Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute idopathic pericarditis can be accompanied by myocarditis, and in all types of acute pericarditis there are electrocardiographic signs of myocardial lesions. In order to determine the severity of the myocardial disease in acute idiopathic pericarditis, a prospective study has been carried out in a group of 25 patients with this diagnosis. The clinical evaluation included phonomecardiographic measurements of the systolic intervals, Weissler index in 24 cases, and echocardiographic study of the left ventricle in eight cases. Besides that, the serum levels of the myocardial enzymes (GOT, GPT, CPK, and LDH and its isoenzymes) were determined in all cases. The results showed a gallop rhythm in 8 percent of the cases, supraventricular arrhythmias in 4 percent, dysfunction of the left ventricle by systolic intervals and/or echocardiography in 32 percent, and increase of the myocardial enzymes in 24 percent, which represents a global incidence of myocardial disease of 44 percent. However, only three patients presented clinical manifestations of myocardial disease, although the congestive cardiac failure was always secondary to cardiac tamponade and not to myocardial failure. The increase of myocardial enzymes can determine important problems of differential diagnosis with an acute myocardial infarction. The clinical course was favourable in all of the cases, including the ones which showed myocardial disease.
...
PMID:[Myocardial disease in acute idiopathic pericarditis (author's transl)]. 736 77

The value of serum creatine kinase B subunit activity (CK B) in the diagnosis of acute myocardial infarction was studied in 238 consecutive cases. All were admitted to a coronary care unit because of suspected acute myocardial infarction. Serum CK B activity was determined by an immunoinhibition procedure, using a CK M subunit inhibiting antibody (anti-M). For the evaluation of serum CK B, patients were classified into acute myocardial infarction and non-acute myocardial infarction groups. This classification was based on electrocardiographic findings, on quantitative determinations of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total serum creatine kinase (CK) activities, and on qualitative electrophoretic determinations of serum CK and serum lactate dehydrogenase (LD) isoenzymes. The prevalence of acute myocardial infarction in the patient material was 0.47. Serum CK B subunit activity was found to be a highly selective indicator of acute myocardial infarction with a predictive value of a positive test result of 0.97 and a predictive value of a negative test result of 0.99. The serum CK B activity increased above the acute myocardial infarction discrimination limit within 12 hours from onset of symptoms. Two non-acute myocardial infarction patients, who were resuscitated after cardiac arrest, had increased serum CK B values caused by the transient presence of CK isoenzyme BB in serum.
...
PMID:Serum creatine kinase B subunit activity in diagnosis of acute myocardial infarction. 737 10

A complex of enzymatic tests, characterizing the liver function and cellular cytolysis in patients with acute myocardial infarction of various severities (without complications and with various types of complications and outcomes) was used in examinations over the first week of the disease. Significant changes in five of the seven tested enzymes were found: aspartate aminotransferase, glutamate dehydrogenase, sorbitol dehydrogenase, cholinesterase, alanine aminotransferase, the degree and incidence of changes in their activities being the lowest in the patients with acute myocardial infarction without complications, higher in those with this condition with isolated complications, still higher in those with combined complications and a favorable outcome, and the highest in those with combined complications and a lethal outcome. Secondary hepatopathy in patients with acute myocardial infarction augments as the complications develop, particularly in arrhythmia, disordered conductivity, and combined complications. Measurements of glutamate dehydrogenase and sorbitol dehydrogenase are recommended starting from the first day of the disease, of cholinesterase from the third day of the disease for a dynamic monitoring of the liver status in order to timely detect and correct hepatopathy and assess the status of patients with complicated acute myocardial infarction.
...
PMID:[Enzyme diagnosis of liver dysfunction in acute myocardial infarct and its complications]. 800 Jul 90

We report here our experience with serum troponin T (TnT), measured with the sandwich immunoassay introduced by Boehringer Mannheim as a marker for myocardial infarction. We assayed TnT in serial serum samples from 30 patients with time courses of serum CK, CK-MB, AST, and LD that we consider typical of acute myocardial infarction (MI). In every patient but one, TnT rose in parallel with both CK-MB and AST, but remained elevated significantly longer. The ratios of the elevations of the different markers varied from patient to patient with marked variation in the ratio of TnT to CK-MB. There appeared to be a significant association between the magnitude of that ratio with the level of ALT.
...
PMID:Troponin-T as a serum marker for myocardial infarction. 913 99

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
...
PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

We conducted a phase I/II study of combination chemotherapy with nedaplatin (NDP) and irinotecan to determine the effects against advanced non-small-cell lung cancer (NSCLC) and to determine the qualitative and quantitative toxicities of the combination chemotherapy. NDP was given on day 1 and irinotecan on days 1 and 8. The treatment cycle was designed to be repeated every 3 weeks. We fixed the dose of irinotecan as 60 mg/m(2) and escalated the NDP dose from a starting dose of 50 mg/m(2) by 10-mg/m(2) increments until the maximum tolerated dose (MTD) was reached. The MTD was defined as the dose level at which at least two of three or three of six patients experienced a dose-limiting toxicity (DLT). Between April 1997 and November 2000, 42 patients were registered in the study. Of the 42 patients, 37 had no prior treatment, 3 had received whole-brain irradiation, 1 had undergone surgical resection, and 1 had had one regimen of chemotherapy before enrolling in this study. In the phase I study, we observed DLTs such as grade 4 neutropenia lasting 7 days and grade 3 diarrhea lasting 1 day in one patient at level 2, grade 3 elevated of GPT in one patient at level 3, and acute myocardial infarction in one patient at level 6. We could not determine the MTD until dose level 6 was reached, so decided on a recommended dose of 100 mg/m(2) NDP, which is recommended for NDP-alone chemotherapy. Because of prolonged neutropenia in the phase I study, we repeated the treatment every 4 weeks in the phase II study. In the phase II study, a total of 16 patients, including 6 patients from the phase I study, were registered and a total of 42 cycles were administered. Grade 3 or 4 neutropenia, grade 3 anemia and grade 3 or 4 thrombocytopenia occurred in 50%, 12% and 7% of cycles, respectively. Febrile neutropenia occurred in eight cycles (19%) but there were no severe infections. Grade 3 elevation of GPT occurred in one patient. Of the 16 patients, 7 had an objective response. Of the 42 patients, 13 achieved a partial response (PR) and the overall response rate was 31.0%. The median duration of PRs was 226 days (range 59 to 646 days). The median survival time was 341 days and the 1-year survival rate was 45.2%. In conclusion, the combination of NDP and irinotecan was highly effective and well tolerated in NSCLC.
...
PMID:Phase I/II study of escalating doses of nedaplatin in combination with irinotecan for advanced non-small-cell lung cancer. 1275 Aug 39

The cytokine erythropoietin protects the heart from ischaemic injury, in part by preventing apoptosis. But appropriate dose of erythropoietin for the protection of injured heart has not been studied. While we were researching the cardiac protective effects of erythropoietin in acute myocardial infarction, we experienced two cases of accidental nearly ten times overdose administration of erythropoietin up to 318,000 units instead of 33,000 units on the second day of three scheduled days of treatment. So a total of 384,000 units of erythropoietin were administered during three days. In case 1, the ALT level soared up to 386 U/l on the second day of administration and decreased slowly. It was back to normal state 3 months later. The AST level increased slowly up to 391 U/l and normalized 3 months later. Haemoglobin level was elevated up to 15.7 g/dl (14.7 g/dl at admission) and, 3 months later, normalized to 14.8 g/dl. In case 2, the ALT level was elevated up to 98 U/l on the second day of administration and decreased slowly. Three months later, the ALT level was normalized. The AST level also increased slowly up to 71 U/l and normalized 3 months later. Haemoglobin level was elevated up to 15.6 g/dl (13.8 g/dl at admission) and, 3 months later, normalized to 13.6 g/dl. In these two cases reported, these patients, even after massive overdose, tolerated it relatively well and the only side-effects we found were elevated liver enzyme and haemoglobin levels.
...
PMID:Accidental ten times overdose administration of recombinant human erythropoietin (rh-EPO) up to 318,000 units a day in acute myocardial infarction: report of two cases. 1644 99

Hepatitis B surface antigen positivity (HBsAg(+)) was believed to be an exclusion for kidney donation. However, in the presence of an organ shortage, allocation of kidneys from HBsAg(+) donors to recipients with anti-HBsAb(+) might be allowed. We examined the 10-year outcomes of kidney transplants (KT) from HBsAg(+) donors to natural or vaccine-induced anti-HBsAb(+) recipients (Group 1). Hepatitis B hyperimmune globulin (HBIG) and lamivudine were not used at any time. We compared the 10-year outcomes of patients who had HBsAg(+) prior to KT and received kidneys from HBsAg(-) donors (Group 2). The endpoint was patient survival determined by Kaplan-Meier and Cox proportional hazard methods. A total of 41 patients were transplanted from 1991-1997. There were 14 Group 1 patients and 27 Group 2 patients. Anti-HBsAb titer ranged from 10 to >1000 mIU/mL. Actuarial 10-year patient survivals were 92.8% and 62.5% for Group 1 and Group 2. Only 1 patient in Group 1 died; this case was due to an acute myocardial infarction. Eleven deaths occurred among Group 2; they were due to chronic active hepatitis (n = 5), hepatoma (n = 3), acute fibrosing cholestatic hepatitis (n = 1), and stroke (n = 2). More than 2 times elevated ALT occurred among 45% of Group 2 but none in Group 1. No patients in Group 1 had positive HBsAg and HBV DNA at last follow-up. Four patients in Group 2 displayed seroconversion to positive HBeAg after KT. Secondary analysis examining the impact of KT on patient life expectancy (from the start of dialysis until last follow-up) used Cox regression, revealing that KT was significantly associated with an increased risk for death within 12 months after transplantation (RR = 30, P = .005) but a decreased risk for death thereafter (RR = .03, P = .005) for Group 2. However, KT did not have significant impact on the risk for death within the first year for Group 1 (P = .61). Our results showed that the 10-year survival of KT from HBsAg(+) donors to recipients with anti-HBsAb(+) was good. This was not associated with evidence of active liver disease. The presence of HBsAg(+) in donors thus should not be considered an exclusion for kidney donation for anti-HBsAb(+) recipients.
...
PMID:Ten-year follow-up of kidney transplantation from hepatitis B surface antigen-positive donors. 1924 16

(2E)-2-{6-[(E)-2-carboxyvinyl]-2,3-dihydroxyphenyl}-3-(3,4-dihydroxyphenyl) propenoic acid, a novel compound designated SMND-309, is a new derivate of salvianolic acid B. The present study was designed to investigate the cardioprotective potential of SMND-309 and to elucidate the possible mechanisms on the basis of biochemical, histopathological and immunohistochemical studies in a rat model of acute myocardial infarction induced by permanent ligation of the left coronary artery. The results showed that treatment with SMND-309 via tail vein at doses of 10 and 20 mg/kg significantly prevented the elevation in ST segment level and the increase in serum creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase and cardiac troponin T content. Meanwhile, SMND-309 significantly increased the activities of superoxide dismutase, catalase and glutathione peroxidase, decreased the content of malondialdehyde in myocardium, and reduced the myocardium necrosis scores and the number of apoptosis cardiocytes in accordance with the up-regulated expression of anti-apoptotic protein, Bcl-2 and the down-regulated expression of proapoptotic protein, Bax. Moreover, SMND-309 exhibits significantly higher potency compared to salvianolic acid B at the same mg/kg but not the same mol/kg. These findings indicate that SMND-309 has a protective potential against myocardial infarction injury and the protective effects may be due to its scavenging lipid peroxidation products, increasing endogenous antioxidant defence enzymes and attenuating cardiocyte apoptosis.
...
PMID:Cardioprotective effect of SMND-309, a novel derivate of salvianolic acid B on acute myocardial infarction in rats. 1991 62

This study was designed to investigate the therapeutic effect of sodium formononetin-3'-sulphonate (Sul-F), a water-soluble derivate of formononetin, on acute myocardial infarction in rats. The results showed that treatment with Sul-F significantly prevented the elevation of ST-segment level, decreased the contents of creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase and cardiac troponin T in serum and reduced the myocardium necrosis scores. The number of apoptosis cardiocytes is well accordance with the up-regulated expression of Bcl-2 and the down-regulated expression of Bax. Meanwhile, Sul-F significantly increased the cardiac mitochondrial ATP content, improved ATP synthase activity, decreased thiobarbituric acid-reactive substances content and attenuated the decrease in superoxide dismutase and glutathione peroxidase activities. These findings indicate that Sul-F has a protective potential against myocardial infarction injury. A possible mechanism for the protective effect is the elevated expression of endogenous antioxidant defence enzymes degraded lipid peroxidation products and improved energy metholism of cardiac mitochondrial, thus attenuating cardiocyte apoptosis.
...
PMID:Cardioprotective effect of sulphonated formononetin on acute myocardial infarction in rats. 2123 20


<< Previous 1 2 3 4 5 Next >>

---