The response of pituitary hormones to exogenous stimulation by hypothalamic hormones (TRH and LH-RH) in patients with endogenous depression.
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Biomedical subjects
Publications and source records attributed to S Czekalski.
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The effects of thymus factor (TFX) and levamisole on the clinical picture and some indices of cellular immunity have been evaluated in 10 patients with nephrotic syndrome due to membranoproliferative glomerulonephritis Type I. The patients revealed decreased T-lymphocyte number and impaired responsiveness to phytohaemagglutinin (PHA) stimulation before treatment. An association between the slight diminution of proteinuria and the increase of E-rosette forming lymphocytes, increased responsiveness to PHA and return to normal of previously elevated B-cell percentages, was observed in four patients treated with TFX and one patients treated with levamisole.
In phosphate deprivation, the kidney is resistant to the phosphaturic effects of several well-established phosphaturic stimuli, including PTH. We examined whether a low-phosphate diet would render rats unresponsive to the phosphaturic effects of glucocorticoids in the presence and absence of PTH. Treatment with triamcinolone (1 or 50 mg/kg/day) caused phosphaturia in rats fed a low-phosphate diet and also restored rhe phosphaturic effects of PTH. Plasma phosphate was significantly increased with both doses of glucocorticoid. There were no changes in acid-base parameters with the low dose and a compensated metabolic acidosis with the high dose of glucocorticoid. Renal gluconeogenesis was stimulated at both doses and was further enhanced by PTH at the higher dose. We conclude that glucocorticoids reverse the resistance to the phosphaturic phosphate and/or enhanced renal gluconeogenesis.
Thyroid function was evaluated in a group of 36 patients with acute renal failure (ARF) during the oliguric/anuric, polyuric and postpolyuric phase. Serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased in the oliguric/anuric phase, as compared with the mean values obtained in the post-polyuric phase and with controls. In contrast to T3 and T4, the concentration of serum reverse triiodothyronine (rT3) was elevated in the oliguric/anuric phase and normal in the polyuric phase. The sephadex-T3-binding index (T3I) was significantly increased in oliguric/anuric patients and in the polyuric phase. The levels of serum thyreotropin were significantly elevated during all phases of ARF as compared with the controls. From the results obtained it is concluded that abnormal peripheral metabolism of T4 seems to be the primary cause of altered plasma concentrations of thyroid hormones in patients with ARF.
Serum reverse triiodothyronine (reverse T3), triiodothyronine (T3), thyroxine (T4) and thyrotropin (TSH) concentrations were determined by radioimmunoassay in end-stage chronic renal failure, hypothyroidism and control subjects. In advanced chronic renal failure serum reverse T3 was normal or elevated and serum T3 concentrations were frequently, and serum T4 occasionally, lowered. Serum TSH was normal even where serum T3 and T4 concentrations were low. Normal or elevated serum reverse T3 associated with normal serum TSH in chronic renal failure clearly differentiates this disease from primary hypothyroidism in which low serum reverse T3 and high serum TSH are constantly found.
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In the course of investigations on experimental arterial hypertension in rats, it has been stated, that imipramine prevents the development of hypertension and that is simultaneously causes an accumulation of cAMP in the vessel walls. The relationship between the two phenomena has been discussed.
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The purpose of the study was the evaluation of nephrogenous adenosine 3'5' monophosphate (ncAMP) determinations in the diagnosis of hyperparathyroidism (HPT) in chronic renal disease (CRD). The ratio of cAMP clearance to creatinine clearance (CcAMP/Ccr) was applied as the index of the participation of ncAMP in 24 hr urinary cAMP excretion. In seventy CRD patients, the mean CcAMP/Ccr value was higher than in healthy individuals. A good correlation between plasma iPTH and CcAMP/Ccr ratio was noted. In patients with a ratio higher than 2.5, the signs of HPT were found. The determination of CcAMP/Ccr ratio in CRD may be of value in the assessment of parathyroid hyperactivity.
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The purpose of this study was to estimate whether target tissues other than the kidney are responsive to parathyroid hormone (PTH) and calcitonin (CT) in anephric man. Twenty subjects were studied: 12 normal, 4 anephric, 4 anuric ('anephric') individuals. PTH infused into 6 normal subjects produced several fold increase in plasma level of cAMP, whereas CT caused minimal increase in the same number of normal individuals. In 4 anephrics PTH infusion resulted in a delayed rise of plasma cAMP. CT administration to 4 'anephrics' did not change plasma cAMP. In all subjects PTH and CT failed to modify plasma electrolytes level. The data indicate that the kidneys are the main source of cAMP after PTH administration and in anephric subjects extrarenal tissues are the source of circulating cAMP.
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