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To explore the effects of different fluid replenishment methods on the internal environment, body thermal regulatory response and severe heatstroke of 5-km armed cross-country training soldiers. Methods A Special Force officers and soldiers who participated in 5-km armed cross-country training (2-3 times a week, 25-30 minutes each time for 3 weeks) during summer training from June to July in 2018 were enrolled, and they were divided into three groups according to the random number table, with 300 trainees in each group. 200 mL of drinking fluids were given to each group 15 minutes before and after each 5-km armed cross-country training: A group with boiled water, B group with purified water, and C group with beverage prepared by pharmaceutical laboratory of the 990th Hospital of PLA Joint Logistics Support Force (100 mL containing 6 g carbohydrates, 42 mg sodium, and 11 mg potassium). The venous blood was collected before and after the last training or during the onset of severe heatstroke to do the following tests: serum cardiac troponin I (cTnI, chemiluminescence), MB isoenzyme of creatine kinase (CK-MB, immunosuppressive), serum creatinine (SCr, enzymatic method), urea nitrogen (BUN, enzymatic method), alanine aminotransferase (ALT, tryptase), aspartate transaminase (AST, tryptase), and Na+, K+, Cl- (electrode method). The heart rate (HR) and core temperature (Tc, anal temperature) were monitored at the same time. The amount of sweat in training and the occurrence of severe heatstroke were also recorded. Results There was no significant difference in heart, liver, kidney function, electrolyte and body heat regulation reaction among three groups of 5-km armed cross-country trainees before training. Compared with before training, the levels of serum cTnI, CK-MB, SCr, BUN, ALT, AST, HR and Tc were significantly increased after training or during the onset of severe heatstroke in three groups, while the contents of Na+, K+, Cl- were significantly decreased, but the increase or decrease of group C was relatively smaller compared with group A and group B [cTnI (μg/L): 0.9 (0.6, 1.4) vs. 1.1 (0.7, 2.8), 1.0 (0.6, 3.3); CK-MB (U/L): 7.0 (5.0, 11.0) vs. 9.0 (6.0, 14.5), 8.0 (6.0, 15.0); SCr (μmol/L): 92.09±18.64 vs. 102.78±18.77, 103.64±20.07; BUN (mmol/L): 7 (6, 9) vs. 9 (8, 11), 10 (8, 13); ALT (U/L): 27 (22, 34) vs. 36 (30, 43), 34 (27, 43); AST (U/L): 37 (31, 48) vs. 41 (34, 50), 39 (34, 51); HR (bpm):87.01±17.07 vs. 95.88±21.06, 96.59±22.04; Tc (℃): 37.73±0.81 vs. 38.03±1.05, 38.10±1.04; Na+ (mmol/L):150.14±3.86 vs. 144.18±8.89, 144.04±9.39; K+ (mmol/L): 4.32±0.57 vs. 4.15±0.62, 4.13±0.51; Cl- (mmol/L):100.43±3.71 vs. 98.42±4.24, 98.41±4.58; all P < 0.01]. The incidence of severe heatstroke in group C was significantly lower than that in group A and group B [1.67% (5/300) vs. 5.00% (15/300), 5.33% (16/300), χ2 = 6.424, P = 0.040]. There was no significant difference in sweating volume in groups A, B, C (g: 370.47±48.71, 370.85±50.66, 370.17±50.21, F = 0.014, P = 0.986). There was no significant difference in the above indexes between group A and group B (all P > 0.05). Bi-classification Logistic regression analysis showed that the increase of HR, Tc and excessive loss of Na+, K+, Cl- were risk factors for severe heatstroke [odds ratio (OR) was 0.848, 0.138, 1.565, 17.996 and 2.328 respectively, all P < 0.01]. Conclusions Timely supplementation of carbohydrate, sodium and potassium ions can effectively change the internal environment and body heat regulation reaction of 5-km armed cross-country trainees, so as to reduce the occurrence of severe heatstroke. The increases of HR, Tc and excessive loss of Na+, K+, Cl- are risk factors for severe heatstroke.
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Objective To evaluate the early diagnostic value of circulating microRNA-1 (miR-1) on acute myocardial infarction (AMI). Methods A prospective cohort study was conducted. The patients with chest pain admitted to the Second People's Hospital of Wuxi from November 2012 to June 2015 were enrolled. According to AMI diagnostic criteria, the patients were divided into AMI group and non-AMI group, and healthy individuals during the same period were served as heath controls. The venous samples of the onset patients were collected within 3 hours after admission. The plasma miR-1 was determined by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR), and the levels of plasma cardiac troponin I (cTnI) and MB isoenzyme of creatine kinase (CK-MB) were measured by electrochemiluminescence. The correlation between plasma miR-1 and cTnI as well as CK-MB was performed by Spearman analysis. The early diagnostic performance of plasma miR-1, cTnI, and CK-MB for AMI was estimated by receiver operating characteristic (ROC) curve analysis. Results There were 127 patients in AMI group, and 107 in non-AMI group, including 82 patients with angina pectoris, 2 with pulmonary embolism, 3 with aortic dissection, 2 with acute pericarditis, 3 with myocarditis, 13 with acute heart failure, and 2 with peptic ulcer. Ninety volunteers were served as healthy controls. There was no difference in clinical characteristics including gender and hyperlipidemia between AMI group and non-AMI group. The expressions of plasma miR-1, cTnI and CK-MB were significantly increased in AMI patients as compared with those of the healthy controls [miR-1 (2-ΔΔCt): 4.32±2.60 vs. 1.44±0.75 and 0.98±0.18, cTnI (μg/L): 3.23 (0.63, 10.70) vs. 0.02 (0.00, 0.17) and 0.00 (0.00, 0.00), CK-MB (U/L): 32.40 (14.20, 95.40) vs. 14.40 (11.20, 17.10) and 8.90 (8.28, 9.50), all P < 0.01]. The expression of plasma miR-1 had a significantly positive correlation with cTnI and CK-MB in AMI patients (r1 = 0.395, r2 = 0.490, both P < 0.000). It was demonstrated by ROC curve analysis that the area under ROC curve (AUC) for the diagnostic value of miR-1 on AMI was 0.905 [95% confidence interval (95%CI) = 0.860-0.950, P = 0.000], the sensitivity was 86.6%, and the specificity was 95.4%; the AUC for cTnI was 0.908 (95%CI = 0.870-0.946, P = 0.000), the sensitivity was 81.9%, and the specificity was 95.9%; the AUC for CK-MB was 0.795 (95%CI = 0.736-0.854, P = 0.000), the sensitivity was 63.0%, and the specificity was 92.9%. Conclusions Plasma miR-1 has the capacity in early diagnosis of AMI, superior to CK-MB, and equal to cTnI. It can provide additional diagnostic information beyond cTnI. The diagnostic accuracy for early AMI can be improved with the combination of plasma miR-1 and cTnI.
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Objective To analyze the profile of dermcidin (DCD) changes in different stages of acute coronary syndrome (ACS) by quantifying the serum 4 183Da DCD peptide fragment deriving from different ACS patients treated with early antithrombotic therapy.Methods A total of 118 patients with confirmed diagnosis of ACS were enrolled. Immediately after visiting a doctor, the venous blood was collected and afterwards instantly the patient was given orally 300 mg of aspirin and 300 mg clopidogrel, and according to the patient's condition and the consent of his/her or acknowledgement of family members achieved, emergency percutaneous coronary interference (PCI) or thrombolysis or conservative treatment was adopted separately. After anti-thrombotic treatment, at 2, 4, 6, 8, 10, 12, 16, 20, 24, 32, 40, 48, 60 and 72 hours, venous blood was collected and serum isolated respectively. The concentration of 4 183Da DCD fragment in serum was determined by matrix assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS). Simultaneously, the myoglobin (Myo), cardiac troponin I (cTnI) and MB isoenzyme of creatine kinase (CK-MB) were also detected.Results The mean relative strength of nature logarithmic transformations of 4 183Da DCD fragment of 118 patients with ACS was 2.75±1.02 before treatment on admission, and after intervention therapy (mainly antithrombotic therapy) it was decreased to 1.84±1.19 (P = 0.005) and 1.74±1.12 (P = 0.000) at 2 hours and 4 hours, respectively, and then after 4 hours it was slightly elevated. 4 183Da polypeptide increased earlier than myocardial injury markers.Conclusion Aspirin and clopidogrel can significantly decrease the concentration of 4 183Da DCD peptide fragment in serum in patients with ACS, which indicates that the DCD fragment could be used as one of the indexes for observation on early efficacy of antithrombotic therapy.
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ObjectiveTo investigate the diagnostic value of N-terminal pro-brain natriuretic peptide (NT-proBNP) and MB isoenzyme of creatine kinase (CK-MB) for heart failure (HF) in pneumonia children.MethodsThe NT-proBNP and CK-MB were assayed in 132 pneumonia children with HF, 138 pneumonia children without HF and 62 healthy children were recruited into this study. A receiver operating characteristics (ROC) curve and a logistic regression model were employed to assess the diagnostic accuracy of NT-proBNP and CK-MB for HF in pneumonia children.ResultsPneumonia children with HF had higher blood NT-proBNP and CK-MB than those in pneumonia children without HF and healthy controls (P<0.01 for both). Pneumonia children with HF had higher blood NT-proBNP and CK-MB than the pneumonia children without HF. The area under curves (AUCs) of NT-proBNP and CK-MB for HF were 0.85 and 0.72, respectively. The AUC for their combinational usage was 0.87.ConclusionBoth NT-proBNP and CK-MB are effective markers as diagnostic adjuncts for HF in pneumonia children. Combination of NT-proBNP and CK-MB can improve the diagnostic accuracy for HF in pneumonia children.
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One hundred and fifty-one type 2 diabetic patients with coronary heart disease ( T2 DMC) and 142 cases of type 2 diabetes mellitus were included for analyzing the influence of different glucose-lowering rates on MB isoenzyme of creatine kinase (CKMB) and muscle hemoglobin level changes to search for the rational glucose-lowering rate.The level of CKMB in type 2 deabetes mellitus group was significantly lower( P＜0.05 ) at follow-up than that before and after intensive therapy.In type 2 diabetes mellitus group,when the fasting or postprandial glucose-lowering rate was not greater than 6 mmol· L-1 · d-1,the level of CKMB and muscle hemoglobin were significantly lower at follow-up than that before intensive therapy ( P＜0.05 ).When the fasting glucose-lowering rate is greater than 6 mmol· L-1 · d-1,the level of CKMB is significantly higher after intensive therapy than that before glucose-lowering ( P＜0.05 ).In T2DMC group,when the fasting or postprandial glucose-lowering rate was not greater than 4 mmol· L-1 · d-1,the level of CKMB and muscle hemoglobin was significantly lower at follow-up than that before intensive therapy(P＜0.05 or P＜0.01 ),buthigher at follow-up when the fasting glucose-lowering rate was greater than 4 mmol· L-1 · d-1(P＜0.05).
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Objective To explore the myocardial damage and the changes of MB isoenzyme of creatine kinase(CK-MB) and cardial troponin I(cTnI) of rat with endotoxemia at early stage.Methods Sixty SD rats were randomly divided into lipopolysaccharide(LPS) group(LPS group,n=48) and control group(n=12).Rats in LPS group were injected intraperitoneally with LPS(5 mg/kg) and then divided into 6 subgroups according sacrificed time after injection(0.5,1.0,2.0,3.0,12.0,24.0 h).CK-MB/ cTnI in blood was determined with chemiluminescent technique and myocardial pathological damage was observed under the light and transmission electron microscope.Control group was subjected to normal sodium and divided randomly into the same subgroups too.Results The rat diminished their action after beening injected endotoxin 15 minutes,and their reaction were slow.One hour later,they were short of action and reaction.Three hours later,they almost did not move at all,and the glossiness of their pelage were faint.Twenty-four hours later,their foodintake was diminished,their shout were weakened,and their response to stimulus were very thin,the glossiness of pelage were insufficient.Compared with control group,CK-MB increased significantly at 1.0,2.0,3.0,12.0,24.0 h(Pa
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0.05).Conclusion BNP and hsCRP may be involved in the occurrence and sustainment of atrial fibrillation.The serum levels of BNP and hsCRP may serve as independent indexes of atrial fibrillation.CK-MB may be not involved in the incidence and development of atrial fibrillation.