Biomedical subjects

K Saeki

Publications and source records attributed to K Saeki.

At least 109 records · Page 6Linked to original sources

PubMed1999

Repetitive monomorphic ventricular tachycardia of left coronary cusp origin.

Repetitive monomorphic ventricular tachycardia with a morphology of inferior axis and left bundle branch block pattern in patients without structural heart disease commonly originates from the right ventricular outflow tract. We report the case of a 22-year-old man with an incessant, monomorphic ventricular tachycardia with a similar morphology originating from the left coronary cusp, which was confirmed by perfect pace mapping, local ventricular activation preceding the onset of QRS by 25 mse, and eliminated by a single delivery of low-energy (11 W) radiofrequency currents.

Adult↗

PubMed1999

Apoptosis-inducing activity of polyphenol compounds derived from tea catechins in human histiolytic lymphoma U937 cells.

Polyphenolic compounds derived from tea catechins were examined for apoptosis-inducing activity in human histiolytic lymphoma U937 cells. (-)-Epigallocatechin gallate, theasinensin D, compound OH-5, theaflavin, and theaflavin digallate induced apoptosis as evidenced by DNA ladder formation, its inhibition by a caspase inhibitor, and chromatin condensation. Theasinensin D was the most potent inducer and the data suggest the importance of the number and three dimensional localization of their phenolic groups in this activity. These apoptosis-inducible compounds may be useful as a cancer chemopreventive and chemotherapeutic agent.

Antineoplastic Agents, Phytogenic↗

PubMed1999

[Development of professional competence in public health nurses].

PURPOSE: Significant changes that are occurring in the community health care system, require that public health nurses who work for local governments to not only provide direct care but also to coordinate health care teams and participate in policy making. The purpose of this study is to investigate the current system of developing professional competence in public health nurses, and to consider ways to improve it. METHOD: The subjects, randomly chosen, were 100 chief public health nurses and 298 staff nurses in Hokkaido. Sixty-four chief nurses, 44 beginner nurses, 87 proficient nurses and 88 expert nurses responded. The data were collected with a self-administered questionnaire which necessitated the subjects to make a self evaluation of their practical competence and circumstances of its development. RESULT: Self evaluated competence, in making accurate assessments of individual needs and initiating direct care, developed with their experiences in the job, and was generally high. However, the questionnaire showed that self evaluation of their work and ability to do theoretical analysis and research was low and did not progress in conjunction with the length of work experience. Policy making experience was limited and policy making competence was evaluated as low, but there was an expectation that this competence would develop in time. Almost all of the respondents expected their professional competence to progress to higher levels. In particular, beginner nurses wanted to gain practical care competence; proficient and expert nurses wanted to develop their powers of theoretical analysis and do more research, while chief nurses were keen to gain competence in the area of policy making. The respondents reported that they sometimes attended academic conferences, but hardly did any research. CONCLUSION: Low self-evaluation of public health nurses reflect a basic immaturity as a profession. They need to establish their profession and to increase their self-evaluated competencies as their careers develop. These findings showed the importance of establishing a system of continuing education that will cultivate competence in various aspects of their job and also motivate self study. These findings also reveal the importance of collaboration between the university as a vehicle for theoretical work and research and the work place as the embodiment of practical application.

Clinical Competence↗

PubMed1999

AFM study of citric acid-ferric chloride etching characteristics of dentin.

PURPOSE: To determine the etching characteristics of 10% citric acid etchant with 3% ferric chloride (10-3) compared with related etchants without ferric chloride (10-0), or one of similar pH (36% citric acid). MATERIALS AND METHODS: Atomic force microscopy (AFM) was used to measure the surface recession and morphology of dentin. AFM images were taken of the same samples at seven steps of an etching and drying procedure using 10-3 (pH = 1.09), 10-0 (pH = 1.87) or 36% (pH = 1.08) citric acid solutions: at baseline, after etching 15 s, after 5-s air-drying, after rewetting, after 24-hr desiccation, after 30 s rewetting and after 24 hrs rewetting in filtered and purified water. RESULTS: 10-3 etched surfaces receded more than either 10-0 or 36% etched surfaces, and underwent greater collapse on 5-s air-drying. On rewetting all surfaces re-expanded to near their as-etched level. Following prolonged desiccation (24 hrs) all samples collapsed to the level seen after brief air-drying. 30-s rewetting did not restore the surface, but re-expansion of the collapsed collagen matrix was seen at 24 hrs.

Acid Etching, Dental↗

PubMed1998

Sequence analysis and expression of a novel mouse homolog of Escherichia coli recA gene.

Escherichia coli recA and its yeast homologs RAD51 and DMC1 play crucial roles in mitotic and/or meiotic recombination and in repair of double-strand DNA breaks. We have identified a murine novel recA-like gene (MmTRAD). The predicted 329 amino acid protein showed significant homology to mouse Rec2, Rad51, Dmc1 (or Lim15) and E. coli RecA. Northern blot analysis revealed that MmTRAD was ubiquitously transcribed in various tissues.

Amino Acid Sequence↗

PubMed1998

Antimutagenic structural modification of quinoline assessed by an in vivo mutagenesis assay using lacZ-transgenic mice.

Quinoline, a hepatocarcinogen, mutates the bacterial tester strains in the presence of the rat liver microsomal enzymes and induces GST-P (placental glutathione S-transferase)-positive foci in a medium-term bioassay system for hepatocarcinogenesis. On the other hand, 3-fluorinated quinoline was neither mutagenic nor carcinogenic in the same assay systems, whereas, 5-fluoroquinoline was mutagenic and carcinogenic. Quinoline was recently demonstrated to be mutagenic in an in vivo mutagenicity assay system using the lacZ-transgenic mouse (MutaMouse). The present study was undertaken to know whether 3-fluoroquinoline would be devoid of in vivo mutagenicity in MutaMouse. Quinoline and 5-fluoroquinoline were also tested in the same system. Mutagenicity was evaluated in the liver, the target organ of quinoline carcinogenesis, and also in the bone marrow and testis. The results strongly indicate that fluorine-substitution at the position-3 of quinoline could be an anti-genotoxic structural modification of quinoline in a wide range of its genotoxic end-points.

Animals↗

PubMed1998

In vivo mutagenesis by the hepatocarcinogen quinoline in the lacZ transgenic mouse: evidence for its in vivo genotoxicity.

Quinoline is carcinogenic to the liver of rats and mice and mutagenic to bacterial tester strains in the presence of rat liver microsomal enzymes. The unscheduled DNA synthesis (UDS) study suggested that quinoline might be a non-genotoxic carcinogen because of the lack of UDS-inducing capacity. In order to determine whether or not cancer induction is initiated by mutagenic DNA lesions, the present study was undertaken to evaluate the mutagenicity of quinoline in an in vivo mutation assay system using the lac Z transgenic mouse (Muta Mouse). Mutation was only induced in the liver, the target organ of carcinogenesis by quinoline, but not in the other organs examined, i.e. lung, kidney and spleen. Mutant frequency in the liver was 4-fold higher than in the untreated control animals. Dimethylnitrosamine, used as a positive control, induced mutation at a frequency 5-fold higher in the liver and 3-fold higher in the spleen than in their respective control organs. It can be concluded that the genotoxicity of quinoline is responsible for its hepatocarcinogenesis, although UDS was not induced under the conditions previously reported.

Animals↗

PubMed1998

Potent inhibition of cell density-dependent apoptosis and enhancement of survival by dimethyl sulfoxide in human myeloblastic HL-60 cells.

Human myeloblastic cell line HL-60 cells undergo apoptosis during in vitro culture in a cell density-dependent manner, and this cell density-dependent apoptosis was observed when the concentration of cultured cells exceeded 8-10 x 10(5) cells/ml. Dimethyl sulfoxide (DMSO), a differentiation inducer of HL-60 cells, did not amplify, but rather potently inhibited, this apoptosis. In a low density culture condition, DMSO attenuated proliferation of HL-60 cells in spite of its inhibition of apoptosis. In contrast, DMSO did support cell survival under high cell density conditions, and DMSO-treated HL-60 cells reached an extremely high concentration of 2-3 x 10(6) cells/ml, a condition which could never be possible in a usual culture environment. Thus, DMSO exerted dual effects on cell proliferation, i.e., growth inhibition and apoptosis inhibition, and the sum of these effects resulted in an apparently distinct phenomenon according to the culture conditions including cell density.

Administration, Topical↗

PubMed1998

Differential receptor-functionality of the two distinct receptor proteins for mouse hepatitis virus.

We compared the virus-binding activity and receptor-functionality of the receptor proteins isolated from mouse hepatitis virus (MHV)-susceptible BALB/c mice (MHVR1) and MHV-resistant SJL mice (MHVR2). By using a soluble receptor protein which lacked the transmembrane and intracytoplasmic domains, virus overlay protein blot assay and neutralization tests showed that MHVR1 bound to JHM cl-2 virus with 300-500 times higher efficiency than to MHVR2. MHVR1 was revealed to have 10-30 fold higher receptor-functionality than MHVR2 when examined by measuring virus-binding to the receptor expressed on the cell surface. These findings suggested that the differences in susceptibility between BALB/c and SJL mice may depend upon the genotype of the MHV receptor.

Animals↗

PubMed1998

Isolation and characterization of murine coronavirus mutants resistant to neutralization by soluble receptors.

Murine coronavirus mutants resistant to neutralization with soluble receptors were isolated to study the receptor-binding site on the S proteins since such mutants were expected to have mutations in an important site for receptor-binding. We have isolated five soluble receptor-resistant (srr) mutants which had mutations of a single amino acid at 3 different positions in S protein. Srr mutant 11 with an amino acid change at position 65 (Leu to His) in the S1 subunit showed an extremely reduced binding by virus overlay protein blot assay. However srr mutants with a mutation at 1114 (Leu to Phe) (srr mutants 3, 4 and 7) or 1163 (Cys to Phe) (srr mutant 18) in the S2 subunit had receptor-binding activity similar to that of wild type cl-2. These results suggest that an amino acid at position 62 located in a conserved region among MHV strains is in particular important for receptor binding. We also discuss why srr mutants with a mutation in S2 showed high resistance to neutralization by soluble receptor, irrespective of their binding to MHV receptors.

Animals↗

PubMed1998

The rnf gene products in rhodobacter capsulatus play an essential role in nitrogen fixation during anaerobic DMSO-dependent growth in the dark

The rnf genes in Rhodobacter capsulatus are essential for nitrogen fixation in the light. Because R. capsulatus grows readily on N2 in the dark by anaerobic respiration with dimethylsulfoxide, the diazotrophic capacities of various strains in the dark were examined. No rnf mutants tested grew diazotrophically, and a nonpolar fdxN-null mutant showed decreased diazotrophic growth in the dark, suggesting that the Rnf and FdxN proteins form the primary electron donor pathway to nitrogenase in the dark as well as in the light. Nonphotosynthetic mutants lacking the component of cyclic electron transport grew diazotrophically and the levels of Rnf proteins were similar to those of the wild-type. These results indicate that rnf gene products play an essential role in nitrogen fixation without any functional link to the cyclic electron transport system.

Journal Article↗

PubMed1998

Localization of a serine proteinase inhibitor, B-43, in the bovine pancreas.

B-43, a serine proteinase inhibitor belonging to the ovalbumin branch of the serpin superfamily, was purified and cloned from bovine brain. Since [35S]-labeled B-43 forms SDS-stable complexes with pancreatic serine proteinases, trypsin, alpha-chymotrypsin, and kallikrein, it has been suggested that B-43 is capable of inhibiting these serine proteinases and that B-43 may be present in the pancreas. In the present study, we investigated the localization of B-43 in the bovine pancreas immunohistochemically and examined the effect of B-43 on the amidolytic activities of pancreatic serine proteinases. Strong B-43-like immunoreactivity was localized in acinar cells, especially in the basal sides of the cells where the rough endoplasmic reticulum is located. The nuclei of the subpopulation of acinar cells were also immunoreactive for B-43. The recombinant glutathione S-transferase-B-43 fusion protein inhibited the amidolytic activity of trypsin and, to a lesser extent, alpha-chymotrypsin and kallikrein, but not elastase. These results suggest a role of B-43 in regulating serine proteinases both in the cytoplasm and the nucleus.

Animals↗

PubMed1998

Characterization of brain-type ryanodine receptor permanently expressed in Chinese hamster ovary cells.

To clarify a function of brain-type ryanodine receptor (RyR3) and its regulation, we established a stable cell line expressing rabbit RyR3 by transfection of Chinese hamster ovary cells (CHO cells) with the cDNA and investigated characteristics of the RyR3. Scatchard analysis of [3H]-ryanodine binding to the membrane from CHO cells expressing RyR3 showed two distinct binding sites. The Kd values of high and low affinity binding sites were 1.92 and 25.9 nM, respectively. [3H]-ryanodine binding to the membrane from CHO cells expressing RyR3 was dependent on pCa. Extracellular Ca2+ (2-10 mM) and high concentration (more than 30 mM) of caffeine activated the RyR3 in CHO cells and increased its intracellular Ca2+ concentration. The enhancement of [3H]-ryanodine binding to the membrane from CHO cells expressing RyR3 was observed by bromoeudistomin D (BED), a caffeine-like powerful Ca2+ releaser, at pCa 5.5. Stably expressed RyR3 in CHO is useful for characterization of its function.

Animals↗

PubMed1998

Effects of cumulus cell density during in vitro maturation of the developmental competence of bovine oocytes.

To determine the role of cumulus cells in oocyte maturation, we carried out an investigation on the effects of addition of cumulus cells to the maturation medium on the developmental competence of corona-enclosed oocytes and oocytes denuded from their somatic cells. The addition of cumulus cell (1.6 x 10(6) cells/mL) improved the development of bovine corona-enclosed oocytes, however, addition of a similar number of cumulus cells as cumulus-oocyte-complexes (COCs, cumulus cell density: 4.2 x 10(6) cells/mL) had no effect on the development of oocytes denuded from their somatic cells. To determine if corona-enclosed oocytes can obtain developmental competence without the addition of extra cumulus cells, the effects of cell density during in vitro maturation on the developmental competence were studied. A density of 1.6 to 3.2 x 10(6) cumulus cells/mL was the most effective for in vitro maturation of oocytes with intact gap junctions. The effects of the medium conditioned by COCs on the developmental competence of oocytes was also examined. It was demonstrated that COC-conditioned medium improved the development of bovine oocytes to the blastocyst stage. These data suggest that the developmental competence of bovine oocytes surrounded with corona cells is supported in a cell density-dependent manner in the maturation medium. In addition, the data indicate that cumulus cells benefit bovine oocyte development either by secreting soluble factors which induce developmental competence or by removing an embryo development-suppressive component from the medium.

Animals↗

PubMed1998

The expression and localization of serine proteinase inhibitor PI-6 mRNA in developmental and ischemic mouse brain.

A serine proteinase inhibitor, PI-6, is a member of the serine proteinase inhibitor (serpin) superfamily. In the present study, we investigated the developmental expression of PI-6 in the mouse brain and the effect of experimental ischemia on the expression of PI-6 in the adult brain. Northern blot analysis showed a high level of expression of PI-6 mRNA in brain stem and diencephalon as compared with other regions in the adult brain. The expression of PI-6 mRNA in the whole brain was increased gradually until 11 days after birth and was decreased again in the adult brain. In situ hybridization analysis revealed that the mRNA was localized in pyramidal cell layer of the post-natal hippocampus, especially in CA3 region, and in layer V of the cerebral cortex. In the brain stem, two specific motor nuclei, the facial nucleus and the motor nucleus of trigeminal nerve, which are important to active feeding, were strongly positive for PI-6 mRNA. Brain ischemia induced by bilateral ligation of the common carotid artery led to an increase in PI-6 mRNA expression in the whole brain, accompanied by the degeneration of hippocampal pyramidal cells. These results indicate distinct temporal and spatial expression of PI-6 in the mouse brain and suggest the involvement of PI-6 in the maturation of neurons and degenerative and regenerative processes.

Age Factors↗

PubMed1998

Cooperative stimulatory effects of tumor necrosis factor and granulocyte-macrophage colony-stimulating factor on the particular respiratory burst activity in human neutrophils: synergistic priming effect on concanavalin A-induced response, no interactive priming effect on the chemotactic peptide-induced response and additive triggering effect.

Tumor necrosis factor (TNF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) rapidly primed human neutrophils for enhanced superoxide (O2-) release, and membrane depolarization stimulated by chemotactic peptide (N-formyl-methionyl-leucyl-phenylalanine), interleukin 8, concanavalin A (Con A) and ionomycin. Combined stimulation of human neutrophils with the optimal concentrations of TNF plus GM-CSF showed no additive or synergistic effects according to the subsequent stimuli and within the parameters tested. Particularly, a high synergistic priming effect of these two cytokines was observed when Con A was used as a triggering agonist of O2- release. The priming of human neutrophils with the optimal concentrations of TNF plus G-CSF, however, always resulted in the same effect as TNF alone. TNF and GM-CSF triggered O2- release directly in human neutrophils for prolonged time periods, and combined stimulation of human neutrophils with the optimal concentrations of TNF plus GM-CSF triggered an added amount of O2- release. TNF and GM-CSF by themselves induced an increase in cytoplasmic pH (intracellular alkalinization), an important signaling event for functional activation of neutrophils, though combined stimulation of human neutrophils with the optimal concentrations of the two cytokines had no additive effects on cytoplasmic pH. The present results show cooperative interaction between TNF and GM-CSF in their stimulatory effects on particular functions in human neutrophils, and these synergistic effects are probably mediated via a mechanism distal to or independent of intracellular alkalinization.

Concanavalin A↗

PubMed1998

Tyrosine phosphorylation of proteins in primary human myeloid leukemia cells stimulated by cytokines: analysis of the frequency of phosphorylation, and partial identification and semi-quantification of signaling molecules.

We investigated tyrosine phosphorylation of proteins in primary human leukemia cells stimulated by granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), interleukin-3 (IL-3), tumor necrosis factor (TNF), thrombopoietin (TPO) and phorbol myristate acetate (PMA) in 61 patients with acute myeloid leukemia (AML), nine patients with chronic myeloid leukemia (CML) in blastic crisis and four patients in chronic phase, and compared these data of leukemia with those of normal human immature hematopoietic cells. These cytokines and PMA induced tyrosine phosphorylation of proteins in a manner characteristic for each cytokine or PMA in AML cells. G-CSF, GM-CSF and IL-3 frequently phosphorylated p92, p80, p70, p44 and p42. p95 was frequently phosphorylated by G-CSF, and was phosphorylated in one third of the cases by TPO. On the other hand, TNF selectively induced tyrosine phosphorylation of p42, and PMA selectively induced that of p44 and p42. In marked contrast to AML cells, CML cells responded poorly to cytokines with protein tyrosine phosphorylation, and normal human bone marrow mononuclear cells and CD34-positive cells also showed poor response to cytokines. The results of the immunoprecipitation studies showed tyrosine phosphorylation of signal transducers and activators of transcription (Stat) 5 induced by G-CSF, GM-CSF, IL-3 and/or TPO in six cases, that of extracellular signal-regulated kinase (ERK) by GM-CSF in two cases and that of p38 by TNF in three cases. Intracellular amount of Stat5 was markedly increased in AML cells compared with that in CML cells and normal human bone marrow cells. whereas intracellular amount of ERK and p38 was uniformly abundant in both leukemic and normal cells. These results show cytokine-specific and amplified tyrosine phosphorylation of proteins in AML cells and suggest that amplified response might, at least in part, result from the increased amount of signaling molecules such as Stat5.

Acute Disease↗

PubMed1998

Changes in monoamine turnover in the brain of cachectic mice bearing colon-26 tumor cells.

Patients with cancer cachexia often suffer from psychiatric disorders. In the present study, we investigated the changes in monoaminergic activities in the brain in tumor-bearing mice with reference to the development of cachexia. Two clones, clone-5 (noncachectic clone) and clone-20 (cachectic clone), derived from the murine Colon-26 adenocarcinoma cell line (Nippon Roche Research Center), were inoculated subcutaneously at 1 x 10(6) cells/0.2 ml into the right lower back of BALB/c mice. In clone-20 mice, body weight and locomotor activity decreased significantly 10-15 days after tumor inoculation. The levels of noradrenaline, dopamine, and 3,4-dihydroxyphenylacetic acid showed no significant change among the three groups. The noradrenaline turnover rate in clone-20 mice was increased in cerebral cortex, hypothalamus, and midbrain. The 5-hydroxytryptamine turnover rate in clone-20 mice was increased in hippocampus, cerebral cortex, midbrain, and pons-medulla oblongata. In contrast, the dopamine turnover rate in clone-20 mice was decreased markedly in hippocampus, cerebral cortex, striatum, hypothalamus, and cerebellum. There was no significant change in amine turnover between control and clone-5 mice except for dopamine in hippocampus, cerebral cortex, and striatum and 5-hydroxytryptamine in striatum. No significant change in the levels of amino acids in the brain was observed among the three groups of mice. It is concluded that some of the psychiatric disorders from which cancer cachectic patients suffer might be ascribable to changes in monoaminergic activities in the brain.

Adenocarcinoma↗