• Investigative Magnetic Resonance Imaging
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• v.22 no.1
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• pp.26-36
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• 2018

Purpose: Children born with single ventricle physiology demonstrate poor growth rate and suffer from malnutrition, which lead to increased morbidity and mortality in this population. We assume that an anabolic steroid, oxandrolone, will promote growth in these infants by improving myocardial energy utilization. The purpose of this paper is to study the efficacy of oxandrolone on myocardial energy consumption in these infants. Materials and Methods: We modeled single ventricle physiology in a lamb by prenatally shunting the aorta to the pulmonary artery and then postnatally, we monitored cardiac energy utilization by quantitatively measuring the first order reaction rate constant, $k_f$ of the creatine-kinase reaction in the heart using magnetization transfer $^{31}P$ magnetic resonance spectroscopy, home built $^1H/^{31}P$ transmit/receive double tuned coil, and transmit/receive switch. We also performed cine MRI to study the structure and dynamic function of the myocardium and the left ventricular chamber. The spectroscopy data were processed using home-developed python software, while cine data were analyzed using Argus software. Results: We quantitatively measured both the first order reaction rate constant and ejection fraction in the control, shunted, and the oxandrolone-treated lambs. Both $k_f$ and ejection fraction were found to be more significantly reduced in the shunted lambs compared to the control lambs, and they are increased in oxandrolone-treated lambs. Conclusion: Some improvement was observed in both the first order reaction rate constant and ejection fraction for the lamb treated with oxandrolone in our preliminary study.

• Journal of Chest Surgery
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• v.20 no.4
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• pp.643-654
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• 1987

The effect of prostacyclin[PGI, ] on myocardial preservation during global ischemia was studied in the isolating working rabbit heart model. Forty hearts underwent a 15 minute period of retrograde nonworking perfusion with Krebs-Henseleit buffer solution [37*C] and were switched over to the working mode for 15 minutes. After baseline measurement of heart rate, peak aortic pressure, aortic flow, and coronary flow, all hearts were subjected to 60 minutes of ischemic arrest at 10*C induced with St. Thomas Hospital cardioplegic solution: Group I had single dose cardioplegia, Croup II double dose, Croup III oxygenated double dose, and Group IV single dose with PCI, infusion [10ng/min./gm heart weight]. Hearts were then revived with 15 minute period of nonworking reperfusion at normothermia, followed by 30 minutes of working perfusion. Repeat measurements of cardiac function were obtained and expressed as a percent of the preischemic baseline values. Oxygen content of arterial perfusate and coronary effluent was measured by designed time interval. Leakage of creatine kinase was determined during post-ischemic reperfusion period. Finally wet hearts were weighed and placed in 120*C oven for 36 hours for measurement of dry weight. In the PGI, treated group [IV], heart rate increased consistently throughout the period of reperfusion from 100*5.0% [p<0.001] to 107*6.2% [p<0.001]. The percent recovery of aortic flow showed 95*5.7% [p<0.001] at the first 3 minute and full recovery through the subsequent time. Coronary flow was augmented significantly in the 3 minute [96*6.2%, p<0.001] and then sustained above baseline values. Among the Croup I, II, and III, all hemodynamic values were significantly below preischemic levels. PGI2 relatively increased oxygen delivery [1.22*0.19ml/min, p<0.001] and myocardial oxygen consumption [0.90*0.13ml/min, p<0.001] during reperfusion period. Leakage of creatine kinase in the PGI2 group was 9.3*1.58IU/15min [p<0.001]. This was significantly lower than Group I [33.0*2.68 IU/15min]. The water content of PCI2 treated hearts [81*0.9%, p<0.001] was also lower than the other groups.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.2
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• pp.213-225
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• 2010

The objective of the current study was to determine factors influencing concentrations of protein-related blood metabolites in indigenous Nguni and crossbred cattle in the semi-arid communal rangelands in South Africa. The body condition scores (BCS), packed cell volume (PCV) and serum concentrations of protein-related metabolites were determined seasonally in 100 cattle raised on communal rangelands from August 2007 to May 2008. Nguni cattle had lower (p<0.05) albumin-globulin ratio, albumin, urea and creatinine, and higher (p<0.05) globulin concentrations than the local crossbreds. Local crossbreds had higher (p<0.05) alanine aminotransferase and alkaline phosphatase concentrations and lower (p<0.05) aspartate aminotransferase concentrations in the postrainy season than Nguni cattle. The creatinine concentrations of Nguni and crossbred cattle were lowest in the sour rangeland during the hot-wet season. The albumin concentrations of Nguni and crossbred cattle were higher (p<0.05) whilst PCV, albumin-globulin ratio and creatine kinase concentration were lower (p<0.05) in the sour rangeland than in the sweet rangeland. Total protein, albumin, globulin, aspartate aminotransferase and creatine kinase concentrations of Nguni and crossbred cattle were lower (p<0.05) in the hot-wet and late cool-dry seasons than in other seasons across rangeland types. Urea concentrations in both breeds were highest in the sweet rangeland in the hot-dry season compared to other seasons. It was concluded that Nguni cattle had lower concentrations of protein metabolites than local crossbreds and protein deficiencies were most prominent in the sweet rangeland during the cool-dry seasons.

• Molecules and Cells
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• v.25 no.4
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• pp.531-537
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• 2008

Abnormal activation of nuclear factor kappa B ($NF-{\kappa}B$) probably plays an important role in the pathogenesis of Duchenne's muscular dystrophy (DMD). In this report, we evaluated the efficacy of curcumin, a potent $NF-{\kappa}B$ inhibitor, in mdx mice, a mouse model of DMD. We found that it improved sarcolemmic integrity and enhanced muscle strength after intraperitoneal (i.p.) injection. Histological analysis revealed that the structural defects of myofibrils were reduced, and biochemical analysis showed that creatine kinase (CK) activity was decreased. We also found that levels of tumor necrosis factor alpha ($TNF-\alpha$), interleukin-1 beta ($IL-1\beta$) and inducible nitric oxide synthase (iNOS) in the mdx mice were decreased by curcumin administration. EMSA analysis showed that $NF-{\kappa}B$ activity was also inhibited. We thus conclude that curcumin is effective in the therapy of muscular dystrophy in mdx mice, and that the mechanism may involve inhibition of $NF-{\kappa}B$ activity. Since curcumin is a non-toxic compound derived from plants, we propose that it may be useful for DMD therapy.

• Journal of Applied Biological Chemistry
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• v.63 no.1
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• pp.69-74
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• 2020

The fruit, leaves, and roots of Elaeagnus multiflora Thunb. have been used in traditional Chinese medicine to treat cough, diarrhea, and itching. However, the anti-fatigue effects of E. multiflora fruit (EMF) extract have not been studied in detail. The aim of this study was to examine the effect of EMF on fatigue and exercise performance in BALB/c mice. EMF was orally administered to mice at four doses (10, 50, 100, and 200 mg/kg/day) for 2 weeks. The anti-fatigue activity was evaluated by determining the exhaustive swimming time. Blood lactate and glucose levels and serum lactate levels after a 10 min swimming time, as well as ammonia, creatine kinase (CK), blood urea nitrogen (BUN), lactate dehydrogenase (LDH), and glycogen contents after exhaustive swimming time were measured. The exhaustive swimming time of the EMF 200 group was significantly increased (p <0.01). The EMF groups showed significantly low levels of CK, BUN, LDH, and lactate compared with the control group (p <0.05). Increased liver glycogen was observed in the EMF 200 group (p <0.05). These results suggest that EMF can be utilized as an efficacious natural resource for its anti-fatigue effects.

• Journal of Ginseng Research
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• v.28 no.1
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• pp.18-26
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• 2004

The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract (100 mg kg$^{-1}$ ) was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from 523$\pm$70 to 381$\pm$53 and 120 h post-exercise from 443$\pm$85 to 327$\pm$75 in treated animals. $\beta$-glucuronidase activity, as indicator of inflammation, showed a significant reduction of about 15-25% in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h post-exercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.

• Journal of Radiation Protection and Research
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• v.18 no.2
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• pp.61-69
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• 1993

We examined various enzyme activity changes by intraperitoneal injection uranium in the carp liver. These enzyme activity changes can be used as biochemical indicators of internal exposure to uranium. The results were followings ; 1) Total protein concentration decreased by intraperitoneal injection in the carp liver. 2) Lysosomal acid pretense and ${\beta}-glucuronidase$ activities increased in the liver until sixth intraperitoneal injection of uranium, but Lysosomal acid phosphatase activities decreased in the liver until the sixth injection of uranium. 3) Alkaline phosphatase activities sharply increased and Glutamate oxaloacetate Transaminase activities steadily decreased in the liver until the sixth injection of uranium. 4) Creatine %kinase activities steadily decreased and malate dehydrogenase activities sharply decreased in the liver after the primary injection of uranium. Any malate dehydrogenase activities was not detected after sixth injection of uranium.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.2
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• pp.79-83
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• 2006

We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.

• Journal of Yeungnam Medical Science
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• v.18 no.1
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• pp.13-29
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• 2001

The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First, creatine kinase ME mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins, troponin T (cTnT) and troponin I (cTnI) appeared and displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. The latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone- or together with myoglobin and CK-ME mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For the diagnosis of patient with chest pain, routinely myoglobin and CK-ME mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later and maintained less than 10% in imprecision.

• Proceedings of the Ginseng society Conference
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• 2002.10a
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• pp.159-175
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• 2002

The effect of Panax ginseng administration in muscle inflammatory process induced after eccentric exercise, that causes myofibrillar disruption, was studied. Changes in lipid peroxidation, inflammation, glycogen levels in muscle and release of myocellular proteins to blood were measured. The analyses were performed immediately after eccentric exercise and over week since this period are necessary for the muscle damage-repair cycle. The ginseng extract $(100\;mg\;kg^{-1})$ was orally administered to rats for three months, before the eccentric exercise performance. The results showed the protective role of ginseng against skeletal muscle damage. This effect could be associated with their membrane stabilising capacity since creatine kinase (CK) activity was significantly decreased 96 h post-exercise from $523{\pm}70\;to\;381{\pm}53$ and 120 h post-exercise from $443{\pm}85\;to\;327{\pm}75$ in treated animals. ${\beta}-glucuronidase$ activity, as indicator of inflammation, showed a significant reduction of about $15-25\%$ in soleus, vastus and triceps in these post-exercise times. The lipid peroxidation, measured by malondyaldehyde levels, was significantly decreased in the 24 h postexercise period in soleus and vastus intermedius muscles and on the recovery period. Finally ginseng administration reduced significantly the decrease of the glycogen levels immediately after exercise and when the regenerative process took place (72-168 h post exercise). Collectively, the results have showed that ginseng did not inhibit the vital inflammatory response process associated with the muscle damage-repair cycle but presumably ameliorate the injury.