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M Nishizawa

Publications and source records attributed to M Nishizawa.

At least 37 records · Page 2Linked to original sources
PubMed2001

Advances in the Pauson-Khand reaction: development of reactive cobalt complexes.

Three conceptually new methods employing reactive cobalt carbonyl complexes have been developed for the Pauson-Khand reaction. The first method involves activation of alkyne-dicobalt hexacarbonyls with "hard" Lewis bases. Primary amines dramatically promote the stoichiometric Pauson-Khand reaction. The active cobalt complexes produced in the system exhibit high reducing ability. The second method involves activation of dicobalt octacarbonyl with less electron-donating "hard" Lewis bases such as 1,2-dimethoxyethane and water. These Lewis bases were successfully utilized as a promoter for the catalytic Pauson-Khand reaction. The third method employs methylidynetricobalt nonacarbonyl cluster, which exhibits high reactivity in the catalytic Pauson-Khand reaction in the absence of activator. This may be due to facile coordination of the substrate to the metal center through dissociative and associative mechanisms and/or cleavage of one of the cobalt-cobalt bonds.

Journal Article↗
PubMed2001

Meiotic instability of the CAG repeats in the SCA6/CACNA1A gene in two Japanese SCA6 families.

Intergenerational stability of the CAG repeat number has been considered to be a specific molecular feature of SCA6 compared with other CAG repeat diseases. Nevertheless, we showed meiotic instability of the CAG repeats in the SCA6/CACNL1A gene in two Japanese SCA6 families, including de novo expansion. In one family, the CAG20 allele expanded to the CAG26 one during paternal transmission, and in the other family, the CAG19 allele expanded to the CAG20 one during maternal transmission. Although it is controversial as to whether the CAG20 allele is pathological or not, this is the first case of haplotype analysis-proven de novo expansion in SCA6, confirming the derivation of an expanded allele from one normal allele. We should carefully follow up the individuals carrying the CAG20 allele in our family who show normal neurological and radiological findings at present.

Adult↗
PubMed2001

A large Japanese SPG4 family with a novel insertion mutation of the SPG4 gene: a clinical and genetic study.

We studied a large Japanese family with autosomal dominant pure hereditary spastic paraplegia (ADPHSP) clinically and genetically. To date, seven loci causing ADPHSP have been mapped to chromosomes 14q, 2p, 15q, 8q, 12q, 2q, and 19q. Among these loci, the SPG4 locus on chromosome 2p21--p22 has been shown to account for approximately 40% of all autosomal dominant hereditary spastic paraplegia (ADHSP) families. Very recently, Hazan et al. identified the SPG4 gene encoding a new member of the AAA (ATPases associated with diverse cellular activities) protein family, named spastin. We found a novel insertion mutation (nt1272--1273insA) in exon 8 of the SPG4 gene in the present family. Our study is the first to confirm the causative mutation of the SPG4 gene in Japanese. Clinically, it is noteworthy that the disease progression in the patients of this family was slow in spite of the late onset, and more than half of the patients showed severe constipation in addition to pure spastic paraplegia.

Adenosine Triphosphatases↗
PubMed2001

Electron spin resonance observation of the Si(111)-(7x7) surface and its oxidation process.

Electron spin resonance (ESR) observation of dangling-bond states on the Si(111)-(7x7) surface is demonstrated for the first time. The ESR spectra clearly show that a reaction of molecular oxygen with the Si(111)-(7x7) surface is associated with the appearance of a new dangling-bond center at unreacted Si adatoms. Most of the oxidized surface sites do not show ESR signals, but in a minor part of the surface another new type of surface defect is detected. The well known P(b) center at the SiO2/Si interface is found to evolve at an oxide thickness as thin as 0.3 nm.

Journal Article↗
PubMed2001

A set of Hox proteins interact with the Maf oncoprotein to inhibit its DNA binding, transactivation, and transforming activities.

Maf oncoprotein is a basic-leucine zipper (bZip) type of transcriptional activator. Since many transcription factors are known to form functional complexes, we searched for proteins that interact with the DNA-binding domain of Maf using the phage display method and identified two homeodomain-containing proteins, Hoxd12 and MHox/Prx1/Phox1/Pmx1. Studies with mutants of Hox and Maf proteins showed that they associate through their DNA-binding domains; the homeodomain of Hox and the bZip domain of Maf, respectively. Reflecting the high similarity of the bZip domain, all other Maf family members tested (c-/v-Maf, MafB, MafK, MafF, and MafG) also associated with the Hox proteins. Pax6, whose homeodomain is relatively similar to MHox, also could interact with Maf. However, two other bZip oncoproteins, Fos and Jun, failed to associate with the Hox proteins, while a distantly related Hox family member, Meis1, could not interact with Maf. Through interactions with the bZip domain, the Hox proteins inhibited the DNA binding activity of Maf, whereas the binding of Hox proteins to their recognition sequences was not abrogated by Maf. We further showed that coexpression of the Hox proteins repressed transcriptional activation and transforming activity of Maf. These results suggested that the interaction of a set of Hox proteins with Maf family members may interfere not only with their oncogenicity but also with their physiological roles.

Amino Acid Sequence↗
PubMed2001

Pho85 kinase, a yeast cyclin-dependent kinase, regulates the expression of UGP1 encoding UDP-glucose pyrophosphorylase.

The PHO85 gene is a negative regulator of the PHO system in the yeast Saccharomyces cerevisiae and encodes a protein kinase (Pho85) highly homologous to the Cdc28 kinase (Cdc28). Ten cyclin-like proteins are known to interact with Pho85, and combination with different cyclins is believed to be responsible for distinct Pho85 functions, including phosphate metabolism, carbon source utilization and cell cycle regulation. However, only a limited number of substrates of Pho85 kinase, including Pho4, Gsy2 and Sicl, have so far been identified. To search for more targets of Pho85 and to clarify the genetic control mechanisms by Pho85 kinase in these cellular functions, we carried out a genome-wide analysis of the effect of a pho85Delta mutation on gene expression. We found that expression of various genes involved in carbon metabolism are affected by the mutation and that among them, UGP1 promoter activity was increased in the absence of Pho85 kinase. This increase in the promoter activity was not observed in a pho4Delta mutant or with a mutant UGP1 promoter that is devoid of putative Pho4 and Bas2 binding sites, suggesting that UGP1 expression is modulated by Pho85 through Pho4. We also found that expression of several Pho85-cyclin genes were altered by the carbon source, the growth phase and Pho85 kinase itself.

Blotting, Northern↗
PubMed2001

A microbial chip combined with scanning electrochemical microscopy.

A microbial chip for bioassay was fabricated and its performance was characterized by scanning electrochemical microscopy (SECM). The microbial chip was prepared by spotting a suspension of Escherichia coli on a polystyrene substrate by using a glass capillary pen. The respiration activity of the E. coli spot was imaged with SECM by mapping the oxygen concentration around the spot. The SECM images of the microbial chips clearly showed spots with lower reduction currents, indicating that E. coli in the spots uptake oxygen by respiration. The bactericidal effects of antibiotics (streptomycin and ampicillin) were measured using the E. coli-based microbial chip, and discussed in comparison with the minimum inhibitory concentration (MIC) determined by an agar plate dilution method.

Ampicillin↗
PubMed2001

Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene.

Friedreich ataxia (FRDA), the most common autosomal recessive neurodegenerative disease among Europeans and people of European descent, is characterized by an early onset (usually before the age of 25), progressive ataxia, sensory loss, absence of tendon reflexes and pyramidal weakness of the legs. We have recently identified a unique group of patients whose clinical presentations are characterized by autosomal recessive inheritance, early age of onset, FRDA-like clinical presentations and hypoalbuminemia. Linkage to the FRDA locus, however, was excluded. Given the similarities of the clinical presentations to those of the recently described ataxia with oculomotor apraxia (AOA) linked to chromosome 9p13, we confirmed that the disorder of our patients is also linked to the same locus. We narrowed the candidate region and have identified a new gene encoding a member of the histidine triad (HIT) superfamily as the 'causative' gene. We have called its product aprataxin; the gene symbol is APTX. Although many HIT proteins have been identified, aprataxin is the first to be linked to a distinct phenotype.

Amino Acid Sequence↗
PubMed2001

Platelet-activating factor acetylhydrolase isoforms I and II in human uterus. Comparisons with pregnant uterus and myoma.

The concentrations of platelet-activating factor (PAF) that possesses the ability to stimulate myometrial contraction are partially regulated by intracellular type of platelet-activating factor acetylhydrolase (PAF-AH) in many tissues. Tissue cytosol contains at least two intracellular PAF-AH, isoforms I and II. To examine the relationship between the activity and isoforms of intracellular PAF-AH in human uterine myometrium and myoma, we assayed the PAF-AH activity and identified the PAF-AH isoforms I and II by Western blot analysis. The intense bands of the alpha2 and ss subunits of PAF-AH isoform I were detected in nonpregnant uterus; however, the specific bands of the alpha1 subunit of PAF-AH isoform I and the PAF-AH isoform II were extremely weak. The levels of the alpha2 and ss subunits and PAF-AH activity in pregnant uterus (37-39 wk gestation) were significantly lower than those in nonpregnant uterus. On the other hand, the level of ss subunit and the PAF-AH activity in myoma were significantly higher than those in nonpregnant uterus. No significant difference was found in the expression of the PAF-AH isoform II among three tissues. These results indicate that the change in the PAF-AH activity observed in pregnant uterus and myoma are due to the lower or higher protein expression of the PAF-AH isoform I, especially the alpha2 and/or ss subunits. The decrease of the uterine PAF-AH activity in the late stage of pregnancy may facilitate the action of PAF to stimulate myometrial contraction.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2001

Removal of anterior clinoid process for basilar tip aneurysm: clinical and cadaveric analysis.

The difficulty in the operation for basilar tip aneurysm is the restriction in surgical working space. To resolve this problem, aggressive skull base surgery has been reported, but these techniques are not prevalent. Pterional and subtemporal approaches are commonly used for basilar tip aneurysms. In an attempt to increase the surgical working space during the pterional approach, the anterior clinoid process and the roof of the optic nerve were removed extradurally to increase the mobilization of the intracranial internal carotid artery and optic nerve. The effects of removing the anterior clinoid process and microanatomy in the perioptic area were analyzed by cadaveric procedures in 10 cases (20 sides). With this procedure, the internal carotid artery can be retracted medially with a spatula 6.1 +/- 0.8 mm (mean +/- SD). The length and the area of dural fold in the bone defect region in the optic canal roof are 2.1 mm and 13.6 mm. In 10 clinical cases, this procedure allowed enough space to approach the basilar tip aneurysm without disturbing the internal carotid artery blood flow. The clinical outcome was satisfactory.

Basilar Artery↗
PubMed2001

Method to improve cosmetic outcome following craniotomy.

This technical note describes a simple method for reducing the dead space created by craniotome due to the loss of bone dust and improving the cosmetic outcome following a craniotomy. After drilling the burr holes for the craniotomy, the bone between the holes is drilled away in a standard fashion except that multiple regions of about 1 cm in length are left intact. These intact regions are broken using a periosteal elevator and fixed like a bridge when the bone is replaced. The resulting bone flap is readily returned to its original position without making the dead space created by regular craniotomy. The amount of the dead space caused by losing the bone dust is reduced and a good cosmetic recovery is obtained. This technique is useful for both craniotomy and facial bone surgery, which requires cosmetic results.

Bone and Bones↗
PubMed2001

Effects of amino acids on the amidation of polyaromatic carboxylic acids by Bacillus cereus.

The soil bacterium Bacillus cereus Tim-r01 efficiently transformed polyaromatic carboxylic acids (PACA) such as 4-biphenylcarboxylic acid (4-BPCA), 4-biphenylacetic acid, and 4-phenoxybenzoic acid into their corresponding amides. The amidation activity was expressed at 37 degrees C (pH 7-8) in the presence of grown cells in nutrients under an aerobic atmosphere. Other strains of B. cereus, IFO 3001 and IAM 1229, also gave the amide from 4-BPCA. In phosphate-buffered saline (PBS), the addition of normal amino acids was essential, while sulfur-containing amino acids such as methionine and cysteine drastically inhibited the amidation. Tracer experiments using N-15-isoleucine and N-15-alanine showed that the nitrogen atom of the amide came from an amino group of amino acids but not from ammonia or alkylamines.

Amides↗
PubMed2001

[Hereditary ataxias-overview].

Many of autosomal dominant spinocerebellar ataxias (SCA) are now shown to result from the expansion of unstable trinucleotide repeats. In most SCAs, these repeats are present within coding sequences of the causative genes and translated into polyglutamine tracts. In this overview clinical and molecular genetic features of newly identified group of diseases in this category are briefly summarized. Expanded polyglutamine repeats are supposed to mediate some toxic effects on a certain population of neurons that result in neuronal dysfunction. The current progress in these molecular biological studies on their pathophysiology is also reviewed. In Japan, Friedreich ataxia with intoronic GAA repeat expansions has not been known. Instead, early onset ataxia with Friedreich phenotype, associated with ocular motor apraxia in childhood and with hypoalbuminemia in adult, is the predominant ataxia with Friedreich phenotype, the causative mutation of which was very recently identified.

Animals↗
PubMed2000

Immunoassay of the MRSA-related toxic protein, leukocidin, with scanning electrochemical microscopy.

Scanning electrochemical microscopy (SECM) was applied to the immunoassay of leukocidin, which is a toxic protein produced by methicillin-resistant Staphylococcus aureus (MRSA), with the intention of developing and early diagnostic for MRSA infection. An antibody-chip for leukocidin was prepared by self-assembling of anti-leukocidin on a protein A-coated glass substrate. A sample solution containing leukocidin was spotted onto the antibody-chip, followed by labeling with horseradish peroxidase (HRP) via a sandwich method. The reduction current of the oxidized form of ferrocenylmethanol generated by the HRP reaction was monitored to view SECM images of the spot of captured leukocidin. The amplitude of reduction current depended on the concentrations of sample solutions used for making spots. This SECM-based immunoassay detects as low as 5.25 pg mL(-1) leukocidin.

Electrochemistry↗