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Takashi Uehara

Publications and source records attributed to Takashi Uehara.

5 recordsLinked to original sources

Immobilization stress-induced increment of lactate metabolism in the basolateral amygdaloid nucleus is attenuated by diazepam in the rat.

Using in vivo microdialysis technique, extracellular lactate levels were measured in the basolateral amygdaloid nucleus of the rat under immobilization stress. Immobilization stress (40 min) led to a tetrodotoxin-reversible increase in dialysate lactate levels. Diazepam (1.0 mg/kg, i.p.) reduced the ability of immobilization stress to increase lactate levels. Furthermore, the attenuation of the immobilization stress-induced increase of lactate levels by diazepam was antagonized by pretreatment with flumazenil (15 mg/kg, i.p.), a selective antagonist at benzodiazepine receptors. These findings suggest that immobilization stress increases lactate levels in rat basolateral amygdaloid nuclei, which is attenuated by stimulation of benzodiazepine receptors.

Amygdala↗

Correlation between delayed neuronal cell death and selective decrease in phosphatidylinositol 4-kinase expression in the CA1 subfield of the hippocampus after transient forebrain ischemia.

Transient forebrain ischemia induces a delayed neuronal death in the CA1 area of the hippocampus. However, the mechanism leading to this phenomenon has yet to be established. The authors used an mRNA differential-display method to isolate genes for which mRNA levels change only in the hippocampus during ischemia/reperfusion. They succeeded in identifying the product of one down-regulated gene as phosphatidylinositol 4-kinase (PI 4-K). Compared with control levels, PI 4-K mRNA expression in the hippocampus, but not the cerebral cortex, was significantly decreased by 30% and about 80% 1 and 7 days after ischemia/reperfusion, respectively. Interestingly, PI 4-K and PI bisphosphate levels were selectively decreased in the CA1 region, but not other regions, whereas TUNEL-positive cells could be detected 3 days after ischemia. Consistent with these results, PI 4-K expression was suppressed by hypoxia in SK-N-MC neuroblastoma cells before loss of cell viability. Overexpression of wild-type PI 4-K, but not the kinase-negative mutant of PI 4-K (K1789A), recovered the loss of viability induced by hypoxia. These findings strongly suggest that a prior decrease in PI 4-K and PI bisphosphate levels caused by brain ischemia/hypoxia is partly involved in delayed neuronal cell death.

1-Phosphatidylinositol 4-Kinase↗

Dumbbell C2 schwannomas involving both sensory and motor rootlets: report of two cases.

OBJECTIVE AND IMPORTANCE: Intradural-extradural dumbbell C2 schwannomas are rare. This report concerns two such cases with the intradural compartment located ventral to the spinal cord and involving both sensory and motor rootlets. CLINICAL PRESENTATION: One patient was a 57-year-old woman with sensory disturbances in the right extremities and hyperreflexia in the left extremities. The other patient was a 73-year-old man who presented with tetraparesis, walking disability, atrophy of the nuchal and bilateral shoulder muscles, and pain in the right C2 dermatome. INTERVENTION: The extradural component of the tumor was removed first; next, the intradural component was removed successfully via the posterior approach combined with a C1-C2 laminectomy. The patients experienced symptomatic improvement without further deficits except for sensory impairment of the C2 dermatome in one of the patients. CONCLUSION: Intradural-extradural dumbbell C2 schwannomas can be satisfactorily managed with a posterior approach. Removal of the extradural component and opening of the dural ring of the C2 nerve root are necessary for safe extraction of the intradural ventrally located component after debulking. These tumors may arise extradurally within the nerve sheath, extend intradurally and ventrally toward the spinal cord, and involve both sensory and motor rootlets.

Aged↗

Role of ubiquilin associated with protein-disulfide isomerase in the endoplasmic reticulum in stress-induced apoptotic cell death.

Up-regulation of several stress proteins such as heat-shock proteins and glucose-regulated proteins participate in tolerance against environmental stress. Previously, we found that protein-disulfide isomerase (PDI) is specifically up-regulated in response to hypoxia/brain ischemia in astrocytes. In addition, the overexpression of this gene into neurons protects against apoptotic cell death induced by hypoxia/brain ischemia. To address the detailed function of PDI, we screened for proteins that interact with PDI using the yeast two-hybrid system. We report here that PDI interacts with ubiquilin, which has a ubiquitin-like domain and a ubiquitin-associated domain. Interestingly, ubiquilin is also up-regulated in response to hypoxia in glial cells with a time course similar to that of PDI induction. In hypoxia-treated glial cells, the endogenous ubiquilin and PDI were almost completely co-localized, suggesting that ubiquilin is an endoplasmic reticulum-associated protein. Overexpression of this gene in neuronal cells resulted in significant inhibition of the DNA fragmentation triggered by hypoxia, but not that induced by nitric oxide or staurosporine. Moreover, ubiquilin has the ability to attenuate CHOP induction by hypoxia. These observations suggested that ubiquilin together with PDI have critical functions as regulatory proteins for CHOP-mediated cell death, and therefore up-regulation of these proteins may result in acquisition of tolerance against ischemic stress in glial cells.

Adaptor Proteins, Signal Transducing↗

[The frequency profiles of size of two-step tuberculin skin tests with histories of BCG vaccinations and tuberculin tests among hospital employees].

In 1998, Prevention Committee of the Japanese Society for Tuberculosis announced guidelines for dealing with nosocomial tuberculosis infections. These guidelines recommended the two-step tuberculin tests (TST) as baseline data for each medical employee when they started to work. If accurate records of previous TSTs are available in addition to baseline data, they are useful to evaluate the presence of tuberculosis infection when they started to work. We therefore studied the frequency profile of size of TST among medical employees in INBA-HITEC Medical Center and discussed methods to improve investigative measures for tuberculosis infection, and prior to skin testing we asked self-reporting questionnaires regarding history of previous BCG vaccinations and TSTs. We expected that their records of previous TSTs were accurately preserved, however, records of previous TSTs reported by medical employees were found to be inaccurate. From two-step TSTs results, the magnitude of booster phenomenon was defined by diameter of erythema and induration. Results demonstrated that the increase of induration size was larger in subjects > or = 41-years-old than in subjects < 41-years-old. Regarding booster phenomenon, no statistically significant differences were detected according to type of duty post. Many subjects with size of TST erythema > or = 30 mm on the first test showed increase erythema > or = 10 mm on the second test. We therefore suggest that the second test be made for those showing reaction size > or = 30 mm on the first test.

Adult↗