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Biomedical subjects

M Oishi

Publications and source records attributed to M Oishi.

At least 109 records · Page 6Linked to original sources
PubMed1997

Difference in P300 latency in two types of leukoaraiosis.

P300 examination was performed in patients with periventricular leukoaraiosis and in patients with leukoaraiosis in the centrum semiovale. Ten patients with periventricular leukoaraiosis, ten patients with leukoaraiosis in centrum semiovale and ten age-matched controls without leukoaraiosis were studied. The P300 was measured with an evoked potential recorder using an oddball paradigm. The mini-mental state examination score was significantly lower and the P300 latency was significantly longer in the leukoaraiosis in the centrum semiovale group than in the periventricular leukoaraiosis group and the control group. Leukoaraiosis in centrum semiovale may be related to dementia and the prolongation of P300 latency.

Aged↗
PubMed1997

Cerebral blood flow and cerebrovascular response to acetazolamide in patients with chronic alcoholism.

Cerebral blood flow and cerebrovascular response to acetazolamide were studied in 12 patients with chronic alcoholism and 12 age matched healthy controls. Blood flows in the cerebral cortex, thalamus, and putamen were significantly lower in the chronic alcoholic group than in the healthy control group. The increase in blood flow caused by acetazolamide did not show any significant difference between the two groups. These findings suggest that the decreased cerebral blood flow in chronic alcoholism is due to decreased cerebral metabolism.

Acetazolamide↗
PubMed1997

Cerebral blood flow in single and multiple lacunar infarctions.

BACKGROUND AND PURPOSE: Single and multiple lacunar infarctions may have some difference in underlying diseases and cerebral blood flows. To determine the difference, we investigated underlying diseases and cerebral blood flows in single and multiple lacunar infarctions. METHODS: Fifteen cases of lacunar infarction, 10 cases of multiple lacunar infarctions, and 16 control subjects were studied. Regional cerebral blood flow was measured within 14 days after stroke onset with the stable xenon CT method. RESULTS: The rate of association of diabetes mellitus was higher in the multiple lacunar infarctions group than in the single lacunar infarction group. The blood flow in the cerebral cortex was significantly lower in the multiple lacunar infarctions group than in the single lacunar infarction group. The blood flow change by acetazolamide in the cerebral cortex was significantly lower in the multiple lacunar infarctions group than in the single lacunar infarction group. CONCLUSIONS: There is some difference in underlying diseases and cerebral blood flows between single and multiple lacunar infarctions.

Acetazolamide↗
PubMed1997

Movement-related cortical potentials and contingent negative variation in olivopontocerebellar atrophy.

Movement-related cortical potentials (MRCPs) and contingent negative variation (CNV) were recorded in 8 cases of olivopontocerebellar atrophy (OPCA) and 8 age-matched healthy controls. The amplitude of the negative slope (NS') was smaller in the OPCA group than in the healthy control group. The amplitude of late CNV was smaller in OPCA group than in the healthy control group. These abnormalities in MRCPs and CNV were improved by intravenous infusion of thyrotropin releasing hormone.

Aged↗
PubMed1997

Japanese experience with micropremies weighing less than 600 grams born between 1984 to 1993.

The viability limit defined by the Japanese Eugenic Protection Act was amended from 24 to 22 completed weeks of gestation in 1991. To testify if the amendment is appropriate, we conducted a survey on the mortality and morbidity rates of infants less than 600 g born in Japan between 1984 to 1993. Questionnaires were mailed to 205 hospitals with neonatal intensive care units (NICUs) and 165 (80%) responded. Of 1655 infants <600 g birth weight and admitted to the NICUs included in this survey, 457 (28%) survived to hospital discharge. The survival rates of infants born <24 weeks and >==24 weeks of gestation were 17% (128/748) and 36% (329/903), respectively; and of infants <500 g and 500 to 599 g at birth were 16% (82/510) and 32% (375/1145), respectively. None of the infants <==20 weeks of gestational age and <==350 g at birth survived, but 4% (2/49), 12% (27/218), 21% (99/474), and 34% (131/381) born at 21, 22, 23, and 24 weeks of gestation survived, respectively. The majority (68%) died within 1 week after birth and only 10% died after the neonatal period. The main causes of death were: acute respiratory failure (33%), intraventricular hemorrhage (20%), infection (16%), and heart failure (10%). Of 457 survivors, 65% were free from handicaps. The incidence of mental retardation (DQ < 70), visual disturbance, and CP were 15%, 14%, and 11%, respectively. Admission of micropremies to NICU increased markedly after the amendment of the Eugenic Protection Act, despite a marked decline in birth rate. The survival rate increased from 22% to 33% after generalized use of surfactant in 1988, but the handicap rate (35%) among survivors remained unchanged. The new viability limit of 22 complete weeks of gestation was feasible, since survival of less than 22 weeks was exceptional while survival of 22 to 23 weeks was 18%.

Cause of Death↗
PubMed1997

Histological comparison of early wound healing following dense hydroxyapatite granule grafting and barrier placement in surgically-created bone defects neighboring implants.

The purpose of this study was to examine early wound healing following grafting of dense hydroxyapatite granules (HA granules) and barrier placement in surgically-created bone defects surrounding implants. Eight healthy adult dogs with an average weight of 15 kg were used in this study. Thirty-two bone defects measuring 4 mm x 4 mm were removed with a surgical bur to form continuous bucco-lingual bone defects and 32 implants (16 titanium [Ti]) and 16 hydroxyapatite-coated [HA]) were then placed into the defects. Four implant groups were created: 1) grafting HA; 2) covering with an expanded polytetrafluoroethylene (ePTFE) membrane; 3) grafting HA and covering with ePTFE membrane; and 4) control (no treatment). Animals were sacrificed 28 days after surgery. Histological sections revealed large amounts of newly-formed bone in all bone defects surrounding the implants treated with ePTFE membranes alone. Fibrous encapsulation of HA granules was observed in the defects of the HA granules grafting group. In the group with grafting of HA granules and covering with ePTFE membranes, small amounts of bone tissue were observed among HA granules, but most HA granules were surrounded with fibrous tissue. Bone defects were completely filled with connective tissue in the control group. There were no differences in the histological findings between Ti and HA-coated implants in all cases. Histomorphometric data disclosed that the presence of HA granules in the bone defects significantly arrested bone formation. Our study suggests that the grafting of dense HA into bone defects surrounding implants will result in fibrous healing during the early healing stage.

Alveolar Bone Loss↗
PubMed1997

Failing hollow implants examined by light microscopy and image processing.

The purpose of this study was to evaluate the radiologic, histologic, and histometric findings of three failing hollow implants. On periapical radiographs, these implants showed vertical bone loss up to the hollow portion around the implant. Examination of the histologic sections disclosed that the hollow portions of all the implants were almost filled with bone tissue, although slight bone resorption and presence of granulation tissue infiltrated with inflammatory cells was observed coronal to the hollow portion. Histometric analysis disclosed that the average percent bone contact was 93.1% in case 1, 90.9% in case 2, and 84.3% in case 3 and the average percent bone filling was 42.1%, 50.5%, and 33.8%, respectively. Consequently, there seems to be some potential for successful treatment of these implants because the destructive changes were limited to the coronal aspects of the implant.

Alveolar Bone Loss↗
PubMed1997

Abscess formation around a hydroxyapatite-coated implant placed into the extraction socket with autogenous bone graft. A histological study using light microscopy, image processing, and confocal laser scanning microscopy.

The purpose of this study was to evaluate the radiologic, histologic, and histometric findings for a retrieved hydroxyapatite (HA)-coated implant which had been placed into a fresh extraction socket with autogenous bone graft 3 months previously. A periapical radiography disclosed a vertical bone loss around the implant cervix. Examination of histologic section disclosed that granulation tissue including bone chips around the cervix, and newly-formed bone tissue around the grafted bone tissue on the HA coated surface. In the confocal laser scanning microscopic findings toluidine blue-negative bone tissue showed autofluorescence. Histometric analysis indicated that the average percent bone contact was 29.2% (ranged 26.4% to 34.1%). Suspected reasons for failure were an early exposure of the barrier membrane, its early removal, the implant placement into an infected site, inadequate antibiotic premedication, and/or poor control of infections around teeth prior to implant surgery and around implants before and after placement of barrier membrane.

Abscess↗
PubMed1997

A candidate case for lymphocytic infundibulo-neurohypophysitis mimicking a neurohypophysial tumor.

A 56-year-old Japanese man presented with a 2-month duration of polyuria and polydipsia. The diagnosis of diabetes insipidus was confirmed by water deprivation and vasopressin injection. The secretory function of the adenohypophysis was estimated as normal by a variety of provocative tests. Magnetic resonance imaging (MRI) displayed the loss of the hyperintense signal of the neurohypophysis and a tumor-like lesion confined to the neurohypophysis. The tissue specimen resected at transsphenoidal surgery showed diffuse lymphocytic infiltration. These findings suggest that this is a candidate case for lymphocytic infundibuloneurohypophysitis (LIN) that is not identical to classical lymphocytic hypophysitis. This patient will be followed up to determine whether this case simply represents an early stage of classical hypophysitis or a different clinical entity.

Diabetes Insipidus↗
PubMed1997

P300 and cerebral blood flow before and after TRH in olivopontocerebellar atrophy.

Ten cases of olivopontocerebellar atrophy (OPCA) (mean age 56 +/- 9 years) and 8 healthy controls (mean age 58 +/- 9 years) were studied. The P300 was measured with a Synax 1100 evoked potential recorder and the regional cerebral blood flow was measured using the stable xenon computed tomography method. The P300 latency was significantly longer in the OPCA group than in the healthy control group. The P300 latency after the intravenous infusion of thyrotropin releasing hormone (TRH) in the OPCA group was significantly shorter than that before the intravenous infusion of TRH. The blood flows in all the measured areas (the cerebellar cortex, the cerebellar white matter, the brainstem, the thalamus, the basal ganglia, the frontal lobe cortex and the frontal lobe white matter) were significantly lower in the OPCA group than in the healthy control group. The blood flows in the cerebellar cortex and in the frontal lobe cortex after the intravenous infusion of TRH were significantly higher than those before the intravenous infusion of TRH. The prolongation of P300 latency in the OPCA group suggests that subclinical disturbance in recognition function is present in OPCA and may be related to the blood flow decrease outside the cerebellum.

Aged↗
PubMed1997

The cytoplasmic domain of Alzheimer's amyloid precursor protein is phosphorylated at Thr654, Ser655, and Thr668 in adult rat brain and cultured cells.

BACKGROUND: The cytoplasmic domain of the Alzheimer's disease amyloid precursor protein (APP) is phosphorylated in vitro at Thr654 and Ser655, and both in vitro and in intact cells at Thr668 (numbering for APP695 isoform). MATERIALS AND METHODS: We have developed phosphorylation state-specific antibodies to each of the sites, and we have used these to analyze the phosphorylation of APP in adult rat brain and in cultured cell lines. RESULTS: We demonstrate that all three sites in APP are phosphorylated in adult rat brain. Phosphorylation at Thr654, Ser655, and Thr668 was also observed in several cultured cell lines. In PC12 cells, phosphorylation at Ser655 was increased more than 10-fold by treatment with okadaic acid, a specific inhibitor of protein phosphatases 1 and 2A, but was not affected by activators of protein kinase C. In HeLa cells, phosphorylation at Thr668 was regulated in a cell cycle-dependent manner with near-stoichiometric phosphorylation being observed at the G2/M phase of the cell cycle. In general, phosphorylation at Ser655 was found to be highest in mature APP isoforms, whereas phosphorylation of Thr668 was highest in immature APP isoforms in cultured cells. CONCLUSIONS: The results demonstrate that phosphorylation of the cytoplasmic domain of APP occurs at Thr654, Ser655, and Thr668 under physiological conditions. The further characterization of APP phosphorylation using phosphorylation-specific antibodies may help in the elucidation of the biological function of APP.

Alzheimer Disease↗
PubMed1996

Expression of the protein tyrosine phosphatase beta2 gene in mouse erythroleukemia cells induces terminal erythroid differentiation.

We have cloned cDNA for protein tyrosine phosphatase beta2, which had been implicated in erythroid differentiation of mouse erythroleukemia cells. Expression of cDNA constructs, in which beta2 cDNA is placed under the control of mouse metallothionein-I promoter, by ZnCl2 converted a significant portion (20 to 38%) of the cells to erythroid-like cells, which is 25-50% of the erythroid differentiation efficiency observed by conventional erythroid-inducing agents. Furthermore, introduction and expression of altered protein tyrosine phosphatase beta2 cDNA constructs designed to produce the enzyme lacking the phosphatase activity inhibited erythroid differentiation by 100-20%, depending upon the concentration of erythroid-inducing agents employed. These results strongly suggest that protein tyrosine phosphatase beta2 is involved in triggering erythroid differentiation in mouse erythroleukemia cells.

5-Aminolevulinate Synthetase↗
PubMed1996

In vitro transcription of a poly(dA) x poly(dT)-containing sequence is inhibited by interaction between the template and its transcripts.

Transcription of poly(dA) x poly(dT)-containing sequences was investigated in vitro using plasmids carrying a (dA)34 x (dT)34 tract in the coding region of the lacZ gene. The efficiency of transcription of the (dT)34 sequence on the transcribing strand by Escherichia coli RNA polymerase was substantially lower (approximately 60%) than that of the (dA)34 sequence or of the control lacZ gene. Analysis of the transcription process of the (dT)34 sequence by T3 RNA polymerase showed that the transcription was frequently arrested or terminated at the middle as well as immediately proximal of the (dA)34 x (dT)34 tract, and it occurred more prominently following accumulation of transcription products. This inhibition was strongly enhanced by the addition of the oligonucleotide (dT)34 or poly(U) to the reaction mixture, while (dA)34 and the duplex (dA)34 x (dT)34 suppressed the inhibition. A similar transcriptional inhibition was also observed in transcription mediated by T7 RNA polymerase and eukaryotic RNA polymerase II. We also demonstrated RNA x DNA complex formation of the (dA)34 x (dT)34 tract with poly(U), but not with poly(A). These findings strongly suggest that poly(dT)-containing template sequences interact and form a complex with its transcription products, possibly an RNA x DNA triplex, which blocks further transcription. This would explain the instability of the plasmids transcribing mRNAs with poly(U) but not poly(A) tracts and the underrepresentation of poly(U) but not poly(A) tracts in mRNAs.

DNA↗
PubMed1996

N-Shc: a neural-specific adapter molecule that mediates signaling from neurotrophin/Trk to Ras/MAPK pathway.

Shc has been implicated in a variety of growth factor- and cytokine receptor-signaling through its specific binding to phosphotyrosine residues of the activated receptors. In neuronal cells, such as PC12, Shc has been shown to be involved in Ras-dependent MAP kinase activation following Trk receptor stimulation with NGF. While the ubiquitous role of Shc as an adaptor molecule in signal transduction is increasing in both neuronal and non-neuronal cells and tissues, the expression level of Shc is surprisingly low in the brain. We demonstrated here the isolation of a neural-specific member of the Shc family. This novel protein, named N-Shc (neuronal Shc), contains two potential phosphotyrosine-binding domains, PTB and SH2, and is expressed exclusively in the brain; whereas Shc is present in all other non-neuronal tissues. As in Shc, N-Shc can bind activated EGF receptor, become tyrosine phosphorylated, and form a complex with Grb2 adapter protein following EGF stimulation. Furthermore, N-Shc can bind activated TrkB receptor following the stimulation with brain-derived neurotrophic factor (BDNF), which is the most abundant neurotrophin in the brain. These data suggest that N-Shc, rather than Shc, mediates neurotrophin and other neuronal signalings in the central nervous system.

3T3 Cells↗