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T Matsuishi

Publications and source records attributed to T Matsuishi.

At least 19 recordsLinked to original sources
PubMed2006

Endothelial dysfunction in MELAS improved by l-arginine supplementation.

The authors evaluated endothelial function in patients with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke) by flow-mediated vasodilation (FMD) and found a significant decrease vs controls. Two years of supplementation with oral l-arginine, a nitric oxide precursor, significantly improved endothelial function to control levels and was harmonized with the normalized plasma levels of l-arginine in patients. l-Arginine therapy improved endothelial dysfunction and showed promise in treating strokelike episodes in MELAS.

Administration, Oral↗
PubMed2003

Observation of B0-->pLambda(pi)(-).

We report the first observation of the charmless hyperonic B decay, B0-->pLambda(pi)(-), using a 78 fb(-1) data sample recorded on the Upsilon(4S) resonance with the Belle detector at KEKB. The measured branching fraction is B(B0-->pLambda(pi)(-))=(3.97(+1.00)(-0.80)+/-0.56)x10(-6). Searches for B0-->pLambda(K)- and pSigma(0)pi(-) yield no significant signals and we set 90% confidence-level upper limits of B(B0-->pLambda(K)-)<8.2x10(-7) and B(B0-->pSigma(0)pi(-))<3.8x10(-6).

Journal Article↗
PubMed2003

Observation of B0 -->D0K0 and B0 -->D0K*0 decays.

We report on a search for B(0)-->D(*0)K(*0) decays based on 85 x 10(6) BB events collected with the Belle detector at KEKB. The B(0)-->D0K(0) and B(0)-->D0K(*0) decays have been observed for the first time with the branching fractions B(B(0)-->D0K(0))=(5.0(+1.3)(-1.2)+/-0.6)x10(-5) and B(B(0)-->D0K(*0))=(4.8(+1.1)(-1.0)+/-0.5)x10(-5). No significant signal has been found for the B(0)-->D(*0)K*0) and B(0)-->D(*0)K(*0) decay modes, and upper limits at 90% C.L. are presented.

Journal Article↗
PubMed2003

Perinatal bile acid metabolism: analysis of urinary unsaturated ketonic bile acids in preterm and full-term infants.

AIM: To compare urinary concentrations of unsaturated ketonic bile acids in preterm and full-term infants. METHODS: Urinary unsaturated ketonic bile acids were determined using gas chromatography-mass spectrometry. RESULTS: Urinary concentrations of total bile acids in early preterm infants (of less than 29wk gestational age) exceeded concentrations in late preterm (between 30 and 37 wk) and full-term infants (between 38 and 41 wk; p < 0.01). The percentage of ketonic bile acids (7alpha, 12alpha-dihydroxy-3-oxo-4-cholenoic acid and 7alpha-hydroxy-3-oxo-4-cholenoic acid) among total urinary bile acids in full-term infants (20.2 +/- 14.1%) was higher than that in early preterm infants (8.94 +/- 8.1%; p < 0.05). The percentage of unsaturated bile acids (3beta-hydroxy-delta5-bile acids) among total bile acids in urine did not differ greatly between groups. CONCLUSION: The percentage of 3-oxo-delta4 bile acids among total bile acids in urine gradually increased from early to late preterm infants, while healthy full-term infants excreted large amounts of 3-oxo-delta4 bile acids in urine at delivery.

Bile Acids and Salts↗
PubMed2002

Measurement of the B(0)-B(0) mixing parameter Deltam(d) using semileptonic B0 decays.

We present a measurement of the B0-Bmacr;(0) mixing parameter Deltam(d) using neutral B meson pairs in a 29.1 fb(-1) data sample collected at the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy e(+)e(-) collider. We exclusively reconstruct one neutral B meson in the semileptonic B0-->D(*-)l(+)nu decay mode and identify the flavor of the accompanying B meson from its decay products. From the distribution of the time intervals between the two flavor-tagged B meson decay points, we obtain Deltam(d)=(0.494+/-0.012+/-0.015) ps(-1), where the first error is statistical and the second error is systematic.

Journal Article↗
PubMed2002

Enlarged bronchial arteries in a fetus with transposition of the great arteries and intact ventricular septum.

Enlarged bronchial arteries are associated in some patients with transposition of the great arteries and intact ventricular septum. The etiology of these enlarged bronchial arteries is not yet known. In this report, we describe a case of TGA/IVS in which enlarged bronchial arteries were demonstrated from the prenatal period. The arteriogram at one year after arterial switch repair demonstrated enlarged bronchial arteries. This prenatal information may be useful for deciding on a strategy for postnatal treatment and counseling the family members.

Angiography↗
PubMed2002

Observation of B+/- -->omegaK+/- decay.

We report the first observation of the charmless two-body mode B+/--->omegaK+/- decay, and a new measurement of the branching fraction for the B+/--->omegapi(+/-) decay. The measured branching fractions are B(B+/--->omegaK+/-)=(9.2(+2.6)(-2.3)+/-1.0)x10(-6) and B(B+/--->omegapi(+/-))=(4.2(+2.0)(-1.8)+/-0.5)x10(-6). We also measure the partial rate asymmetry of B+/--->omegaK+/- decays and obtain A(CP)=-0.21+/-0.28+/-0.03. The results are based on a data sample of 29.4 fb(-1) collected on the Upsilon(4S) resonance by the Belle detector at the KEKB e(+)e(-) collider.

Journal Article↗
PubMed2002

Severe infantile measles encephalitis occurred three months after neonatal measles.

A 3-month-old girl who developed severe measles encephalitis after neonatal measles is reported. Her mother had measles when she was ten days old and she was admitted to our hospital with low grade fever, Koplik spot, and mild exanthema seventeen days after birth, and she recovered in 7 days without any complication. At three months of age, she was readmitted because of intractable seizures. The levels of IgM and IgG antibodies against measles in the cerebrospinal fluid were elevated. The measles virus genome, amplifying the region encoding the nucleocapsid protein, was detected from the brain specimen by reverse transcriptase-polymerase chain reaction. Magnetic resonance imaging showed a focal destructive lesion and diffuse cerebral atrophy. The electroencephalogram did not show periodic synchronous discharges. Although the neonatal measles was believed to be relatively mild in severity, the possible development of measles encephalitis should be carefully monitored in an infant who had neonatal measles.

Encephalitis, Viral↗
PubMed2002

Soluble forms of the selectin family in children with Kawasaki disease: prediction for coronary artery lesions.

AIM: To investigate the relationship between the plasma levels of soluble forms of the selectin family and the incidence of coronary artery lesions (CALs) in patients with Kawasaki disease (KD). METHODS: Thirty-three patients with KD, including group A patients (n = 22) who had no CALs and group B patients (n = 11) who had CALs, as well as age-matched febrile (n = 10) and afebrile controls (n = 11), were studied. RESULTS: Peak plasma E-selectin levels (172.0 +/- 58.6 ng ml(-1)) occurred during the acute phase of KD, while peak plasma P-selectin levels (260.3 +/- 43.2 ng ml(-1)) occurred during the subacute phase of the illness (p<0.05). Plasma L-selectin levels (1757.3 +/- 244.3 ng ml(-1)) during the convalescent phase tended to be higher than in either the acute or the subacute phase (not significant). Before intravenous immunoglobulin treatment, the plasma levels of E- (225.1 +/- 46.8 ng ml(-1)) and P-selectin (259.4 +/- 76.2 ng ml(-1)) of patients with CALs (n = 11) were significantly higher than those of patients (n = 22) with no CALs (E-selectin, 131.6 +/- 36.9 ng ml(-1); P-selectin, 184.9 +/- 84.6 ng ml(-1); p < 0.05). When a plasma E-selectin value before immunoglobulin treatment of >184.7 ng ml(-1) was used as the cut-off point, the sensitivity and specificity for the incidence of CALs were 81.8% and 90.9%, respectively. These findings demonstrate the relationship between plasma levels of selectins and disease severity of Kawasaki vasculitis. CONCLUSION: Higher plasma levels of E-selectin may have potential as a predictor of the incidence of coronary artery lesions in Kawasaki disease patients.

Child↗
PubMed2001

Decreased cerebrospinal fluid levels of beta-endorphin and ACTH in children with infantile spasms.

To investigate the pathophysiology of infantile spasms (IS), we measured the cerebrospinal fluid (CSF) levels of beta-endorphin (beta-EP), adrenocorticotropic hormone (ACTH), and corticotropin-releasing hormone (CRH) in 20 patients with IS, including 11 with the secondary form and 9 with the cryptogenic form of the disease. The findings were compared with those obtained in age-matched controls without neurologic disease. The CSF levels of beta-EP and ACTH were significantly lower in patients with IS than those in the controls. The CSF levels of CRH in patients with IS were lower, although, this trend was not significant. These reductions in the CSF levels of these neuropeptides could explain the impairment of the brain-adrenal axis in such patients. These results might support the hypothesis that, instead of originating from an increased abundance of CRH, which can act as a rapid and potent convulsant, some infantile seizures could be caused by an ACTH deficiency.

Adolescent↗
PubMed2001

Reduced expression of neuropeptides can be related to respiratory disturbances in Rett syndrome.

We immunohistochemically examined neurotransmitter systems, which function in the brainstem and are involved in neuronal organization of respiration, in an autopsy brain from a patient with Rett syndrome (RS). Immunoreactivity (IR) for tyrosine hydroxylase, a functional marker for catecholaminergic neurons, was severely reduced in the locus ceruleus, while that for tryptophan hydroxylase involved in serotonin synthesis was spared in the raphe nuclei. In the brainstem, IR for substance P (SP) was reduced in the parabrachial complex and that for methionine-enkephalin (met-enk) was affected in the parabrachial, hypoglossal, dorsal vagal and solitary nuclei. In addition, expressions of these neuropeptides were also disturbed in the basal ganglia. A widespread altered expression of antagonistic neuropeptides, SP and met-enk, may be involved in the pathogenesis of RS, especially in its respiratory manifestation.

Adolescent↗
PubMed2001

Mutation analysis of the methyl-CpG-binding protein 2 gene (MECP2) in Rett patients with preserved speech.

Genomic DNAs from 35 Japanese sporadic patients with Rett syndrome (RTT) were screened for DNA mutations in the entire coding region and exon-intron boundaries of methyl-CpG-binding protein 2 (MECP2). We detected mutations in 30 (85.7%) of 35 patients. Among these 35 RTT patients, five patients (14%) had the preserved speech variant of this disease. Four respective mutations (R133C, R306C, R294X, 2 base pair (bp) deletion) were found in these five patients. Two patients had the same missense mutation, R133C. The patients with the R133C mutation and one with frameshift mutation presented the relatively mild clinical presentation, and the R133C mutation was not found in any other patient without preserved speech. We confirmed that the preserved speech variant is one of the clinical phenotypes of RTT and is also caused by MECP2 mutation. We speculated that the clinical phenotype of patients with the R133C missense mutation might be mild.

Adult↗
PubMed2001

Neurobiology and neurochemistry of Rett syndrome.

The current status of neurobiological and neurochemical research on Rett syndrome is reviewed, and correlations are developed with previously described neurophysiological, neuroimaging, neuropathological, and immunohistochemical changes. We review the abnormalities reported in the biogenic amine neurotransmitters/receptor systems, and of beta-phenylethylamine, an endogenous amine synthesized by the decarboxylation of phenylalanine in dopaminergic neurons of the nigrostriatal system. We also discuss the roles of other neurotransmitters, including beta-endorphin and substance P, and neurotrophic factors, including nerve growth factors. Recently, DNA mutations in the methyl-CpG binding protein 2, mapped to Xq28, have been identified in some patients with Rett syndrome. The multiple abnormalities in the various neurotransmitters/receptor systems explain the pervasive effects of Rett syndrome.

Adolescent↗
PubMed2001

Platelet monoamine oxidase B and plasma beta-phenylethylamine in Parkinson's disease.

OBJECTIVE: To evaluate the correlation between changes in platelet monoamine oxidase type B (MAO-B) activity and plasma beta-phenylethylamine (PEA) concentrations in patients with Parkinson's disease and controls. METHODS: Platelet MAO-B activity and plasma PEA were measured with gas chromatography-mass spectrometry (GC-MS) in patients with Parkinson's disease treated with levodopa (12 men and 12 women) or selegiline (three men and three women), and physically healthy subjects as a control group (10 men and 10 women). RESULTS: Platelet MAO-B activity was significantly higher in the Parkinson's disease group (mean 542 (SD 318) pmol/10(7) platelets/30 min) than in the control group (mean 349 (SD 307) pmol/10(7) platelets/30 min) (p<0.05). By contrast, the plasma PEA concentrations in patients with Parkinson's disease were significantly lower than in the control group (mean 532 (SD 243) pg/ml; 931 (SD 560) pg/ml) (p<0.01). The plasma PEA concentrations in patients with Parkinson's disease treated with selegiline were prominently higher than in patients with no selegiline treatment (p<0.001). There was a significantly negative correlation between platelet MAO-B activity and plasma PEA concentrations in patients (n=24, r=-0.466, p<0.001). CONCLUSIONS: The increase in platelet MAO-B activity and decrease in plasma PEA concentrations in patients with Parkinson's disease may be involved in the pathophysiological processes of the disease, and these changes are reversed by treatment with selegiline.

Aged↗