Acute neurochemical changes in mouse brain following cerebral ischemia

Acute changes in neurochemical levels induced by ischemia were studied in the mouse brain. Contents of neurochemicals in the frontal, parietal and occipital cortices and hippocampus were determined immediately after 15 min of ischemia (0), and then at 15, 30, 90 and 180 min after recirculation following ischemia. These data were compared with those for sham-operated control mice. Choline (Ch) contents in ischemic animals increased by 530–630% from control levels immediately after ischemia, and returned to control levels by 90 min. Decreases in levels of norepinephrine (NE) and serotonin (5-HT) were observed during 30 min after recirculation. There were no significant changes in levels of acetylcholine (ACh) or dopamine (DA), throughout recirculation. On the other hand, DA and 5-HT metabolites (3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid) significantly increased. Thus, comprehensively investigating the various neurotransmitters will provide meaningful information regarding the disturbance of central nervous system induced by cerebrovascular disease.     

Cyclic thrombocytopenia associated with IgM anti-GPIIb-IIIa autoantibodies

Summary. We studied a female patient with cyclic fluctuation in platelet count following splenectomy for autoimmune thrombocytopenia. The cyclical fluctuation appeared to be in phase with her menstrual cycle and her platelet count was low during menses. Bone marrow examinations performed at the peak as well as the bottom of the platelet count showed normal or increased numbers of megakaryocytes. The patient's platelet count increased rapidly after intravenous gamma-globulin (IVIgG) therapy, suggesting that a failure of platelet production is unlikely to account for the cycle. Platelet-associated IgM (PAIgM) was markedly elevated, whereas PAIgG was normal at any stage of the cycle. MACE assay demonstrated that PAIgM contained IgM anti-glycoprotein (GP) IIb-IIIa autoantibodies. Comparison between MACE assay using untreated and EDTA-treated platelets at 3 7°C demonstrated that the platelet-associated IgM autoantibodies mainly recognized divalent cation-dependent conformation(s) of GPUb-IIIa. No antibodies were, however, detected in her serum. The levels of IgM anti-GPIIb-IIIa showed an inverse relationship with the platelet count. In spite of the marked increase in platelet count after IVIgG, however, the levels of IgM anti-GPIIb-IIIa remained elevated. These findings suggest that plateletassociated IgM anti-GPIIb-IIIa autoantibodies are of pathogenic significance in this patient.     

Decreased cerebrospinal fluid levels of β-endorphin in Japanese patients with Joseph disease

We measured the cerebrospinal fluid (CSF) levels of β-endorphin in 7 Japanese patients with Joseph disease and compared them with control values. The 7 patients included 4 with type I and 3 with type II disease; their mean age was 45.7 ± 12.09 years. Diseased controls were matched in age to the patients studied. In these patients, CSF β-endorphin level was significantly lower than in the controls (40% of normal values). An alteration in CSF β-endorphin level may explain some of the neurological impairment found in Joseph disease.     

A novel vitamin E derivative (TMG) protects against gastric mucosal damage induced by ischemia and reperfusion in rats

The aim of the present study was to investigate the antioxidative effects of water-soluble vitamin E derivative, 2-(-d-glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol (TMG), on ischemia–reperfusion (I/R) -induced gastric mucosal injury in rats. Gastric ischemia was induced by applying a small clamp to the celiac artery and reoxygenation was produced by removal of the clamp. The area of gastric mucosal erosion, the concentration of thiobarbituric acid-reactive substances, and the myeloperoxidase activity in gastric mucosa significantly increased in I/R groups compared with those of sham-operated groups. These increases were significantly inhibited by pretreatment with TMG. The contents of both mucosal TNF- and CINC-2 in I/R groups were also increased compared with the levels of those in sham-operated groups. These increases of the inflammatory cytokines were significantly inhibited by the treatment with TMG. It is concluded that TMG inhibited lipid peroxidation and reduced development of the gastric mucosal inflammation induced by I/R in rats.