Neuronal degeneration and glial cell-responses following trimethyltin intoxication in the rat

Trimethyltin (TMT) preferentially induces neuronal changes in the hippocampus and pyriform cortex. In the present study we investigated the time course of microglial and astroglial responses associated with neurodegeneration after the administration of TMT (i.p. 9 mg/kg or 12 mg/kg body weight) in the rat. At a dosage of 9 mg/kg TMT, neurodegeneration was clearly demonstrated in the CA1 and CA3 regions of the hippocampus as argyrophilic (dark) neurons by day 4 using the Gallyas-Braak (G-B) impregnation method that has been shown to be sensitive and specific for neurodegeneration. Early microglial response was immunohistochemically shown with anti-microglial response factor-1 (MRF-1) antibody in the CA3 by day 1, preceding neurodegeneration morphologically detected by the G-B method. Activation of astrocytes was revealed by immunohistochemical staining for glial fibrillary acidic protein (GFAP) by day 2. In parallel with the maximal neurodegeneration, large numbers of hypertrophied microglia and astrocytes were observed in the CA1 and CA3 by day 7. Numbers of degenerative neurons appeared to be closely associated with adjacent microglia by the double staining of G-B impregnation and MRF-1 immunohistochemistry. The number of reactive microglia considerably decreased to the resting state by day 14, while hypertrophied astrocytes were still prominent in the CA3 up to day 21. With the high dose of TMT, granule cells in the dentate gyrus and CA1 and CA3 pyramidal cells were significantly impregnated. After TMT treatment, accompaning neurodegeneration we observed early response of microglia and prolonged activation of astrocytes, suggesting an individual role of glial cells in maintenance and repair of damaged neurons following brain injury.     

Effect of duodenectomy on gastric motility and gastric hormones in dogs

OBJECTIVE: To test the hypothesis that the duodenum is required to coordinate interdigestive insulin secretion with gastrointestinal motility and to determine whether duodenectomy alters the interdigestive cycles of plasma motilin and insulin levels and their relations to insulin secretion and motility. METHODS: Adult mongrel dogs were chronically implanted with force transducers in the stomach, duodenum, and upper jejunum to monitor contractile activity. Eight healthy mongrel dogs were divided into control and duodenectomized dogs. Insulin secretion, gastrointestinal motility, and plasma concentrations of motilin during the interdigestive period were measured in normal and duodenectomized dogs. RESULTS: After duodenectomy, no obvious phase III contractions were seen in the gastric antrum, but migrating phase III contractions were seen in the upper jejunum. The plasma motilin concentration did not fluctuate as it does in normal dogs, and remained low. After duodenectomy, insulin secretory cycles were not coordinated with either cycles of interdigestive motility or the plasma concentration of motilin. Exogenous motilin administration stimulated endogenous insulin release significantly compared with saline-treated controls. The contractile response of the stomach to exogenous motilin after duodenectomy was similar to that of intact dogs. CONCLUSIONS: Duodenectomy disrupts the relation between cycles of both interdigestive gastrointestinal motility and insulin secretion. These effects of duodenectomy may be attributable to interruption of the duodenopancreatic neural connections, hormonal abnormalities, or loss of vagus-sensitive humoral factors. The duodenum, which stores motilin, seems to play an important role in the relations between gastric migrating motor complexes and the concomitant increase of insulin secretion in fasted dogs. The mechanism responsible for the effect of motilin in both duodenectomized and normal dogs may involve a cholinergic pathway.     

Syringohydromyelia in Hajdu-Cheney syndrome

We report the case of a 10-year-old boy with typical manifestation of Hajdu-Cheney syndrome. MRI demonstrated syringohydromyelia involving almost the entire spinal cord, although neurological symptoms had not yet developed. Syringohydromyelia is considered to be a sequel to progressive basilar invagination and is one of the essential features of this rare osteolytic bone dysplasia.     

Lack of specific binding of anticardiolipin antibodies to intact platelets.

The aims of this study were to investigate whether anticardiolipin antibodies (aCL) bind to intact (resting or activated) platelets in vitro. Suspensions of resting, activated (with a mixture of thrombin and collagen) and freeze-thawed platelets from healthy subjects were incubated with either affinity-purified aCL or pooled normal human immunoglobulin G (IgG). Platelet-bound IgG was measured by flow cytometric analysis of platelets incubated with a fluorescein-conjugated polyclonal goat anti-human IgG. There was no significant binding of IgG aCL to intact resting or activated platelets, while significant specific binding to freeze-thawed platelets was demonstrated. These results question the theory that aCL bind/activate intact platelets in vivo.     

Successful surgery for an acute type A aortic dissection following repair of a descending thoracic aortic aneurysm

Acute type A aortic dissection in the presence of a previously repaired atherosclerotic descending thoracic aortic aneurysm is rarely reported. We experienced a patient who underwent an ascending aortic replacement with reconstruction of the aortic arch 16 months after repair of a descending thoracic aortic aneurysm. We succeeded in the redo operation with comprehensive techniques involving selective cerebral perfusion, deep hypothermia, early antegrade systemic circulation for cerebral protection, and femoro-femoral bypass with occlusion of the descending aorta for lower systemic perfusion as well as renal perfusion. The patient recovered and is doing well one year after the redo operation.     

Immuno-electron-microscopic localization of complements in amyloid fibrils of senile plaques

Summary The presence of components of immunoglobulins (Ishii et al. 1975) and complements (Eikelenboom and Stam 1982) in senile plaques suggests that the immunologic mechanisms are involved in the causation of pathologic processes in the brain of patients with Alzheimer's disease. Senile plaques consists of amyloid degenerated neuritis and glia, and exact localization of complements among these tissue elements will provide an important clue to the pathogenesis of the Alzheimer brain. This report deals with light- and electronmicroscopic localization of complements in amyloid fibrils of senile plaques by immunoperoxidase histochemistry. The presence of C_1q, C₄, and C₃ is confirmed light-microscopically. At the ultrastructural level, anti-complement C_1q, C₄, and C₃ peroxidase reaction products are exclusively localized on the amyloid fibrils, but no other tissue elements, such as normal or degenerated neurites, neurofibrillary tangles, or glia. The results indicate the presence of immune complex in amyloid fibrils of senile plaques, and little association of complements in senile plaques with neurofilament protein.Supported in part by a grant for the study of neurologic diseases from the Ministry of Health, Japan