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Biomedical subjects

J Stessman

Publications and source records attributed to J Stessman.

At least 55 records · Page 3Linked to original sources
PubMed1986

The cyclic AMP second messenger system in man: the effects of heredity, hormones, drugs, aluminum, age and disease on signal amplification.

The intracellular effects of a number of hormonal signals are mediated by the cyclic AMP second messenger system in man and the ubiquitous distribution of hormone-stimulated adenylate cyclase suggests the importance of this enzyme complex in normal aging and pathophysiological states. Various vectors including heredity, endogenous catecholamines, steroid hormones, and drugs affect the activity of hormone-stimulated adenylate cyclase in man. The effect of heredity was studied using lymphocytes obtained from monozygotic twin pairs and age and sex-matched sib pairs. Only for forskolin-stimulated activity is a significant proportion of individual variance attributable to heredity, suggesting the relative stability of the catalytic subunit. Beta-adrenergic and prostaglandin E-1 activity are "state" characteristics and their activities are controlled by environmental parameters. A significant reduction in isoproterenol-stimulated cyclic AMP accumulation between the menses and luteal phase of the menstrual cycle is observed in lymphocytes obtained from 11 female subjects. The lowest level of beta-adrenergic receptor activity is associated with the highest levels of progesterone and estradiol hormone levels in blood. Lithium at therapeutic concentrations markedly inhibits adenylate cyclase activity in platelet membranes. Moreover, marked individual differences are observed in sensitivity to lithium as determined by Dixon plot derived Ki values for 9 normal, healthy subjects. Human adenylate cyclase obtained from platelets and lymphocytes is activated by micromolar amounts of aluminum in the presence of NaF. Irreversible activation of adenylate cyclase by aluminum is suggested as a possible mechanism of this metal's neurotoxicity. The biochemical basis for the age-associated decline in beta-adrenergic responsiveness in man is discussed. Several investigations suggest a deficit at two levels in the adenylate cyclase complex: an impaired coupling of the receptor/N protein subunits and an additional lesion distal to the receptor at the level of N/C coupling. Perfusion studies with salbutamol suggest that the decline in beta-adrenergic sensitivity is general and not restricted to lymphocytes. Possible abnormalities in cyclic AMP signal amplification and recognition in various disease states is discussed. Increased prostaglandin E-1-stimulated cyclic AMP accumulation is observed in lymphocytes obtained from patients with Alzheimer's disease compared to age-matched controls and correlated with severity of the disease state.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMed1986

Laetrile intoxication and hepatic necrosis: a possible association.

A 65-year-old woman with cirrhosis and hepatoma lapsed into deep coma, hypotension, and acidosis after ingestion of 3 gm of Laetrile, a cyanogenetic glucoside. After initial treatment, the patient regained consciousness, but massive hepatic damage led to her death. We suggested a possible relationship between Laetrile poisoning and massive hepatic necrosis.

Aged↗
PubMed1985

Beta-adrenergic-stimulated adenylate cyclase activity in normal and EBV-transformed lymphocytes.

Beta-adrenergic-associated cyclic AMP accumulation was studied in intact lymphocytes before and after transformation with Epstein-Barr virus into immortal cell lines. Although a marked reduction in isoproterenol-stimulated cyclic AMP synthesis was observed in transformed cells, forskolin-stimulated cyclic AMP accumulation was preserved. A parallel loss of 125-iodocyanopindolol binding sites suggests that the reduction in beta-adrenergic-stimulated AMP synthesis is due to receptor down-regulation.

Adenylyl Cyclases↗
PubMed1985

Nifedipine in the treatment of hypertension in the elderly.

The effect of nifedipine monotherapy, retard tablets, 20 mg bid, was evaluated in 23 hypertensive patients, mean age, 79 +/- 2 years. Twenty-one patients completed an eight-week study. Blood pressure (BP) decreased to 160/90 mm Hg in 15 patients; in four additional patients diastolic BP dropped by 15% to 28%. In a subset of five patients with isolated systolic hypertension, a significant reduction in systolic BP was noted. Side effects were relatively mild and only two patients discontinued the study. The results suggest that nifedipine monotherapy offers an alternative, logic, therapeutic approach to hypertension in the elderly.

Age Factors↗
PubMed1985

The effect of age on beta-adrenergic function in man: a review.

The structure and function of the beta-adrenergic adenylate cyclase complex in the elderly is reviewed. The function of the beta-adrenergic receptor in man is modulated by levels of circulating catecholamines, noncatecholamine hormones, drugs, disease, and age. Although a number of clinical observations demonstrate an age-related decrease in catecholamine responsiveness, the molecular basis of this phenomenon is unknown. Simple reduction in beta-receptor number does not appear to explain age-associated loss of catecholamine responsiveness. Recent investigations from our laboratory employed salbutamol-induced rise in plasma cyclic AMP (cAMP) levels to study the molecular basis for this phenomenon. In young individuals there was a threefold increase in plasma cAMP levels after salbutamol infusion. In older subjects only a 50% rise in plasma cAMP levels was observed. These results suggest that the basis for reduced catecholamine responsiveness in the elderly is due to a defect in the peripheral beta-receptor-linked adenylate cyclase complex. The finding of reduced beta-adrenergic-stimulated adenylate cyclase activity in the aged prompted us to determine the specificity of this decline by measuring the activity in older and younger individuals of another hormone-sensitive adenylate cyclase. However, no effect of subject age was observed on glucagon-sensitive adenylate cyclase activity, suggesting that the blunted response of the beta-receptor adenylate cyclase complex in the elderly represents a specific loss of function and is not due to a general age-associated decline in hormone-stimulated cyclase function. Specific molecular defects which could account for decline in beta-adrenergic responsiveness in the elderly are discussed.

Adenylyl Cyclases↗
PubMed1985

Erythrocyte Na+-K+ cotransport in elderly hypertensive subjects.

Na+-K+ cotransport was measured in 21 hospitalized geriatric patients, all recovering from hip surgery. Twelve of these had hypertension, and the other 9 were the control group. Although both groups were comparable for age, blood pressure was significantly different. Mean cotransport values in red blood cells showed no significant difference between the two groups. While Na+-K+ cotransport activity may be hereditary, the authors do not feel the test may be used as a genetic marker for hypertension.

Aged↗
PubMed1984

Acute desensitization of lymphocyte beta-adrenergic-stimulated adenylate cyclase in old age and Alzheimer's disease.

The effect of prior incubation with a single concentration of isoproterenol (10(-4) M) for 2 hours at 37 degrees C on isoproterenol-stimulated cyclic AMP accumulation in intact lymphocytes from young, old and subjects with Alzheimer's disease was studied. In lymphocytes from all three subjects groups prior incubation of cells with isoproterenol resulted in a significant reduction of cyclic AMP accumulation upon subsequent stimulation with isoproterenol.

Adenylyl Cyclases↗
PubMed1984

Alzheimer's disease: isoproterenol and prostaglandin E1-stimulated cyclic AMP accumulation in lymphocytes.

Reduced lymphocyte beta-adrenergic receptor activity was observed in patients with Alzheimer's disease and in aged controls; a parallel decline in lymphocytic prostaglandin E1 receptor activity was seen in the aged controls. In the Alzheimer patients, however, such lymphocytic prostaglandin E1 receptor activity was significantly raised and correlated with a rating scale for severity of dementia.

Adult↗
PubMed1984

Deterioration of beta-receptor-adenylate cyclase function in elderly, hospitalized patients.

Salbutamol infusion was used to study the molecular basis for reduced catecholamine responsiveness in a group of elderly hospitalized individuals. Salbutamol-induced plasma cyclic 3', 5'-adenosine monophosphate (cyclic AMP) rise in a group of 10 elderly (mean age 77 years) patients, 8 of whom were hospitalized 6 to 8 weeks after femoral fracture, and 10 younger (mean age 27 years) individuals was compared. Parallel clinical response was monitored by changes in pulse rate and blood pressure. In the younger group there was a three-fold increase in plasma cyclic AMP levels after salbutamol infusion. In the older adults only a one-and-one-half-fold rise in plasma cyclic AMP levels was observed. There was an increase in pulse rate and systolic blood pressure and a decrease in diastolic blood pressure in the younger group compared with the older participants. These results suggest that the basis for reduced catecholamine responsiveness in elderly hospitalized individuals is due to a defect in the peripheral beta-receptor-linked adenylate cyclase complex.

Adult↗
PubMed1983

Effects of subminimal inhibitory concentrations of aminoglycosides on the penicillinase production of Staphylococcus aureus.

The effects of subminimal inhibitory concentrations of kanamycin, amikacin and gentamicin on the production of penicillinase by Staphylococcus aureus were tested on 12 penicillin-resistant strains. Of the 36 experiments performed, 16 (44%) displayed an increase and 9 (25%) produced a decrease in the penicillinase activity of the strains. These effects were observed at concentrations ranging from 1:2 to 1:2,048 of the respective minimal inhibitory concentration, irrespective of the susceptibility of the strain to the aminoglycoside drug.

Aminoglycosides↗
PubMed1983

Erythrocyte Na+, K+ cotransport and blood pressure in identical twins.

The erythrocyte Na+, K+ cotransport system was studied in ten pairs of identical twins. Cation fluxes were remarkably similar in each pair of twins, which supports the concept of a genetic determinant for the cotransport system. There was, however, no apparent correlation between cotransport values and the family history of hypertension.

Adolescent↗
PubMed1983

The combination of propranolol and nifedipine in the treatment of hypertension: acute and long term effects.

The long term efficacy and tolerability of nifedipine combined with propranolol was assessed in a group of hypertensive patients inadequately controlled on propranolol alone. Twenty-six subjects were initially treated with propranolol in a constant daily dose of 160-240 mg, for up to 4 weeks. Nifedipine, 30 mg/day, was added and the dose was titrated upwards to 90 mg/day to achieve normal blood pressure. In 22 patients receiving the combined therapy for 14-30 weeks, mean arterial pressure dropped from 138 +/- 3 mmHg to 102 +/- 2 mmHg. Thirteen patients experienced untoward effects, and 4 discontinued the study. In the remaining 9, side effects were mild and well tolerated. Seventeen patients were subsequently treated sequentially with propranolol alone, combined therapy and nifedipine alone, to assess the efficacy of each regimen and the additive effect of each drug. The combined regimen was found to be more effective than either drug alone. A subgroup continued either combined therapy (14) or nifedipine monotherapy (3) and was followed for up to 9 months. Blood pressure control was maintained in the majority, but 4 more patients dropped out because of side effects. We conclude that the long term use of nifedipine combined with propranolol is effective and relatively well tolerated, and may offer an alternative approach to the treatment of moderately severe hypertension.

Adult↗
PubMed1981

Acute myocardial infarction caused by blast injury of the chest.

A 51-year-old healthy man was hit in the chest by the shock-waves generated by an explosion, without being injured by any physical object. He felt immediate chest pain, but, in spite of electrocardiographic tracings highly suspicious for an acute anteroseptal infarction in the emergency room, he was discharged from hospital. The electrocardiogram recorded three weeks later was pathognomonic of anteroseptal infarction. Coronary arteriography performed four months later showed a complete obstruction of the left anterior descending coronary artery, with retrograde filling from the right coronary artery. It is assumed that the myocardial infarction was caused by the blast injury which induced an intimal tear and/or a subintimal haemorrhage in the left anterior descending artery with subsequent thrombosis. The lack of atherosclerosis in any other coronary arteries in this patient is noteworthy.

Blast Injuries↗
PubMed1980

Orthotopic renal autotransplantation in the treatment of renovascular hypertension.

Severe hypertension non-responsive to medical therapy was discovered in a 27-year-old woman in the third trimester of pregnancy. Renal arteriography after delivery revealed bilateral renal artery stenosis. The right kidney was smaller than the left one. The differential renal function studies, rather than the renal vein renin measurements, identified which side was causing the hypertension. An attempt at primary repair of the right renal artery failed. Orthotopic renal autotransplantation, using saphenous vein grafts that were interposed between the renal veins and the inferior vena cava, and between the segmental renal arteries and the abdominal aorta, reduced the blood pressure to normal values.

Adult↗