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Biomedical subjects

Y Mizuno

Publications and source records attributed to Y Mizuno.

At least 181 records · Page 10Linked to original sources
PubMed2000

[Anosognosia for hemiplegia in a patient with pontine infarction].

We report a patient with anosognosia for hemiplegia associated with a right pontine infarction. A 51-year-old woman with histories of hypertension and diabetes mellitus was admitted because of weakness of her left upper and lower extremities. On neurologic examination, she was alert and oriented without dementia. Visuospatial hemineglect was not present. Hemiparesis of her left upper and lower extremities was noted. Her brain MRIs showed a large infarction in the right pons. On admission, she could recognize her illness but was indifferent to her hemiplegia, so she said that there was not well-off for her life. Two weeks after the onset, her neurological symptoms gradually improved. Simultaneously, her interest in her hemiparesis increased. We proposed that, in the present patient, anosognosia for hemiplegia was caused by the pontine infarction. Since pontine anosognosia for hemiplegia has been rarely reported to date, it is expected that the findings of the present patient will be useful to the better understanding of mechanisms underlying anosognosia.

Agnosia↗
PubMed2000

[C3 deficiency].

Explore the source record for details and available documents.

Anti-Infective Agents↗
PubMed2000

[A 57-year-old woman with progressive disturbance of gait and mental deterioration].

We report a 57-year-old woman with progressive gait disturbance and mental deterioration. She was well until March 1995, when she was 54 years of the age. At that time she noted a gradual onset of tremor and difficulty using her hand. Similar symptoms appeared in her right hands, and she visited another hospital, where 300 mg of levodopa and 7.5 mg of bromocriptine were prescribed. These medication did not help her symptoms. In the summer of 1996, she became to fall down easily. In September of the same year, she started to repeat the same words many times. She was unable to stop it. She was hospitalized to our service on January 25, 1997. On admission, she was alert but demented moderately; her Hasegawa dementia scale was 15/30. She showed palilallia, logoclonia, and echolalia. She showed constructional apraxia and questionable left-right disorientation. She had marked vertical gaze palsy with preserved oculocephalic response. She had masked face and small voice. Her gait was wide based with small steps. No muscle atrophy or weakness was noted. She showed only mild rigidity in the neck, but no rigidity was noted in the limb. No tremor was noted. She was bradykinetic. Deep tendon reflexes were symmetric and within normal limits. Laboratory findings on admission was unremarkable. MRI showed atrophy of the brain stem as well as cerebral cortical areas, particularly in the fronto-temporal region. Her hospital course was complicated with paralytic ileus and septicemia. She developed hypotension and pronounced dead on July 28, 1998. She was discussed in the neurological CPC. The chief discussant arrived at a conclusion that the patient had progressive supranuclear palsy and died of septic shock. All the participants wondered between PSP and CBD, but majority agreed with this diagnosis of the chief discussant. Only one thought that she might have had corticobasal degeneration rather than PSP, because of dementia, cortical atrophy in MRI, and lack of limb rigidity. Postmortem examination revealed cortical and brain stem atrophy. In the premotor cortex, marked astrocytosis and ballooned neurons were seen. Furthermore, astrocytic plaques were seen; this is considered to be pathognomonic for CBD. The substantia nigra showed marked neuronal loss and gliosis, but no neurofibrillary tangles or Lewy bodies were seen. Gliosis was also seen in the globus pallidus and in the medial thalamus. The pathologic diagnosis was corticobasal degeneration. This patient was very interesting case, in that the clinical manifestations appeared to be consistent with PSP, yet pathologic diagnosis was CBD. Lack of limb rigidity may be atypical for advanced PSP. In addition, palilalia appears to be more associated with CBD.

Brain↗
PubMed2000

[Prevention and care management of influenza infection in institutions for the elderly and high risk groups].

Influenza infection is a serious problem in institutions for the elderly and those with increased risk factors because of the high pneumonia complication rate and a significant increase in mortality. An outbreak of influenza is mainly caused by contact from the staff to residents, therefore the health care of the staffs and prevention of influenza should be a high priority in institutions such as nursing homes. To prevent influenza epidemics, institutionalised elderly and high risk groups should be vaccinated more actively. The rapid test for diagnosis of influenza viral infection permits the timely administration of antiviral agents and infection control among institutionalised elderly and high risk groups. Amantadine and neuraminidase inhibitors could be used for treatment and prophylaxis of influenza among institutionalised elderly and high risk group patients.

Aged↗
PubMed2000

[Autosomal recessive juvenile parkinsonism: its pathogenesis is involved in the ubiquitin-proteasome pathway].

The contribution of genetic factors in the pathogenesis of PD is supported by the demonstration of the high concordance in twins studies using PET, the increased risk among relatives of PD patients in case control and family studies, and the existence of familial PD and parkinsonism by single gene defect. Recently, two genes such as alpha-synuclein and parkin have been identified. alpha-Synuclein is involved in a rare dominant form of familial PD with dopa responsive parkinsonian features and Lewy body positive pathology. In contrast, parkin is responsible for autosomal recessive form (AR-JP) of early onset PD with Lewy body-negative pathology. To date, variable mutations such as deletions or point mutations have been reported in AR-JP patients from world wide. In addition, the localization of parkin indicates parkin may are involved in the axonal transport system. More recently, we have found that parkin interacts with ubiquitin-conjugating enzyme, UbcH 7, and is functionally linked to the ubiquitin-proteasome pathway as a ubiquitin ligase. These findings fit the characteristics of lack of Lewy bodies which are cytoplasmic inclusions considered a pathological hallmark. Our findings should enhance the exploration of the mechanisms of neuronal death in PD as well as other neurodegenerative disorders of which variable inclusion bodies are observed.

Cysteine Endopeptidases↗
PubMed1999

Autosomal-recessive juvenile parkinsonism in a Jewish Yemenite kindred: mutation of Parkin gene.

We report a Jewish family of Yemenite origin in which three brothers born from a consanguineous marriage had juvenile parkinsonism. The DNA samples from three affected brothers and one healthy brother were analyzed for the linkage to markers covering the autosomal-recessive juvenile parkinsonism (AR-JP) locus. A perfect homozygous cosegregation to the markers was found, giving a maximal lod score of 3.11 at D6S1579, D6S305, and D6S411, all of which are 0 cm apart from each other (nonparametric linkage score, 8.041; p = 0.000977). Exon 3 of the Parkin gene was homozygously deleted in all patients. The AR-JP gene also exists in the Jewish population.

DNA↗
PubMed1999

An automated interpretation of MALDI/TOF postsource decay spectra of oligosaccharides. 1. Automated peak assignment.

A computer program has been developed that helps the interpretation of MALDI/TOF postsource decay (PSD) spectra of N-linked oligosaccharides of a protein. The program includes routines for automated peak assignment and generation of a simulated PSD spectrum. From a raw spectrum, peaks are assigned automatically; i.e., numbers of saccharide residues removed from the parent ion are calculated. If the structure of the oligosaccharide is known, a simulated PSD spectrum of the oligosaccharide will be generated. The simulated PSD spectrum helps interpretation of the observed spectrum. While, in a case where several candidate structures are given, one can narrow the field of plausible structures for the unknown oligosaccharide by comparing the observed spectrum with the simulated PSD spectra. Using a Pentium 233-MHz microprocessor, it takes only a few seconds to interpret a spectrum.

Algorithms↗
PubMed1999

Cardiac angiotensin-converting enzyme activity in myocardial infarction.

The cardiac renin-angiotensin system is regarded as an important modulator in the infarct heart. Little is known about their presence and regulation in human hearts. We measured angiotensin-converting enzyme (ACE) and renin activities at the aortic root and anterior interventricular vein (AIV) in 51 patients with previous myocardial infarction (MI): anterior wall MI in 31 and inferior wall MI in 20 and 33 control subjects. In the anterior wall MI group, the serum ACE activity was increased significantly in the AIV than in the aortic root (16.2 +/- 5.3 vs 15.3 +/- 5.0 nmol/min/ml, p <0.001), whereas the activity was not different between the aortic root and AIV in the control (14.4 +/- 3.7 vs 14.4 +/- 3.7 nmol/min/ ml) and in the inferior wall MI (16.5 +/- 4.8 vs. 17.0 +/-5.2 nmol/min/ml) groups. On the other hand, there was no significant difference in plasma renin activity between the AIV and aortic root in the 3 groups (control group, 1.0 +/- 0.5 vs 1.0 +/- 0.5 pg/ml/hour; anterior wall MI group, 1.3 +/- 0.8 vs 1.3 +/- 0.8 pg/ml/hour; inferior wall MI group, 1.2 +/- 0.7 vs 1.3 +/- 0.8 pg/ml/ hour). The difference in serum ACE activity between the AIV and aortic root had a significant positive linear correlation with pulmonary capillary wedge pressure (r = 0.606, p <0.001), and had a significant negative linear correlation with left ventricular ejection fraction (r = -0.620, p <0.001) in the anterior wall MI group. Serum ACE activity from the infarct region of the left ventricle was augmented in patients with MI, and the activity was increased in proportion to the severity of left ventricular dysfunction.

Adult↗
PubMed1999

Brain-derived growth factor and nerve growth factor concentrations are decreased in the substantia nigra in Parkinson's disease.

Using highly sensitive sandwich enzyme-linked immunosorbent assays (ELISA), we measured for the first time the concentrations of brain-derived growth factor (BDNF) in the brain (substantia nigra, caudate nucleus, putamen, cerebellum, and frontal cortex) from control and parkinsonian patients. BDNF in the human brain (the order of ng/mg protein) was significantly lower specifically in the nigrostriatal dopamine (DA) regions from parkinsonian patients than in those from control patients. The concentration of nerve growth factor (NGF) was also significantly decreased in the substantia nigra of parkinsonian patients in comparison with that in the controls. Since BDNF and NGF may play important roles in survival and differentiation of neuronal cells, the present data indicate that the lack of neurotrophins, especially BDNF, may be involved in the pathogenesis of PD during progress of neurodegeneration of the nigrostriatal DA neurons.

Adult↗
PubMed1999

Methylglyoxal modification of protein. Chemical and immunochemical characterization of methylglyoxal-arginine adducts.

Methylglyoxal (MG), an endogenous metabolite that increases in diabetes and is a common intermediate in the Maillard reaction (glycation), reacts with proteins and forms advanced glycation end products. In the present study, we identify a novel MG-arginine adduct and also characterize the structure of a major fluorescent adduct. In addition, we describe the immunochemical study on the MG-arginine adducts using monoclonal antibody directed to MG-modified protein. Upon incubation of Nalpha-acetyl-L-arginine with MG at 37 degrees C, two nonfluorescent products and one fluorescent product were detected as the major products. The nonfluorescent products were identified as the Ndelta-(5-hydro-5-methyl-4-imidazolon-2-yl)-L-ornithine derivatives (5-hydro-5-methylimidazolone) and a novel MG-arginine adduct having a tetrahydropyrimidine moiety (Ndelta-(4-carboxy-4,6-dimethyl-5, 6-dihydroxy-1,4,5,6-tetrahydropyrimidine-2-yl)-L-ornithine). On the basis of the following chemical and spectroscopic evidence, the major fluorescent product, putatively identified as Ndelta-(5-methylimidazolon-2-yl)-L-ornithine (5-methylimidazolone), was found to be identical to Ndelta-(5-hydroxy-4, 6-dimethylpyrimidine-2-yl)-L-ornithine (argpyrimidine): (i) the low and high resolution fast atom bombardment-mass spectrometry gave a molecular ion peak at m/z of 297 (M+H) and a molecular formula of C10H25O6N4, respectively, which coincided with argpyrimidine; (ii) the 1H NMR spectrum of this product in d6-Me2SO showed a singlet at 2.10 ppm corresponding to six protons; (iii) the peak corresponding to the 5-methylimidazolone derivative was not detected by the liquid chromatography-mass spectrometry with the mode of selected ion monitoring; (iv) incubation of 5-hydro-5-methylimidazolone, a putative precursor of 5-methylimidazolone, at 37 degrees C for 14 days scarcely generated 5-methylimidazolone. On the other hand, as an immunochemical approach to the detection of these MG adducts, we raised the monoclonal antibodies (mAb3C and mAb6B) directed to the MG-modified protein and found that they specifically recognized the major fluorescent product, argpyrimidine, as the dominant epitope. The immunohistochemical analysis of the kidneys from diabetic patients revealed the localization of argpyrimidine in intima and media of small artery walls. Furthermore, the accumulation of argpyrimidine was also observed in some arterial walls of the rat brain after middle cerebral artery occlusion followed by reperfusion. These results suggest that argpyrimidine may contribute to the progression of not only long term diabetic complications, such as nephropathy and atherosclerosis, but also the tissue injury caused by ischemia/reperfusion.

Animals↗
PubMed1999

Remnant lipoprotein levels in fasting serum predict coronary events in patients with coronary artery disease.

BACKGROUND: Remnant lipoproteins are atherogenic, but assays of remnants have not been available in routine clinical laboratories because of the lack of practical and validated methods. A simple and reliable method for such an assay, using an immunochemical approach, has recently been developed. This study prospectively examined whether remnant lipoprotein levels in fasting serum, measured by our method, may have prognostic value in patients with coronary artery disease (CAD). METHODS AND RESULTS: Remnant lipoprotein levels in fasting serum were measured in 135 patients with CAD by an immunoaffinity mixed gel containing anti-apolipoprotein (apo) A-1 and anti-apoB-100 monoclonal antibodies. Patients were followed up for </=36 months until occurrence of 1 of the following clinical coronary events: recurrent or refractory angina pectoris requiring coronary revascularization, nonfatal myocardial infarction, or cardiac death. Kaplan-Meier analysis demonstrated a significantly higher probability of developing coronary events in patients with the highest tertile of remnant levels (>5.1 mg cholesterol/dL; 75th percentile of distribution of remnant levels) than in those with the lowest tertile of remnant levels (</=3.3 mg cholesterol/dL; 50th percentile of the distribution). Higher levels of remnants were a significant and independent predictor of developing coronary events in multivariate Cox hazard analysis including the following covariates: extent of coronary artery stenosis, age, sex, smoking, hypertension, diabetes mellitus, hypercholesterolemia, low HDL cholesterol, and hypertriglyceridemia. CONCLUSIONS: Higher levels of remnant lipoproteins in fasting serum predict future coronary events in patients with CAD independently of other risk factors. Thus, measurement of fasting remnant levels, assessed by the current immunoseparation method, may be helpful in assessment of CAD risk.

Adult↗
PubMed1999

Folate and homocysteine metabolism in copper-deficient rats.

To investigate the effect of copper deficiency on folate and homocysteine metabolism, we measured plasma, red-cell and hepatic folate, plasma homocysteine and vitamin B-12 concentrations, and hepatic methionine synthase activities in rats. Two groups of male Sprague-Dawley rats were fed semi-purified diets containing either 0. 1 mg (copper-deficient group) or 9.2 mg (control group) of copper per kg. After 6 weeks of dietary treatment, copper deficiency was established as evidenced by markedly decreased plasma and hepatic copper concentrations in rats fed the low-copper diet. Plasma, red-cell, hepatic folate, and plasma vitamin B-12 concentrations were similar in both groups, whereas plasma homocysteine concentrations in the copper-deficient group were significantly higher than in the control group (P<0.05). Copper deficiency resulted in a 21% reduction in hepatic methionine synthase activity as compared to the control group (P<0.01). This change most likely caused the increased hepatic 5-methyltetrahydrofolate and plasma homocysteine concentrations in the copper-deficient group. Our results indicate that hepatic methionine synthase may be a cuproenzyme, and plasma homocysteine concentrations are influenced by copper nutriture in rats. These data support the concept that copper deficiency can be a risk factor for cardiovascular disease.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1999

Synthesis of 2,8-disubstituted imidazo[1,5-a]pyrimidines with potent antitumor activity.

Seventeen 1,2,3,4-tetrahydroimidazo[1,5-a]pyrimidine derivatives bearing electron-withdrawing substituents were designed and synthesized by novel ring closure as potential antitumor agents. They were screened for their activities against mouse leukemia L1210 and human oral epidermoid carcinoma KB cell lines, and relationships of structure and antitumor activity in vitro are discussed. It was found that 8-thiocarbamoyl-1,2,3,4-tetrahydroimidazo[1, 5-a]pyrimidin-2(1H)-thione (8c) exhibited activity comparable to that of 5-fluorouracil against both L1210 and KB cells. The existence of both 2-thioxo and 8-substituent with a thioxo group in the molecule is crucial for the cytotoxicity against L1210 and KB cells. A novel procedure for introduction of a double bond between C-3 and C-4 in 8c was developed. Introduction of the 3,4-double bond increased the activity against L1210, but against KB cells the activity decreased by 4-fold. Cytotoxicity of compounds 8c and 8-thiocarbamoyl-1,2-dihydroimidazo[1,5-a]pyrimidin-2(1H)-thione (11c) against human solid tumor and leukemia cell lines was further evaluated. The saturation of the 3,4-double bond led to a significant increase in cytotoxicity against tumor cell lines tested.

Animals↗
PubMed1999

Increased specificity of reverse transcription priming by trehalose and oligo-blockers allows high-efficiency window separation of mRNA display.

We have developed a method for high-efficiency window separation of cDNA display by increasing the specificity of priming in reverse transcription. In the conventional method, two-base anchored oligo(dT) primers (5'dT16VN3', where N is any base and V is G, A or C) are used to make windows for the display of transcripts. However, reverse transcriptase often extends misprimed oligonucleotides. To avoid mispriming from dT16VN primers, we have developed two new technologies. One is higher temperature priming with reverse transcriptase thermoactivated by the disaccharide trehalose. The other is the use of competitive oligonucleotide blockers that hybridize to the non-selectively primed mRNAs, preventing the mispriming from the VN site. These methods were combined to improve restriction landmark cDNA scanning (RLCS), resulting in the elimination of the redundant signals that appear in different windows. This was achieved by the increased specificity of initiation of reverse trans-cription from the beginning of poly(A) sites. This method paves the way for the precise visualization of transcripts to allow expression profiles in individual tissues and at each developmental stage to be understood.

Animals↗
PubMed1999

Polymorphism in the parkin gene in sporadic Parkinson's disease.

We report polymorphism of the parkin gene in 160 sporadic Parkinson's disease (PD) patients and controls. Three polymorphisms were found: a G-to-A transition in exon 4 (S/N167), a C-to-T transition in exon 10 (R/W366), and a G-to-C transition in exon 10 (V/L380). Genotype distributions and allele frequencies of S/N167 and V/L380 did not differ significantly between the two groups. The R/W366 allele frequency was significantly lower in PD patients (1.2 vs 4.4%). The level of protection from PD provided by this allele was 3.60 (95% CI; range, 0.45-6.50), suggesting that it may be a protective factor against PD.

Aged↗
PubMed1999

Immunohistochemical and subcellular localization of Parkin protein: absence of protein in autosomal recessive juvenile parkinsonism patients.

Autosomal recessive juvenile parkinsonism (AR-JP) is a distinct clinical entity characterized by a selective degeneration of nigral neurons. Recently, the parkin gene responsible for AR-JP has been identified. Now, we report the subcellular localization of Parkin protein in patients with AR-JP or Parkinson's disease (PD) and in controls by immunoblotting and immunohistochemistry using antibodies raised against the Parkin molecule. Parkin protein was absent in all regions of the brains of patients with AR-JP. Parkin protein was not decreased in the brains of sporadic PD patients. Immunoreactivity was detected in a few Lewy bodies. Parkin protein was located in both the Golgi complex and cytosol.

Brain↗