Humans ; Alzheimer Disease ; Cross-Sectional Studies ; Creatine Kinase ; Brain/metabolism*

Acute Disease ; Carbon Monoxide Poisoning ; enzymology ; physiopathology ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; Echocardiography ; Heart ; physiopathology ; Humans ; Hyperbaric Oxygenation ; Isoenzymes ; metabolism ; Myocardium ; enzymology

Animals ; Creatine Kinase ; blood ; Energy Metabolism ; Lactate Dehydrogenases ; blood ; Male ; Pressure ; adverse effects ; Rabbits ; Serum ; enzymology

OBJECTIVETo explore the effects of hippophae juice on free radical metabolism of rat skeletal muscle and partial biomarkers in blood.

METHODSRandomly dividing the 30 SD rats into 3 groups (n = 10): sedentary group, training group and hippophae training group. Measuring related indices of skeletal muscle and blood in rat after 6 week training and hippophae juice supplement.

RESULTSCompared with training group, hippophae training group showed obviously longer exhaustive time, significantly increased antioxidant enzyme in skeletal muscle, remarkably decreased malonaldehyde (MDA) content in skeletal muscle, obviously increased testosterone (T) and hemoglobin (Hb) content in blood, significantly decreased creatine kinase (CK).

CONCLUSIONHippophae juice can impove the antioxidant ability of rat skeletal muscle, the level of T and Hb in blood, delay fatigue, therefore effectively enhance the aerobic stamina of rat.

Animals ; Creatine Kinase ; blood ; Free Radicals ; metabolism ; Hemoglobins ; metabolism ; Hippophae ; Male ; Muscle, Skeletal ; metabolism ; Rats ; Rats, Sprague-Dawley ; Testosterone ; blood

OBJECTIVETo investigate the clinical significance of myocardial enzymes in patients with acute tetramine (TEM) poisoning.

METHODSThe dynamic changes of the activity of myocardial enzymes and ECG were observed in 67 patients with acute TEM poisoning as well as in 67 healthy people for medical checkup at outpatient department as the control group.

RESULTSMyocardial enzymes of the patients with acute TEM poisoning were increased to different extents on the first day. There was significant difference in the activity of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) and CPK isoenzyme MB (CK-MB) between the patients and the healthy people in the control group (P < 0.01). There was significant difference in the myocardial enzymes at different time points among the patients with mild, middle and severe poisoning (P < 0.01). The severer the TEM poisoning was, the higher the activity of myocardial enzymes and the abnormal rate of ECG were. The activity of CPK was the earliest to rise with the highest aptitude of fluctuation and the longest time of elevation. The change of the myocardial enzymes was earlier than that of ECG. The abnormal rate of AST, CPK, CK-MB, LDH, alpha-HBDH was 86.57%, 98.51%, 94.03%, 89.55% and 79.10% respectively. The abnormal rate of ECG was 49.3% on the third day of poisoning. Measurement of myocardial enzymes was better than ECG in sensitivity.

CONCLUSIONAcute tetramine poisoning can damage myocardium, which is reversible. CPK is a typical marker for the damage and can serve as one of the important clinical monitoring indices.

Acute Disease ; Adolescent ; Adult ; Aspartate Aminotransferases ; metabolism ; Bridged-Ring Compounds ; poisoning ; Child ; Child, Preschool ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; metabolism ; Electrocardiography ; Female ; Humans ; Hydroxybutyrate Dehydrogenase ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Male ; Middle Aged ; Myocardium ; enzymology

To explore the potential of lipoteichoic acid (LTA) induced cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts and whether endogenous nitric oxide (NO) participates in the protection, the rats were pretreated with LTA (1 mg/kg, i.p.) 24 h before the experiment, and the isolated hearts were subjected to 30 min no-flow normothermic global ischemia and 60 min reperfusion after a 20-min stabilization period by the langendorff method. Cardiac functions were evaluated at the end of stabilization, and at 30 min, 60 min of reperfusion. The amounts of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase(LDH) and total NO oxidation products in the coronary effluent were measured spectrophotometrically at the end of reperfusion. It was revealed that pretreatment with LTA could significantly improve the recovery of cardiac function, reduce the release of CK-MB and LDH, and increase the concentrations of NO in coronary effluent. The protective effects were abrogated by pretreatment of the rats with L-NAME. It was concluded that LTA could induce the delayed cardioprotection against I/R injury, and endogenous NO may be involved in the mechanisms.
Animals ; Cardiotonic Agents ; pharmacology ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; In Vitro Techniques ; Ischemic Preconditioning, Myocardial ; Isoenzymes ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lipopolysaccharides ; pharmacology ; Male ; Myocardial Reperfusion Injury ; prevention & control ; Nitric Oxide ; metabolism ; Rats ; Rats, Wistar ; Teichoic Acids ; pharmacology

OBJECTIVETo find a better index for detecting myocardial lesion in patients with acute ammonia poisoning.

METHODSCardiac troponin T (cTnT), creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB), and electrocardiogram (ECG) were determined and compared in patients with acute ammonia poisoning and healthy controls.

RESULTSIn severe ammonia poisoning patients, the levels of cTnT [(1.285 +/- 2.650) micro g/L], CK [(257.636 +/- 362.719) IU/L], CK-MB [(20.909 +/- 19.770) IU/L] were significantly higher than those in healthy control [(0.035 +/- 0.014) micro g/L, (82.050 +/- 36.302) IU/L, (8.350 +/- 2.455) IU/L respectively, P < 0.05]. The levels of cTnT, CK and CK-MB in mild ammonia poisoning patients [(0.039 +/- 0.016) micro g/L, (78.200 +/- 28.401) IU/L and (8.467 +/- 2.669) IU/L respectively], and moderate ammonia poisoning patients [(0.054 +/- 0.043) micro g/L, (99.786 +/- 71.941) IU/L and (9.429 +/- 3.857) IU/L were not significantly different from those of healthy controls (P > 0.05)]. cTnT positive detection rate (68.2%) was significantly higher than CK (36.4%), CK-MB (31.2%) and ECG (31.2%) (P < 0.05).

CONCLUSIONcTnT is a better index to detect myocardial lesion in severe ammonia poisoning.

Acute Disease ; Adolescent ; Adult ; Ammonia ; poisoning ; Child ; Child, Preschool ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; Electrocardiography ; Female ; Heart ; drug effects ; physiopathology ; Humans ; Isoenzymes ; metabolism ; Male ; Middle Aged ; Myocardium ; pathology ; Occupational Diseases ; chemically induced ; diagnosis ; metabolism ; Troponin T ; metabolism

OBJECTIVE: To compare the changes in muscle enzyme between children with myocarditis and Duchene/Becker muscular dystrophy (DMD/BMD), and to seek the explanations for variation.
 METHODS: The retrospective analysis for 83 myocarditis children (myocarditis group) and 69 DMD/BMD children (DMD/BMD group), who were collected from Department of Pediatric of Shengjing Hospital affiliated to China Medical University since January 2008 to May 2015, was carried out. At the same time, 24 healthy children from the Department of Pediatric Development served as a control group. The examination indexes included creatine kinase (CK), creatine kinase-isoenzyme MB (CK-MB), creatine kinase isoenzyme MB mass (CK-MB mass), cardiac troponin I (cTnI) and high-sensitive-cTnT (hs-cTnT).
 RESULTS: 1) In the myocarditis group, the CK increased from 100 to 1 000 U/L, reached a peak after 5 days, which lasted for a week and then dropped to the normal; the CK-MB reached a peak after 5 to 7 days and dropped to the normal a month later; the CK-MB mass reached a peak on the first day and dropped to the normal after 3 weeks; the cTn reached to a peak after 5 days and dropped to the normal after about 17 days; hs-cTnT reached to a peak on the first day and dropped to the normal after about 19 days. 2) In the DMD/BMD group, the CK increased significantly and 27 cases had a CK value of more than 10 000 U/L. After the treatment for 1 to 2 weeks, their enzyme rose again after a slight drop. In terms of cTnI, 6 cases showed a moderate increase, 5 of them couldn't drop to the normal level until more than 3 weeks later; the hs-cTnT increased in the 45 cases, which lasted for more than 3 weeks in the 31 cases of them and showed a tendency of persisting increase.
 CONCLUSION The cTnI and hs-cTnT rise significantly and possess wider observation window than CK and CK-MB mass in myocarditis children, with more sensitive and specific changes. The myocardial damage can occur before myasthenia and keep this trend for a long time in the DMD/BMD children. The trend of cTnI change in myocarditis children is similar to hs-cTnT, while hs-cTnT in DMD/BMD children is more sensitive than cTnI.
Biomarkers ; Child ; China ; Creatine Kinase ; blood ; metabolism ; Creatine Kinase, MB Form ; blood ; metabolism ; Female ; Humans ; Male ; Muscle Weakness ; enzymology ; Muscular Dystrophy, Duchenne ; enzymology ; therapy ; Myocarditis ; enzymology ; therapy ; Retrospective Studies ; Time Factors ; Troponin I ; blood ; metabolism ; Troponin T ; blood ; metabolism

OBJECTIVETo explore the changes of brain energy metabolism following acrylamide (ACR) poisoning.

METHODSCreatie kinase (CK), adenosine triphosphate (ATP), adenosine diphosphate(ADP), adenosine 5'-monophosphate(AMP) and glucose contents in brain were observed in O1a mice and 6J mice following ACR intoxication by enzyme analytical method.

RESULTSATP, CK and glucose levels decreased transiently in O1a mice, while ATP level in 6J mice was significantly decreased (1.76 mumol/g, P < 0.01), as compared to the control (2.53 mumol/g) but ADP and AMP were increased, glucose was decreased. The activity of CK in poisoned group (1.13 mumol/g, P < 0.01) was lower than that of control (3.16 mumol/g and lasted for 5 weeks).

CONCLUSIONThe influence of ACR on O1a mice was slight and reversible but on 6J mice was severe and lasting. There was severe damage to the potential energy supply compensation, which might be the biochemical basis of neuron damage induced by acrylamide.

Acrylamide ; poisoning ; Adenosine Triphosphate ; analysis ; Animals ; Brain ; drug effects ; metabolism ; Creatine Kinase ; analysis ; Energy Metabolism ; drug effects ; Glucose ; analysis ; Mice

OBJECTIVE: To investigate the changes of creatine kinase-MB (CK-MB) and heat shock protein 60 (HSP 60) in rats without electric marks after electric injury, to identify the relationship of the CK-MB, HSP 60 and the time of electric injuries, and to evaluate the damage to cells after electric injury. METHODS: The animal model of electric injury without electric marks was established by alternating current (voltage 110 V). Automatic biochemistry analyzer was used to detect the serum CK-MB and immunohistochemical staining technology was used to analyze the tissues of myocardium and left lobe of liver. RESULTS: The amount of serum CK-MB was increased when the rats were injuried, and reached the peak at 30min. Then the amount of CK-MB began to decrease and showed a slight downward trend in 3-5 h after electric injury, and leveled off at 6 h. Immunohistochemistry staining also showed the changes of HSP 60 of rats' myocardial cells and hepatic cells regularly after electric injury. CONCLUSION The regular changes of serum CK-MB and tissular HSP 60 in rats can be used to diagnosis electric injury and assess the injury of internal organs after the electric injury without electric marks.
Animals ; Chaperonin 60/metabolism* ; Creatine Kinase, MB Form/metabolism* ; Electric Injuries/complications* ; Immunohistochemistry ; Liver/pathology* ; Myocardium/pathology* ; Rats