Interactions of neurons and astrocytes during growth and development of human fetal brain in vitro.
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Biomedical subjects
Publications and source records attributed to B H Choi.
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Malignant atrophic papulosis (Kohlmeier-Degos disease) is reported for the first time with pathologic verification of central nervous system involvement in a child. The disease began in infancy with rare recurring skin lesions; the child died at the age of 7, after progressive neurologic deterioration. Diagnosis was suspected clinically and confirmed by biopsy of a typical skin lesion. Recognition of this disorder by its dermatologic manifestations may obviate invasive diagnostic procedures.
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Catecholamine (CA) containing neurons and processes of the putative locus coeruleus (LC) of human fetal brain have been identified by the use of a modified Falck-Hillarp fluorescence histochemical technique and have been examined by light and electron microscopy. Fetuses were received as surgical specimens following abortion by hysterotomy. Estimated gestational ages varied between 11 and 18 weeks. Small granular vesicles (SGV) ranging from 450 to 650 A and large granular vesicles (LGV) ranging from 700 to 1050 A were identified in variable numbers along with agranular vesicles in the cell bodies and processes of neurons in the LC of all fetal specimens examined by electron microscopy. The occurrence of SGV in association with green fluorescence within the LC of a 12-week-old human fetus suggests a relatively early ontogenetic development of a storage mechanism for CA within this nucleus.
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The specific activity of protein L-isoaspartyl methyltransferase, an enzyme implicated in the metabolism of damaged, isoaspartate-containing proteins, has been measured in postmortem samples of parietal cortex from 30 individuals (19 with Alzheimer's disease and 11 controls). Methyltransferase specific activity was positively correlated with age at death, increasing by 2.9 pmol/min/mg of protein for every ten years of age (r = .51, p less than 0.005). This correlation was significant in the control and Alzheimer's disease groups alike. Specific activity also appeared to be about 15% higher in females than in age- and diagnosis-matched males (p less than 0.05). No significant differences were observed between age- and sex-matched Alzheimer patients and controls, suggesting that a deficiency in this enzyme is not responsible for the accumulation of abnormal proteins in Alzheimer's disease.
A marked and significant reduction of protease nexin-1 (PN-1) and PN-2/amyloid beta protein precursor (A beta PP) was observed in selected regions of Alzheimer's disease (AD) brains as compared to those of aged-matched controls. Correlative analysis indicated a relationship between PN-1 reduction and the severity of pathologic alterations. A statistically significant inverse correlation was noted between the level of PN-1 activity and the density of tau-positive dystrophic neurites in the hippocampus. In view of the ability of thrombin and PN-1 activity to regulate neurite outgrowth, it is possible that abnormal thrombin and PN-1 interactions may play a role in dystrophic neurite formation. The presence of clusters of dystrophic neurites around the capillaries suggests that blood-brain barrier (BBB) dysfunction may enhance such abnormal interactions. The decrease in PN-2/A beta PP levels in AD brains could possibly contribute to neuronal degeneration in AD in view of the ability of PN-2/A beta PP to protect neurons against the toxic effects of the A beta.
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OBJECTIVE: To evaluate the effects of low-intensity ultrasound (LIUS) stimulation on the anabolic state of human cartilage from patients with osteoarthritis (OA). METHODS: Explant cultures of human OA cartilage were stimulated for 10 min every day for 7 consecutive days using continuous-wave sonication at a frequency of 1 MHz with spatial and temporal average intensities of 0 (control), 40, 200, 500, or 700 mW/cm2. The effects of LIUS on cell proliferation were evaluated by 3H-thymidine incorporation. Proteoglycan synthesis was evaluated by the incorporation of 35S-sulfate and by Safaranin O staining. Collagen synthesis was evaluated by 3H-proline incorporation and immunohistochemistry. RESULTS: At an intensity of 200 mW/cm2, LIUS treatment induced the expression of collagen type II and proteoglycan measured by the incorporation of radioactivity and specific staining of the cartilage explants. However, the expression decreased again at the higher intensities of 500 or 700 mW/cm2. Ultrasound had no stimulatory effect on cell proliferation at any intensity. CONCLUSION: LIUS has anabolic effects on human cartilage in explant cultures, indicating a potentially important method for the repair of osteoarthritic cartilage.
Detailed clinical and neuropathological studies have been made in two fullterm newborn human infants who were exposed to methylmercury in utero as a result of maternal ingestion of methylmercury-contaminated bread in early phases of pregnancy. High levels of mercury were detected in various regions of the brain at autopsy. Study of the brains revealed a disturbance in the development in both cases, consisting essentially of an incomplete or abnormal migration of neurons to the cerebellar and cerebral cortices, and deranged cortical organization of the cerebrum. There were numerous heterotopic neurons, both isolated and in groups, in the white matter of cerebrum and cerebellum and the laminar cortical pattern of the laminar cortical pattern of the cerebrum was disturbed in many regions as was shown by the irregular groupings and the deranged alignment of cortical. Prominent in the white matter of the cerebrum and the cerebellum was diffuse gemistocytic astrocytosis accompanied by an accumulation of mercury grains in their cytoplasm. These findings indicate a high degree of vulnerability of human fetal brain to maternal intoxication by methylmercury. A major effect appears to be related to faulty development and not to destructive focal neuronal damage as has been observed in mercury intoxicaiton in adults and children exposed postnatally.
The aim of this study was to investigate whether a new periodontal ligament attachment will form on titanium implants when they are implanted with cultured periodontal ligament cells. Periodontal ligament cells obtained from the teeth of 3 dogs were cultured and attached to the surface of titanium implants. The implants with the cultured autologous periodontal ligament cells were placed in the mandibles of the dogs. After 3 months of healing, histologic examination revealed that, on some implant surfaces, a layer of cementum-like tissue with inserting collagen fibers had been achieved. These results demonstrated that cultured periodontal ligament cells can form tissue resembling a true periodontal ligament around implants.