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Biomedical subjects

L Shenkman

Publications and source records attributed to L Shenkman.

At least 73 records · Page 4Linked to original sources
PubMed1981

An immunodeficient child with inflammatory bowel disease: involvement of cyclic nucleotides and effects of lithium.

A 3-year-old male with inflammatory bowel disease and hypogammaglobulinemia was found to have decreased T lymphocyte function. His serum was shown to depress normal T cell proliferative responses to phytohemagglutinin. Incorporation of lithium chloride to in vitro cultures enhanced autologous lymphocyte responses to phytohemagglutinin. Since lithium acts by inhibiting cAMP production, the child's lymphocytes were postulated to have increased levels of cAMP. Both lymphocytes and serum were shown to contain elevated levels of cAMP. In vivo therapy with lithium citrate was initiated and enhanced T cell numbers and function were observed concomitantly. Serum cAMP was also reduced to normal levels. The patient showed initially marked clinical improvement as assessed by mood, weight gain, and diminution of diarrhea. This clinical improvement was unfortunately not sustained despite the continued improvement in immune parameters and cAMP levels.

Agammaglobulinemia↗
PubMed1980

Lithium as an immunologic adjuvant.

Lithium, an adenylate cyclase inhibitor, stimulates a variety of in vitro indices of immune function, including proliferation of lymphocytes in response to mitogens, rosette formation by T-cells and phagocytosis by macrophages. Lithium enhances these immunologic responses at concentrations comparable to those achieved in patients receiving lithium for treatment of manic-depressive disorders. Lithium may prove to have important therapeutic applications as an immune adjuvant, particularly in immune deficiency states associated with excessive C-AMP production.

Adjuvants, Immunologic↗
PubMed1980

Pheochromocytoma: an animal model.

A reproducible animal model for studying pheochromocytoma is described. Rat pheochromocytoma cells (PC-12 line) maintained in tissue culture and injected subcutaneously into rats produce a functioning tumor at the side of inoculation. Animals harboring these tumors develop alterations characteristic of pheochromocytoma including weight loss, hypertension and a contracted blood volume. This model provides an easily reproducible system for studying the pathophysiologic features of pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1980

Adenosine deaminase deficiency without immunodeficiency: clinical and metabolic studies.

A child diagnosed at birth as deficient in red blood cell adenosine deaminase (ADA) but with substantial residual lymphocyte ADA has been evaluated for two and one-half years. The only immunologic abnormality observed was hypogammaglobulinemia during the fifth month of life. This was unexpected because children with total ADA deficiency either have severe combined immunodeficiency or selectively greater impairment of cellular than humoral immunity. The absence of severe combined immunodeficiency in this child was associated with normal lymphocyte content of ATP, dATP, and cyclic 3'5'-adenosine monophosphate, potentially toxic metabolites which are elevated in ADA-deficient immunodeficient children.

Adenosine Deaminase↗
PubMed1979

Haloperidol-induced syndrome of inappropriate secretion of antidiuretic hormone.

Several psychotropic drugs have been associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We report here a patient who on two occasions developed clinically significant hyponatremia while receiving the antipsychotic drug, haloperidol. The criteria for the syndrome of inappropriate secretion of ADH were fulfilled and other causes of SIADH were excluded. We documented inability in this patient to excrete a water load while on haloperidol and normal ability in its absence. This case therefore illustrates SIADH due to haloperidol.

Haloperidol↗
PubMed1979

Yersinia enterocolitica antibodies in thyroid disorders.

Yersinia enterocolitica agglutinating antibodies were present in 42% of 36 patients with thyroid disease and in none of 77 control subjects. Since the frequency of Yersinia infections in Israel is low, the association of thyroid diseases with Yersinia antibodies is of particular interest. The significance of this finding is discussed in view of some recent observations.

Antibodies, Bacterial↗
PubMed1978

Activation of rat pheochromocytoma tyrosine hydroxylase by a cyclic AMP-dependent protein kinase in a cell-free system.

Short term exposure of PC-12 cells to dibutyryl cyclic AMP (dB-cAMP) results in an activation of tyrosine hydroxylase. In the cell-free system the PC-12 tyrosine hydroxylase activity is stimulated by addition of c-AMP, Mg+2 and ATP. Exogenous c-AMP dependent protein kinase further stumulates tyrosine hydroxylase activity. The kinetic data suggests that the PC-12 tyrosine hydroxylase in the basal state is in a non-phosphorylated form but under phosphorylating conditions the enzyme is activated and its kinetics properties are altered.

Cell Line↗
PubMed1978

Massive osteolysis. An unusual cause of bone destruction.

A patient who presented with multiple lytic lesions of bone was found to have massive osteolysis. The clinical course of this patient is described and the literature on massive osteolysis reviewed. This disease of uncertain etiology is pathologically marked by resorption of bone, and replacement by angiomas and fibrosis. X-ray findings are usually more severe than expected from the patients' clinical presentation. Laboratory studies, including attempts at biopsy, are generally unrevealing. Drug therapy is of no value, and success of surgical attempts at bone union are unpredictable. Massive osteolysis should be considered in the differential diagnosis of osteolytic lesions, particularly since this disorder can result in serious morbidity.

Bone Neoplasms↗
PubMed1977

Diabetes insipidus following cardiorespiratory arrest.

Diabetes insipidus following cardiac arrest and hypoxemic encephalopathy occurred in two patients. In both, severe hypoxemic brain damage was followed within three days by clinical and laboratory features of diabetes insipidus, which were corrected by administration of exogenous vasopressin. Hypothalamic injury resulting in diabetes insipidus should be considered in the differential diagnosis of polyuria and dehydration occurring in critically ill patients who have suffered cardiorespiratory arrest.

Adult↗