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Creatine Kinase (creatine + kinase)
Kinds of Creatine Kinase Terms modified by Creatine Kinase Selected AbstractsThe clinical features of dermatomyositis in a South Australian populationINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 2 2007Vidya LIMAYE Abstract Aim:, To review the clinical features of dermatomyositis (DM) in a South Australian population. Methods:, Retrospective review of medical records of patients with biopsy-proven DM in South Australia from 1990 to 2005. Results:, There were 21 cases of biopsy-proven DM in SA (62% F, mean age 49.7 ± 18.4 years) and clinical details were available in 20 of these. Malignancy was identified in 9/20 patients; in five this followed the diagnosis of DM, with three malignancies seen within 3 months of disease onset. Three patients had a clearly defined immune insult prior to the diagnosis of DM; one patient had Mycoplasma pneumoniae infection 23 days prior to DM, two had pneumococcal and influenza vaccinations 5 and 14 days prior to the onset of DM, respectively. Two of three patients with anti-Jo-1 antibody experienced thromboembolism within 2 months of DM onset and three patients had interstitial lung disease (2 with anti-Jo-1 antibody). Creatine kinase (CK) was elevated in 15/20 cases and showed strong correlation with transaminases, and notably not with traditional inflammatory markers. Conclusions:, This retrospective review of patients with biopsy-proven DM suggests a role for infection/vaccination in triggering disease onset. A particularly strong association with malignancy was observed and it is suggested that DM may predispose to thrombosis. Transaminases, in addition to CK may be used to monitor disease activity, and traditional inflammatory markers have little role in this. [source] Cardiac Troponin I in Pastured and Race-Training Thoroughbred HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2003Wade Phillips Cardiac troponin I (cTnI), a myocardial polypeptide, is a highly sensitive and specific biomarker of myocardial injury in people and dogs. The structure of cTnI is highly conserved across species, and equine myocardium has high reactivity with human immunoassays. The purpose of this study was to describe cTnI concentrations in normal pastured and race-training Thoroughbred horses. Ten horses on pasture and 10 horses in race training were studied. Horses were considered normal on the basis of physical examination, training performance, electrocardiography (ECG), and echocardiography. Serum cTnI concentrations were determined with a colorimetric immunoassay. The assay has an analytical sensitivity of 0.04 ng/mL. Serum cTnI concentrations in race-training horses were not significantly different from those of pastured horses. When groups were combined, mean cTnI concentration (±SD) was 0.047 ± 0.085 ng/mL, and the median was 0 (range, 0-0.35 ng/mL). The 90th percentile for both groups combined was 0.11 ng/mL. This study establishes a preliminary reference range for serum cTnI in normal Thoroughbred horses. Key words: Cardiac disease; Cardiac markers; Creatine kinase; Myocarditis. [source] The three-dimensional structure of cytosolic bovine retinal creatine kinaseACTA CRYSTALLOGRAPHICA SECTION D, Issue 2 2001Dominic Tisi Creatine kinase (CK) catalyses the reversible transfer of the phosphate moiety from phosphocreatine (PCr) to ADP, generating creatine and ATP. The crystal structure of a cytosolic brain-type creatine kinase is reported at 2.3,Å. The biological dimer sits on a crystallographic twofold axis. The N-terminal residues of both subunits come very close to the crystallographic twofold at the dimer interface. The electron density observed is consistent with two alternative conformations for the N-termini, as previously found for chicken brain-type creatine kinase. [source] Oxidative Stress Alters Creatine Kinase System in Serum and Brain Regions of Polychlorinated Biphenyl (Aroclor 1254)-Exposed Rats: Protective Role of MelatoninBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2009Prabhu Venkataraman Creatine kinase plays a key role in energy metabolism of nervous tissue and might be one of the targets for reactive oxygen species. Melatonin, an indoleamine, plays an important role in neurodegenerative diseases as an antioxidant and neuroprotector. The objective of the present study was to investigate the protective role of melatonin on polychlorinated biphenyl (Aroclor 1254)-induced oxidative stress and the changes in creatine kinase activity in brain regions of adult rats. Group I: rats were intraperitoneally (i.p.) administered with corn oil (vehicle) for 30 days. Group II: rats injected i.p. with Aroclor 1254 at 2 mg/kg body weight (bw)/day for 30 days. Groups III and IV: rats i.p. received melatonin (5 or 10 mg/kg bw/day) simultaneously with Aroclor 1254 for 30 days. After 30 days, rats were killed and the brain regions were dissected to cerebral cortex, cerebellum and hippocampus. Lipid peroxidation, hydroxyl radical and hydrogen peroxide (H2O2) levels were determined. The activity of creatine kinase was assayed in serum and brain regions, and its isoenzymes in serum were separated electrophoretically. Activity of creatine kinase was decreased while an increase in H2O2, hydroxyl radical and lipid peroxidation was observed in brain regions of polychlorinated biphenyl-treated rats. Also polychlorinated biphenyl exposure showed a significant increase in serum creatine kinase level and its isoforms such as BB-creatine kinase, MB-creatine kinase, and MM-creatine kinase. Administration of melatonin prevented these alterations induced by polychlorinated biphenyl by its free radical scavenging mechanism. Thus, polychlorinated biphenyl alters creatine kinase activity by inducing oxidative stress in brain regions, which can be protected by melatonin. [source] Retrospective Review: The Incidence of Non-ST Segment Elevation MI in Emergency Department Patients Presenting With Decompensated Heart FailureCONGESTIVE HEART FAILURE, Issue 6 2003W. Frank Peacock MD The authors performed a 6-month review of heart failure patients presenting to a teaching hospital emergency department to determine the rate of positive serum myocardial infarction markers. All patients with an emergency department discharge diagnosis of heart failure were included; those with a creatinine level >2.0 mg/dL were excluded. There were 151 patients who met the entry criteria, with a mean age of 68.6±13.6 years, and 84 (56%) were men. The mean ejection fraction was 32%, and the mean Framingham score was 3.8±1.6. Twenty (14%) had positive markers. Troponin T was positive in 17 (11%), and creatine kinase was positive in nine (6%). Both markers were positive in six (4%). Chest pain was absent in 70% of the positive marker group. The authors conclude that elevated cardiac markers are not rare in decompensated heart failure. These pilot data suggest these tests should be routinely obtained on heart failure patients. [source] A cytoskeletal tropomyosin can compromise the structural integrity of skeletal muscleCYTOSKELETON, Issue 9 2009Anthony J. Kee Abstract We have identified a number of extra-sarcomeric actin filaments defined by cytoskeletal tropomyosin (Tm) isoforms. Expression of a cytoskeletal Tm (Tm3) not normally present in skeletal muscle in a transgenic mouse resulted in muscular dystrophy. In the present report we show that muscle pathology in this mouse is late onset (between 2 and 6 months of age) and is predominately in the back and paraspinal muscles. In the Tm3 mice, Evans blue dye uptake in muscle and serum levels of creatine kinase were markedly increased following downhill exercise, and the force drop following a series of lengthening contractions in isolated muscles (extensor digitorum longus) was also significantly increased in these mice. These results demonstrate that expression of an inappropriate Tm in skeletal muscle results in increased susceptibility to contraction-induced damage. The extra-sarcomeric actin cytoskeleton therefore may have an important role in protecting the muscle from contractile stress. Cell Motil. Cytoskeleton 2009. © 2009 Wiley-Liss, Inc. [source] Insulin resistance Type A and short 5th metacarpalsDIABETIC MEDICINE, Issue 6 2003Vinod K. Patel Abstract Background/aims Insulin resistance is associated with a number genetic syndromes and a variety of defects of insulin action. Methods We describe three members of an extended family spanning two generations with insulin resistance Type A and short 5th metacarpals. The proband had secondary amenorrhoea, male pattern hair distribution, acne, hirsutism, deep voice, acanthosis nigricans, polycystic ovaries, diabetes, features of acromegaly, raised creatine kinase and triglyceride levels and short 5th metacarpals. Her growth hormone, adrenal steroid and testosterone levels were normal. The proband's daughter had severe acne, hirsutism, acanthosis nigricans, polycystic ovaries, raised triglyceride, glucose and testosterone level short metacarpals and normal insulin receptor gene. The proband's son had a muscular build, raised creatine kinase, hypertriglyceridaemia and short 5th metacarpals. His fasting insulin levels were normal but pro-insulin was raised. Result/conclusion There are many familial and genetic syndromes associated with insulin resistance. This family was diagnosed as having insulin resistance Type A. This family does not conform entirely to any of the previously described syndromes and a number of family members have the phenotype of short 5th metacarpals, which appears to be associated with the features of insulin resistance Type A. Diabet. Med. 20, 500,504 (2003) [source] In vitro effects of lidocaine on the contractility of equine jejunal smooth muscle challenged by ischaemia-reperfusion injuryEQUINE VETERINARY JOURNAL, Issue 1 2010M. GUSCHLBAUER Summary Reasons for performing study: Post operative ileus (POI) in horses is a severe complication after colic surgery. A commonly used prokinetic drug is lidocaine, which has been shown to have stimulatory effects on intestinal motility. The cellular mechanisms through which lidocaine affects smooth muscle activity are not yet known. Objectives: To examine the effects of lidocaine on smooth muscle in vitro and identify mechanisms by which it may affect the contractility of intestinal smooth muscle. Hypothesis: Ischaemia and reperfusion associated with intestinal strangulation can cause smooth muscle injury. Consequently, muscle cell functionality and contractile performance is decreased. Lidocaine can improve basic cell functions and thereby muscle cell contractility especially in ischaemia-reperfusion-challenged smooth muscle. Methods: To examine the effects of lidocaine on smooth muscle function directly, isometric force performance was measured in vitro in noninjured and in vivo ischaemia-reperfusion injured smooth muscle tissues. Dose-dependent response of lidocaine was measured in both samples. To assess membrane permeability as a marker of basic cell function, release of creatine kinase (CK) was measured by in vitro incubations. Results: Lidocaine-stimulated contractility of ischaemia-reperfusion injured smooth muscle was more pronounced than that of noninjured smooth muscle. A 3-phasic dose-dependency was observed with an initial recovery of contractility especially in ischaemia-reperfusion injured smooth muscle followed by a plateau phase where contractility was maintained over a broad concentration range. CK release was decreased by lidocaine. Conclusion: Lidocaine may improve smooth muscle contractility and basic cell function by cellular repair mechanisms which are still unknown. Improving contractility of smooth muscle after ischaemia-reperfusion injury is essential in recovery of propulsive intestinal motility. Potential relevance: Characterisation of the cellular mechanisms of effects of lidocaine, especially on ischaemia-reperfusion injured smooth muscle, may lead to improved treatment strategies for horses with POI. [source] Effect of conditioning horses with short intervals at high speed on biochemical variables in bloodEQUINE VETERINARY JOURNAL, Issue S36 2006A. LINDNER Summary Reasons for performing study: There is limited published work on the effect of training using intensive and short intervals of exercise to condition horses for racing. Objectives: To examine the effect of conditioning horses 1, 2 or 3 x a week using 2 short fast exercise intervals on blood lactate (LA), plasma ammonia (NH3) and urea (urea) as well as creatine kinase (CK) activity. Methods: Thoroughbreds (age 4,5 years) were conditioned at near maximal speed (12,14 m/sec) over 100 m, on 2 occasions separated by a 10 min period at walk, on dirt track (conditioning exercise; CE) during a 6 week conditioning period (CP). The CE was undertaken either once (5 horses), twice (5 horses) or 3 times a week (4 horses) during a CP. Before, every 2 weeks during and after the CP, blood was drawn during the CE at 0, 2 and 4 min after each run and additionally 6 min after the 2nd run to measure blood LA and determine the maximal LA post exercise (LAmax). Plasma NH3 was measured in the same samples and the maximal NH3 post exercise (NH3max) determined. Additional blood samples were taken from the horses when stabled before the CE, and 12 and 24 h after to measure urea and CK activity in plasma. Results: There was no differential effect of the number of weekly CE on LAmax, NH3max, LA and NH3 immediately after exercise (LAO and NH30). Conditioning did not have an effect on LAmax and LAO after the 1st interval (P>0.05), but LAO after the 2nd interval was lower after conditioning. NH3max after the 1st and 2nd exercise interval decreased in response to the conditioning, but not NH3 immediately after exercise (P>0.05). Median plasma CK activity 12 h after exercise was higher than before exercise and returned to pre-exercise levels 24 h post exercise when horses were exercised once and twice/week. In contrast, the median plasma CK activity of horses exercising 3 times/week remained at the pre-exercise level 12 and 24 h post exercise (P>0.05). Conclusion: Conditioning horses with 2 intervals of 100 m at near maximal speed had a positive effect on blood LA and plasma NH3. Potential relevance: With the type of exercise examined, the fitness of racing horses can be maintained and eventually improved. In further studies the effect of increasing the number of runs in one exercise session should be investigated. [source] The efficacy of dantrolene sodium in controlling exertional rhabdomyolysis in the Thoroughbred racehorseEQUINE VETERINARY JOURNAL, Issue 7 2003J. G. T. Edwards Summary Reasons for performing study: Dantrolene sodium (Dantrium) has been used extensively for the treatment of myopathies in man and anecdotal evidence suggests it is of clinical benefit in the control of exercise-induced rhabdomyolysis (ER) in racehorses, although data to support this are currently lacking. Objectives: To investigate the efficacy of oral dantrolene sodium in controlling ER in a randomised, double-blind, placebo-controlled crossover trial involving 77 Thoroughbred racehorses in Newmarket, UK. Methods: Horses were treated on 2 occasions 1 week apart, with treatment days coinciding with a return to exercise following 2 days box rest on each occasion. For the first treatment, each horse was randomly selected to receive either 800 mg dantrolene sodium or a colour- matched placebo administered orally 1 h before exercise. This was followed by crossover to the other treatment on the second occasion, with each horse thereby acting as its own control. Degree of ER was assessed using rising serum creatine kinase (CK) levels, by subtracting pre-exercise blood CK levels from those measured in 6 h post exercise blood samples. For each horse, the difference in change between pre- and post exercise CK values between placebo and dantrolene treatments was calculated, with positive values indicating a greater rise with placebo than with dantrolene sodium treatment. Results: The overall mean difference for all horses was +104.8 iu/l and the null hypothesis, that there was no true difference in non-normally distributed post exercise rises in CK values between placebo and dantrolene treatments, was rejected (P = 0.0013) using the nonparametric Wilcoxon signed rank test. Additionally, no horses given dantrolene sodium showed clinical signs of ER, whereas 3 horses given the placebo developed ER following exercise. The incidence of ER in the study was 4% (3/77). Conclusions: The results confirmed that oral administration of dantrolene sodium, 1 h before exercise, had a statistically significant effect on reducing the difference between pre - and post exercise plasma CK levels compared with a placebo in the same animals, and preventing clinical ER in susceptible individuals. Potential relevance: This study suggested that dantrolene sodium is of use in controlling ER in the Thoroughbred racehorse. Further investigation into pre- and post exercise myoplasmic calcium levels and the repeat of the study late in the season when horses receive a much higher energy ration and more strenuous exercise would appear to be warranted. [source] D-2-Hydroxyglutaric acid inhibits creatine kinase activity from cardiac and skeletal muscle of young ratsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2003C. G. Da Silva Abstract Background, Tissue accumulation of high amounts of D-2-hydroxyglutaric acid (DGA) is the biochemical hallmark of the inherited neurometabolic disorder D-2-hydroxyglutaric aciduria (DHGA). Patients affected by this disease usually present hypotonia, muscular weakness, hypothrophy and cardiomyopathy, besides severe neurological findings. However, the underlying mechanisms of muscle injury in this disorder are virtually unknown. Materials and methods, In the present study we have evaluated the in vitro role of DGA, at concentrations ranging from 0·25 to 5·0 mm, on total, cytosolic and mitochondrial creatine kinase activities from skeletal and cardiac muscle of 30-day-old Wistar rats. We also tested the effects of various antioxidants on the effects elicited by DGA. Results, We first verified that total creatine kinase (CK) activity from homogenates was significantly inhibited by DGA (22,24% inhibition) in skeletal and cardiac muscle, and that this activity was approximately threefold higher in skeletal muscle than in cardiac muscle. We also observed that CK activities from mitochondrial (Mi-CK) and cytosolic (Cy-CK) preparations from skeletal muscle and cardiac muscle were also inhibited (12,35% inhibition) by DGA at concentrations as low as 0·25 mm, with the effect being more pronounced in cardiac muscle preparations. Finally, we verified that the DGA-inhibitory effect was fully prevented by preincubation of the homogenates with reduced glutathione and cysteine, suggesting that this effect is possibly mediated by modification of essential thiol groups of the enzyme. Furthermore, ,-tocopherol, melatonin and the inhibitor of nitric oxide synthase L-NAME were unable to prevent this effect, indicating that the most common reactive oxygen and nitrogen species were not involved in the inhibition of CK provoked by DGA. Conclusion, Considering the importance of creatine kinase activity for cellular energy homeostasis, our results suggest that inhibition of this enzyme by increased levels of DGA might be an important mechanism involved in the myopathy and cardiomyopathy of patients affected by DHGA. [source] Pure quadriceps myopathy in two sistersEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2003I. Mahjneh The authors carried out a clinical, laboratory and muscle computed tomographgy CT follow-up study of 18,21 years on two sisters affected by quadriceps myopathy (QM). The onset in the fourth decade was a weakness in the thighs. During the follow-up study, the patients showed only vasti muscles involvement, normal creatine kinase (CK) levels, myopathic muscle biopsy and electromyography (EMG) and normal membrane protein expression on immunocytochemical analysis. Therefore, all muscle pathologies known to have quadriceps involvement as a leading feature have been ruled out. We conclude that our patients have pure QM with probable autosomal recessive inheritance. [source] Interaction of a novel mitochondrial protein, 4-nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1), with the amyloid precursor protein familyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2010Hemachand Tummala Abstract Amyloid precursor protein (APP) and its paralogs, amyloid precursor-like protein-1 and amyloid precursor-like protein-2, appear to have redundant but essential role(s) during development. To gain insights into the physiological and possibly pathophysiological functions of APP, we used a functional proteomic approach to identify proteins that interact with the highly conserved C-terminal region of APP family proteins. Previously, we characterized an interaction between APP and ubiquitous mitochondrial creatine kinase. Here, we describe an interaction between APP and a novel protein, 4-nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1). The interaction between APP and NIPSNAP1 was confirmed both in transiently transfected COS7 cells and in the mouse brain, where NIPSNAP1 is expressed at a high level. We demonstrate that NIPSNAP1 is targeted to the mitochondria via its N-terminal targeting sequence, and interacts with mitochondrial chaperone translocase of the outer membrane 22. Mitochondrial localization of NIPSNAP1 appears to be critical for its interaction with APP, and overexpression of APP appeared to disrupt NIPSNAP1 mitochondrial localization. Moreover, APP overexpression resulted in downregulation of NIPSNAP1 levels in cultured cells. Our data suggest that APP may affect mitochondrial function through a direct interaction with NIPSNAP1 as well as with other mitochondrial proteins. [source] Substrate Channelling in a Creatine Kinase System of Rat Skeletal Muscle Under Various pH ConditionsEXPERIMENTAL PHYSIOLOGY, Issue 1 2003M. Gregor The aim of this study was to evaluate myofibrillar creatine kinase (CK) activity and to quantify the substrate channelling of ATP between CK and myosin ATPase under different pH conditions within the integrity of myofibrils. A pure myofibrillar fraction was prepared using differential centrifugation. The homogeneity of the preparation and the purity of the fraction were confirmed microscopically and by enzymatic assays for contaminant enzyme activities. The specific activity of myofibrillar CK reached 584 ± 33 nmol PCr min,1 mg,1 at pH 6.75. Two methods were used to detect CK activity: (1) measurement of direct ATP production, and (2) measurement of PCr consumption. This method of evaluation has been tested in experiments with isolated creatine kinase. No discrepancy in CK activity between the methods was observed in the pH range tested (6.0-7.5). However, the same procedures resulted in a significant discrepancy between the amounts of reacted PCr and produced ATP within the pure myofibrillar fraction. This discrepancy represents the portion of ATP produced by the CK reaction, which is preferentially channelled to the myosin ATPase before diffusing into the bulk solution. The maximum evaluated difference reached 42.3 % at pH 6.95. The substrate channelling between myofibrillar-bound CK and myosin ATPase was evaluated under various pH levels within the physiological range and it reached a maximum value in a slightly acidic environment. These results suggest that ATP/ADP flux control by the CK system is more important at lower pH, corresponding to the physiological state of muscle fatigue. [source] Mitochondrial affinity for ADP is twofold lower in creatine kinase knock-out musclesFEBS JOURNAL, Issue 4 2005Possible role in rescuing cellular energy homeostasis Adaptations of the kinetic properties of mitochondria in striated muscle lacking cytosolic (M) and/or mitochondrial (Mi) creatine kinase (CK) isoforms in comparison to wild-type (WT) were investigated in vitro. Intact mitochondria were isolated from heart and gastrocnemius muscle of WT and single- and double CK-knock-out mice strains (cytosolic (M-CK,/,), mitochondrial (Mi-CK,/,) and double knock-out (MiM-CK,/,), respectively). Maximal ADP-stimulated oxygen consumption flux (State3 Vmax; nmol O2·mg mitochondrial protein,1·min,1) and ADP affinity (; µm) were determined by respirometry. State 3 Vmax and of M-CK,/, and MiM-CK,/, gastrocnemius mitochondria were twofold higher than those of WT, but were unchanged for Mi-CK,/,. For mutant cardiac mitochondria, only the of mitochondria isolated from the MiM-CK,/, phenotype was different (i.e. twofold higher) than that of WT. The implications of these adaptations for striated muscle function were explored by constructing force-flow relations of skeletal muscle respiration. It was found that the identified shift in affinity towards higher ADP concentrations in MiM-CK,/, muscle genotypes may contribute to linear mitochondrial control of the reduced cytosolic ATP free energy potentials in these phenotypes. [source] Inhibition of creatine kinase activity by 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one in the cerebral cortex and cerebellum of young ratsJOURNAL OF APPLIED TOXICOLOGY, Issue 6 2010Rodrigo Binkowski de Andrade Abstract In the present study, we investigated the potential in vitro toxicity of the tellurium compound 3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on creatine kinase activity in cerebral cortex and cerebellum of 30-day-old Wistar rats. First, enriched mitochondrial and cytosolic fractions from the two tissues were pre-incubated for 30,min in the presence or absence of 1, 5 or 20,µm of organotellurium and the creatine kinase activity was measured. The organochalcogen reduced creatine kinase activity in a concentration-dependent pattern in the two tissues studied. Furthermore, the enzyme activity was performed after pre-incubation for 30, 60 or 90,min in the presence of 5,µm of the organotellurium. The compound inhibited creatine kinase activity in a time-dependent way in the enriched mitochondrial fraction of both tissues, but not in the cytosolic fraction, indicating different mechanisms for the organochalcogen in the mitochondrial and in the cytosolic creatine kinase. Pre-incubation of tellurium compound with reduced glutathione suggests that creatine kinase activity inhibition might be caused by direct interaction with thiol groups or by oxidative stress. Our findings suggest that creatine kinase inhibition may be one of the mechanisms by which this organotellurium could cause toxicity to the rat brain. Copyright © 2010 John Wiley & Sons, Ltd. [source] Daidzein but not other phytoestrogens preserves bone architecture in ovariectomized female rats in vivoJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2008D. Somjen Abstract Ovariectomy of immature female rats, results in significant decrease of trabecular bone volume and in cortical bone thickness. Previously, we found that estradiol-17, (E2) restored bone structure of ovariectomized (Ovx) female rats to values obtained in intact sham-operated female rats. E2 also selectively stimulated creatine kinase (CK) specific activity a hormonal-genomic activity marker. In the present study, we compared the effects of E2 and the phytoestrogens: daidzein (D), biochainin A (BA), genistein (G), carboxy-derivative of BA (cBA), and the SERM raloxifene (Ral) in Ovx, on both histological changes of bones and CK, when administered in multiple daily injections for 2.5 months. Bone from Ovx rats, showed significant disrupted architecture of the growth plate, with fewer proliferative cells and less chondroblasts. The metaphysis underneath the growth plate, contained less trabeculae but a significant increased number of adipocytes in the bone marrow. D like E2 and Ral but not G, BA, or cBA, restored the morphology of the tibiae, similar to that of control sham-operated animals; the bony trabeculeae observed in the primary spongiosa was thicker, with almost no adipocytes in bone marrow. Ovariectomy resulted also in reduced CK, which in both epiphysis and diaphysis was stimulated by all estrogenic compounds tested. In summary, only D stimulated skeletal tissues growth and differentiation as effectively as E2 or Ral, suggesting that under our experimental conditions, D is more effective in reversing menopausal changes than any of the other isolated phytoestrogens which cannot be considered as one entity. J. Cell. Biochem. 103: 1826,1832, 2007. © 2007 Wiley-Liss, Inc. [source] The study of the creatine kinase in rat brain during ischemia by magnetization transfer and biochemical analysisJOURNAL OF NEUROCHEMISTRY, Issue 2003D. Dobrota Various methods are used to study the biochemical changes in the central nervous system under normal and pathological conditions. The magnetization transfer 31P magnetic resonance technique was used here to measure the creatine kinase (CK) reaction rate constant in vivo in rats with cerebral ischemia. The measurements indicated that the rate constant of the CK reaction was significantly reduced in the case of chronic brain ischemia in aged rats. The similar reduction of the creatine kinase activity was found in the ischemic rat brain homogenate measured by biochemical analysis. At the same time, corresponding conventional phosphorus magnetic resonance spectra showed negligible or no change in signal intensities of compounds containing macroergic phosphates. Acknowledgements: This work was supported by the Grant Category C and Comenius University Grant No. X/2003. [source] Preventive effect of Aegle marmelos leaf extract on isoprenaline-induced myocardial infarction in rats: biochemical evidenceJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 10 2005P. Stanely Mainzen Prince We have evaluated the preventive effects of an aqueous Aegle marmelos leaf extract (AMLEt) in isoprenaline (isoproterenol)-induced myocardial infarction in rats. Rats were pretreated with AMLEt (50, 100 or 200 mg kg,1) for 35 days. After the treatment period, isoprenaline (200 mg kg,1) was administered subcutaneously to rats at an interval of 24 h for two days. The activity of creatine kinase (CK) and lactate dehydrogenase (LDH) was significantly increased in serum and significantly decreased in heart of isoprenaline-treated rats. Pretreatment with AMLEt decreased the activity of CK and LDH in serum and increased them in the heart. The activity of sodium-potassium dependent adenosine triphosphatase (Na+K+ATPase) was significantly decreased while the activity of calcium dependent adenosine triphosphatase (Ca2+ATPase) was simultaneously increased in the heart and aorta. AMLEt pretreatment increased the activity of Na+K+ATPase and decreased the activity of Ca2+ATPase in the heart and aorta simultaneously. The levels of cholesterol and triglycerides increased, while the levels of phospholipids decreased in the heart and aorta of isoprenaline-treated rats. In AMLEt-pretreated rats the levels of cholesterol and triglycerides decreased whereas phospholipids increased in heart and aorta. All the deranged biochemical parameters were restored with 200 mg kg,1 AMLEt. Similarly ,-tocopherol (60 mg kg,1)-pretreatment to isoprenaline-treated rats exhibited a significant effect on all the parameters studied. The results from this study may have clinical relevance. [source] Comparison of measurements of 18 analytes in canine and feline blood samples using the in-practice Falcor 350 and the reference KoneLab 30i analysersJOURNAL OF SMALL ANIMAL PRACTICE, Issue 10 2008K. Papasouliotis Objectives: Falcor 350 (A. Menarini Diagnostics) is a wet-reagent biochemistry analyser that is available for in-house use. The aim of this study was to compare the results produced by this analyser with those obtained by a wet-reagent analyser (KoneLab 30i; Thermo Clinical Labsystems) that served as the reference instrument. Methods: Blood samples from 120 clinical cases (60 dogs and 60 cats) were analysed for 18 analytes (urea, creatinine, total proteins, albumin, creatine kinase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, amylase, lipase, glucose, triacylglycerol, cholesterol, total calcium, phosphate, sodium and potassium) using both the reference and Falcor instruments. Results: Good to excellent correlations (rs value) (canine/feline) were identified for urea (0·87/0·86), creatinine (0·96/0·99), total proteins (0·91/0·95), albumin (0·96/0·93), creatine kinase (0·98/0·99), aspartate aminotransferase (0·95/0·98), alanine aminotransferase (0·99/0·99), alkaline phosphatase (0·99/0·98), total bilirubin in dogs (0·88), amylase (0·99/0·87), lipase in dogs (0·88), glucose (0·97/0·98), triacylglycerol (0·93/0·97), cholesterol (0·99/0·99), total calcium (0·88/0·89), phosphate (0·94/0·97) and potassium (0·96/0·97). The correlations for sodium (0·41/0·61), total bilirubin in cats (0·78) and lipase in cats (0·25) were considered unacceptable. Clinical Significance: For 13 of the 18 analytes (creatinine, total proteins, albumin, creatine kinase, aspartate aminotransferase, alanine aminotransferase, amylase, glucose, cholesterol, triacylglycerol, phosphate, potassium and urea) in both canine and feline samples, the two instruments produce values that are closely related to each other (excellent correlation) and are sufficiently similar to allow them to be used interchangeably without the need for additional correction factor computations (good agreement). Because of differences in the methodologies, the Falcor results for alkaline phosphatase, total calcium, sodium, lipase and total bilirubin cannot be used interchangeably with those generated by the KoneLab and should be interpreted using reference intervals established from the Falcor analyser. [source] Hypoadrenocorticism in a catJOURNAL OF SMALL ANIMAL PRACTICE, Issue 4 2001J. Stonehewer Primary hypoadrenocorticism was diagnosed in an eight-year-old neutered male cat. The predominant presenting complaint was dysphagia. Other historical signs included lethargy, weight loss, polydipsia, polyuria, muscle weakness and occasional vomiting. The signs had waxed and waned over the two months before presentation and had improved when the cat was treated with enrofloxacin and prednisolone by the referring veterinarian. On referral, dehydration, depression and poor bodily condition were found on physical examination. Results of initial laboratory tests revealed mild anaemia, hyperkalaemia, hyponatraemia, hypochloraemia and elevations in serum creatinine and creatine kinase. The diagnosis of primary adrenocortical insufficiency was established on the basis of results of an adrenocorticotropic hormone (ACTH) stimulation test and endogenous plasma ACTH determination. Initial therapy for hypoadrenocorticism included intravenous administration of 0,9 per cent saline and dexamethasone, and oral fludrocortisone acetate. Within one week the cat was clinically normal and two years later was still alive and well on fludrocortisone acetate treatment only. [source] Review article: the gastrointestinal complications of myositisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2010E. C. EBERT Aliment Pharmacol Ther,31, 359,365 Summary Background, The inflammatory myopathies are a group of acquired diseases characterized by a proximal myopathy caused by an inflammatory infiltrate of the skeletal muscle. The three major diseases are dermatomyositis, polymyositis and inclusion body myositis. Aims, To review the gastrointestinal manifestations of myositis. Methods, Over 110 articles in the English literature were reviewed. Results, Dysphagia to solids and liquids occurs in patients with myositis. The pharyngo-oesophageal muscle tone is lost and therefore patients develop nasal speech, hoarseness, nasal regurgitation and aspiration pneumonia. There is tongue weakness, flaccid vocal cords, poor palatal motion and pooling of secretions in the distended hypopharynx. Proximal oesophageal skeletal muscle dysfunction is demonstrated by manometry with low amplitude/absent pharyngeal contractions and decreased upper oesophageal sphincter pressures. Patients exhibit markedly elevated creatine kinase and lactate dehydrogenase levels consistent with muscle injury. Myositis can be associated with inflammatory bowel disease, coeliac disease and interferon treatment of hepatitis C. Corticosteroids and other immunosuppressive drugs comprise the mainstay of treatment. Inclusion body myositis responds poorly to these agents and therefore a myotomy is usually indicated. Conclusion, Myositis mainly involves the skeletal muscles in the upper oesophagus with dysphagia, along with proximal muscle weakness. [source] Thrombin generation during reperfusion after coronary artery bypass surgery associates with postoperative myocardial damageJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 7 2006P. RAIVIO Summary.,Background: Cardiopulmonary bypass and coronary artery bypass grafting (CABG) result in significant thrombin generation and activation of fibrinolysis. Thrombin contributes to myocardial ischemia,reperfusion injury in animal studies, but the role of thrombin in myocardial damage after CABG is unknown. Objectives: We measured thrombin generation and fibrin turnover during reperfusion after CABG to evaluate their associations with postoperative hemodynamic changes and myocardial damage. Methods: One hundred patients undergoing primary, elective, on-pump CABG were prospectively enrolled. Plasma prothrombin fragment F1+2 and D-dimer were measured preoperatively and at seven time points thereafter. Mass of the Mb fraction of creatine kinase (Ck-Mbm) and troponin T (TnT) were measured on the first postoperative day. Results: Reperfusion induced an escalation of thrombin generation and fibrin turnover despite full heparinization. F1+2 during early reperfusion associated with postoperative pulmonary vascular resistance index. F1+2 at 6 h after protamine administration correlated with Ck-Mbm (r = 0.40, P < 0.001) and TnT (r = 0.44, P < 0.001) at 18 h postoperatively. Patients with evidence of myocardial damage (highest quintiles of plasma Ck-Mbm and TnT) had significantly higher F1+2 during reperfusion than others (P < 0.002). Logistic regression models identified F1+2 during reperfusion to independently associate with postoperative myocardial damage (odds ratios 2.5,4.4, 95% confidence intervals 1.04,15.7). Conclusions: Reperfusion caused a burst in thrombin generation and fibrin turnover despite generous heparinization. Thrombin generation during reperfusion after CABG associated with pulmonary vascular resistance and postoperative myocardial damage. [source] Effects of Lidocaine Infusion during Experimental Endotoxemia in HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 4 2010J.R. Peiró Background: The clinical efficacy of IV infusion of lidocaine for treatment of equine endotoxemia has not been studied. Hypothesis: Lidocaine infusion after exposure to lipopolysaccharide (LPS) will inhibit the inflammatory response and have inhibitory effects on the hemodynamic and cytokine responses to endotoxemia. Animals: Twelve horses. Methods: Two equal groups (n = 6): saline (GI) and lidocaine (GII). In all animals, endotoxin (500 ng/kg body weight [BW]) was injected intraperitoneally over 5 minutes. Twenty minutes later, animals received a bolus of GI or GII (1.3 mg/kg BW) over 5 minutes, followed by a 6-hour continuous rate infusion of GI or GII (0.05 mg/kg BW/min). Treatment efficacy was judged from change in arterial blood pressure, peripheral blood and peritoneal fluid (PF) variables (total and differential cell counts, enzyme activities, and cytokine concentrations), and clinical scores (CS) for behavioral evidence of abdominal pain or discomfort during the study. Results: Compared with the control group, horses treated with lidocaine had significantly lower CS and serum and PF tumor necrosis factor-, (TNF-,) activity. At several time points in both groups, total and differential cell counts, glucose, total protein and fibrinogen concentrations, and alkaline phosphatase, creatine kinase, and TNF-, activities were significantly different from baseline values both in peripheral blood and in PF. Conclusions and Clinical Importance: Lidocaine significantly decreased severity of CS and inhibited TNF-, activity in PF. [source] Measurement of spin-lattice relaxation times and chemical exchange rates in multiple-site systems using progressive saturationMAGNETIC RESONANCE IN MEDICINE, Issue 1 2007Craig J. Galbán Abstract A new method for measuring spin-lattice relaxation times and chemical exchange (CE) rate constants in multiple-site exchanging systems is described. The method, chemical exchange and T1 measurement using progressive saturation (CUPS), was applied to determine T1s and analyze phosphorus exchange among phosphocreatine (PCr), ATP, and inorganic phosphate (Pi), mediated by creatine kinase (CK) and ATP synthase, using 31P-MRS. Two-site exchange was analyzed in vitro and in the rat leg, and three-site exchange was analyzed in the rat heart. Data were fitted to a model of progressive saturation incorporating T1 relaxation and CE. For the in vitro system at 8.45T, we found T1(PCr) = 2.86 s and T1(,-ATP) = 1.72 s. For the rat gastrocnemius at 1.9T, we found T1(PCr) = 6.60 s and T1(,-ATP) = 2.06 s. For the rat heart at 9.4T, we found T1(PCr) = 3.35 s, T1(,-ATP) = 0.69 s, and T1(Pi) = 1.83 s. All of these values were within 20% of literature values. Similarly, the determined exchange rates were in the same range as published values. Using simulations, we compared CUPS with transient saturation transfer as a method for measuring T1s and rates. The two methods showed similar sensitivity to noise. We conclude that CUPS is a viable alternative for measuring T1s and CE rates in exchanging systems. Magn Reson Med 58:8,18, 2007. © 2007 Wiley-Liss, Inc. [source] Serum creatine kinase levels in spinobulbar muscular atrophy and amyotrophic lateral sclerosisMUSCLE AND NERVE, Issue 1 2009Nizar Chahin MD Abstract We compared serum creatine kinase (CK) levels between spinobulbar muscular atrophy (SBMA) and amyotrophic lateral sclerosis (ALS) and reviewed available histochemical studies of frozen sections of muscle biopsies. CK levels and the frequency of patients with elevated CK levels were significantly higher in the SBMA group when compared with the ALS group. CK levels occasionally approached values up to 8 times the upper limit of normal in the SBMA group. In addition to the chronic neurogenic changes in the muscle biopsy, all SBMA patients showed one or more myopathic changes. Increased numbers of markedly hypertrophic fibers were consistently seen in all patients. It is not clear whether the elevated CK level is directly related to the increased number of hypertrophic fibers or to other myopathic features. Based on these findings, we recommend genetic testing for SBMA in cases of male patients with motor neuron disease who present with a significantly elevated serum creatine kinase level, even when other characteristic clinical features of SBMA are absent. Muscle Nerve 40: 126,129, 2009 [source] Neuromuscular manifestations of critical illness,MUSCLE AND NERVE, Issue 2 2005Charles F. Bolton MD Abstract Critical illness, more precisely defined as the systemic inflammatory response syndrome (SIRS), occurs in 20%,50% of patients who have been on mechanical ventilation for more than 1 week in an intensive care unit. Critical illness polyneuropathy (CIP) and myopathy (CIM), singly or in combination, occur commonly in these patients and present as limb weakness and difficulty in weaning from the ventilator. Critical illness myopathy can be subdivided into thick-filament (myosin) loss, cachectic myopathy, acute rhabdomyolysis, and acute necrotizing myopathy of intensive care. SIRS is the predominant underlying factor in CIP and is likely a factor in CIM even though the effects of neuromuscular blocking agents and steroids predominate in CIM. Identification and characterization of the polyneuropathy and myopathy depend upon neurological examination, electrophysiological studies, measurement of serum creatine kinase, and, if features suggest a myopathy, muscle biopsy. The information is valuable in deciding treatment and prognosis. Muscle Nerve, 2005 [source] Hyper-CK-emia as the sole manifestation of myotonic dystrophy type 2MUSCLE AND NERVE, Issue 6 2005Luciano Merlini MD Abstract A 49-year-old man had an 8-year history of persistent, isolated elevation of serum creatine kinase (hyper-CK-emia) without muscle symptoms, and no electromyographic evidence of myotonia; his muscle biopsy showed features reminiscent of myotonic dystrophy (DM), with morphometric findings consistent with those described in DM type 2 (DM2). Genetic studies excluded mutations in the DM type 1 (DM1) gene, but revealed a CCTG repeat expansion in the ZNF9 gene, which is associated with DM2. Our data suggest that in asymptomatic patients with persistent hyper-CK-emia, DM2 should be considered in the differential diagnosis. Muscle Nerve, 2005 [source] Creatine transporter and mitochondrial creatine kinase protein content in myopathiesMUSCLE AND NERVE, Issue 5 2001M.A. Tarnopolsky MD Abstract Total creatine or phosphocreatine, or both, are reduced in the skeletal muscle of patients with inflammatory myopathy, mitochondrial myopathy, and muscular dystrophy/congenital myopathy. We used Western blotting techniques to measure skeletal muscle creatine transporter protein and sarcomeric mitochondrial creatine kinase (mtCK) protein content in patients with inflammatory myopathy (N = 8), mitochondrial myopathy (N = 5), muscular dystrophy (N = 7), and congenital myopathy (N = 3), as compared to a control group without a neuromuscular diagnosis (N = 8). Creatine transporter protein content was lower for all groups compared to control subjects (P < 0.05; P < 0.01 for congenital myopathy). Mitochondrial CK (mtCK) was lower for inflammatory myopathy (P < 0.05), higher for mitochondrial myopathy (P < 0.05), not different for muscular dystrophy, and markedly lower for the congenital myopathy group (P < 0.01), compared to control subjects. Together, these data suggest that the reduction in total creatine or phosphocreatine in patients with certain myopathies is correlated with creatine transporter and not mtCK protein content. This further supports the belief that creatine monohydrate supplementation may benefit patients with low muscle creatine stores, although the reduction in creatine transporter protein may have implications for dosing. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 682,688, 2001 [source] Reversible acute renal failure associated with hypothyroidism: Report of four cases with a brief review of literatureNEPHROLOGY, Issue 2 2003Ahmad MOORAKI SUMMARY: ,,We present four adult cases of acute renal failure associated with hypothyroidism. All patients presented with symptoms suggestive of moderate to severe hypothyroidism, such as cold intolerance, constipation, muscle weakness, and lower extremity oedema. Initial serum creatinine levels ranged between 115 and 203 µmol/L (1.3 and 2.3 mg/dL), with creatinine clearances (CrCl) ranging between 0.58 and 0.97 mL/s (34.5 and 58 mL/min). After 6,12 weeks of treatment with levothyroxin, serum creatinine levels decreased to the range of 80 and 124 µmol/L (0.9 and 1.4 mg/dL) and CrCl increased to 0.74,1.64 mL/s (44,98 mL/min). One patient had proteinuria of 800 mg/day, which decreased to the normal range (<200 mg/day) after levothyroxin treatment. One patient developed acute gouty arthritis before normalization of thyroid-stimulating hormone (TSH), which was successfully managed with prednisone therapy. All of our patients had increased creatine kinase (CK), ranging between 1000 and 2360 U/L (normal range, 22,165 U/L), which normalized after 6 weeks of levothyroxin treatment. [source] | ||||||||||||||||||||||||||||||||||||||||