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Biomedical subjects

M Tachikawa

Publications and source records attributed to M Tachikawa.

At least 19 recordsLinked to original sources
PubMed2005

Fukutin and alpha-dystroglycanopathies.

Fukuyama-type congenital muscular dystrophy (FCMD), Walker-Warburg syndrome (WWS), and muscle-eye-brain (MEB) disease are clinically similar autosomal recessive disorders characterized by congenital muscular dystrophy, lissencephaly, and eye anomalies. We identified the gene for FCMD and MEB, which encodes the fukutin protein and the protein O-linked mannose beta1, 2-N-acetylglucosaminyltransferase (POMGnT1), respectively. Recent studies have revealed that posttranslational modification of alpha-dystroglycan is associated with these congenital muscular dystrophies with brain malformations. All are characterized by hypoglycosylated alpha-dystroglycan. Fukutin's function and the relation with other alpha-dystroglycanopathies are discussed.

Animals↗
PubMed2001

Evaluation of atomic integrals for hybrid Gaussian type and plane-wave basis functions via the McMurchie-Davidson recursion formula.

A convenient formalism is developed for the evaluation of atomic integrals composed of a hybrid Gaussian type function and plane-wave (GTF-PW) basis set, based upon the recursion scheme proposed by McMurchie and Davidson [L. E. McMurchie and E. R. Davidson, J. Comput. Phys. 26, 218 (1978)] which was originally for Gaussian type basis functions. We show that revisions of recursion relations in the original article are necessary in order to allow systematic production of overlap, kinetic energy, nuclear attraction, and electron repulsion integrals in compact forms. Involving easy calculation of complex incomplete gamma functions, the recursion relations enable the use of hybrid GTF-PW basis functions with arbitrarily large angular momentum. This basis function can be applied to the first-principle calculation for solids involving localized electron orbitals.

Journal Article↗
PubMed2000

Age and origin of the FCMD 3'-untranslated-region retrotransposal insertion mutation causing Fukuyama-type congenital muscular dystrophy in the Japanese population.

Fukuyama-type congenital muscular dystrophy (FCMD), an autosomal recessive disorder with a high prevalence in the Japanese population, is characterised by severe muscular dystrophy associated with brain malformation (cortical dysgenesis) and mental retardation. In Japan, 87% of FCMD-bearing chromosomes carry a 3-kb retrotransposal insertion of tandemly repeated sequences within the disease gene recently identified on chromosome 9q31, and most of them share a common founder haplotype. FCMD is the first human disease known to be caused primarily by an ancient retrotransposal integration. By applying two methods for the study of linkage disequilibrium between flanking polymorphic markers and the disease locus, and of its decay over time, the age of the insertion mutation causing FCMD in Japanese patients is calculated to be approximately 102 generations (95% confidence interval: 86-117 g), or slightly less. The estimated age dates the most recent common ancestor of the mutation-bearing chromosomes back to the time (or a few centuries before) the Yayoi people started migrating to Japan from the Korean peninsula. This finding makes the molecular population genetics of FCMD understandable in the context of Japan's history and the founder effect consistent with the prevalent theory on the origins of the modern Japanese population.

Asian People↗
PubMed1998

Demonstration of a Directly Photopatternable Spin-On-Glass Based on Hydrogen Silsesquioxane and Photobase Generators.

A commercially available spin-on-glass material, hydrogen silsesquioxane, has been rendered photopatternable to micrometer dimensions by the introduction of a photobase generator at concentrations of <5 wt %. The cure process proceeds via hydrolysis of the silyl hydride linkage by residual water in the film, as activated by a photogenerated base catalyst. Subsequent reaction of the generated silanol with neighboring silyl hydride groups yields a thermally stable siloxane cross-link. The photochemical cross-linking of hydrogen silsesquioxane shows high sensitivity (<40 mJ/cm2) and is not inhibited by molecular oxygen. The resultant oxide films can be further cured at elevated temperature either under an inert atmosphere to minimize the dielectric constant or heated in an air atmosphere to complete the conversion to silica glass. The oxidative nature of both the photo and thermal cure processes and the release of only traces of hydrogen as byproduct results in minimal weight loss in the film during processing.

Journal Article↗
PubMed1997

Metabolic methylation is a possible genotoxicity-enhancing process of inorganic arsenics.

To elucidate if the metabolic methylation participates in the induction of inorganic arsenic-responsible genetic damage, arsenite (ARS) and its methylated metabolites, methanearsonic acid (MMAA) and dimethylarsinic acid (DMAA), were comparatively assayed for the induction of DNA damage by determining DNA repair synthesis using polymerization inhibitors such as aphidicolin (aph) and hydroxyurea (HU). When human alveolar epithelial type II (L-132) cells in culture were exposed to either one of these three arsenic compounds, DNA single-strand breaks resulting from the inhibition of repair polymerization were remarkably produced by exposure to DMAA at 5 to 100 microM, while not by that to ARS and MMAA even at 100 microM. Furthermore, a bromodeoxyuridine (BrdrU)-photolysis assay indicated that the induction of DNA repair synthesis was observed only in the case of exposure to DMAA. When L-132 cells were exposed to 100 microM MMAA in the presence of 10 mM S-adenosyl-L-methionine (SAM), which is a well-known methyl-group donor in metabolic methylation of arsenics, DNA repair synthesis was induced along with an increase in the amount of dimethylarsenic in the cells. These results indicate that metabolic methylation of inorganic arsenics to dimethylarsenics is predominantly involved in the induction of DNA damage.

Arsenic Poisoning↗
PubMed1997

A 260-kDa filamin/ABP-related protein in chicken gizzard smooth muscle cells is a new component of the dense plaques and dense bodies of smooth muscle.

A 260-kDa protein, termed cgABP260, which localized in the dense plaques and dense bodies of smooth muscle cells, was found in a low-salt alkaline extract of chicken gizzard smooth muscle. An antibody against cgABP260 was used to screen a chicken gizzard cDNA library, and the nucleotide sequence of the partial cDNA encoding this protein was determined. Comparison of predicted amino acid sequences revealed that the protein had significant homology with human ABP-280 and chicken retina filamin [Barry, C.P. et al. (1993) J. Biol. Chem. 268, 25577-25586], but despite the high homology, cgABP260 was immunologically distinguishable from filamin. Immunoblot analysis showed that an anti-cgABP260 antibody reacted exclusively with the cgABP260 band of smooth, skeletal, and cardiac muscle tissues. By indirect immunofluorescence, the membrane-affinity-purified antibody against cgABP260 intensely stained the dense plaques of the isolated smooth muscle cells. Immunoelectron microscopy showed that immunogold particles representing cgABP260 were found abundantly on the dense plaques and less abundantly on the dense bodies. Its amino acid sequence, molecular size, immunological reactivity, and localization in smooth muscle thus indicated that cgABP260 is a new component of the dense plaques and dense bodies of smooth muscle cells.

Amino Acid Sequence↗
PubMed1996

A comparative study of dynamic structures between phage 434 Cro and repressor proteins by normal mode analysis.

Two DNA binding proteins, Cro and the amino-terminal domain of the repressor of bacteriophage 434 (434 Cro and 434 repressor) that regulate gene expression and contain a helix-turn-helix (HTH) motif responsible for their site-specific DNA recognition adopt very similar three-dimensional structures when compared to each other. To reveal structural differences between these two similar proteins, their dynamic structures, as examined by normal mode analysis, are compared in this paper. Two kinds of structural data, one for the monomer and the other for a complex with DNA, for each protein, are used in the analyses. From a comparison between the monomers it is found that the interactions of Ala-24 in 434 Cro or Val-24 in 434 repressor, both located in the HTH motif, with residues 44, 47, 48, and 51 located in the domain facing the motif, and the interactions between residues 17, 18, 28, and 32, located in the HTH motif, cause significant differences in the correlative motions of these residues. From the comparison between the monomer and the complex with DNA for each protein, it was found that the first helix in the HTH motif is distorted in the complex form. While the residues in the HTH motif in 434 Cro have relatively larger positive correlation coefficients of motions with other residues within the HTH motif, such correlations are not large in the HTH motif of 434 repressor. It is suggestive to their specificity because the 434 repressor is less specific than 434 Cro. Although a structural comparison of proteins has been performed mainly from a static or geometrical point of view, this study demonstrates that the comparison from a dynamic point of view, using the normal mode analysis, is useful and convenient to explore a difference that is difficult to find only from a geometrical point of view, especially for proteins very similar in structure.

Amino Acid Sequence↗
PubMed1995

In vitro effect of chromium and other trace metals on mouse hepatotoxicity induced by carbon tetrachloride exposure.

Using primary cultured mouse hepatocytes, in vitro study was performed to discuss the effect of Cr(III) and several other trace metals, Cr(VI), Mn(II), Zn(II), Co(II), Cu(II), Ni(II), and Ga(III) on acute liver damage induced by CCl4 exposure. 1) The LDH activity 60 min after CCl4 exposure increased dose-dependently with CCl4 concentrations in all of the trace metal pretreatment groups, except for the Cr(VI) pretreatment group, which showed a significant protective effect even after 30 min of CCl4 exposure. 2) LDH leakage was not observed 10 min after CCl4 exposure at 3 or 5 mM, while lipid peroxidation was increased dose-dependently with CCl4 concentrations in all groups except the Cr(VI) pretreatment group, in which the production of peroxidated lipid was significantly inhibited. 3) Similarly to the pretreatment with Cr(VI), LDH leakage 30 min after exposure to 5 mM CCl4 was inhibited by pretreatment with such antioxidants as N,N'-diphenyl-p-phenylenediamine or DL-alpha-tocopherol. 4) The Cr(VI) uptake was about 50% of the added amount, whereas the Cr(III) uptake was only 5% of the added amount. 5) 90% or more of the intracellular chromium was reduced to Cr(III) 10 min after Cr(VI) treatment. The results suggested that the in vitro protective effect of pretreatment with Cr(VI) was due to a rapid reduction of Cr(VI) to Cr(III), and the radical scavenger-like effect of the produced Cr(III) was the same effect as in vivo Cr(III); it therefore suggests that Cr(III) contributes to protective effect on CCl4-induced hepatotoxicity.

Animals↗
PubMed1991

Differences between freshwater and seawater killifish (Oryzias latipes) in the accumulation and elimination of pentachlorophenol.

Freshwater and seawater acclimated (FWA and SWA) killifish (Oryzias latipes) were exposed to pentachlorophenol (PCP) for 3-10 days. Uptake and clearance rates of FWA and SWA killifish were determined. The estimated bioaccumulation factors (BCF) of PCP for FWA and SWA killifish were 1680 and 370, respectively. The smaller uptake rate and faster clearance rate resulted in the lower BCF for SWA killifish. Fresh- and seawater killifish excreted the PCP metabolites, the glucuronide and sulfate conjugates of PCP; the major metabolite of freshwater killifish was PCP sulfate; for seawater acclimated fish, it was PCP glucuronide. The greater excretion of PCP glucuronide by seawater killifish may be responsible for the rapid elimination of PCP. PCP accumulation in killifish decreased with higher pH levels in both freshwater and seawater environments, but these differences were less than the effect of salinity. The results indicate that salinity can affect the accumulation and elimination of environmental pollutants in killifish.

Animals↗