Search PubMed⌕ Search

Biomedical subjects

K Moriyama

Publications and source records attributed to K Moriyama.

At least 91 records · Page 5Linked to original sources
PubMed1997

[Minimally invasive technique for mitral valve repair--the importance of intraoperative transesophageal echocardiography].

A 65-year-old male with mitral regurgitation was scheduled for the mitral valve repair by means of minimally invasive technique. The technique, which requires a 10-cm right parasternal incision, offers minimal discomfort, less postoperative pain, quick functional recovery and excellent cosmetic healing. However, the intraoperative monitoring by the transesophageal echocardiography was required to evaluate the mitral valve function and to confirm the complete removal of air from the apex of the left ventricle and right upper pulmonary vein due to the small operative field. In addition, the monitoring of the short-axis view of the left ventricle makes it possible to evaluate and to confirm the preload and the left ventricular contractility. We considered that the transesophageal echocardiography is essential and useful for the minimally invasive mitral valve repair.

Aged↗
PubMed1996

Reduced precore transcription and enhanced core-pregenome transcription of hepatitis B virus DNA after replacement of the precore-core promoter with sequences associated with e antigen-seronegative persistent infections.

Hepatitis B virus variants harboring nucleotide alterations in the preC-C promoter have been detected in fulminant hepatitis B as well as in HBeAg-seronegative persistent infection. However, it has not been demonstrated that variants with nucleotide alterations in the preC-C promoter cause various disease states. We replaced the preC-C promoter region of a wild-type genome with the most frequent naturally occurring mutated form and introduced it into HepG2 cells. The mutant with coexisting A1762T and G1764A substitutions produced less than one-fifth of the wild-type level of HBeAg. Conversely, the mutant generated 2.4 times more core particle antigen and showed a high-replicator phenotype. RNase protection and quantitative 5' RACE showed a 16- to 32-fold reduction of preC transcripts and a 4-fold induction of C transcripts of the mutant compared to wild-type. The preC transcript of the mutant had a more heterogeneous 5' end than that of the wildtype. However, the mutations did not alter the initiation sites of C transcription. When the promoter region was cloned into CAT plasmids, the mutations had dual effects on preC and C promoter activities, decreasing and increasing them, respectively. These results suggest that these mutations are responsible for the reduced HBeAg production as well as the enhanced replication and core production. Analysis of revertants with either single point mutation showed that T at 1762 is critical for the mutant phenotype.

Amino Acid Sequence↗
PubMed1996

Tertiary structure of destrin and structural similarity between two actin-regulating protein families.

Destrin is an isoprotein of cofilin that regulates actin cytoskeleton in various eukaryotes. We determined the tertiary structure of destrin by triple-resonance multidimensional nuclear magnetic resonance. In spite of there being no significant amino acid sequence homology, we found that the folding of destrin was strikingly similar to that of repeated segments in the gelsolin family, which resulted in a new protein fold group. Sequential dissimilarity of the actin-binding helix of destrin to that of gelsolin explains the Ca2+-independent actin-binding of destrin. Possible mechanisms of phosphorylation-sensitive phosphoinositide-competitive actin binding, of pH-dependent filament severing, and of nuclear translocation with actin in response to stresses, are discussed on the basis of the tertiary structure.

Actin Depolymerizing Factors↗
PubMed1996

Characterization of a novel variant of apolipoprotein E, E2 Fukuoka (Arg-224 --> Gln) in a hyperlipidemic patient with xanthomatosis.

A new variant of apolipoprotein (apo) E, designated apo E2 Fukuoka, was identified in a 54-year-old Japanese woman who suffered from hyperlipoproteinemia (total cholesterol 29.7 mmol/l, triglyceride 12.0 mmol/l, when she was 48-year-old) with the presence of xanthoma in the palms, bones, and ocular fundi, and other sites. Foam-cell macrophages were observed in bone marrow specimens. Analysis of apo E phenotype showed the E3/E2 isoform on isoelectric focusing performed on plasma, but the E3/E3 isoform on restriction-fragment-length polymorphism of the apo E gene. This discrepancy indicated that the apo E had an amino-acid substitution outside of amino-acid residues at 112 and 158. Sequence analysis of the patient's DNA, which was amplified by PCR and subcloned, revealed a single substitution from arginine (CGG) to glutamine (CAG) at residue 224, thereby adding one negatively charged unit to apo E3. Recombinant apo E2 Fukuoka produced in COS-1 cells showed almost the same binding activity to the LDL receptor on human skin fibroblasts as compared with recombinant apo E3. Recombinant apo E2 Fukuoka showed the same heparin binding ability than recombinant apo E3. Findings indicated that apo E2 Fukuoka was not the primary cause of the hyperlipoproteinemia observed in this case.

Apolipoprotein E2↗
PubMed1996

Herbimycin A, a tyrosine kinase inhibitor, impairs hypercalcemia associated with a human squamous cancer producing interleukin-6 in nude mice.

Interleukin-6 (IL-6) is a multifunctional cytokine that is produced not only by a variety of normal cells but also by cancer cells. IL-6 produced by cancer cells stimulates the proliferation of these cancer cells in an autocrine/ paracrine manner and causes paraneoplastic syndromes including hypercalcemia, cachexia, and leukocytosis. We have reported previously that a human oral squamous cancer associated with hypercalcemia produces large amounts of IL-6, that animals bearing this cancer exhibit elevated levels of plasma IL-6, and that neutralizing antibodies to human IL-6 reverse hypercalcemia in tumor-bearing animals, indicating an important role of IL-6 in the hypercalcemia in this model. Because these cancer cells overexpress epidermal growth factor receptors (EGFR) with intrinsic tyrosine kinase (TK) activity similar to many other squamous cancers, we examined the effects of herbimycin A, a tyrosine kinase inhibitor, on IL-6 production and hypercalcemia in animals bearing this cancer to develop a new approach to treat the hypercalcemia associated with malignancy. Intraperitoneal administration (once a day for 2 days) of herbimycin A to cancer-bearing hypercalcemic mice reduced the plasma levels of human IL-6 and impaired the hypercalcemia. During 2-day treatment with herbimycin A, no changes were observed in tumor size. Of interest, plasma levels of mouse, but not human, soluble IL-6 receptors were also elevated. However, herbimycin A showed no effects on plasma levels of mouse soluble IL-6 receptors. Herbimycin A suppressed the tyrosine autophosphorylation of EGFR and IL-6 mRNA expression and production, all of which were stimulated by EGF. The data raise the possibility that TK inhibitors may be potential mechanism-based therapeutic agents for the treatment of hypercalcemia associated with squamous cancers which overexpress EGFR.

Animals↗
PubMed1996

Phosphorylation of Ser-3 of cofilin regulates its essential function on actin.

BACKGROUND: Cofilin is a low-molecular weight actin-modulating protein, and is structurally and functionally conserved in eucaryotes from yeast to mammals. The functions of cofilin appear to be regulated by phosphorylation and dephosphorylation. RESULTS: A proteolytic study of phosphorylated porcine cofilin and expression of a mutated cofilin in cultured cells revealed that Ser-3 is the unique phosphorylation site. Phosphorylated cofilin was found not to bind to either F- or G-actin while unphosphorylated cofilin binds to both. S3D-cofilin, in which Ser-3 was replaced with Asp, did not bind in vitro to actin while S3A-cofilin did. The transient over-expression of wild-type or S3A-cofilin in cultured cells caused disruption of preexisting actin structures and induced cytoplasmic actin bundles. Heat shock-induced nuclear or NaCl buffer-induced cytoplasmic actin/cofilin rods contained the expressed cofilin. In contrast, the over-expression of S3D-cofilin did not alter the actin structures. Induced actin rods did not contain S3D-cofilin. S3D-porcine cofilin did not complement the lethality associated with delta cof1 mutations in Saccharomyces cerevisiae while wild-type and S3A-cofilin did. Furthermore, we found that S2A/S4D- and S2D/S4D-yeast cofilin mutants were not viable. CONCLUSION: We conclude that the function of cofilin is negatively regulated in vivo by phosphorylation of Ser-3 and that cells require the function of unphosphorylated cofilin for viability.

Actin Depolymerizing Factors↗
PubMed1996

Lymphokine-activated killer cells can discriminate CD34+ leukemia cells from normal hematopoietic progenitor cells.

The ability of lymphokine-activated killer (LAK) cells to discriminate between CD34+ leukemia cells and hematopoietic progenitor cells was investigated. As effector cells, CD4(-)-LAK generated from a CD4- subset of allogeneic peripheral blood lymphocytes were used. The target cell samples were obtained from peripheral blood stem cell (PBSC) collections. Detection of residual tumor cells was performed using a polymerase chain reaction (PCR) technique for chimeric bcr/abl messenger RNA. When PBSC were obtained from patients with seminoma and lung cancer, treated with the CD4(-)-LAK for 12 h and the CD34+ cells were isolated, colony formation (CFU-GM) by these cells was preserved. When PBSC were obtained from a patient with PCR-positive acute lymphocytic leukemia and treated with the CD4(-)-LAK for 3 h, reexamination showed conversion to PCR negativity. Furthermore, when the CD34+ cells isolated from the negative converted PBSC were cultured, they still exhibited colony formation. These results suggest that the CD4(-)-LAK can kill the CD34+ leukemia cells, discriminating from the normal hematopoietic progenitors.

Antigens, CD34↗
PubMed1996

Identification of two apolipoprotein variants, A-I Karatsu (Tyr 100-->His) and A-I Kurume (His 162-->Gln).

We identified two apolipoprotein (apo) A-I variants, using isoelectric focusing gel electrophoresis: apo A-I Karatsu, which had a relative charge of +1 compared to normal apo A-I4, and apo A-I Kurume, which had a relative charge of -1. Direct sequence analysis of the PCR-amplified DNA from the proband of apo A-I Karatsu revealed a single substitution of tyrosine (TAC) for histidine (CAC) at position 100. Sequence analysis of apo A-I Kurume revealed a single substitution of histidine (CAT) for glutamine (CAG) at position 162. Probands of these two mutants and limited family study showed no accelerated atherosclerosis.

Adult↗
PubMed1996

A cysteine-containing truncated apo A-I variant associated with HDL deficiency.

We identified a 50-year-old Japanese woman with a novel mutation in the apolipoprotein (apo) A-I gene causing high-density lipoprotein (HDL) deficiency. The patient had extremely low HDL cholesterol and apo A-I levels (0.14 mmol/L and 0.8 mg/dL, respectively) but no evidence of coronary heart disease. However, she had bilateral xanthomas of the Achilles tendon, elbow, and knee joint as well as corneal opacities. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of serum followed by immunoblotting revealed that the patient's apo A-I had a lower molecular weight (24,000) than normal apo A-I. A partial gene duplication encompassing 23 nucleotides was found by DNA sequence analysis, resulting in a tandem repeat of bases 333 to 355 from the 5' end of exon 4. This tandem repeat caused a frameshift mutation with premature termination after amino acid 207. The frameshift gives rise to a predicted protein sequence that contains two cysteines. We designated this mutant as apo A-ISasebo. Apo A-ISasebo formed heterodimers with apo A-II and apo E in the patient's plasma and was associated with both the low-density lipoprotein and HDL fractions. The patient's cholesterol esterification rate and lecithin-cholesterol acyltransferase activity were reduced to about 30% of normal, although specific enzyme activity was unaffected, suggesting that it remained functionally normal. In addition, cholesteryl ester transfer activity was reduced to about half of normal. Thus, apo A-ISasebo was associated with complex derangements of lipoprotein metabolism.

Amino Acid Sequence↗
PubMed1996

A role of cofilin/destrin in reorganization of actin cytoskeleton in response to stresses and cell stimuli.

1. Cofilin is an essential actin-regulating protein widely distributed in all eucaryotes. The structure and function of cofilin are conserved during evolution. 2. Cofilin depolymerizes F-actin in vitro at alkaline pH and severs F-actin in vitro at pH lower than 7.3. Overexpression of cofilin in viable cells induced bundles of actin filaments suggesting that the severing activity rather than the actin-depolymerizing or monomeric actin-sequestering activity is physiologically significant in vivo. 3. The actin bundle formation induced by overexpression of cofilin is accompanied with an increase in cell motility of Dictyostelium cells. 4. In higher vertebrates, the actin-binding activity of cofilin is negatively regulated by phosphorylation on its Ser-3 residue. The actin-binding activity is essential for yeast cells to grow. 5. Stresses and various cell stimuli activate cofilin by inducing dephosphorylation of cofilin in resting vertebrate cells. 6. Cofilin has an nuclear localization signal sequence and translocates into the nucleus together with actin in response to various stresses. Functional roles of cofilin/actin in the nucleus remain to be elucidated. 7. Tertiary structure of destrin (cofilin) resembles that of gelsolin segment 1 and well explains its functions such as Ca(2+)-independent actin binding activity.

Actin Depolymerizing Factors↗
PubMed1996

Purification and characterization of a lectin from Amaranthus hypochondriacus var. Mexico seeds.

A lectin from Amaranthus hypochondriacus var. Mexico (AHML) was purified by affinity chromatography using asialofetuin-Sepharose 4B. AHML is specific for N-acetyl-D-galactosamine as are the other Amaranthus lectins. AHML has no carbohydrate moiety and requires no metal ion for the hemagglutination activity. The pI of AHML is 6.8. AHML has a native molecular mass of 45.0 kDa and is composed of homo-subunits having molecular masses of 36.8 kDa.

Amino Acids↗
PubMed1996

Properties of magnetically attractive experimental resin composites.

SUS444 stainless steel filled chemically cured resin composites that can attract magnet were fabricated. The filler was treated with various concentrations of silane. The experimental composite was easy to handle and showed a good shelf life. The maximal properties obtained are as follows; The attraction force to a magnetic attachment was 1/3-1/4 lower than the commercially available magnet-keeper system for dental magnetic attachment. Flexural strength and Knoop hardness of the composite were 76MPa (7.7 kgf/mm2) and 64 KHN. These values were lower than the commercially available chemically cured composite used as a reference. Eluted metal from the composite in 1% lactic acid solution for 7 days showed 0.7 mg/cm2, but in 0.9% NaCl solution for 7 days, it could not be detected.

Composite Resins↗
PubMed1996

Identification of two apolipoprotein variants, A-I Kaho (Asp 51-->Val) and A-I Lys 107 deletion.

We have identified two apolipoprotein (apo) A-I variants using isoelectric focusing gel electrophoresis: apo A-I Kaho which has a relative charge of +1 compared to normal apo A-I4, and apo A-I Nanakuma2 which has a relative charge of -1. Sequence analysis of PCR-amplified DNA from the proband of apo A-I Kaho revealed a single substitution of aspartic acid (GAC) for valine (GTC) at residue 51. Sequence analysis of PCR-amplified DNA from the proband of apo A-I Nanakuma2 revealed a three-base (AAG or AGA) deletion between bases 186 and 193 from the 5' end of exon 4 that leads to deletion of Lys 106 or 107. This mutation may be the same as that of apo A-I Marburg or A-I Munster-2 reported by Rall et al. (Rall SC Jr, Weisgraber KH, Mahley RW, Ogawa Y, Fielding CJ, Utermann G, Haas J, Steinmetz A, Menzel HJ, and Assmann G, J Biol Chem, 259: 10063-10070, 1984). Because of its unique sequence between 185 and 193 from the 5' end of exon 4 of apo A-I gene, we could not define whether AAG or AGA is deleted by DNA sequencing.

Adult↗
PubMed1996

[Usefulness of reaction times in high-cortical recognition tasks].

We compared reaction times for high-cortical recognition tasks with kana-searching test in a group of 46 normal individuals aged 21 to 83 who gain a full score in Mini-Mental State. The following tasks of reaction time were used; simple reaction time (SRT), choice reaction time (CRT), memory scanning time (MST), and visual searching time (VST). The results were consistent and demonstrated that mean reaction time of 46 individuals increased in difficult tasks such as MST or VST. All reaction times increased depending on aging, which became longer in difficult tasks. Score of kana-searching test was correlated with MST and VST, but did not correlate with SRT and CRT. These findings suggest that reaction times may be useful for mass-screening of high-cortical functions in different ages as well as the kana-searching test.

Adult↗