[Visual-speech disconnexion syndrome of the right visual cortex after transection of the splenium of the corpus callosum].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Iwata.
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.
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.
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.
The widespread N18 potential in median nerve SEP was studied in normal subjects and in patients with high cervical, brain-stem and thalamic lesions who had profound disturbances of deep sensation. N18 was well identified in the HSi-CV2 derivation in every normal subject as a broad elevation from the baseline lasting about 20 msec. The cortical N20 was absent in all patients. N18 was absent in a patient with a dorsal column lesion at C1-2 level. The amplitude and configuration of N18 were normal in all other patients with brain-stem and thalamic lesions, including a patient with a lesion at the ponto-medullary junction. The sagittal distribution of N18 was studied in a patient with a thalamic lesion and an oblique distribution with the maximum region between Cz and nasion was demonstrated. The present results indicate that at least the greater part of N18 is generated at the caudal most brain-stem or through branches from this level. Taking previous animal and intraoperative studies into consideration, we think it most probable that the main part of N18 corresponds to the ventro-rostral negative pole of the dipolar potential generated at the cuneate nucleus by the primary afferent depolarization of presynaptic terminals of dorsal column fibers.
Explore the source record for details and available documents.
PURPOSE: Interferon (IFN)-gamma induces major histocompatibility complex (MHC) class II and intercellular adhesion molecule-1 (ICAM-1) expression on human corneal epithelial (HCE) cells. So far, it has not been clarified whether both inductions by IFN-gamma use the same signal transduction pathway. Therefore, in the present study, we tried to determine the significance of the protein tyrosine kinase (PTK)-dependent signaling pathway in the induction of both MHC class II and ICAM-1 expression by IFN-gamma in cultured HCE cells. METHODS: Cultured HCE cells were treated with human recombinant IFN-gamma. The induction of protein tyrosine phosphorylation of proteins including PTKs, janus kinase (JAK)1, and JAK2, was examined by Western blotting and immunoprecipitation. The effects of treatment of HCE cells with specific PTK inhibitors on IFN-gamma-induction of MHC class II and ICAM-1 expression were examined by flow cytometry. RESULTS: IFN 1 (Interferon) induced tyrosine phosphorylation of multiple substrates, particularly that of 75,000; 90,000; 130,000; and 160,000 molecular weight proteins including JAK1 and JAK2 in cultured HCE cells. The PTK inhibitors, herbimycin A and genistein, inhibited tyrosine phosphorylation of those proteins. Also, these PTK inhibitors prevented IFN-gamma-induction of MHC class II synthesis and surface expression. However, neither herbimycin A nor genistein had any effect on IFN-gamma-induction of ICAM-1 expression. CONCLUSIONS: Tyrosine phosphorylation of proteins including JAK1 and JAK2 is essential for IFN-gamma-induction of MHC class II expression, but not critical for that of ICAM-1 expression in cultured HCE cells. In addition, it is suggested that the IFN-gamma-induction of MHC class II requires PTK activities not only in the primary JAK-signal transducers and activators of transcription (STAT) pathway but also in the subsequent pathway mediated by IFN-gamma-induced intermediate proteins.
Explore the source record for details and available documents.
The purpose of this study was to determine whether the force of a finger could be measured with a new system based on an attachment to the Kin-Com dynamometer, and to define the reproducibility of the finger force measurement. Eleven male subjects (age, 27.6 +/- 6.12 years) took part. All were free of orthopedic problems in the tested hand. Mean forces of the index and little finger for concentric and eccentric motion were measured using the new system. Overall coefficients of variation (OCVs) were calculated as an index of reproducibility. The reproducibility of force curves was considered good when an OCV was less than 20%. The OCVs for mean force of the index finger and for eccentric motion of the little finger were less than the 20% standard, at 10.7 and 14.0, respectively. The OCV for concentric motion of the little finger was greater than 20%. The findings suggest that measurement of finger force is feasible with the new Kin-Com attachment.
Pattern reversal visual evoked potentials (PVEPs) were recorded in 20 patients with migraine with aura (MA), 19 patients with migraine without headache (migraine equivalent; ME) during interictal periods, and 34 normal subjects. All migraine patients had hemianopsia or fortification spectra during attacks. In both MA and ME patients of less than 49 years of age, there were significant (p<0.01) differences in amplitude of PVEPs at the mid-occipital and contralateral to visual aura electrode sites compared to normal subjects. Amplitude of PVEPs in MA and ME showed significant (p<0.001) increases when recorded soon after attacks, especially within 10 days. There was a significant (p<0.01) correlation between percentage asymmetries and the duration of illness in both MA and ME. We conclude from our PVEP findings that cortical spreading depression remains the most likely explanation for the migraine visual aura.