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Biomedical subjects

E Shane

Publications and source records attributed to E Shane.

67 records · Page 4Linked to original sources
PubMed1984

The end phase of analysis: indicators, functions, and tasks of termination.

This paper considers the end phase of analysis. Beginning with a brief review of the literature on termination, specifically the indicators for initiating the termination process, we identify the structural attainments necessary for the patient to successfully complete the analysis and to maintain smooth post-analytic functioning. We stress in this regard the significance of self-analytic functions and the relative immutability of the transference neurosis. These points are illustrated with clinical examples. Our paper concludes with a discussion of the tasks and contributions of the analyst during the termination process. We make special reference to countertransference vulnerability resulting from the analyst's own termination experiences.

Adult↗
PubMed1984

Reticulocyte cytosol activator protein: its actions upon the beta adrenergic receptor and the N-proteins of adenylate cyclase.

Rat reticulocytes contain a cytosol activator protein (RCAP) that augments catecholamine-sensitive adenylate cyclase activity in reticulocyte membranes. A partially purified preparation of RCAP was obtained by Sephacryl S-200 chromatography and used to elucidate further its mechanism of action. The specific activity of the S-200 fraction to augment isoproterenol responsiveness is increased approximately 1100-fold over the starting material from 1.2 nmoles to 1300 nmoles cyclic AMP formed per milligram of RCAP. The molecular weight is approximately 20,000. In addition to its effects on catecholamine-responsive adenylate cyclase, RCAP is associated with significant increases in basal (0.9 +/- 0.2 to 1.5 +/- 0.4 nmol/mg; p less than 0.02), guanyl-5'-yl imidodiphosphate [Gpp(NH)p]; (3.9 +/- 0.9 to 4.4. +/- 1.1 nmol/mg; p less than 0.005) and fluoride (4.1 +/- 0.6 to 4.8 +/- 0.6 nmol/mg; p less than 0.005) associated activities. RCAP stimulates isoproterenol responsiveness in wild type S49 cell membranes but is inactive in the mutant line, cyc-. RCAP alters the characteristics of agonist binding to the beta-adrenergic receptor of reticulocyte and wild S49 cell membranes, causing a significant increase in the IC50 for isoproterenol. Direct assessment of Ns and Ni components of the adenylate cyclase complex demonstrates that RCAP inhibits cholera toxin-specific ADP-ribosylation of the 42K subunit of Ns and stimulates pertussis toxin-specific ADP ribosylation of the 39K subunit of Ni.

Adenosine Diphosphate↗
PubMed1982

Therapy of hypercalcemia due to parathyroid carcinoma with intravenous dichloromethylene diphosphonate.

Dichloromethylene diphosphonate (Cl2MDP) a potent inhibitor of osteoclast-mediated bone resorption, lowers serum calcium in hypercalcemia associated wit malignancies and with primary hyperparathyroidism, and reduces excess calcium mobilization from bone in multiple myeloma and in Paget's disease. We have evaluated the effectiveness of intravenously administered Cl2MDP in five patients with parathyroid carcinoma, a disorder characterized by severe hypercalcemia, very high parathyroid hormone (PTH) levels, and marked osteoclast-mediated bone resorption. All patients had biopsy-proved metastatic parathyroid carcinoma and hypercalcemia which persisted after multiple surgical procedures and other attempts at management. During a three-day observation period, each patients continued to demonstrate stable or progressive hypercalcemia despite infusion with saline solution and furosemide. Cl2MDP was administered over 2 hours at 2.5 mg/kg on day 1 and 5 mg/kg on days 2 through 7. Response was noted in all five patients; there was a gradual decline in the average serum calcium from 16.0 +/- 1.1 mg/dl (SEM) to 11.1 +/- 0.9 mg/dl by the eighth day (p less than 0.01). There were concomitant reductions in urinary calcium excretion, from 798 +/- 153 mg/g creatinine to 350 +/- 96 mg/g creatinine (p less than 0.05) and in the urinary hydroxyproline excretion, from 155 +/- 38 mg/g creatinine to 94 +/- 29 mg/g creatinine (p less than 0.02). Serum PTH levels remained markedly elevated (460 +/- 141 micrograms eq/ml to 493 +/- 169 micrograms eq/ml). In three patients, all indices returned to pretreatment levels by 10 days after the last infusion. In two of these patients there was a response to retreatment with Cl2MDP with a fall in calcium from 16.9 +/- 0.5 mg/dl to 12.4 +/- 1.5 mg/dl. There was no response in one patient. No adverse reactions to Cl2MDP were observed. The decrease in serum calcium and concomitant declines in urinary calcium and hydroxyproline suggest that Cl2MDP can effectively inhibit the excessive bone resorption associated with parathyroid carcinoma.

Aged↗
PubMed1981

Hypercalcemia of malignancy: treatment with intravenous dichloromethylene diphosphonate.

Twelve patients with hypercalcemia associated with various malignancies were treated with intravenous dichloromethylene diphosphonate (Cl2MDP), a potent inhibitor of osteoclastic bone resorption, in doses of 2.5 mg/kg of body weight initially and 5.0 mg/kg thereafter for up to 7 days. Mean serum calcium concentration fell from 13.8 +/- 0.6 mg/dL (SEM) before Cl2MDP to 9.8 +/- 0.7 mg/dL (SEM) (p less than 0.001) after 7 days. Urine calcium excretion fell from 775 +/- 95 mg/g creatinine (SEM) to 272 +/- 70 mg/g creatinine (SEM) (p less than 0.005), and urine hydroxyproline excretion fell from 144 +/- 28 mg/g creatinine (SEM) to 78 +/- 18 mg/g creatinine (SEM) (p less than 0.05) after treatment with Cl2MDP. The Cl2MDP was well tolerated, and adverse effects were limited to asymptomatic hypocalcemia in two patients. The ability of Cl2MDP to correct hypercalcemia and reduce urine calcium and hydroxyproline excretion in these patients is consistent with the hypothesis that increased bone resorption is primarily responsible for this complication of malignancy and suggests that Cl2MDP may be highly useful in managing this condition.

Adult↗
PubMed1981

Effects of dichloromethylene diphosphonate on serum and urinary calcium in primary hyperparathyroidism.

Dichloromethylene diphosphonate (Cl2MDP), an inhibitor of osteoclast function, was evaluated for its ability to lower the serum and urinary calcium in 14 patients with primary hyperparathyroidism. The study was double-blind, placebo-controlled, and cross-over in design. All patients received 12 weeks of Cl2MDP (1600 mg daily) and 12 weeks of placebo in a randomized sequence. The average serum calcium was lowered by Cl2MDP from 11.5 +/- 0.1 mg/dL to 10.8 +/- 0.2 mg/dL (p less than 0.001). In the 3-month follow-up after drug administration, the average serum calcium (11.0 +/- 0.2 mg/dL) remained significantly below pretreatment levels (p less than 0.01). The reduction in serum calcium was accompanied by a significant decline in the urinary hydroxyproline excretion from 37 +/- 3 to 28 +/- 2 mg/g creatinine (p less than 0.01) and by a 40% reduction in the average urinary calcium excretion from 185 +/- 29 to 113 +/- 23 mg/g creatinine (p less than 0.01). Administration of Cl2MDP was not associated with any significant changes in parathyroid hormone levels or in urinary cyclic adenosine monophosphate excretion. No side effects were observed. We conclude that Cl2MDP lowers the serum and urinary calcium in patients with primary hyperparathyroidism.

Adult↗
PubMed1980

A radioreceptor assay for propranolol and 4-hydroxypropranolol.

A radioreceptor assay for the measurement of propranolol and 4-hydroxypropranolol levels in plasma is described. Maximum sensitivity for propranolol was 1.2 +/- 0.15 ng/ml and for 4-hydroxypropranolol 4.2 +/- 0.4 ng/ml. Interassay and intra-assay variations for both were under 10%. Modifications in the radioreceptor assay permitted the measurements of total beta-adrenergic blocking activity and the separate contributions of parent drug and metabolite. When 4-hydroxypropranolol was stabilized, a composite level of total beta-adrenergic blocking activity in plasma was obtained. When the 4-hydroxy metabolite was oxidized, only the stable parent drug was detected. The difference in values between measurements made under these conditions was equivalent to the amount of 4-hydroxypropranolol in the sample. The radioreceptor assay was also used to measure the amount of free propranolol and 4-hydroxypropranolol. Under identical experimental conditions, more 4-hydroxypropranolol than propranolol circulated in the free form. These observations establish the feasibility of adapting the radioreceptor assay for propranolol to the measurement of total beta-adrenergic blocking activity and its components in plasma as well as to the measurement of free drug and metabolite levels.

Animals↗
PubMed1980

Hypoparathyroidism and elevated muscle enzymes.

We studied a patient with hypocalcemia and increased serum activity of sarcoplasmic enzymes. Idiopathic hypoparathyroidism was established by history, low serum parathyroid hormone content, and marked responsiveness of urinary cyclic AMP and phosphate to parathyroid hormone. Muscle-associated isoenzymes of creatine phosphokinase and lactic dehydrogenase were increased, but there was no concomitant muscle weakness. Muscle biopsy was normal by morphologic and histochemical examination. The patient was treated with calcium and vitamin D. As the calcium rose, there were corresponding decreases in the serum activities of creatine phosphokinase and lactic dehydrogenase, with correlation coefficients of -0.88 and -0.64, respectively (p less than 0.01).

Adult↗
PubMedDate not supplied

Osteoporosis and low bone mass in premenopausal and perimenopausal women.

OBJECTIVE: To characterize the historical, clinical, and biochemical features of 111 young women (age, <55 years) referred for evaluation of osteoporosis or low bone mass. METHODS: Women with a bone mineral density T score < or = -2.0 (N = 111) at one or more anatomic sites (by dual-energy x-ray absorptiometry) were assessed relative to anthropomorphic and biochemical characteristics and risk factors for osteoporosis. RESULTS: Of 111 women with low bone mass or osteoporosis, 73 (66%) had identifiable causes of bone loss, of which estrogen deficiency (menopause, premenopausal estrogen deficiency) and conditions associated with estrogen deficiency (anorexia nervosa, cancer chemotherapy) were the most common. Prolonged use of glucocorticoids was the most common secondary cause of osteoporosis. Of 38 women with no identifiable cause of bone loss, 21 were premenopausal (mean age, 38 +/- 10 years [standard deviation]) and 17 were perimenopausal (mean age, 50 +/- 3 years). The mean lumbar spine T score was -2.18 +/- 1.0 in the premenopausal and -2.51 +/- 0.6 in the perimenopausal women. Nontraumatic fractures were reported by 42% of the premenopausal women and 18% of the perimenopausal women. A family history of osteoporosis was reported by 71% of the premenopausal and 47% of the perimenopausal women. CONCLUSION: Most young women with osteoporosis or low bone mass had estrogen deficiency or another secondary cause of premature bone loss (or both). A subset of premenopausal and perimenopausal women, however, had no identifiable cause of bone loss. The strong family history of osteoporosis, especially in the premenopausal women, provides further support for current theories of a genetic predisposition to osteoporosis.

Adult↗