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Biomedical subjects

M Oishi

Publications and source records attributed to M Oishi.

At least 91 records · Page 5Linked to original sources
PubMed1998

Blood flow differences between leuko-araiosis with and without lacunar infarction.

BACKGROUND: The present study was designed to find the differences in regional cerebral blood flow and cerebrovascular acetazolamide reactivity between leuko-araiosis with and without lacunar infarction. METHODS: Fifteen cases of leuko-araiosis with lacunar infarction, 15 cases of leuko-araiosis without lacunar infarction and 15 age-matched controls in which leuko-araiosis and cerebrovascular diseases are absent (control group) were studied. The regional cerebral blood flow was measured using the stable xenon computed tomography method before and 20 minutes after intravenous injection of 17 mg/kg acetazolamide. RESULTS: The blood flows in the leuko-araiosis area and the lacunar area were significantly lower than the blood flow in the cerebral white matter. The blood flows in the cerebral cortex and the cerebral white matter were significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group. The cerebrovascular acetazolamide reactivity in the leuko-araiosis area and the lacunar area was significantly lower than that in the cerebral white matter. The cerebrovascular acetazolamide reactivity in the cerebral cortex and the cerebral white matter was significantly lower in the leuko-araiosis with lacunar infarction group than in the leuko-araiosis without lacunar infarction group and the control group. CONCLUSIONS: The degree of arteriolosclerosis is considered to be more severe and the rate of association of hypertension was higher in leuko-araiosis with lacunar infarction than in leuko-araiosis without lacunar infarction.

Acetazolamide↗
PubMed1998

beta-Thromboglobulin and 11-dehydrothromboxane B in tension-type headache.

Platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were investigated in tension-type headache. Ten cases of episodic tension-type headache (mean age 42.5 years), 10 cases of chronic tension-type headache (mean age 45.3 years), and 10 age-matched healthy controls were studied. The platelet factor 4, beta-thromboglobulin, thromboxane B2 and 11-dehydrothromboxane B2 concentrations in the plasma were significantly higher in the episodic tension-type headache group than in the chronic tension-type headache and healthy control groups. Platelets may be involved in episodic tension-type headache.

Adult↗
PubMed1998

Effectiveness of traditional Chinese medicine in Alzheimer disease.

Effects of traditional Chinese medicine on dementia, P300, cerebral blood flow, and cerebrospinal fluid (CSF) examination were investigated. Ten patients with Alzheimer disease (AD) who agreed to take traditional Chinese medicine were studied. The traditional Chinese medicine was given for 3 months and the Mini-Mental State Examination (MMSE), P300 examination, cerebral blood flow examination, and CSF examination were performed before and after taking the traditional Chinese medicine. The scores of the MMSE, the P300 latency, and blood flow in the cerebral cortex in AD improved with treatment with the traditional Chinese medicine. The concentration of alpha-aminobutyric acid in the CSF decreased with treatment with the traditional Chinese medicine. The improvement is considered to be not a placebo effect. Key Words: T

Aged↗
PubMed1998

Correlations between P300 components and neurotransmitters in the cerebrospinal fluid.

P300 and cerebrospinal fluid neurotransmitter metabolites and amino acids were examined in 10 patients with Alzheimer's disease, 9 patients with vascular dementia and 10 healthy controls. A negative correlation between P300 amplitude and MHPG concentration, negative correlation between P200 and N200 latencies and norepinephrine concentration, positive correlation between N200 latency and lysine concentration and positive correlation between N100 amplitude and tyrosine concentration were statistically significant. These findings suggest that the noradrenergic system influences P300 amplitude, and that multiple systems may influence P300 components.

3-Methoxy-4-hydroxyphenylethanol↗
PubMed1998

Correlation between contingent negative variation and regional cerebral blood flow.

The relationship between contingent negative variation (CNV) and regional cerebral blood flow was investigated, using the stable xenon computed tomography method. Seventeen cases of chronic multiple cerebral infarction in the perforating artery areas (vascular dementia, mean age 67.0), 6 cases of Alzheimer's disease (mean age 69.5) and 8 healthy controls (mean age 62.5) were studied. Regional cerebral blood flows in the frontal, temporal, parietal and occipital cortex, frontal, temporal and occipital white matter, caudate nucleus, putamen and thalamus were measured. The amplitude of early CNV was significantly smaller in the vascular dementia group than in the healthy control group. The blood flows in the parietal cortex and thalamus were significantly lower in the vascular dementia group than in the healthy control group. There was a significant positive correlation between the amplitude of early CNV and frontal cortex blood flow. No significant correlations were present between the CNV and the other regional cerebral blood flows nor in healthy controls. The amplitude of CNV has been reported to be decreased in dementia. From the present study, the amplitude of early CNV was considered to be influenced by the blood flow in the frontal cortex.

Aged↗
PubMed1998

Improvement of P300 latency by treatment in non-insulin-dependent diabetes mellitus.

P300 event-related potentials were investigated in 24 cases of non-insulin-dependent (Type II) diabetes mellitus (NIDDM) without apparent central nervous system (CNS) symptoms and without cerebrovascular diseases on head magnetic resonance imaging, and in 16 age-matched healthy control subjects. N200 and P300 latencies were significantly prolonged and N200 and P300 amplitudes were significantly smaller in the NIDDM group than in the healthy control group. P300 latency was significantly shorter after the treatment than before. N200 and P300 waves have been recognized as useful indicators of cognitive function. The present study suggests that cognitive function is impaired in NIDDM patients and may improve with treatment of hyperglycemia.

Cognition↗
PubMed1998

Clinical manifestations due to a point mutation of the mitochondrial tRNAleu(UUR) gene in five families with diabetes mellitus.

It has been shown that an adenine (A) to guanine (G) transition at position 3243 of the mitochondrial transfer RNA(tRNA)leu(UUR) gene is associated with a subgroup of diabetes mellitus. Therefore, we screened for this transition in 86 patients with non-insulin-dependent diabetes mellitus (NIDDM) in which two or three generations were affected with diabetes, in 14 patients with insulin-dependent diabetes mellitus, and in 9 families with diabetes mellitus and/or associated disorders suggesting mitochondrial gene abnormalities. We failed to identify the mutation in 100 diabetic patients, 86 NIDDM and 14 insulin-dependent diabetes mellitus (IDDM). Out of the latter 9 families, we identified an A to G transition in 14 individuals in 5 families. Diabetes mellitus was shown to be maternally inherited in one family. In 9 of 14 patients with the mutation, insulin was required to treat diabetes mellitus, indicating impaired insulin secretion. A hyperglycemic clamp test performed in one subject revealed significant impairment of insulin secretion, whereas euglycemic clamp test showed normal insulin sensitivity in this patient. The heteroplasmy of the mutant mitochondrial DNA (mtDNA) in leukocytes does not appear to correlate with the severity of diabetes in terms of the insulin therapy required. Body mass index of the affected individuals was less than 23.3. In one family, in addition to diabetes mellitus and hearing loss, hypoparathyroidism was associated with the mutation, suggesting that hypoparathyroidism is caused by the impaired processing and/or secretion of proparathyroid hormone due to the mutation. In addition, the affected subjects presented with proteinuria at the time of diagnosis of diabetes mellitus which appeared not to be related with diabetic nephropathy.

Adolescent↗
PubMed1998

Magnetic resonance imaging findings of the skeletal muscle of a patient with nemaline myopathy.

This is the first magnetic resonance imaging (MRI) report of nemaline myopathy in which muscle atrophy was not apparent clinically in the lower extremities because of subcutaneous fat. The patient is a 38-year-old woman who was admitted to our hospital because of muscle weakness of the four extremities. Until the age of 17 years, she was asymptomatic except that her running speed was slow. The T1-weighted image of muscle MRI at the mid-thigh level showed hyperintensity of the quadriceps femoris muscle and relatively spared hamstring muscle. The T2-weighted image of muscle MRI at the maximum diameter of the lower leg showed hyperintensity of the tibialis anterior muscle and a relatively spared triceps surae muscle. The biopsy specimen of the right deltoid muscle showed nemaline bodies and type II fiber deficiency.

Adipose Tissue↗
PubMed1998

[Myopathy with cerebral white matter abnormality--a case report].

A 45-year-old man noticed mild numbness of the feet at the age of 40 years and difficulty in standing up from squatting position at 43 years. His birth and developmental milestones were normal and the family history was unremarkable. He was alert and intelligent with global IQ of 91. There was mild muscle weakness as well as atrophy in bilateral hips and thighs. The serum creatine kinase level was 542 U/l. On computed tomography, the hamstrings were preferentially involved. The biopsied specimens from the right quadriceps femoris and peroneal muscles showed myogenic changes with evidence of necrotic and regenerating process. Dystrophin, dystrophin-associated glycoproteins and merosin were normally expressed. From the clinical and pathologic findings, he was diagnosed as having myopathy. The electroencephalogram was normal but the P300 latency was prolonged. T2-weighted head magnetic resonance imaging showed diffuse high intensity in the cerebral white matter. Myopathy with cerebral white matter abnormality in adult patients has not yet been reported. Asymptomatic cerebral white matter abnormality should be considered in adult patients with myopathy.

Brain Diseases↗
PubMed1998

[A case of chronic inorganic mercury poisoning with progressive intentional tremor and remarkably prolonged latency of P300].

A 59-year-old man showed slowly progressive intentional tremor for 40 years prior to first visit to us in 1996. He was exposed to mercury vapor for about 3 years (1956-1959) and the diagnosis of chronic inorganic mercury poisoning was made. Hasegawa dementia scale-revised (HDS-R), mini-mental state (MMS) examination and P300 examination were performed. HDS-R and MMS were within normal range but the latency of P300 was remarkably prolonged. His tremor was considered to be due to chronic inorganic poisoning because there were no other causes and the frequency of his tremor was 3-4 Hz. which was lower than that in essential tremor. The prolonged P300 latency was also considered to be due to the same cause because there were no other causes and the head MRI were normal. Chronic inorganic mercury poisoning has been reported to produce organic changes in the brain and P300 is considered to be useful to detect these changes.

Brain↗
PubMed1998

[Correlation between event-related potentials and regional cerebral blood flow in chronic alcoholism].

We report a correlation between P300 and cerebral blood flow in 11 patients with chronic moderate alcoholism. The patients had been drinking more than 83 ml pure alcohol equivalent everyday for more than 10 years and did not have any other neurological diseases. The P300 latency was significantly longer in the chronic alcoholism group than in the age-matched healthy control group. There was a significant negative correlation between the P300 latency and the thalamus blood flow in the chronic alcoholism group. These findings suggest that there is a subclinical disturbance of cognitive function in chronic alcoholism and that the prolongation of P300 latency is related to the decrease in thalamus blood flow in chronic alcoholism.

Aged↗
PubMed1998

[Regional cerebral blood flow and cerebrospinal fluid amino acid analysis in elderly dementia].

Regional cerebral blood flow and amino acid concentration in the cerebrospinal fluid were studied in 12 cases of vascular dementia, 12 cases of Alzheimer's disease, 12 cases of chronic alcoholism, and 12 age-matched healthy controls. In vascular dementia, blood flows were decreased in the cerebral cortex, frontal white matter, thalamus, caudate nucleus, and putamen and alpha-aminobutyric acid and glutamic acid concentrations were increased in the cerebrospinal fluid. In Alzheimer's disease, blood flows were decreased in the frontal cortex, parietal cortex, temporal cortex, and frontal white matter and alanine concentration was increased in the cerebrospinal fluid. In chronic alcoholism, blood flows were decreased in the cerebral cortex, thalamus, and putamen and urea, alanine, and glycine concentrations were increased in the cerebrospinal fluid.

Alcoholism↗
PubMed1997

Induction of protein tyrosine phosphatase epsilon transcripts during NGF-induced neuronal differentiation of PC12D cells and during the development of the cerebellum.

We have investigated a possible role played by protein tyrosine phosphatase epsilon (PTPepsilon), which was recently cloned and predominantly expressed in brain, in neural differentiation and function. During neuronal cell differentiation of PC12D cells triggered by NGF or FGF, PTPepsilon transcripts were transiently induced at a time between the appearance of transcripts for immediate-early genes and for neuronal cell-specific markers. PTPepsilon was the only PTPase whose transcripts were induced during PC12D cell differentiation among over two dozen PTPase transcripts so far examined. Moreover, in situ hybridization revealed that PTPepsilon transcripts were detected in the neural tube of day 12 postcoitum embryo, and in the nervous system including brain, spinal cord, and ganglions in a ubiquitous manner in late gestational stages. In 4-day-old neonatal mice, the transcripts were widely distributed in the central nervous system where the strongest expression was detected in the hippocampus, cerebral cortex, and olfactory bulb. Interestingly, in day 7 and 16 neonatal brains, the strongest PTPepsilon gene expression was localized in the granular cells of cerebellum, which might indicate that PTPepsilon is involved in the differentiation of the granular cells. The biological significance of PTPepsilon in neuronal differentiation and brain functions is discussed.

Animals↗
PubMed1997

Enrichment of oligo(dG).oligo(dC)-containing fragments from human genomic DNA by Mg 2+-dependent triplex affinity capture.

Oligo(dG).oligo(dC)- or short poly(dG).poly(dC)-containing fragments were enriched and cloned by means of Mg2+-dependent triplex affinity capture and subsequent cloning procedures. A library constructed after three cycles of enrichment showed that approximately 80% of the clones in the supercoiled form formed a complex with labeled oligonucleotide (dG)34. However, while the rest of the clones retained the ability to form a complex (type I clones), 90.9% failed to form a complex when they were linearized. This group of DNA was abundant in the genomic DNA, although it showed only approximately 3-fold enrichment by one cycle of affinity capture. This group was further classified into two species (types II and III) based on complex formation ability after phenol extraction. Type II clones retained the complex formation ability after treatment, while the human telomere [(TTAGGG)n] and telomere-like [(TGGAA)n] or [(TGGAG)n] sequences belonging to type III clones did not. Serial deletion experiments and the binding assays using oligonucleotides confirmed that the repetitive units containing T(G)nT ( n = 3-5) tracts or (G)n-motifs (n >/= 3) were the sites of complex formation for type II and III clones. On the other hand, type I clones contained poly(dG).poly(dC) tracts at least 10 nt long, and DNase I-footprinting analysis indicated that these tracts were the sites of complex formation.

Cloning, Molecular↗
PubMed1997

Phosphorylation of Alzheimer beta-amyloid precursor-like proteins.

Amyloid precursor-like proteins (APLPs), APLP1 and APLP2, are members of a gene family which include the Alzheimer beta-amyloid precursor protein (APP). APLP1, APLP2, and APP contain highly homologous amino acid sequences, especially in their cytoplasmic domains, although APLPs lack the beta-amyloid domain derived by proteolytic processing from APP. APP is phosphorylated at three sites in the cytoplasmic domain in cultured cells and adult rat brain [Suzuki et al. (1994) EMBO J. 13, 1114-1122; Oishi, et al. (1997) Mol. Med. 3, 109-121] and at sites in the extracellular domain in cultured cells [Knops et al. (1993) Biochem. Biophys. Res. Commun. 197, 380-385; Hung & Selkoe (1994) EMBO J. 13, 534-542; Walter et al. (1997) J. Biol. Chem. 272, 1896-1903]. We report here that a cytoplasmic domain peptide from APLP1 is phosphorylated in vitro by protein kinase C and that a cytoplasmic domain peptide from APLP2 is phosphorylated in vitro by protein kinase C and cdc2 kinase. APLP2 is phosphorylated by cdc2 kinase at a site homologous to the cdc2 kinase site phosphorylated in APP. Furthermore, phosphorylation of this site occurs in a cell cycle-dependent manner in cultured cells. These findings indicate that in intact cells the phosphorylation of APLP2 appears to be regulated in a similar fashion to that of APP.

Alzheimer Disease↗