Previous studies reported controversial results concerning alterations of astrocytes in schizophrenia. Because S100B may be regarded as a marker for astrocytes, the objective of this study was to examine S100B serum concentrations in 30 patients with schizophrenia with a monoclonal two-site immunoluminometric assay that specifically detects S100B. An ANOVA revealed medication ( p < 0.005) and deficit vs. nondeficit syndrome ( p < 0.05) as factors that influenced S100B significantly. S100B was higher in schizophrenic patients treated with antipsychotic drugs for approximately 3 weeks (241.1 F 152.5 ng/l) in comparison with unmedicated patients (111.4 F 31.8 ng/l, p < 0.005), and healthy age-matched controls (112.8 F 53.4 ng/l, p < 0.001; Bonferroni corrected two-tailed Student's t-test). There was no difference of S100B between unmedicated patients and controls ( p>0.05). Patients with deficit (250.6 F 154.9 ng/l) had higher S100B levels than patients with nondeficit schizophrenia (146.7 F 107.2 ng/l, p < 0.05) or controls ( p < 0.005). S100B was positively correlated with the subscore 'thought disturbance' of the Brief Psychiatric Rating Scale ( p < 0.05). In summary, increased serum levels of S100B may indicate alterations of astrocytes during early treatment with antipsychotics and in deficit schizophrenia. Whether S100B is elevated due to injured astrocytes and a disrupted blood -brain barrier, or by active secretion of S100B by astrocytes, has to be clarified by further studies. D

Studies were performed on 72 anesthetized mongrel dogs. Upon injection or infusion of secretin into the portal vein, the pancreatic volume and bicarbonate response was found to be significantly smaller than following administration into the femoral vein, but only when low doses of secretin (0.25 clin U/kg/h or smaller) were applied. No difference was observed in pancreatic protein and enzyme secretion after cholecystokinin, when both high and low doses were applied to the portal or femoral vein. The injection of secretin and cholecystokinin into the renal artery causes a loss of biological activity of 75 and 60%, respectively, as compared to femoral administration. Ligature of the blood vessels of both kidneys resulted in an increase in the biological activity of secretin of 80% and of cholecystokinin of 50%. The slopes of the flow rate curves determined upon secretin injection were smaller after ligature of the renal blood vessels. The biological half-life of secretin increased from an average of 2.9 to 4.8 min. These results indicate that the kidneys play a role in the catabolism of exogenous secretin and cholecystokinin, whereas the blood and the liver (at least for cholecystokinin) seem to be of small importance.