmax. At the end of the experiment, hearts were harvested for histopathological assessment and infarct size determination. Results: Compared with I/R group, rats treated with low dose CP showed a significant recovery in myocardial function with improved LVSP (88 11 vs 69 11 mmHg of 3 h; 92 11 vs 64 14 mmHg of 12 h; 90 11 vs 64 14 mmHg of 24 h; p < 0.01 respectively). The dp/dtmax also had the similar trends. The myocardial infarct size was reduced in CP group compared to that in I/R group; the infiltration of polymorph nuclear leukocytes (PMNs) in myocardium was decreased in CP group. The histopathological damage score was also attenuated. Conclusions: These findings suggest that low dose CP rescues cardiac function from ischemia-reperfusion injury by alleviating histopathological damage in rat myocardium. # 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

To evaluate the effect of alprazolam use on psychological status and hospitalization cost in patient with paroxysmal supraventricular tachycardia underwent electrophysiology studies or radiofrequency catheter ablation.In this prospective, randomized, double-blind, placebo-controlled study, 142 inpatients [77 males, mean age (43.1 +/- 14.5) years] were randomly assigned to receive alprazolam (0.4 mg qd at 10PM for 3 days, n = 72) or placebo (n = 70) 3 days before scheduled electrophysiology studies or radiofrequency catheter ablation. All patients were examined by the Chinese version of Symptom Checklist-90 (SCL-90) at 24 hours before the procedure.Compared with the placebo group, the scores of somatization (1.38 +/- 0.40 vs. 1.65 +/- 0.56, P0.01), anxiety (1.50 +/- 0.39 vs. 1.69 +/- 0.50, P0.05), phobic anxiety (1.24 +/- 0.36 vs. 1.47 +/- 0.57, P0.01), psychotism constructs (1.24 +/- 0.34 vs. 1.35 +/- 0.30, P0.05) and global severity index (1.36 +/- 0.35 vs. 1.49 +/- 0.37, P0.05) were significantly decreased in alprazolam group. The hospitalization costs were also significantly lower in alprazolam group (32 498 +/- 1170) yuan compared to placebo group (32 947 +/- 1096) yuan, P0.05.The alprazolam use before electrophysiology studies and radiofrequency catheter ablation can improve the patients' psychological status and reduce the hospitalization costs.

To investigate the effect of acupoint injection of oxymatrine (OM) on experimental hepatocellular carcinoma and the mechanism.The rats of hepatocellular carcinoma induced by 2-acetoaminoflurence (2-AAF) were randomly divided into a normal control group (group N), a model group (group M), a control group of oxymatrine intraperitoneal injection (OM ip group) and a treatment group of small dose oxymatrine injection into Zusanli (OM ZSL group). At the end of 12h week, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (gamma-GT) were determined. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expressions of cyclin D1 and cyclin-dependent kinase 4 (CDK4) mRNA in hepatocellular carcinoma tissues.The number of cancer nodes on the surface of liver in th Om ip group and the Om ZSL group was lower than in the group M, with the serum ALT, AST, and gamma-GT levels significantly decreased (P0. 01), and significantly inhibited expressions of cyclin D1, CDK4 mRNA (P0. 01).OM ip and small dose oxymatrine injection into ZSL can treat or delay hepatocarcinogenisis of hepatocellular carcinoma induced by 2-AAF. Partial mechanism of this anti-carcinoma is protecting hepatocytes possibly through improving hepatic functions, and inhibiting excessive proliferation of liver cancer cells via inhibiting the expressions of cyclin Dl, CDK4 mRNA.