Black Cumin Seed Oilas Hepatoprotector in Decreasing SGPT and SGOT Activity and Increasing P53 Gene Expression in Sprague Dawley Rats Induced by Alloxan

The objective of this research was to determine the effect of BCSO on SGPT/SGOT levels and p53 expression in rats induced by alloxan. This study applied a post test only control group design. A total of 42 SD rats were divided into 6 groups. Group I was normal rats. Group II (negative control) was given alloxan. Group III and IV (treatment groups) were given BCSO with equivalent doses of 6.8 mg/kg and 68 mg/kg thymoquinone, respectively (BCSO 6.8 and BCSO68 groups). Group V (positive control) was given vitamin C. Group VI (control media) were given DMSO. BCSO and Vitamin C are given for 1 week. Alloxan was given on 7th day, i.p. On the 8th day did blood sampling for measurement of SGPT and SGOT levels. Liver retrieval was performed on the 9th day continued immunohistochemistry staining. The average levels of SGPT/SGOT were then analyzed with ANOVA test. p53 expression was analyzed by Kolmogorov Semirnov and Levene then followed by Kruskal Wallis and Mann-Whitney. Statistical tests performed on 95% confidence level. The results showed that the induction of alloxan increased levels of SGPT/SGOT. BCSO68 reduced SGPT /SGOT levels in alloxan-induced rats (p < 0.05). Both BCSO 6.8 and BCSO68 increased the expression of p53 in liver tissue of alloxan – induced rats. Average percentage of p53 expression in group I to group VI were 11.12 ± 0.37; 19.24 ± 4.47; 30.31 ± 1.59; 40.43 ± 1.74; 29.67 ± 0.47; 12.02 ± 1.01, respectively. The result of statistical analysis showed the value of p < 0.05 in all groups except in group III. It can be concluded that BCSO may have hepatoprotective effect and increase the expression of p53 in the liver of alloxan-induced rats

Interval Running Exercise Reduces Running TIME of 800 Meters Dash Without Causing Increased Level of Sgot – Sgpt in Male Students of the Faculty of Sports Sciences, Manado State University

The effort to gain best achievement in sports by means of exercise has twodilemmatic sides, both for the coaches and sport promoters. On one side, exercise shouldbe done intensely and maximally, but on the other side, it is a known fact that excessiveand maximal exercises can damage the body organs. The purposes of this study were toobserve the side effects of interval running exercise of 800 meters, to find out level offatigue by examining lactate acid produced by each model, and to assess the negativeeffects on organs as indicated by the level of SGOT-SGPT. The exercise model appliedin the study comprised interval running of 2 x 800 meters, 4 x 400 meters, 8 x 200meters, 16 x 100 meters and one standard of comparison exercise, which was runningexercise of 2 x 800 meters with passive rest. This study was true experimental usingrandomized pre-test-post-test control group design. Samples of this study were 27 malestudents of the Faculty of Sports Sciences, Manado State University, who were dividedinto five groups. Group 1 was with interval running exercise of 2 x 800 meters. Group 2was assigned to interval running exercise of 4 x 400 meters. Group 3 was with intervalrunning exercise of 8 x 200 meters. Group 4 was with interval running exercise of 16 x100 meters. Group 5 as comparison standard was with running exercise of 2 x 800 meterspassive rest. All the exercise models were carried out for six weeks, each with afrequency of three times a week. Results of the study showed that the five groupsdemonstrated reduction of running time of 800 meters dash (p<0.05), lactate acidproduction differed in some of the groups (p>0.05), levels of SGOT and SGPT of allgroups did not show significant increase (p>0.05). From the above findings, it can beconcluded that all exercise models of interval running 2 x 800 meters, 4 x 400 meters, 8 x200 meters, 16 x 100 meters and 2 x 800 meters with passive rest lowered the runningtime of 800 meters dash and did not increase level of SGOT-SGPT

A neuro-fuzzy approach as medical diagnostic interface

In contrast to the symbolic approach, neural networks seldom are designed to explain what they have learned. This is a major obstacle for its use in everyday life. With the appearance of neuro-fuzzy systems which use vague, human-like categories the situation has changed. Based on the well-known mechanisms of learning for RBF networks, a special neuro-fuzzy interface is proposed in this paper. It is especially useful in medical applications, using the notation and habits of physicians and other medically trained people. As an example, a liver disease diagnosis system is presented

Comparative study of the hypoglycemic and biochemical effects of Catharanthus roseus (Linn) g. apocynaceae (Madagascar periwinkle) and chlorpropamide (diabenese) on alloxan-induced diabetic rats

The effect of the aqueous extracts of Catharanthus roseus and chlorpropamide (Diabenese) on the levels of serum cholesterol, total protein, lipid peroxidation, blood glucose and liver enzymes were compared in alloxan-induced diabetic rats. Four groups namely A, B, C and D comprising of nine rats each were used. A and B were administered with chlorpropamide and C. roseus extracts respectively, while C and D served as diabetic and non-diabetic controls respectively. The results showed comparatively significant reductions (P�0.05) in the levels of glucose, protein, cholesterol, lipid peroxidation and liver enzymes in the groups administered C. roseus extracts and chlorpropamide relative to the controls. The reductions were higher in the groups treated with C. roseus extract than in the groups treated with diabenese

Redemptive benefit of atorvastatin in the risk factors of coronary artery disease

Cardiovascular disease, in particular coronary artery disease (CAD), is the principal cause of mortality in developed countries. The classical acute phase protein, C-reactive protein (CRP) is an exquisitely sensitive systemic marker of disease with broad clinical utility for monitoring and differential diagnosis. In recent years, acute phase reactants have been shown to predict future cardiovascular events in individuals with and without established CAD. Atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, substantially reduce cardiovascular morbidity and mortality, and recently their anti-inflammatory properties have been investigated. The present study was therefore designed to determine the effects of atorvastatin on CRP in patients with CAD. Ninety two patients with or without or at the risk of CAD were recruited for the study, of which 35 belongs to control (untreated) and 57 were test group, in which, 30 of them received daily with 20 mg/day of atorvastatin and the remaining 27 were untreated. The patients were followed for over a period of 6 weeks. For entire study population, CRP along with lipid profile, SGOT, SGPT, urea and creatinine were measured 1st day and at the end of 6th week of the treatment. For patients with or at risk of CAD, the reduced rate of progression of atherosclerosis associated with intensive atorvastatin treatment, as compared with control is significantly related to greater reduction in the levels of both atherogenic lipoproteins and CRP. This may be important with respect to the early benefits of atorvastatin therapy

Pharmacologic modulation of experimental postischemic hepatic function

The present study, evaluated and compared the effects of SRI 63-441, a potent platelet activating factor antagonist, superoxide dismutase (SOD), an oxygen free radical scavenger, and ibuprofen, a cyclooxygenase inhibitor on hepatic function after 90 minutes of warm ischemia. After warm ischemia, livers were harvested and underwent 90 minutes of warm, oxygenated, sanguinous perfusion on an isolated liver perfusion apparatus. Pretreatment of donor animals with 20 mg/kg intravenous (I.V.) SRI 63-441 5 minutes before induction of total hepatic ischemia resulted in significantly increased bile production, a significant decrease in transaminase release, and a higher tissue adenosine triphosphate (ATP) content when compared with ischemic non-treated controls. SOD resulted in improved bile production and decreased transaminase liberation only when present in the perfusate at the time of in vitro reperfusion. Ibuprofen did not improve postischemic hepatic function in this model. Electron microscopy revealed patchy hepatocellular vacuolization with an intact sinusoidal endothelium in all ischemic livers. However, the degree of damage was less severe in the livers from those rats pretreated with 20 mg/kg SRI 63-441. This study demonstrates that SRI 63-441 pretreatment significantly reduces hepatic warm ischemic injury, and in the present model, appears superior to two other agents that have been advanced in the treatment of ischemic injury. The use of such agents singly or in combinations have important implications as regards gaining a better understanding of he basic mechanisms in organ ischemia, and moreover, for therapeutic applications in organ ischemia and preservation

Factors determining short- and long-term survival after orthotopic liver homotransplantation in the dog

Without azathioprine therapy, the operative risk with orthotopic liver transplantation is small. Twenty-two of 23 animals survived 2 days or more, and 19 for 6 days or longer. All eventually died of rejection within 10 days. Changes in homograft histology and function were similar to those previously reported, with cellular infiltration and hepatocyte necrosis which was heavily concentrated in the centrilobular areas. In individual experiments, there was little evidence of immunologically induced segmental hepatic arterial or portal venous occlusion; hepatocyte loss was homogeneous, and fibrinoid vascular lesions were uncommon. There was, however, some evidence of damage to the sinusoidal endothelium by adherent mononuclear cells. The changing character of the mononuclear infiltration of the homograft was reflected by widespread proliferation of similar cells in the host lymphoid tissue. Specific changes in other host organs were not noted. Some of the biochemical and histologic alterations caused by unmodified rejection can also be produced by azathioprine. In 18 nontransplanted dogs, acute rises in SGOT, SGPT, and alkaline phosphatase, unaccompanied by hyperbilirubinemia, were noted within a few days after beginning administration of this agent. Although these abnormalities tended to regress within the 40 day period of observation, more than two thirds of the livers showed histologic evidence of centrilobular hepatocyte damage or necrosis-often with intrahepatic cholestasis, but always without mononuclear cell infiltration. The hepatotoxicity was not prevented by methionine. Weight loss and progressive anemia also occurred. Lymphoid tissue was depleted. The mortality from the toxicity study was 33 percent. The use of azathioprine to mitigate rejection increased the early mortality after homotransplantation, 32 of 116 dogs dying within the first week (28 percent), most commonly of pulmonary complications. The 84 animals living longer than 7 days had a greatly potentiated homograft survival, exceeding 25 days in 44 dogs, and 50 days in 24. Fifteen animals are still alive from 62 to 324 days postoperatively. Six dogs had all drugs stopped after 116 to 123 days. Only 1 has had a clinically evident late rejection and 5 are still alive from 63 to 204 days later. Three of these animals had repeat biopsies 77 to 182 days after cessation of therapy; one homograft which was normal at 4 months remained so 6 months later, another had an improved histologic appearance, and the third had deteriorated. The longest mean survival was in those animals receiving adjuvant therapy with L-methionine or S35-methionine, but the variability of the results was so great that a statistically significant advantage of these agents could not be demonstrated. Soon after operation red cell survival was decreased, but in chronic survivors there was no evidence of a grafthost reaction. There was great variability in the vigor of rejection, ranging from the uncontrollable (29 percent) to the clinically undetectable (23 percent). Most of the animals (49 percent) had some biochemical evidence of rejection which proved to be spontaneously reversible, to a greater or lesser degree, since intensification of immunosuppressive therapy was not required. These findings correlate well with the histologic studies. In virtually all animals, azathioprine delayed the onset of rejection but in those dying in the second and third postoperative weeks, the pathologic stigmas of rejection were very similar to the untreated controls. As in the untreated animals, the number of proliferating large pyroninophilic cells in the host's lymphoid tissues was roughly proportional to the number of mononuclear cells invading the homograft liver. After this time, the predominant histologic features in most animals were those of repair and regeneration, with either absent or relatively minor degrees or continuing destruction. Since the major rejection damage was centrizonal, the healing was most prominent in these areas with interconecting fibrosis around the central veins, centrilobular bile canalicular dilatation and cholestasis, and pseudolobule formation. In some of the homografts, increased connective tissue was also present in the portal tracts, but in others including the longest survivor there were no residual abnormalities whatever. In azathioprine-treated animals, damage to the vessels in the homograft portal tracts was found in only one liver. With electron microscopy there was some evidence of damage to the sinusoidal endothelium by adherent mononuclear cells, a finding which could be analogous to that described by Kountz and co-workers11 in the peritubular capillaries of renal homografts. If immunologically mediated hemodynamic alterations play an important role in liver homograft rejection by interrupting the blood supply to the hepatocytes, it seems most likely that they occur at this intrasinusoidal capillary level rather than in the larger vessels. © 1965