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Biomedical subjects

J S Scott

Publications and source records attributed to J S Scott.

At least 145 records · Page 8Linked to original sources
PubMed1985

Ovarian strumal carcinoid tumor with amyloid stroma--report of a case with 20-year follow-up.

We report a case of strumal carcinoid tumor arising in the left ovary of a 20-year-old woman. Histologically, microfollicular, solid, and trabecular areas were present, and amyloid stroma was demonstrated. Many cells contained argyrophilic granules, and thyroglobulin and calcitonin were demonstrated immunohistochemically in several areas. Ultrastructurally the cells resembled thyroid follicular cells and contained neurosecretory granules. It is concluded that strumal carcinoid is of endodermal origin, and shows evidence of thyroid and C-cell differentiation.

APUD Cells↗
PubMed1985

A comparison of cobalamin binding by liver and kidney in rat and man.

Binding of cobalamin (Cbl) was compared in liver and kidney plasma membranes prepared from rat and human tissues. Single, high-affinity, saturable (200 pmol/l), binding sites for TC II-Cbl were found in all tissues; by contrast no receptors were present for free cobalamin, for which only non-specific adsorption occurred. Binding constants for TC II-CNCbl determined for liver and kidney plasma membranes were of a similar magnitude. Mean values for Ka (litre/nmol) were 16.7 (rat liver), 18.8 (rat kidney), 8.0 (human liver) and 7.5 (human kidney). Results for binding TC II-OHCbl instead of TC II-CNCbl showed no difference in Ka and Bmax. values, although the non-specific adsorption was decreased to a third. Competitive inhibition results showed that the receptors are specific for the TC II molecule and that binding is unaffected either by the cobalamin moiety or by the presence of free cobalamin. Degradation of the receptor protein molecules by trypsin (10 micrograms/ml) resulted in 90% inhibition of binding. It is concluded that differences between liver and kidney in cobalamin uptake and accumulation cannot be attributed to differences in their TC II receptors.

Animals↗
PubMed1985

The retention of cobalamin by the liver in the cobalamin-deficient rat.

The effect of cobalamin deficiency on whole body cobalamin content and its turnover was examined in the rat. Quantitative and qualitative changes in hepatic cobalamin were also followed and the effect of deficiency on the turnover of this cobalamin was determined in the isolated perfused liver. As cobalamin deficiency developed after total gastrectomy, whole body cobalamin content declined at a constant rate, indicating no attempt to conserve total body cobalamin stores even when depleted (5% of normal). In contrast, the cobalamin concentration of liver declined more slowly, indicating conservation of hepatic cobalamin. Furthermore, the methylcobalamin (MeCbl) content of liver was maintained or even increased. Measurement of the rate of release of cobalamin by the isolated perfused liver at varying times after gastrectomy showed that as depletion of whole body and hepatic cobalamin stores proceeded, the rates of release of hepatic cobalamin into plasma and bile decreased. Regression analysis showed that the fractional rates of release of hepatic cobalamin into plasma (r = 0.9, P less than 0.001, n = 15) and bile (r = 0.65, P less than 0.01, n = 15) were significantly correlated with hepatic cobalamin content. It is concluded that conservation of hepatic cobalamin in deficiency is achieved, at least in part, by a specific decrease in the rate of release of hepatic cobalamin.

Animals↗
PubMed1985

Bronchoalveolar lavage in ponies with recurrent airway obstruction (heaves).

We performed bronchoalveolar lavage (BAL) in 2 groups of ponies. Principal ponies had a history of heaves, a disease characterized by recurrent airway obstruction and airway hyperreactivity when ponies are housed in a barn and fed hay; control ponies had no history of airway obstruction. Ponies were paired (principal and control), and BAL was performed after 2 months of being pastured when principal ponies were in clinical remission (Period A), after barn housing when principal ponies had acute airway obstruction (Period B), and after a 1- and a 2-wk recovery phase of pasture grazing (Periods C and D). At Periods A, C, and D, white blood cell counts and immunoglobulin/albumin ratios in peripheral blood and BAL fluid of principal and control animals did not differ. Peripheral blood white cell counts and immunoglobulin/albumin ratios were unaffected by barn exposure and return to pasture. However, at Period B, neutrophil numbers in the BAL fluid were increased in the principal but not in the control animals. The IgG/albumin ratio of the principal animals increased at Period C. We conclude that in ponies with a history of heaves, barn exposure results in increased neutrophils in BAL fluid. In this pony model of lung disease, pulmonary leukostasis follows a time course similar to that of airway obstruction and airway hyperreactivity.

Albumins↗
PubMed1984

The place of staging laparotomy in the management of Hodgkin's disease.

The results of laparotomy and splenectomy in 225 patients with Hodgkin's disease are presented. The investigation changed the staging of the disease in 35% of patients. It carried no mortality and a low morbidity. It is concluded that the procedure provides information unobtainable accurately by other means and that it should be carried out in adult patients of both sexes and all histological subgroups who have clinical Stage I and II disease.

Adult↗
PubMed1984

The regulatory roles of liver and kidney in cobalamin (vitamin B12) metabolism in the rat: the uptake and intracellular binding of cobalamin and the activity of the cobalamin-dependent enzymes in response to varying cobalamin supply.

To examine possible regulatory roles of liver and kidney in cobalamin metabolism, specific activities of the two cobalamin-dependent enzymes, uptake in vivo of cyano [57Co]cobalamin [( 57Co]CNCbl) and the binding of [57Co]Cbl to intracellular proteins were measured in normal, cobalamin-loaded and cobalamin-deficient rats. Cobalamin deficiency and cobalamin loading produced greater changes in cobalamin concentration in the kidney than in the liver. Although cobalamin deficiency resulted in a decrease in total methylmalonyl-coenzyme A mutase (methylmalonyl-CoA mutase) in both organs, cobalamin loading had no effect. Neither deficiency nor loading altered total methyltransferase activity. The holoenzyme activities of both enzymes correlated with changes in tissue cobalamin levels. Uptake of [57Co]Cbl indicated that the kidney, in contrast to the liver, increased its uptake during loading and reduced it during deficiency, suggesting a possible regulatory role for this organ. In the normal rat, 24 h after injection of [57Co]CNCbl, 0.3% of the administered [57Co]Cbl was present in the liver as free cobalamin. By contrast, in the kidney, over 13% of the [57Co]Cbl was present in the free form. During deficiency free renal [57Co]Cbl was reduced to 0.6% of the administered [57Co]Cbl whereas in cobalamin-loaded rats it was increased to more than 27%. It is concluded that alterations in tissue cobalamin levels resulting from differences in cobalamin supply are due to changes in the large pool of free cobalamin present in the kidney and not to changes in the intracellular binding.

Animals↗
PubMed1983

Connective-tissue disease, antibodies to ribonucleoprotein, and congenital heart block.

The relation between congenital heart block and maternal connective-tissue disease was studied by antibody screening of serum samples obtained in connection with 45 cases of isolated congenital complete heart block. Serum was available from 41 mothers (17 who had connective-tissue disease and 24 who were healthy) and 21 children. Thirty-four mothers had antibody to a soluble tissue ribonucleoprotein antigen called Ro(SS-A), which was identified by immunodiffusion. Anti-Ro(SS-A) was found in seven of eight serum samples collected from affected children when they were less than three months old but in none of 13 samples obtained when these children were older. It appears that maternal anti-Ro(SS-A) antibody crosses the placenta and is a marker for risk of congenital complete heart block; its absence from maternal serum suggests that a child is unlikely to be affected. Anti-Ro(SS-A) or a related antibody is probably involved in the pathogenesis of congenital complete heart block.

Autoantibodies↗