Low cerebrospinal fluid sugar syndromes.
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Biomedical subjects
Publications and source records attributed to L D Prockop.
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The effect of hyperbaric oxygenation (OHP) on survival and quality of survival of guinea pigs afflicted with experimental allergic encephalomyelitis (EAE) was investigated. EAE was induced in Hartley and Strain 13 animals by intradermal injections of whole guinea pig spinal cord in complete Freund's adjuvant. The inoculated animals were divided into control and treatment groups; the treated animals received OHP in a variety of treatment schedules. Clinical signs of EAE were quantitated and mean survival times were measured. When Hartley animals were exposed to 100% O2 at 2.5 atmospheres absolute (ATA) for 2 hr/day from 5--19 days postinoculation, the mean survival time (+/- SE) was 19.1 +/- 1.6 days relative to 15.7 +/- 0.7 days in the control (p less than 0.050). When Strain 13 guinea pigs were treated with 100% O2 at 2ATA for 4 hr/day on 5--16 days, the mean survival time was 21.6 +/- 0.6 days compared to 16.0 +/- 0.4 days for the control (p less than 0.001). Clinical sign measurements demonstrated that the onset of EAE in the treated animals of both strains occurred between 4--6 days after these signs became detectable in control animals. These results suggest that OHP therapy can ameliorate EAE in afflicted guinea pigs.
Epilepsy can be triggered by many unusual mechanisms. Some are exceedingly rare and bizarre, seemingly confined to one patient. This article reports the case of a 20-year-old woman who has had absence epilepsy for 11 years that is evoked by thinking or talking about driving an automobile. This stimulus consistently precipitated absence seizures, as defined by clinical and electroencephalographic criteria. An emotionally traumatic early childhood event may play a role in the triggering mechanism. A similar case has not been reported.
Seven men aged 17 to 22 years developed severe distal symmetrical predominately motor polyneuropathy after repeated inhalation of a commercially available brand of lacquer thinner. Motor nerve conduction velocities were markedly slowed. Fascicular biopsy specimens of sural nerve showed a striking loss of myelinated nerve fibers. Prominent neurofilamentous masses resulted insegmental paranodal distention of axons with secondary thinning and retraction of myelin from the node of Ranvier. Autopsy material from one case revealed central chromatolysis of anterior horn cells in the lumbosacral enlargement and axonal swellings in the fasciculus gracilis. One or more volatile hydrocarbons contained in the lacquer thinner involved may be neurotoxic if inhaled to excess any many cause a neuropathy with characteristic pathological features.
This study evaluates cerebral entry of mouse interferon alpha/beta (MuIFN alpha/beta) or mouse interferon gamma (MuIFN-gamma) following continuous (3 day), subcutaneous infusion of normal or glioma bearing mice. The intracerebral C57BL/6 mouse glioma-26 (G-26) model was used at days 10-14 post tumor implant, the advanced stage of glioma progression as defined by histology and the median survival time (27 +/- 3.8 days). The infusion of horseradish peroxidase (HRP) in vivo at day 10 or 11 post glioma implant showed strong staining in the tumor bed indicating compromised blood-brain barrier (BBB). In addition, histochemistry with Bandeiraea simplicifolia isolectin B4 demonstrated the accumulation and/or activation of macrophage/microglia. The 3 day infusion of mice (day 11-14 post tumor implant) via subcutaneous (sc) osmotic micro-pumps with MuIFN alpha/beta (8x10(5) - 1.7x10(6) international units [IU]/ml) or with recombinant mouse interferon gamma (rMuIFN-gamma) (1x10(6) IU/ml) resulted in a low but detectable (1-5 IU/ml) cerebral level of IFN. The IFN levels in the blood (20-40 IU/ml) and brain, measured by assay of inhibition of viral cytopathic effect (CPE) or ELISA assay for MuIFN-gamma, showed no difference between normal and glioma bearing mice. The lipoxygenase (LO) activity (dioxygenase) of glioma tissue and contralateral control was evaluated in non-treated and MuIFN alpha/beta continuously (3 day) treated mice. The LO activity in glioma tissue was significantly higher (p < 0.05) than the contralateral control in non-treated mice. However, following sc MuIFN alpha/beta infusion the LO activity of glioma decreased to control level.
The in vitro effect of ascorbyl esters (ascorbyl-stearate [As-S] and -palmitate [As-P]) and interferon (recombinant human interferon-a2b [rHuIFN-a2b]) on human glioma (U-373) cell proliferation, viability and glutathione-S-transferase (GST) activity was studied. The effect of As-S, As-P and rHuIFN-a2b on cell proliferation and viability was evaluated by [3H] Thymidine incorporation and colorimetric MTT assays, respectively. Incubation of glioma cells with As-S, As-P or rHuIFN-a2b for 24 h resulted in a dose dependent inhibition of cell proliferation (IC50 = 68.0 microM As-S, 86.0 microM As-P and 47.3 Units/ml rHuIFN-a2b), and moderate decrease of cell viability. It was found that As-S was a more efficient inhibitor of cell proliferation, viability and GST activity than As-P. GST from U-373 cells was purified. The activity of purified GST towards 1-chloro-2,4-dinitrobenzene (CDNB) was inhibited in a dose dependent manner by ascorbyl esters (I-50 = 27.5 microM As-S and 56.0 microM As-P) but not by rHuIFN-a2b. GST activity of cytosol isolated from U-373 cells which were previously treated with As-S (150 microM) or rHuIFN-a2b (150 units/ml) for 0, 2, 5, 10, 20 and 30 min was sharply decreased during 5 to 10 min of treatment and increased at longer durations of treatment.
The effect of mouse interferon-alpha/beta (MuIFN-alpha/beta on growth/viability, cell cycle regulation, 5-lipoxygenase (5-LO) protein expression, leukotriene B4 (LTB4) biosynthesis and glial fibrillary acidic protein (GFAP) expression of mouse glioma (G-26) cells in vitro was studied. The G-26 cells were treated with 800 IU/ml of MuIFN-alpha/beta for 1, 2, 3 and 4 days. The growth and viability of glioma cells was evaluated by [3H]-thymidine incorporation and MTT (3(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazoliumbromi de) assay, resulted in a time dependent decrease in [3H]-thymidine incorporation into DNA and MTT formazan formation, respectively. The cell cycle regulation measured by flow cytometry with propidium iodide staining revealed that the cell multiplication cycle was slowed down due to accumulation of cell in S-phase of the cell cycle, leading to inhibition in G0/G1 phase of the cell cycle. The 5-LO protein expression (measured by Western immunoblot analysis) and LTB4 biosynthesis (measured by enzyme immunoassay) were found to be increased by 2 to 2.4 fold and several fold respectively on days 3 and 4 of MuIFN-alpha/beta treatment. The GFAP protein expression was also found to be increased at least by 3 fold on day 4 of the MuIFN-alpha/beta treatment. These results suggest that inhibition in growth and thereby slowing of the cell multiplication cycle of glioma cells has resulted in upregulation of GFAP expression and 5-LO pathway.