Search

The antiphospholipid antibody syndrome is a multisystem disorder characterized by persistently elevated antiphospholipid antibodies and/or arterial or venous thrombosis, thrombocytopenia and recurrent spontaneous abortion. Anticardiolipin antibodies and the lupus anticoagulant are different classes of antiphospholipid antibodies associated with this disorder. Various hematologic, neurologic, obstetric and cutaneous abnormalities are manifest in this syndrome. This article reviews the characteristic features of the antiphospholipid antibody syndrome.

Overexpression of the nm23H1 gene has been associated with the suppression of metastasis in several solid tumors. However, in colorectal carcinoma and neuroblastoma, increased levels of nm23 H1 nucleoside diphosphate kinase A (NDPKA) mRNA are associated with tumorigenesis. To determine the role of nm23 H1/NDPKA in the prostate, normal and/or malignant tissue samples from 29 consecutive patients were studied. Levels of nm23 H1/NDPKA mRNA and nm23 H1/NDPKA mRNA protein were determined in tissue from 18 and 27 patients, respectively. In all, 16 of the 18 tumor samples expressed increased levels of nm23 H1/NDPKA mRNA as compared with those measured in normal tissue. The level of nm23 H1/NDPKA mRNA was >10-fold higher in a metastatic lymph node than in normal prostate tissue. All cancer specimens and areas of prostatic intraepithelial neoplasia showed immunoreactivity with the nm23 H1/NDPKA antibody; however, normal prostatic tissue was unreactive. These findings suggest that overexpression of the nm23 H1/NDPKA gene occurs frequently in adenocarcinomas of the prostate and may be an early event in prostate cancer tumorigenesis.

Sucralfate, a basic aluminum salt of sucrose, was the first successful drug with a major cytoprotective mechanism of action. It binds bile acids and pepsin and adheres to both ulcerated and nonulcerated mucosa. Sucralfate stimulates the synthesis and release of gastric mucosal prostaglandins as well as bicarbonate and the epidermal growth factor which stimulates healing. Sucralfate is the safest drug available today in the treatment of dyspeptic symptoms and compared to ranitidine and cimetidine it has the following characteristics. (2) The short-term healing of duodenal ulcers is the same for sucralfate, cimetidine and ranitidine. (3) Sucralfate-treated patients have a lower recurrence rate of duodenal ulceration after healing when compared with cimetidine and the recurrence rate is not connected with the presence or absence of Campylobacter pylori.

The responses of gastric inhibitory polypeptide (GIP) and insulin to intraduodenal and IV triglyceride infusions were measured in 11 late fetal and 10 neonatal pigs. Basal plasma glucose, insulin, and GIP concentrations were lower in fetal than in neonatal pigs. In the fetal pigs, plasma glucose increased slightly during intraduodenal and IV triglyceride infusions, whereas plasma insulin remained unchanged during the tests. No significant changes were observed in plasma GIP concentration following intraduodenal triglyceride infusion in the fetal pigs, but plasma GIP fell during the IV infusion of triglyceride in these pigs (p less than 0.01). In the neonatal pigs, plasma glucose and insulin remained unaffected by intraduodenal and triglyceride infusions. Plasma GIP did not change during the IV triglyceride infusion, but exhibited a paradoxical decline after the intraduodenal triglyceride infusion (p less than 0.05). It is concluded that the GIP-cell response to an oral triglyceride load is suppressed in late fetal and neonatal pigs. The abolished GIP response to oral triglycerides could play a causal role in the inactivity of the enteroinsular axis which is seen in both human and animal neonates.

It is generally assumed that C-peptide is not degraded in the liver to any significant extent. This assumption is, however, based on indirect evidence. We therefore measured the hepatic extraction ratio (R) of insulin and C-peptide in anesthetized pigs with simultaneous sampling of portal and hepatic venous blood. Blood samples were taken at one-minute intervals for 10 minutes during basal (unstimulated) experimental conditions as well as after intravenous injection of 1 mg. glucagon into four normal-weight and four obese pigs. The hepatic extraction ratio of insulin or C-peptide was calculated as the portal concentration minus the hepatic concentration divided by the portal concentration. The average pre- and poststimulatory molar ratios of C-peptide to insulin were 1.5 ± 0.11 (S.E.M.) and 1.2 ± 0.06 in portal blood and 3.4 ± 0.21 and 2.2 ± 0.08 in hepatic blood. For all pigs the mean Rc-peptide was 0.30 ± 0.03 and 0.33 ± 0.02 pre- and poststimulatory, respectively. The corresponding figures for Rinsulin (0.71 ± 0.02 and 0.61 ± 0.02) were both significantly higher (p < 0.01). The mean R-values for C-peptide and insulin were consistently higher in obese pigs than in normal-weight pigs (p < 0.01). Additional experiments in two normal-weight pigs showed that ligation of the hepatic artery elicited a significant fall of mean Rc-peptide, which, however, never became less than 0.12. These results suggest that besides the wellknown hepatic extraction of insulin, the livers of anesthetized pigs also extract significant amounts of endogenous C-peptide. Hepatic extraction of C-peptide is, however, about 50 per cent lower than that of insulin.