Search PubMed⌕ Search

Biomedical subjects

S Takemori

Publications and source records attributed to S Takemori.

167 records · Page 10Linked to original sources
PubMedDate not supplied

Adrenal activation of carbon tetrachloride: role of microsomal P450 isozymes.

Previous investigations demonstrated that carbon tetrachloride (CCl4) was activated by adrenal microsomes, resulting in various functional changes and ultimately in necrosis of the zona reticularis of the gland. Experiments were done to identify the adrenal P450 isozyme(s) involved in the bioactivation of CCl4. Incubation of microsomes from the zona reticularis (ZR) of the guinea pig adrenal cortex with CCl4 plus NADPH caused initiation of lipid peroxidation, covalent binding of CCl4-derived radioactivity to protein, and degradation of cytochrome(s) P450. Preincubation of the microsomal preparations with inhibitory antibodies to P450(17 alpha) or P450C21 decreased the corresponding enzyme activities (17 alpha-hydroxylation and 21-hydroxylation), but did not affect the activation of CCl4. 1-Aminobenzotriazole (ABT), a suicide inhibitor of some P450 isozymes, decreased the enzyme activities catalysed by an adrenal 52,000 Da (52 kDa) isozyme, but had no effect on the function of P450(17 alpha) or P450C21. However, ABT completely inhibited the CCl4-induced LP and covalent binding in adrenal microsomes. The results indicate that adrenal CCl4 activation is catalysed by the 52 kDa P450 isozyme and not by the steroid hydroxylases. Localization of the 52 kDa isozyme to the ZR probably accounts for the selective necrosis of this region of the gland by CCl4.

Adrenal Cortex↗
PubMedDate not supplied

Visual suppression of vestibular nystagmus after cerebellar lesions.

Visual suppression of calorically induced vestibular nystagmus was observed following discrete lesions of various structures in the cerebellum. Unilateral lesions of the flocculus resulted in a complete loss or a significant reduction in visual suppression when the quick phase of the nystagmus was directed to the ipsilateral side of the lesions, and bilateral flocculus lesions caused a bilateral loss of suppression. Nodulus lesions resulted in a loss of suppression, and this loss tended to recover in time. Lesions of the dentate nucleus resulted in a very short term loss of suppression. Extirpation or lesions of the uvula, vermis, para-flocculus, cerebellar cortex, or the fastigial or interpositus nuclei had no observed effect on the visual suppression of vestibular nystagmus. The results of this study suggest that the flocculus and nodulus function as intermediators through which the visual system can modify or alter vestibular reflexes. Also, this phenomenon, that is, loss of visual suppression after the flocculus and nodulus lesion, is very useful to diagnose the localized lesion in the cerebellum.

Animals↗
PubMedDate not supplied

Visual suppression test.

Visual suppression of caloric nystagmus was studied in normal adults and in 98 clinical cases in order to justify the application of the procedure as a clinical test. The maximum slow phase velocity during ten seconds in darkness and the slow phase velocity during ten seconds in light were taken from the recordings and measured. The mean values of these slow phase velocities were calculated and the mean slow phase velocity in darkness was assigned a value of 100%. The value which the slow phase velocity in light subtracts from the slow phase velocity in darkness, represents the visual suppression. It was determined that visual suppression of the slow phase velocity of caloric nystagmus was 48 +/- 10% in 22 normal adults. This was caused by the visual fixation mechanisms. Cases in which lesions were diagnosed in the cerebellum, such as spinocerebellar degeneration and cerebelitis, showed reduced or abolished visual suppression. The lesion side can be determined by this test. Compensation following unilateral sudden loss of inner ear function can be measured by the visual suppression test.

Adult↗