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Biomedical subjects

M Ban

Publications and source records attributed to M Ban.

At least 91 records · Page 5Linked to original sources

Systemic lupus erythematosus with vesiculobullous lesions. Immunoelectron microscopic studies.

A 20-year-old man had systemic lupus erythematosus (SLE) and a skin eruption that consisted of pruritic, tense, clear, bullous, and vesicular lesions. Histopathological examination of the bullous lesions disclosed papillary microabscesses of neutrophils and subepidermal bulla formation. Direct immunofluorescence microscopy demonstrated linear bandlike depositions of IgA and IgG at the basement membrane zone in both peribullous and normal-appearing skin. By immunoelectron microscopy, the IgA and IgG deposits were found beneath the basal lamina, extending beyond the anchoring fibril zone into the deeper portion of the dermis. The immunoelectron microscopic features supported the conclusion that this patient had SLE with vesiculobullous lesions rather than SLE concurrent with dermatitis herpetiformis, linear IgA bullous dermatosis, or bullous pemphigoid. Oral dapsone therapy gave the patient dramatic relief from the cutaneous lesions, although he was unable to tolerate extended treatment with the drug.

Adult↗

Diltiazem for treatment of essential hypertension: a double-blind controlled study with reserpine.

In a double-blind, parallel, 12-week trial, antihypertensive effects of diltiazem and reserpine were compared in 107 patients with essential hypertension. Diltiazem reduced blood pressure from 176/100 mmHg to 154/86 mmHg after 12 weeks, and reserpine reduced blood pressure from 171/96 mmHg to 155/85 mmHg. The difference between diltiazem and reserpine was not statistically significant. However, among a subset of patients given 180 mg/day of diltiazem, a significantly better antihypertensive effect was achieved than among a subset given 0.3 mg of reserpine. The incidence of side effects and complications in the diltiazem group was about one half that in the reserpine group (12.3% and 27.1%, respectively). Side effects of diltiazem were mild, and the drug was extremely well tolerated. These results show that diltiazem is an effective antihypertensive drug for the treatment of mild to moderate essential hypertension.

Adult↗

Hyperammonemia in lysinuric protein intolerance.

Two brothers with hyperdibasicaminoaciduria and postprandial hyperammonemia showed characteristics of lysinuric protein intolerance. Intravenous alanine load produced hyperammonemia that was aborted by oral supplementation with arginine in one brother but not in the other, although both patients had almost the same intestinal malabsorption of arginine. This occurrence suggests that even a small amount of arginine, when absorbed into the blood, can normalize the affected ammonia metabolism of lysinuric protein intolerance. Two patients with cystinuria developed marked hyperammonemia when they received an intravenous alanine load after a 19-hour fast. As both patients displayed a reduced plasma concentration of arginine and ornithine at this time, the hyperammonemia was assumed to arise from the low plasma amino acid level. It seems likely that a decrease in plasma levels of urea cycle substrate causes a failure of the tissue urea cycle metabolism. Thus the impaired ammonia metabolism in lysinuric protein intolerance would be attributed to the low plasma arginine and ornithine levels.

Adolescent↗

Induced hepatotoxicity in female rats by aflatoxin B1 and ethynylestradiol interaction.

Female Sprague-Dawley rats were treated with a single ip dose of aflatoxin B1 (AFB1) (3 or 6 mg/kg). Twenty-four hours later and weekly until killed, some of the rats treated with AFB1 were given ethynylestradiol (EE) by gavage at the dose of 13 mg/kg. One, three, six, and nine months following the beginning of the experiment, animals were killed. Light microscopy of liver and histochemical determinations of gamma-glutamyltransferase (GGT) as well as the measurement of hepatic drug-metabolizing enzyme activities were investigated. The results show that AFB1 induced only very weak changes in the levels of different constituents studied. Thus, the mycotoxin did not affect GGT activity and increased epoxide hydrolase activity by a maximum of 42%. In contrast, EE significantly and progressively decreased (20 to 50%) the activity of UDP-glucuronosyltransferase (UDPGT) as well as the concentration of cytochrome P-450 and microsomal proteins. However, the estrogen increased the activity of epoxide hydrolase up to 150% as well as the activity of the hepatic (400%) and plasma (175%) GGT. The results also indicate that AFB1 amplified the EE-induced increase in liver weight and enhanced the depressive effects of the estrogen on microsomal proteins, cytochrome P-450, and UDPGT. Foci of cellular alteration which consisted of clear, acidophilic and basophilic cell lesions were seen in the livers of treated rats examined by light microscopy. These lesions were more prominent in the livers of animals given combinations of AFB1 and EE; they were accompanied by a strong intensity of GGT staining in the periportal area and a marked increase of the enzyme activity in the plasma (324%). From the sixth month, the livers of some animals treated with the combinations of AFB1 and EE showed hyperplastic nodules. This study indicates that the interaction between chronic administration of EE and a single ip injection of AFB1 induces hepatic lesions considered as possible forerunners of liver cell carcinomas. It also shows that GGT is a potential marker of preneoplastic lesions and may be used, therefore, in epidemiologic surveys in humans exposed to liver carcinogens such as the aflatoxins.

Aflatoxin B1↗

Myocardial norepinephrine and cyclic amp concentration following myocardial ischemia--relation to ventricular fibrillation and sudden death.

This study was designed to investigate the relationships of myocardial concentrations of norepinephrine (NE) and cyclic AMP (c-AMP) to the development of ventricular fibrillation (VF) with reference to the effects of a premedication of dibutyryl cyclic AMP (DBC-AMP) and propranolol in dogs with experimental myocardial infarction. Myocardial specimens were obtained serially from the ischemic and the non-ischemic zones by mini-drill biopsy, and NE and c-AMP levels were determined by high-performance liquid chromatography and radioimmunoassay, respectively. Before the occurrence of VF, myocardial NE increased in both the ischemic and the non-ischemic zones, and c-AMP increased significantly in the ischemic zone but did not in the non-ischemic zone. In dogs premedicated with DBC-AMP an increase of c-AMP was observed in both the ischemic and the non-ischemic zones in association with an increased incidence of VF. On the other hand, no significant increase of myocardial c-AMP was observed in both the ischemic and the non-ischemic zones of propranolol-premedicated dogs which were free from VF. A significant increase of myocardial c-AMP in the ischemic zone was observed in dogs which suffered from VF in spite of the premedication of propranolol. The incidence of VF was significantly reduced by 26.5% in dogs pretreated with propranolol. No significant changes in myocardial norepinephrine and c-AMP were observed in dogs which were free from VF throughout the experiments.

Animals↗

Renal transport of lysine and arginine in lysinuric protein intolerance.

In a patient with lysinuric protein intolerance, renal handling of lysine and arginine was examined to study the renal transport mechanism of this disease. The tubular reabsorption of lysine or arginine of the patient, when the filtered load of amino acid was increased by intravenous infusion, was not raised as much as that of control subjects at low filtered loads, but the ability for amino acid reabsorption seemed to exist under these conditions. However, when the filtered load was greatly increased, instead of a net reabsorption, a net secretion of amino acid was obtained. This seems to mean that at low filtered loads the amino acid in the tubular lumen is accumulated by the tubular cell across the intact luminal membrane, leading to a small amino acid excretion in the urine. With a great increase of the filtered load the saturated intracellular amino acid, which is not transported to the capillary because of a transport defect of the basolateral membrane, is assumed to leak back into the lumen. This causes a marked urinary amino acid loss exceeding filtered load at high tubular loads. The intravenous load of lysine depressed the percentage of arginine reabsorption and arginine load depressed lysine reabsorption. The percentage of the depressed amino acid reabsorption of the patient decreased almost linearly with increases of the inhibitor load.

Adolescent↗

SG-75 induction of increased coronary outflow and PGE1 from ischemic areas in dogs with experimental myocardial infarction.

We measured the coronary blood flow and concentrations of prostaglandin E1(PGE1), PGF2 alpha, and lactate from the ischemic myocardium of dogs treated with either SG-75 or indomethacin. There was a significant increase of coronary blood outflow from the ischemic myocardium after ligation in dogs given SG-75 and in control dogs compared with indomethacin-treated dogs. The release of lactate from the ischemic myocardium decreased significantly in dogs with SG-75 compared with the indomethacin and control group. The concentration of PGE1 rose significantly after ligation in dogs with SG-75 compared indomethacin-treated and those in control dogs. A significant release of PGE1 from the ischemic area of the myocardium treated with SG-75 was clearly demonstrated at 60 min after ligation of the LAD coronary artery. Also, a significant release of PGF2 alpha from the ischemic area of the myocardium was demonstrated at 15 min after ligation. There was a significant correlation between the increase of coronary outflow and PGE1 release from the ischemic myocardium ( 4= 0.70, p less than 0.01). However, no significant correlation was demonstrated between the increase of coronary outflow and PGF2 alpha. These results show a close relation ship between increased coronary outflow induced by SG-75 and increased release of PGE1. Thus, a beneficial effect of SG-75 on the ischemic myocardium was demonstrated.

Alprostadil↗

Clinical effectiveness of niludipine in patients with ischemic heart disease.

The antianginal efficacy of niludipine (Bay a 7167), a new calcium antagonistic drug, was investigated in 51 patients with ischemic heart disease. 16 patients were diagnosed as effort angina and 31 patients had both angina at rest and on effort. Six anginal patients had myocardial infarction. One patient was diagnosed as a variant form of angina and 3 others as unstable angina. 11 patients had essential hypertension. 49 completed the study and 2 dropped out. Niludipine (60 mg to 80 mg every 24 h) significantly reduced the mean weekly rate of angina attacks from 6.5 to 2.2 (p less than 0.001). Marked reductions of nitroglycerin requirement were also noted (p less than 0.001). In 71% of the patients complete control of anginal attacks was achieved, and in over 77% the frequency of angina was reduced by at least 50%. Niludipine was at 93.8% effective in patients with ischemic heart disease. It decreased significantly both systolic and diastolic blood pressure in angina patients with essential hypertension, but there were no significant changes of blood pressure in normotensive anginal patients. The agent was tolerated very well and there were no side effects. These findings suggest that niludipine is a highly effective drug for the treatment of both ischemic heart disease and essential hypertension.

Adult↗

The distribution of plasma norepinephrine concentration and the relation of plasma norepinephrine concentration to pulmonary arterial pressure in heart disease.

Plasma norepinephrine (NE) concentration was measured in blood samples from the pulmonary artery (PA), the superior vena cava (SVC), the inferior vena cava (IVC) and the femoral artery (FA) in 34 patients undergoing diagnostic cardiac catheterization. In patients with pulmonary hypertension, the mean plasma NE concentrations in PA, SVC and FA were significantly higher than that of IVC, but no such difference was found in patients without such hypertension. Except in IVC, the plasma NE concentration in patients with pulmonary hypertension was significantly higher than in others. Furthermore, the plasma NE concentration was positively correlated with the mean pulmonary arterial pressure and inversely related to pulmonary arterial oxygen saturation in patients without a shunt. These results suggest the possibility that vasoconstriction by the sympathetic nervous system may contribute to the development of pulmonary hypertension in patients without the shunt.

Adolescent↗

Long-term results of operated and non-operated patients with congenital heart diseases.

The long-term results of 1023 adult patients with congenital heart diseases, operated and non-operated, with atrial septal defect (ASD), patent ductus arteriosus (PDA), pulmonary stenosis (PS) and tetralogy of Fallot, were followed for up to 24 years, and the long-term results of operated and non-operated congenital heart diseases were compared. The survival rate of patients with operated isolated ASD was significantly higher than in patients with non-operated isolated ASD, and that of operated patients with VSD associated with other anomalies was also significantly higher than in non-operated VSD patients with such involvement. The survival rate showed no significant difference in the operated and non-operated patients with PDA, PS and tetralogy of Fallot. In all congenital heart diseases, there was a close correlation between the mean pulmonary artery pressure and the mortality rate both in operated and non-operated patients and a marked improvement of physical capacity of operated patients at the time of the last follow-up examination.

Adolescent↗

Sympathetic nervous systems in chronic cor pulmonale.

Twenty-three patients with chronic respiratory failure and 30 normal subjects were studied to assess the sympathetic nervous activity in chronic hypoxic states, especially in chronic cor pulmonale. Of the 23 patients, 13 had a right ventricular hypertrophy (RVH) pattern on the electrocardiogram. Plasma norepinephrine (NE), dopamine-beta-hydroxylase (DBH), cyclic adenosine 3',5'-monophosphate (cyclic AMP) and cyclic guanosine 3',5'-monophosphate (cyclic GMP) concentrations were measured before and after oxygen inhalation. Plasma NE concentrations were 0.57 +/- 0.07 ng/ml in patients with chronic respiratory failure and 0.22 +/- 0.02 ng/ml in controls (p less than 0.001). Moreover, plasma NE concentrations were higher in patients with RVH than without (p less than 0.05), and these concentrations decreased significantly (p less than 0.05) in the former patients after oxygen inhalation. Plasma cyclic AMP concentrations were 31.2 +/- 2.6 pmol/ml in cases of chronic respiratory failure and 17.4 +/- 0.7 pmol/ml in controls (p less than 0.001) with no difference in plasma cyclic GMP and DBH concentrations. These results suggest that a significant proportion of patients with chronic respiratory failure, especially with cor pulmonale, were in hyper-adrenergic states partially due to hypoxia.

Adult↗

Decreased generation of cyclic AMP in lymphocytes by beta-adrenergic stimulation in heart failure.

Peripheral blood lymphocytes from 31 normal subjects and 29 patients with heart diseases were stimulated by isoproterenol, and cyclic AMP level in lymphocytes was assayed. Simultaneously plasma norepinephrine concentration at rest was measured. In normal subjects the generation of cyclic AMP after the stimulation decreased with age. The response of lymphocytes in patients of NYHA classes III and IV was significantly smaller than in the normal, age-matched control. Plasma norepinephrine concentration of patients of classes II, III, and IV rose significantly above normal. In congestive heart failure, a significant correlation between plasma norepinephrine concentration and increase of lymphocyte cyclic AMP was demonstrated. From these results it was suggested that beta-adrenergic receptors in congestive heart failure were desensitized.

Adrenergic beta-Agonists↗

Plasma level of norepinephrine and cyclic nucleotides following acute myocardial infarction.

The plasma concentrations of norepinephrine (NE), adenosine cyclic 3', 5'-monophosphate (cyclic AMP), and guanosine cyclic 3', 5'-monophosphate (cyclic GMP) were measured serially for 2 weeks after the onset of symptoms in 17 patients with acute myocardial infarction (AMI). The mean concentrations of NE in patients without complications were significantly elevated during the first 2 days following AMI. There was a significant correlation between the maximum concentration of plasma NE and of plasma CK. The mean concentrations of plasma cyclic AMP and cyclic GMP in patients without complications were significantly elevated on the first day and for 8 days respectively following AMI. The concentration of plasma cyclic AMP on admission in patients with complications was significantly higher than that in those without complications. There were significant correlations between the maximum concentration of plasma cyclic AMP and those of plasma CK, GOT, and LDH. Significant but weak correlations between the concentration of plasma NE and those of cyclic AMP and cyclic GMP were found. The results of the present study suggest an enhanced sympathetic nervous system activity at an early stage of AMI, a prolonged enhancement of parasympathetic nervous system activity in the course of AMI, and the potential value of plasma cyclic AMP concentrations as a useful index to estimate the seriousness and size of AMI.

Aged↗