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41.
In the present case, a patient in whom limb apraxia and asymmetrical parkinsonism developed suggesting corticobasal degeneration, is reported. Neuropathologic examination revealed numerous tufted astrocytes in the precentral cortex in addition to the characteristic pathologic findings of PSP. Therefore, on the basis of clinicopathologic features, atypical progressive supranuclear palsy was diagnosed. In addition, the brain tissue of the present patient was investigated with an antibody specific for four‐repeat tau (4R‐tau). In the precentral cortex, numerous tau‐positive tufted astrocytes, pretangles, and threads were positive for 4R‐tau. Using a confocal microscopy we demonstrated that tufted astrocytes positive for 4R‐tau were adjacent to astrocytes positive for GFAP. The present findings suggest that accumulation of four‐repeat tau in astrocytes is a degenerative process rather than a reactive process.  相似文献   
42.
An 8-month-old boy had an anterior type of persistent hyperplastic primary vitreous in the right eye. Results of needle biopsy, performed because of elevated intraocular pressure, disclosed clusters of blastic cells. The eye was enucleated on the suspicion of retinoblastoma. Histological examination showed retrolental fibrovascular tissue and retinal dysplasia. Immunoreactive opsin was detected in the innermost structures and in photoreceptor-like cells of rosettes. We conclude that photoreceptor cells differentiated to express opsin, even when neighbouring cells were abnormally arranged. An immunocytochemical study of glial fibrillary acidic protein demonstrated glial proliferation in the inner layer of the retina but not in the preretinal space.  相似文献   
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Ptosis is known to be associated with thyroid disorders. We describe two biochemically corrected hypothyroid patients presenting with isolated bilateral ptosis. EMG of the orbicularis oculi showed continuous grouped motor unit potentials. In the absence of obvious aetiology, it is hypothesised that focal demyelination of terminal branches to the orbicularis oculi may play a role in the generation of the discharges.  相似文献   
46.
The present study attempted to construct the Japanese version of Revised Self-Monitoring Scale (Lennox & Wolfe, 1984). Factor analysis of this scale yielded two factors: 1) Sensitivity to expressive behavior of others, 2) Ability to modify self-presentation. This scale and its two factors had acceptable internal consistency: these results were almost similar with the original study. In correlational analyses with other personality measures, this scale correlated positively with both Private and Public Self-Consciousness Scale and Maudsley Personality Inventory-E Scale, but positively or negatively with some scales of Yatabe-Guilford Personality Inventory (e.g., G, S: positively. I, T: negatively.). Moreover the correlations between the two factors and the above mentioned measures provided interesting results. The availability of this scale was discussed.  相似文献   
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The lenses of ICR/f-strain rats with hereditary cataract were monitored in situ by laser Raman spectroscopy. The lenses used were within the age of 3-10 weeks before lens opacification became manifest. The reduction of protein SH group content and the increase of protein S-S bond content were observed in ICR/f rats in the precataractous stage. No significant change in the water content was observed.  相似文献   
49.
The antagonist pharmacology of glutamate neurotoxicity was quantitatively examined in murine cortical cell cultures. Addition of 1-3 mM DL-2-amino-5-phosphonovalerate (APV), or its active isomer D-APV, acutely to the exposure solution selectively blocked the neuroexcitation and neuronal cell selectively blocked the neuroexcitation and neuronal cell loss produced by N-methyl-D-aspartate (NMDA), with relatively little effect on that produced by either kainate or quisqualate. As expected, this selective NMDA receptor blockade only partially reduced the neuroexcitation or acute neuronal swelling produced by the broad-spectrum agonist glutamate; surprisingly, however, this blockade was sufficient to reduce glutamate-induced neuronal cell loss markedly. Lower concentrations of APV or D-APV had much less protective effect, suggesting that the blockade of a large number of NMDA receptors was required to acutely antagonize glutamate neurotoxicity. This requirement may be caused by the amplification of small amounts of acute glutamate-induced injury by subsequent release of endogenous NMDA agonists from injured neurons, as the "late" addition of 10-1000 microM APV or D-APV (after termination of glutamate exposure) also reduced resultant neuronal damage. If APV or D-APV were present both during and after glutamate exposure, a summation dose-protection relationship was obtained, showing substantial protective efficacy at low micromolar antagonist concentrations. Screening of several other excitatory amino acid antagonists confirmed that the ability to antagonize glutamate neurotoxicity might correlate with ability to block NMDA-induced neuroexcitation: The reported NMDA antagonists ketamine and DL-2-amino-7-phosphono-heptanoate, as well as the broad-spectrum antagonist kynurenate, were all found to attenuate glutamate neurotoxicity substantially; whereas gamma-D-glutamylaminomethyl sulfonate and L-glutamate diethyl ester, compounds reported to block predominantly quisqualate or kainate receptors, did not affect glutamate neurotoxicity. The present study suggests that glutamate neurotoxicity may be predominantly mediated by the activation of the NMDA subclass of glutamate receptors--occurring both directly, during exposure to exogenous compound, and indirectly, due to the subsequent release of endogenous NMDA agonists. Given other studies linking NMDA receptors to channels with unusually high calcium permeability, this suggestion is consistent with previous data showing that glutamate neurotoxicity depends heavily on extracellular calcium.  相似文献   
50.
Health risk appraisal (HRA) is a new health educational tool widely-used in the United States, which informs clients about how their health habits and lifestyles affect their probability of dying from potentially preventable causes and helps to motivate them to reduce their personal health risks. It personalizes mortality statistics and epidemiologic data by combining these data with a person's risk factors. We have got started the development of HRA for Japanese with reference to a new version of HRA named "Healthier People" revised by the Carter Center of Emory University and the Centers for Disease Control in the United States.  相似文献   
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