Search PubMed⌕ Search

Biomedical subjects

K Mori

Publications and source records attributed to K Mori.

At least 217 records · Page 12Linked to original sources
PubMed2000

Cloning of the fish cell line SSN-1 for piscine nodaviruses.

Six cell clones were derived from the SSN-1 cell line, which is composed of a mixed cell population and persistently infected with a C-type retrovirus (SnRV). These clones were susceptible to 4 piscine nodavirus strains belonging to different genotypes (SJNNV, RGNNV, TPNNV and *BFNNV [striped jack, redspotted grouper, tiger puffer and barfin flounder nervous necrosis viruses]). Three clones, designated A-6, E-9, and E-11, were highly permissive to nodavirus infection and production. The virus-induced cytopathic effects appeared as cytoplasmic vacuoles and intensive disintegration at 3 to 5 d post-incubation. These observations were highly reproducible and formed the basis for a successful virus titration system. Quantitative analysis using the cloned E-11 cell line clearly revealed differences in the optimal growth temperatures among the 4 genotypic variants: 25 to 30 degrees C for strain SGWak97 (RGNNV), 20 to 25 degrees C for strain SJNag93 (SJNNV), 20 degrees C for strain TPKag93 (TPNNV), and 15 to 20 degrees C for strain JFIwa98 (BFNNV). Electron microscopy demonstrated SnRV retrovirus particles only in A-6 and E-9 cells, but PCR amplification for the pol gene and LTR region of the proviral DNA indicated the presence of the retrovirus in the other clones, including E-11. The cell clones obtained in the present study will be more useful for qualitative and quantitative analyses of piscine nodaviruses than the SSN-1 cell line.

Animals↗
PubMed2000

Functional characterization of a mammalian Sac1 and mutants exhibiting substrate-specific defects in phosphoinositide phosphatase activity.

The Saccharomyces cerevisiae SAC1 gene was identified via independent analyses of mutations that modulate yeast actin function and alleviate the essential requirement for phosphatidylinositol transfer protein (Sec14p) activity in Golgi secretory function. The SAC1 gene product (Sac1p) is an integral membrane protein of the endoplasmic reticulum and the Golgi complex. Sac1p shares primary sequence homology with a subfamily of cytosolic/peripheral membrane phosphoinositide phosphatases, the synaptojanins, and these Sac1 domains define novel phosphoinositide phosphatase modules. We now report the characterization of a rat counterpart of Sac1p. Rat Sac1 is a ubiquitously expressed 65-kDa integral membrane protein of the endoplasmic reticulum that is found at particularly high levels in cerebellar Purkinje cells. Like Sac1p, rat Sac1 exhibits intrinsic phosphoinositide phosphatase activity directed toward phosphatidylinositol 3-phosphate, phosphatidylinositol 4-phosphate, and phosphatidylinositol 3,5-bisphosphate substrates, and we identify mutant rat sac1 alleles that evoke substrate-specific defects in this enzymatic activity. Finally, rat Sac1 expression in Deltasac1 yeast strains complements a wide phenotypes associated with Sac1p insufficiency. Biochemical and in vivo data indicate that rat Sac1 phosphatidylinositol-4-phosphate phosphatase activity, but not its phosphatidylinositol-3-phosphate or phosphatidylinositol-3, 5-bisphosphate phosphatase activities, is essential for the heterologous complementation of Sac1p defects in vivo. Thus, yeast Sac1p and rat Sac1 are integral membrane lipid phosphatases that play evolutionary conserved roles in eukaryotic cell physiology.

Amino Acid Sequence↗
PubMed2000

CV-2619 protects cultured astrocytes against reperfusion injury via nerve growth factor production.

In this study, we examined the effect of the neuroprotective agent 2, 3-dimethoxy-5-methyl-6-(10-hydroxydecyl)-1,4-benzoquinone (CV-2619) on reperfusion injury in cultured rat astrocytes after exposure to hydrogen peroxide (H(2)O(2))-containing medium. CV-2619 (10 nM to 10 microM) significantly attenuated the reperfusion-induced decrease in cell viability. The compound showed an anti-apoptotic effect in this astrocyte injury model. Antioxidants such as ascorbic acid, alpha-tocopherol and reduced glutathione also inhibited H(2)O(2) exposure-induced cytotoxicity. CV-2619 did not affect the levels of reactive oxygen species, but it increased nerve growth factor (NGF) production. The effect of CV-2619 on H(2)O(2) exposure-induced cytotoxicity was blocked by cycloheximide and anti-NGF antibody. The protective effect of CV-2619 was antagonized by the mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase inhibitor 2'-amino-3'-methoxyflavone and the phosphatidylinositol-3 kinase inhibitor wortmannin. These findings suggest that the effect of CV-2619 is mediated at least partly by NGF production in astrocytes and that ERK and phosphatidylinositol-3 kinases play a role in the downstream mechanism.

Animals↗
PubMed2000

Epoxidation of alpha,beta-unsaturated ketones using hydrogen peroxide in the presence of basic hydrotalcite catalysts

The basic layered hydrotalcites have been used as catalysts for the epoxidation of alpha,beta-unsaturated ketones in heterogeneous reaction media using hydrogen peroxide as an oxidant. A wide variety of alpha,beta-unsaturated ketones were oxidized to the corresponding epoxyketones in excellent yields under mild reaction conditions. For example, 2-cyclohexen-1-one gave 2,3-epoxycyclohexanone in 91% yield at 40 degrees C for 5 h with high efficiency in hydrogen peroxide. The catalytic activity of the hydrotalcites increased as the basicity of their surfaces increased. In the case of the epoxidation of less reactive substrates, adding a cationic surfactant such as n-dodecyltrimethylammonium bromide (DTMAB) to the above oxidation system accelerated the epoxidation reaction. These hydrotalcite catalysts were easily separated from the reaction mixture and were reusable.

Journal Article↗
PubMed2000

Phosphate regulation of vascular smooth muscle cell calcification.

Vascular calcification is a common finding in atherosclerosis and a serious problem in diabetic and uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMCs cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition. Mechanistic studies revealed that elevated phosphate treatment of HSMCs also enhanced the expression of the osteoblastic differentiation markers osteocalcin and Cbfa-1. The effects of elevated phosphate on HSMCs were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor phosphonoformic acid, to dose dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. With the use of polymerase chain reaction and Northern blot analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. The full text of this article is available at http://www.circresaha.org.

Arteries↗
PubMed2000

Receptor isoform-specific interaction of prostaglandin EP3 receptor with muskelin.

By using the yeast two-hybrid system, muskelin was found to bind with the carboxy-terminal tail of the prostaglandin EP3 receptor alpha isoform but not with either the beta or gamma isoform. A direct interaction between the carboxy-terminal tail of the alpha isoform and muskelin was confirmed in vitro using recombinant fusion proteins. Analysis by confocal microscopy indicated that the isoform and muskelin were distributed at the plasma membrane in transfected cells. When the isoform was stimulated by agonist, the receptor was internalized in the cells expressing the receptor alone, but this internalization was partially inhibited by the cotransfection with muskelin. Furthermore, muskelin enhanced the Gi activity of the isoform. Thus, muskelin appears to be an isoform-specific anchoring protein for the EP3 receptor.

Animals↗
PubMed2000

Two mirror-image sensory maps with domain organization in the mouse main olfactory bulb.

The glomerular sheet in the olfactory bulb (OB) provides an olfactory sensory map identifying which odorant receptors (ORs) in the nose are activated by inhaled odorants. How are the glomeruli spatially arranged in the OB? Using OCAM and neuropilin-1 (NP1) as molecular markers for target glomeruli of distinct subsets of olfactory axons, we demonstrate here that glomeruli are parceled into topographically distinct domains. Spatial arrangement of these domains suggests that each OB contains two mirror-image maps of the glomeruli. In situ hybridization shows that the glomeruli representing the same OR are symmetrically arranged; one in a domain in the lateral hemisphere and the other in a corresponding domain in the medial hemisphere of the OB. These results suggest that OB contains two symmetrical OR maps with similar domain organization.

Animals↗
PubMed2000

Thickness of Retinal Nerve Fiber Layer Decreases after Vitreous Surgery for Idiopathic Macular Hole.

Purpose: The alteration of the retinal nerve fiber thickness (NFLT) before and after vitreous surgery for a macular hole in cases with or without visual field defects was investigated.Methods: The NFLT of 23 eyes with idiopathic macular hole was measured with scanning laser polarimeter up to 12 months after surgery. The NFLT was divided into superior, inferior, nasal, and temporal quadrants. The mean NFLT of each quadrant was analyzed statistically and compared to the results of visual field tests.Results: In all cases, the NFLT decreased significantly up to 3 months after surgery, but increased gradually up to 12 months. In cases with visual field loss, the thickness of the nerve fiber layer that corresponds to the visual field defect diminished strongly, in contrast with other quadrants. Even in cases without visual field loss, the NFLT decreased significantly a month after surgery, especially in the nasal and inferior quadrants.Conclusion: This study demonstrates that the thickness of retinal nerve fiber layer decreases at least one month after surgery, even in cases without visual field defect. This may suggest the existence of a subclinical complication of vitreous surgery.

Journal Article↗
PubMed2000

Pulmonary vascular disease in Down's syndrome with complete atrioventricular septal defect.

We sought to determine the predisposing factors of pulmonary vascular disease (PVD) in complete atrioventricular septal defect. Down's syndrome is considered a risk factor for PVD, but the progression of PVD differs in each case. Morphometric analysis in autopsied hearts showed that Rastelli type A morphology had a narrower left ventricular outlet and a wider right ventricular outlet than did type C. In 81 consecutive patients with Down's syndrome who underwent cardiac catheterization, we estimated the following variables: Rastelli subtypes, pulmonary vascular resistance, pulmonary-to-systemic flow ratio, patients' age, and operative outcome. The hemodynamic variables in those <1 year old did not differ between the groups with type A and type C. However, all 5 patients with fatal pulmonary hypertension in early infancy had type A morphology. The lung histology revealed that 3 of these patients already had irreversible PVD. At >/=1 year old, those with type A showed a significantly higher pulmonary vascular resistance (p <0.001) and a lower pulmonary to systemic flow ratio (p <0.05) than did those <1 year old. In contrast, neither of these variables in the type C group differed between those >/=1 and <1 year old. Moreover, those with type A had a greater risk of being contraindicated for surgical repair (p <0.05). We suspect, therefore, that type A morphology is an independent risk factor for PVD in those with Down's syndrome associated with this anomaly. This hemodynamic influence could become obvious once patients are >/=1 year old. It may also sometimes result in irreversible PVD even in early infancy.

Adolescent↗
PubMed2000

Spontaneous atlantoaxial rotatory fixation in old age after cerebral infarction: case report.

STUDY DESIGN: Case report of spontaneous Fielding and Hawkins Type I atlantoaxial rotatory fixation in a 78-year-old man after hemiplegia and homonymous hemianopsia caused by cerebral infarction. OBJECTIVES: To describe a case of spontaneous atlantoaxial rotatory fixation in old age and review previous adult cases of atlantoaxial rotatory fixation without fracture. SUMMARY OF BACKGROUND DATA: Atlantoaxial rotatory fixation in adults is a relatively rare finding and is mainly caused by trauma. To the author's knowledge, there has been no previous report of spontaneous atlantoaxial rotatory fixation in old age. METHODS: The patient's head was fixed in a 40 degrees left-rotated position. Left hemiplegia and homonymous left-side hemianopsia developed due to cerebral infarction. Computed tomography of the cervical spine clearly showed rotatory fixation of the atlas on the axis. RESULTS: Successful reduction was obtained after 1 day of skull traction. CONCLUSIONS: It was hypothesized that repeated left-rotational stress due to homonymous hemianopsia loaded to the atlantoaxial joint caused abnormal laxity of the joint.

Aged↗
PubMed2000

Induction of protective immunity against pathogenic simian immunodeficiency virus by a foreign receptor-dependent replication of an engineered avirulent virus.

In AIDS vaccine strategies, live attenuated vaccines can confer good resistance against pathogenic virus infections but have the potential risk of inducing disease, whereas safer replication-negative strategies such as DNA vaccinations have so far failed to prevent the disease onset. Here, we developed a novel DNA vaccine strategy to induce restricted replication of an avirulent virus and evaluated it in a simian immunodeficiency virus (SIV) infection model. We generated a chimeric SIV, FMSIV, by replacing SIV env with ecotropic Friend murine leukemia virus (FMLV) env to confine its replication to FMLV receptor (mCAT1)-expressing cells. In primate cells lacking mCAT1, FMSIV did not replicate unless mCAT1 was introduced exogenously. Vaccination to macaques with both the FMSIV DNA and the mCAT1-expression plasmid DNA induced SIV Gag-specific cellular immune responses and resistance against pathogenic SIV(mac239) challenge more efficiently than the replication-negative control vaccination with the FMSIV DNA alone. This strategy may be useful for development of safe and effective vaccines against various kinds of pathogenic viruses.

AIDS Vaccines↗
PubMed2000

Intercellular adhesion molecule-5 induces dendritic outgrowth by homophilic adhesion.

Intercellular adhesion molecule-5 (ICAM-5) is a dendritically polarized membrane glycoprotein in telencephalic neurons, which shows heterophilic binding to leukocyte beta(2)-integrins. Here, we show that the human ICAM-5 protein interacts in a homophilic manner through the binding of the immunoglobulin domain 1 to domains 4-5. Surface coated ICAM-5-Fc promoted dendritic outgrowth and arborization of ICAM- 5-expressing hippocampal neurons. During dendritogenesis in developing rat brain, ICAM-5 was in monomer form, whereas in mature neurons it migrated as a high molecular weight complex. The findings indicate that its homophilic binding activity was regulated by nonmonomer/monomer transition. Thus, ICAM-5 displays two types of adhesion activity, homophilic binding between neurons and heterophilic binding between neurons and leukocytes.

Animals↗
PubMed2000

Pheromonal and kairomonal activities can be separated: synthesis and bioactivity studies of pine bast scale sex pheromones and their analogues.

New syntheses were achieved to secure matsuone (1), the pheromone of the pine scale Matsucoccus matsumurae, that of M. feytaudi (2), and that of M. josephi (3). Five analogues (4-8) of 1, 2, and 3 were synthesized and their bioactivities studied. The pheromone analogue 7 showed relatively strong pheromonal activity toward M. josephi, while it was inactive as a kairomone toward the predator Elatophilus hebraicus. Similarly, analogue 8 acted as a pheromone for M. feytaudi, but it did not attract any of its local predators. The M. feytaudi pheromone 2 exhibited strong kairomonal activity toward E. hebraicus, but was not active as a pheromone mimic to attract M. josephi.

Animals↗
PubMed2000

T-588 inhibits astrocyte apoptosis via mitogen-activated protein kinase signal pathway.

The effect of (1R)-1-benzo[b]thiophen-5-yl-2-[2-(diethylamino)ethoxy]ethan -1-ol hydrochloride (T-588), a cognition enhancer, on reperfusion injury was studied in cultured rat astrocytes. T-588 at 1-10 microM partially protected astrocytes against reperfusion injury after exposure to Ca(2+)-free medium or hydrogen peroxide. Nerve growth factor (NGF) had a similar protective effect. Addition of both T-588 and NGF resulted in complete protection against Ca(2+) reperfusion injury. T-588 did not stimulate NGF production in astrocytes. The effect of T-588 on Ca(2+) reperfusion injury including apoptosis was inhibited by the mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase inhibitor 2'-amino-3'-methoxyflavone (PD98059), but not by the phosphoinositide 3-kinase inhibitor wortmannin. The effect of NGF was inhibited by PD98059 and wortmannin. T-588 stimulated rapidly the phosphorylation of ERK, but did not affect that of Akt in astrocytes. These findings suggest that the ERK MAP kinase pathway has a role in the protective effects of T-588 and NGF.

Androstadienes↗
PubMed2000

Visualization of neurogenesis in the central nervous system using nestin promoter-GFP transgenic mice.

Neurons are generated from neural progenitor cells not only during development but also in the mature brain. To develop an in vivo system for analyzing neurogenesis, we generated transgenic mice expressing green fluorescent protein (GFP) under the control of regulatory regions of the nestin gene. GFP fluorescence was observed in areas and during periods connected with neurogenesis, including embryonic neuroepithelium, neonatal cerebellum, and hippocampal dentate gyrus and rostral migratory pathway from the subventricular zone to the olfactory bulb in the adult. GFP-positive cells in the adult brain included immature neuronal cells expressing polysialylated NCAM. BrdU labeling experiments revealed that newly generated interneurons which migrated rostrally from the subventricular zone expressed GFP until they reached the olfactory bulb. These results indicate that nestin promoter-GFP transgenic mice can be utilized to visualize the regions of neurogenesis throughout the life of the animals and to follow the migration and differentiation of newly generated neurons.

Aging↗
PubMed2000

mRNA splicing-mediated C-terminal replacement of transcription factor Hac1p is required for efficient activation of the unfolded protein response.

Eukaryotic cells control the levels of molecular chaperones and folding enzymes in the endoplasmic reticulum (ER) by a transcriptional induction process termed the unfolded protein response (UPR) according to the needs within the ER. In Saccharomyces cerevisiae, expression of the UPR-specific transcription factor Hac1p is tightly regulated at the level of mRNA splicing that depends on an unconventional system. Thus, HAC1 precursor mRNA is constitutively expressed but not translated. A sensor molecule Ire1p/Ern1p-mediated signaling from the ER specifically removes an intron of 252 nucleotides from the precursor mRNA, and the resulting mature mRNA is translated to produce Hac1p. Because the 5' splice site is located near the C-terminal end of the Hac1p-coding region, this splicing replaces the last 10 codons of the ORF with an exon encoding 18 aa without affecting the N-terminal 220-aa region which contains the DNA-binding domain. Here, we found that this C-terminal 18-aa segment functions as a potent activation domain. Therefore, the splicing event joins the HAC1 DNA-binding domain to its activation domain, allowing rapid posttranscriptional generation of a potent transcriptional activator (238-aa Hac1p) that activates the UPR efficiently. This suggests that the UPR is hardly activated by Hac1p produced without splicing (230-aa Hac1p) which may occur in the absence of Ire1p/Ern1p-mediated signaling from the ER. Based on these and other results, we propose that the control of expression and activity of Hac1p meets the requirements of the ER.

Basic-Leucine Zipper Transcription Factors↗