Biomedical subjects
Publications and source records attributed to L Shenkman.
A 14-year-old patient presented with hypercalcaemia-induced acute renal failure. Investigation yielded a diagnosis of T-cell leukaemia. Chemotherapy resulted in complete remission, a return of serum calcium levels to normal and consequent improvement of renal function.
Five Persian Jews were detected with the polyglandular deficiency syndrome (PDS). Primary hypoparathyroidism and hypogonadism were present in each, adrenal insufficiency in two, and insulin-dependent diabetes mellitus and latent hypothyroidism in single subjects. The percentage of T and B cells, and the mononuclear cell response to phytohemagglutinin and Concanavalin A were normal in all five. IgG and IgA levels and the OKT4+/OKT8+ cell ratio were low in one subject. Antinuclear and antithyroid antibodies were present in one subject. HLA-DR5 was present in 4/4, HLA-24 and B5 (B51) in 3/4 subjects. A single case of isolated hypoparathyroidism (IHP) was detected among 12 first degree relatives. HLA antigens B8, DR3, were absent in all of these subjects. Seven non-Iranian Jews with IHP were also examined. HLA A26 or A25 were present in all seven. Persian Jews appear to have a unique variant of PDS.
Digoxin-like immunoreactivity (DLI) has been found in serum from subjects with a variety of physiological and pathological conditions, including uremia, liver disease, pregnancy, and the neonatal period. The physicochemical nature of this material is still not known. Using gel filtration chromatography, extraction with methylene chloride, and treatment with beta-glucuronidase, we determined that serum DLI exists in three forms: protein-bound, glucuronidated, and free, with respective mol wt of 5000, 400, and 230. In serum, DLI exists in the protein-bound and free forms, while in urine, DLI is found in the glucuronidated and free states.
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Cholinergic muscarinic binding by viable peripheral lymphocytes was assessed by measuring specific binding of the muscarinic antagonist [3H]quinuclidinyl benzylate. After atropine treatment maximal lymphocyte muscarinic binding was increased by about 30%, as it did in the hippocampus of the same rats. Strain-dependent differences in muscarinic binding by peripheral lymphocytes were correlated with similar differences in selective brain regions. Higher muscarinic binding was observed in lymphocytes derived from aged (24 months old) rats. We conclude: atropine treatment causes an increase in lymphocyte muscarinic binding as it does in the brain; strain differences in brain muscarinic binding are paralleled by similar differences in lymphocytes; and in aged rats muscarinic binding capacity by lymphocytes is elevated. The results indicate that circulating lymphocytes may serve as a useful peripheral marker reflecting induced alterations or inherent differences in muscarinic binding.
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In peripheral blood lymphocytes (mixed lymphocytes isolated on a Ficoll-Hypaque density gradient) derived from normal human subjects, cholinergic muscarinic binding capacity was found to increase with age. In contrast, lymphocytes derived from patients with "probable" senile dementia of the Alzheimer type (SDAT) exhibited a marked reduction in binding capacity. Treatment of these patients with antimuscarinic drugs was associated with increased muscarinic binding by lymphocytes. These results indicate that cholinergic muscarinic binding by peripheral blood lymphocytes may be useful in the study of alterations associated with aging and SDAT, as well as in evaluating changes induced by certain cholinergic drug treatments.
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We present an unusual case of torsion of a wandering spleen in a 14 year old boy. Wandering spleen is an entity which has rarely been reported in infants and children. Although patients may be asymptomatic, some may present as an acute surgical emergency if trauma or torsion of the vascular pedicle occurs, as in our case. The treatment of this condition is splenectomy.
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Hypothalamic pituitary function was studied in 13 patients with myasthenia gravis. Gonadotropin, TSH, and prolactin dynamics were investigated using conventional provocative stimuli. No consistent abnormality was found in either gonadotropin or prolactin release. Abnormal TSH responses to TRH administration was present in six of the 13 patients in association with normal free thyroxine indices and the absence of antithyroid antibodies. This latter observation is relevant when the association of myasthenia gravis with hyperthyroidism, thyroiditis and hypothyroidism is considered.
Over a 14-year period, 26 patients with adrenal insufficiency of multiple etiology were evaluated. Eight were diagnosed at autopsy, six of whom had acute bilateral adrenal hemorrhage. Nine had chronic adrenal insufficiency. Of these, five were idiopathic and three had polyglandular disorders. Four others had tuberculosis. Six of nine patients with chronic adrenal insufficiency were hyperpigmented. Unusual manifestations of adrenal hypocorticism included hypercalcemia, flaccid paralysis, and joint contractures. The presence of multiple hormonal deficiencies focused the diagnosis on hypopituitarism. Two cases of isolated ACTH deficiency were detected. Patients with familial Mediterranean fever with amyloidosis commonly presented with reduced adrenal reserve rather than overt insufficiency. Metastatic cancer of the adrenal glands was a rare cause of reduced adrenal reserve.
The study demonstrates that in the hippocampus of inbred Wistar-Kyoto (WKY) rats [3H]choline uptake is 38% higher than in Brown-Norway (BN) rats. In contrast, the maximum binding capacity of [3H]quinuclidinylbenzilate (QNB) is 28% lower in WKY than in BN rats. After immobilization stress there is a reduction in [3H]choline accumulation which is more pronounced in WKY rats. Furthermore, maximal QNB binding after stress is increased only in WKY rats. Choline acetyltransferase activity, which was 83.5% higher in WKY rats, was not altered after stress in both strains. We conclude that: (1) choline accumulation is directly related to choline acetyltransferase activity in hippocampal synaptosomes; (2) maximum cholinergic muscarinic binding capacity is inversely related to the above two presynaptic activities and (3) immobilization stress results in a decreased choline accumulation and may lead to an increased QNB binding. The results imply that reduction in choline accumulation may be a compensatory mechanism of cholinergic synapses during adaptation to lengthly periods of neuronal activity.
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Lithium enhances several in vitro indices of immune function, including thymidine uptake by mitogen-stimulated human mononuclear cells. To further characterize the mechanism of action of lithium and to determine whether it acts by abrogating suppressor cell activity or by enhancing helper cell function, we have compared the effects of lithium on the mitogenic response of normal, suppressor-depleted and suppressor-enriched mononuclear cell preparations. In normal cultures, lithium enhanced thymidine uptake in response to concanavalin A (Con A) and phytohemagglutinin (PHA). In the suppressor-depleted cultures, thymidine uptake after Con A stimulation was significantly higher than in normal cultures, and was further enhanced by lithium. In the suppressor-enriched system, response to PHA was significantly lower than in normal cultures, and addition of lithium reversed the observed suppression. These results indicate that lithium may be enhancing thymidine uptake in response to mitogen at least in part by abrogating suppressor cell activity. The observed increase in thymidine incorporation in the suppressor-depleted cultures suggests that lithium may also have a direct stimulatory effect on helper cell activity.
Ninety-five randomly selected patients attending an ambulatory geriatric medical clinic were tested for the presence in their sera of hepatitis B surface antigen and of antibody to hepatitis B and A viruses. Such evidence of past hepatitis infection was correlated with current liver function and history of having received blood transfusions. The results showed that 94% of patients had antibody to hepatitis A virus, and 32% had antibody to hepatitis B virus. Patients with abnormal liver function tests, or those with a history of blood transfusions were no more likely to have hepatitis B antibody than patients with normal liver function tests or those with no history of transfusion.