A simple method for maintaining neurons in vitro.
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Biomedical subjects
Publications and source records attributed to M L Grunnet.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Germinal plate hemorrhage with intraventricular rupture has been a leading cause of morbidity and mortality among premature neonates. Because germinal plate hemorrhage decreases with increasing gestational age, germinal plate vessel size and/or structure may be an important etiologic factor. Electron micrographs of the cortical and germinal plate blood vessels from 13 premature infants ranging in age from 19-37 weeks gestation were studied; vessel, lumena, and endothelial areas were measured using a digitizing tablet. In infants between 25-32 weeks gestation, the germinal plate vessel and lumenal areas were significantly greater than the areas of cortical vessel and lumena. This finding suggests that one of the factors involved in germinal plate hemorrhage is described by LaPlace's law which states that the larger the vessel diameter, the greater the pressure on the vessel wall.
The ultrastructural changes produced by Mesoridazine and Nortriptyline in neurons and glia in vitro are reported. Concentrically laminated bodies (CLB) and increased numbers of dense bodies were produced by exposure to these drugs. The number and complexity of the CLB increased with increased dose and longer time in vitro and their formation appeared to be reversible.
Cerebrovascular insufficiency in infancy and childhood is well documented and has a diverse and often unknown etiology. Reported here is a polycythemic, microciphalic infant girl of 43 week's gestation with bilateral cerebral infarction occurring in the perinatal period. Infarction was the result of bilateral carotid artery stenosis produced by massive reduplication of the internal elastic lamina. Review of the literature failed to reveal any reports of similar arterial lesions. The angiographical picture was also unique. The etiology of this unusual defect is not known, but we believe the problem was congenital perhaps due to an intrauterine infectious process.
BACKGROUND: The ability to predict treatment responsiveness and survival of patients with glioblastoma multiforme, the most malignant and most common primary brain tumor, would be a valuable asset. Tumor and proliferation markers such as p53 and PCNA have been immunohistochemically defined and have been useful in other tumors in determining prognosis. Therefore, the authors studied the correlation of responsiveness to treatment, time to progression and survival with p53 and PCNA labeling indices in a pre-irradiation chemotherapy study of the glioblastoma multiforme. METHODS: Immunohistopathology for labeling indices for p53 and PCNA using formalin-fixed, paraffin-embedded tissue from the glioblastomas of 23 patients entered into a phase II ECOG trial of pre-irradiation chemotherapy were defined using the streptavidin-peroxidase technique with AEC chromogen. The labeling indices were correlated with response to treatment time to progression and overall survival. Most patients received three cycles of BCNU for three days over three months and cisplatin monthly for three days over three months prior to external beam irradiation. RESULTS: There were no significant differences in treatment response, time to progression or overall survival in glioblastoma, patients with positive p53 labeling index (> 5%) versus a negative p53 labeling index (< or = 5%) or positive PCNA labeling (> 10%) versus a negative labeling index (< or = 10%) or any combination of P53 and PCNA labeling indices. CONCLUSIONS: Using this protocol of pre-irradiation chemotherapy, p53 and PCNA labeling indices in the glioblastoma multiforme did not predict treatment benefit.
Intraventricular hemorrhage (IVH) and classical periventricular leukomalacia complex are considered the two most common forms of perinatal anoxic-ischemic brain injury. However, recently, a third entity, the periventricular leukomalacia complex (PLC) was described and was seen in 31 percent of 61 premature infants coming to autopsy from the University of Connecticut Neonatal Intensive Care Unit (NBIC) and in several other centers. Periventricular leukomalacia complex consists of necrotizing lesions of the periventricular white and grey matter, hippocampus and subiculum, cerebellum and basis pontis. The clinical course of PLC is similar to that of IVH, but it is important to differentiate PLC as the widespread nature of these lesions may lead to a poor neurological outcome.