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Biomedical subjects

M Nishijima

Publications and source records attributed to M Nishijima.

At least 73 records · Page 4Linked to original sources
PubMed1999

Isolation of a chinese hamster ovary (CHO) cDNA encoding phosphatidylglycerophosphate (PGP) synthase, expression of which corrects the mitochondrial abnormalities of a PGP synthase-defective mutant of CHO-K1 cells.

Phosphatidylglycerophosphate (PGP) synthase catalyzes the first step in the cardiolipin (CL) branch of phospholipid biosynthesis in mammalian cells. In this study, we isolated a Chinese hamster ovary (CHO) cDNA encoding a putative protein similar in sequence to the yeast PGS1 gene product, PGP synthase. The gene for the isolated CHO cDNA was named PGS1. Expression of the CHO PGS1 cDNA in CHO-K1 cells and production of a recombinant CHO PGS1 protein with a N-terminal extension in Escherichia coli resulted in 15-fold and 90-fold increases of PGP synthase specific activity, respectively, establishing that CHO PGS1 encodes PGP synthase. A PGP synthase-defective CHO mutant, PGS-S, isolated previously (Ohtsuka, T., Nishijima, M., and Akamatsu, Y. (1993) J. Biol. Chem. 268, 22908-22913) exhibits striking reductions in biosynthetic rate and cellular content of phosphatidylglycerol (PG) and CL and shows mitochondrial morphological and functional abnormalities. The CHO PGS-S mutant transfected with the CHO PGS1 cDNA exhibited 620-fold and 7-fold higher PGP synthase activity than mutant PGS-S and wild type CHO-K1 cells, respectively, and had a normal cellular content and rate of biosynthesis of PG and CL. In contrast to mutant PGS-S, the transfectant had morphologically normal mitochondria. When the transfectant and mutant PGS-S cells were cultivated in a glucose-depleted medium, in which cellular energy production mainly depends on mitochondrial function, the transformant but not mutant PGS-S was capable of growth. These results demonstrated that the morphological and functional defects displayed by the PGS-S mutant are due directly to the reduced ability to make normal levels of PG and/or CL.

Amino Acid Sequence↗
PubMed1999

Requisite Morphologic Interaction for Attachment between Ulva pertusa (Chlorophyta) and Symbiotic Bacteria.

: In order to understand the morphogenesis-inducing mechanism of Ulva pertusa by symbiotic bacteria, we observed the requisite conditions of bacteria for attachment to U. pertusa for algal morphogenesis. Non-morphogenesis-inducing bacterial mutants derived by ultraviolet irradiation did not attach onto the surface of this alga. Scanning electron microscopic observation during the process of morphogenesis in U. pertusa revealed a network-like structure formed on the algal surface within 1 week after application of bacteria. The bacteria attached onto the alga after 2 weeks of incubation. After this attachment process the morphologic change was observed in U. pertusa.

Journal Article↗
PubMed1999

Changes in gastric mucosal ulcerogenic responses in rats with adjuvant arthritis: role of nitric oxide.

AIM: To examine gastric mucosal ulcerogenic responses to indomethacin and HCl/ethanol in adjuvant arthritic (AA) rats. METHODS AND RESULTS: Arthritis was induced in male Dark Agouti (DA) rats by injection of Freund's complete adjuvant (FCA) into the right hind paw. The gastric ulcerogenic response to indomethacin was markedly worsened in AA rats, depending on the degree of arthritic change. This aggravation of indomethacin-induced gastric lesions in AA rats was significantly prevented by NG-nitro-L-arginine methyl ester (L-NAME) and amino-guanidine as well as dexamethasone. In contrast, the mucosal ulcerogenic response to HCl/ethanol was inhibited in AA rats. The suppression of HCl/ethanol-induced gastric lesions in AA rats was reversed almost totally by L-NAME and aminoguanidine as well as dexamethasone and partly by indomethacin. The expression of inducible nitric oxide synthase (iNOS) mRNA was observed in the stomach of AA rats but not of normal rats. Moreover, the luminal releases of nitric oxide (NO) metabolites as well as prostaglandin (PG) E2 were significantly increased in AA rats. CONCLUSIONS: The gastric mucosal ulcerogenic responses were modified in AA rats, in different manners depending on the irritants; an increase in response to indomethacin and a decrease in response to HCl/ethanol. These changes may both be accounted for by increased production of NO by iNOS, and the latter is also partly related to increased production of PGs.

Animals↗
PubMed1999

Effects of pantoprazole, a novel H+/K+-ATPase inhibitor, on duodenal ulcerogenic and healing responses in rats: a comparative study with omeprazole and lansoprazole.

BACKGROUND: Pantoprazole, 2-[(2-pyridylmethyl) sulphinyl] benzimidazole, is a new substituted benzimidazole that inhibits the parietal cell H+/K+-ATPase. METHODS: In the present study, the anti-secretory and anti-ulcer activities of pantoprazole were compared with those of omeprazole and lansoprazole in rats. RESULTS: Pantoprazole (0.3-3 mg/kg, p.o.) as well as omeprazole (1-10 mg/kg, p.o.) and lansoprazole (1-10 mg/kg, p.o.) dose-dependently decreased both basal acid secretion in pylorus-ligated rats and the stimulated acid secretion induced by mepirizole in acute fistula rats, and the effects of pantoprazole were more potent than those of omeprazole and lansoprazole, the ED50 values for the stimulated acid secretion being 0.8, 2.0 and 1.2 mg/kg, respectively. Neither of these drugs had any effect on duodenal HCO3- secretion. These pump inhibitors prevented the development of duodenal lesions in response to mepirizole in a dose-related manner, the ED50 values for pantoprazole, omeprazole and lansoprazole being 0.4, 2.0 and 1.3 mg/kg, respectively. Likewise, pantoprazole showed the healing promoting action on chronic duodenal ulcers induced by acetic acid, and this effect was also more potent when compared to omeprazole or lansoprazole. CONCLUSIONS: We conclude that pantoprazole exhibited both anti-ulcer and healing promoting effects on duodenal ulcers in rats, and the effects may be attributable to its potent anti-secretory action. Other pump inhibitors such as omeprazole and lansoprazole were almost equally effective as pantoprazole, yet this drug was most potent on the basis of ED50 values.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Polyphasic taxonomy of the genus Shewanella and description of Shewanella oneidensis sp. nov.

The genus Shewanella has been studied since 1931 with regard to a variety of topics of relevance to both applied and environmental microbiology. Recent years have seen the introduction of a large number of new Shewanella-like isolates, necessitating a coordinated review of the genus. In this work, the phylogenetic relationships among known shewanellae were examined using a battery of morphological, physiological, molecular and chemotaxonomic characterizations. This polyphasic taxonomy takes into account all available phenotypic and genotypic data and integrates them into a consensus classification. Based on information generated from this study and obtained from the literature, a scheme for the identification of Shewanella species has been compiled. Key phenotypic characteristics were sulfur reduction and halophilicity. Fatty acid and quinone profiling were used to impart an additional layer of information. Molecular characterizations employing small-subunit 16S rDNA sequences were at the limits of resolution for the differentiation of species in some cases. As a result, DNA-DNA hybridization and sequence analyses of a more rapidly evolving molecule (gyrB gene) were performed. Species-specific PCR probes were designed for the gyrB gene and used for the rapid screening of closely related strains. With this polyphasic approach, in addition to the ten described Shewanella species, two new species, Shewanella oneidensis and 'Shewanella pealeana', were recognized; Shewanella oneidensis sp. nov. is described here for the first time.

Animals↗
PubMed1999

Elective induction of labor at 39 weeks of gestation: a prospective randomized trial.

OBJECTIVE: To clarify the safety of elective induction of labor at 39 weeks of gestation. STUDY DESIGN: Prospective randomized study. SUBJECTS AND METHODS: Uncomplicated nulliparas (N = 194) were randomly assigned at 36 weeks of gestation. Labor was electively induced in 63 women at 39 weeks of gestation in the active management group (I group, N = 98). Spontaneous labor onset was expected with semi-weekly nonstress test (NST) and amniotic fluid index (AFI) by 42 weeks of gestation in the expectant group (E group, N = 96). Perinatal events were compared between the 2 groups. RESULTS: A significantly higher incidence of meconium-stained amnios (19.4% vs 3.2%) and fetal resuscitation (16.7% vs 4.8%) was found in the E group than in the I group. Also, although a significantly higher incidence of epidural analgesia was noted in the I group (89%) than in the E group (54%) (labor onset > or = 39 weeks, N = 72), the duration of the 1st stage was shorter in I group and the duration of the 2nd stage was not significantly different. No other significant difference was noted between the 2 groups in terms of the rate of C-section, blood loss, incidence of pathological FHR, birth weight, Apgar score, umbilical arterial pH, or admission to NICU. CONCLUSION: Active management of labor at 39 weeks could be made as safely as expectant management with modified biophysical profile monitoring.

Adult↗
PubMed1999

A typical bacterial ornithine-containing lipid Nalpha-(D)-[3-(hexadecanoyloxy)hexadecanoyl]-ornithine is a strong stimulant for macrophages and a useful adjuvant.

Nalpha-[3-(Hexadecanoyloxy)hexadecanoyl]-ornithine is a typical bacterial ornithine-containing lipid (OL). The configuration of the 3-hydroxy fatty acids in the OL was proved to be D by using HPLC with chiral column. For this analysis, Nalpha-(D or L)-[3-(hexadecanoyloxy)hexadecanoyl]-L-ornithine were synthesized and used as standards. The typical bacterial OL, as well as the synthesized one, exhibited strong interleukin-1- and prostaglandin E2-inducing activities, and further, it induced the production of high IgG anti-tetanus toxoid antibodies in mice. The typical OL is expected to be utilized as a nontoxic, potent adjuvant.

Adjuvants, Immunologic↗
PubMed1999

Perinatal outcome and management of single fetal death in twin pregnancy: a case series and review.

OBJECTIVE: To determine neonatal outcome of single fetal death in twin pregnancy. METHODS: Retrospective study was performed on 30 cases of single fetal death in twin pregnancy during the period from August 1971 to December 1997 at Kitasato university hospital. RESULTS: The incidence of single fetal death in twin pregnancy was 6.2% among total number of 481 twins. Prognosis of surviving infants was satisfactory except in one case, with malformation in 10 cases of dichorionic twins (total 242 sets). In contrast, neonatal death occurred in 6 cases of 20 monochorionic twins (total 239 sets), 4 of which were among 7 cases of twin-to-twin transfusion syndrome (TTTS). Cerebral palsy occurred in 2 infants of monochorionic twins. One case was diagnosed as periventricular leukomalacia (PVL) within one week after birth, and this was the case of delivery 1 day after one twin fetal death. CONCLUSION: Single fetal death itself occurs more often in monochorionic twins. There seems to be a benign outcome for the surviving dichorionic twins. On the other hand, there may be a grave outcome, though infrequent, for monochorionic twins when concomitant TTTS has existed. It is very important to identify the chorionicity by ultrasound examination in early pregnancy.

Diseases in Twins↗
PubMed1999

Nitric oxide, superoxide radicals and mast cells in pathogenesis of indomethacin-induced small intestinal lesions in rats.

We investigated the pathogenic mechanism of indomethacin-induced small intestinal lesions, in relation to nitric oxide (NO), superoxide radicals and mast cells. Rats received indomethacin (1-6 mg/kg) s.c. once daily for 3 days, and the small intestine was examined for lesions 24 hr after the final administration of indomethacin. Indomethacin caused hemorrhagic lesions in the small intestine, mostly in the jejunum and ileum, in dose- and time-dependent manners, with concomitant increase of mucosal microvascular permeability. This treatment also caused an increase of inducible NO synthase (iNOS) activity with the expression of its mRNA, myeloperoxidase (MPO) activity as well as thiobarbituric acid reactants (TRBAS) in the mucosa, and the changes in iNOS activity preceded those in MPO activity and TRBAS as well as lesion development. These lesions induced by indomethacin were prevented by aminoguanidine (a selective inhibitor of iNOS), dexamethasone (an inhibitor of iNOS mRNA transcription), allopurinol (a xanthine oxidase inhibitor), hydroxyurea (a neutrophil reducing agent) and FR167653 (an inhibitor of interleukin-1/tumor necrosis factor-alpha production) as well as 16,16-dimethyl prostaglandin E2ń. Likewise, the severity of these lesions was also reduced by mast cell stabilizers FPL-52694 and disodium cromoglycate and a lipoxygenase inhibitor TMK-688, but not affected by tripelennamine (a histamine H1-receptor antagonist) or methysergide (a serotonin receptor antagonist). These results suggest that: 1) the pathogenic mechanism of indomethacin-induced small intestinal lesions involves superoxide radicals as well as NO produced by iNOS, 2) the deleterious effect of NO may be accounted for by the cytotoxic action of peroxynitrite, produced from NO in the presence of superoxide radicals, and 3) the mast cells may also be involved in the process of small intestinal ulceration, although the mediator responsible remains undefined.

Animals↗
PubMed1998

Mammalian cell mutants resistant to a sphingomyelin-directed cytolysin. Genetic and biochemical evidence for complex formation of the LCB1 protein with the LCB2 protein for serine palmitoyltransferase.

Lysenin, a hemolytic protein derived from the earthworm Eisenia foetida, has a high affinity for sphingomyelin. Chinese hamster ovary (CHO) cells exhibited a high cytolytic sensitivity to lysenin, but treatment with sphingomyelinase rendered the cells resistant to lysenin. Temperature-sensitive CHO mutant cells defective in sphingolipid synthesis were resistant to lysenin, and this lysenin resistance was suppressed by metabolic complementation of sphingolipids. Selection of lysenin-resistant variants from mutagenized CHO cells yielded two types of sphingomyelin-deficient mutants, both of which showed less lysenin binding capability than wild-type cells. One mutant strain was severely defective in sphingomyelin synthesis but not glycosphingolipid synthesis, and another strain (designated LY-B) was incapable of de novo synthesis of any sphingolipid species and had no activity of serine palmitoyltransferase (SPT; EC 2.3.1.50) catalyzing the first step of sphingolipid biosynthesis. LY-B cells lacked the LCB1 protein, a component of SPT, and transfection of LY-B cells with the hamster LCB1 cDNA restored both SPT activity and sphingolipid synthesis to the cells. Expression of an affinity peptide-tagged LCB1 protein in LY-B cells caused the endogenous LCB2 protein to adsorb to a tag affinity matrix. In addition, an anti-hamster LCB2 protein antibody co-immunoprecipitated both SPT activity and the wild-type LCB1 protein with the LCB2 protein. Thus, cell surface sphingomyelin is essential for lysenin-induced cytolysis, and lysenin is a useful tool for isolation of sphingomyelin-deficient mutants. Moreover, these results demonstrate that the SPT enzyme comprises both the LCB1 and LCB2 proteins.

Acyltransferases↗
PubMed1998

Genetic evidence that phosphatidylserine synthase II catalyzes the conversion of phosphatidylethanolamine to phosphatidylserine in Chinese hamster ovary cells.

Phosphatidylserine (PS) in mammalian cells is synthesized through the exchange of free L-serine with the base moiety of phosphatidylcholine or phosphatidylethanolamine (PE). The serine base exchange in Chinese hamster ovary (CHO) cells is catalyzed by at least two enzymes, PS synthase (PSS) I and II. A PSS I-lacking mutant of CHO-K1 cells, PSA-3, which exhibits approximately 2-fold lower serine base exchange activity than CHO-K1, is defective in the conversion of phosphatidylcholine to PS but has the ability to convert PE to PS. The PSA-3 mutant requires exogenous PS or PE for cell growth. In the present study, from PSA-3 mutant cells, we isolated a mutant, named PSB-2, with a further decrease in the serine base exchange activity. The activity in the homogenate of PSB-2 mutant cells was approximately 10% that of PSA-3 mutant cells and approximately 5% that of CHO-K1 cells. The PSB-2 mutant exhibited an approximately 80% reduction in the PSS II mRNA level relative to that in PSA-3 mutant and CHO-K1 cells. These results showed that the PSB-2 mutant is defective in PSS II. Like the PSA-3 mutant, the PSB-2 mutant grew well in medium supplemented with PS. However, in the medium supplemented with PE, the PSB-2 mutant was incapable of growth, in contrast to the PSA-3 mutant. In the medium with exogenous PE, the PSB-2 mutant was defective in PS biosynthesis, whereas the PSA-3 mutant synthesized a normal amount of PS. A metabolic labeling experiment with exogenous [32P]PE revealed that the PSB-2 mutant was defective in the conversion of exogenous PE to PS. This defect and the growth and PS biosynthetic defects of the PSB-2 mutant cultivated with exogenous PE were complemented by the PSS II cDNA. In addition, the cDNA of the other PS synthase, PSS I, was shown not to complement the defect in the conversion of exogenous PE to PS of the PSB-2 mutant, implying that PSS I negligibly contributes to the conversion of PE to PS in CHO-K1 cells. These results indicated that PSS II is critical for the growth and PS biosynthesis of PSA-3 mutant cells cultivated with exogenous PE and suggested that most of the PS formation from PE in CHO-K1 cells is catalyzed by PSS II.

Animals↗
PubMed1998

Control of phosphatidylserine biosynthesis through phosphatidylserine-mediated inhibition of phosphatidylserine synthase I in Chinese hamster ovary cells.

Phosphatidylserine (PtdSer) synthesis in Chinese hamster ovary (CHO) cells occurs through the exchange of L-serine with the base moiety of phosphatidylcholine or phosphatidylethanolamine. The synthesis is depressed on the addition of PtdSer to the culture medium. A CHO cell mutant named mutant 29, whose PtdSer biosynthesis is highly resistant to this depression by exogenous PtdSer, has been isolated from CHO-K1 cells. In the present study, the PtdSer-resistant PtdSer biosynthesis in the mutant was traced to a point mutation in the PtdSer synthase I gene, pssA, resulting in the replacement of Arg-95 of the synthase by lysine. Introduction of the mutant pssA cDNA, but not the wild-type pssA cDNA, into CHO-K1 cells induced the PtdSer-resistant PtdSer biosynthesis. In a cell-free system, the serine base-exchange activity of the wild-type pssA-transfected cells was inhibited by PtdSer, but that of the mutant pssA-transfected cells was resistant to the inhibition. Like the mutant 29 cells, the mutant pssA-transfected cells grown without exogenous PtdSer exhibited an approximately 2-fold increase in the cellular PtdSer level compared with that in CHO-K1 cells, although the wild-type pssA-transfected cells did not exhibit such a significant increase. These results indicated that the inhibition of PtdSer synthase I by PtdSer is essential for the maintenance of a normal PtdSer level in CHO-K1 cells and that Arg-95 of the synthase is a crucial residue for the inhibition.

Animals↗
PubMed1998

Parasitism by a protozoan in the hemolymph of the giant clam, Tridacna crocea.

A parasitism by a protozoan was found in the giant clam, Tridacna crocea. The parasites were spindle-shaped, 8.6 +/- 0.5 micro m in length and 2.5 +/- 0.3 micro m in width. Structural features of the apical complex of the parasite and a molecular phylogenetic analysis of its 18S rRNA gene sequence indicate that the protozoan belongs to the Apicomplexa. No flagellum was observed in the parasitic protozoan. It infected the eosinophilic granular hemocyte, one of the three types of hemocytes in the clam hemolymph, but it is not known whether it influenced the growth of the clam.

Animals↗
PubMed1998

Vasa vasorum of the intracranial arteries.

Most of the major extracranial arteries have vasa vasorum which play an important role in some pathological conditions. However, in the intracranial arteries, the existence of vasa vasorum and their pathological implication have not been adequately investigated. We examined the distribution and incidence of vasa vasorum in the major cerebral arteries and their relationships to certain clinical factors in 50 autopsy cases performed between 1987 and 1994. By light microscopy, vasa vasorum were found in 36 of 50 patients. Of 36 patients, vasa vasorum in 30 cases were localizedly observed in the tunica adventitia and the in other 6 were distributed in the tunica media accompanied by intramural haemorrhage. Existence of vasa vasorum was more common in the proximal arteries (vertebral, internal carotid, and basilar arteries) than in the distal arteries (middle cerebral and anterior cerebral arteries). Vasa vasorum were found more frequently in aged patients with severe atherosclerosis and those with cerebrovascular diseases. Our results indicated that intracranial vasa vasorum existed with a higher frequency in the tunica adventitia of the vertebral and internal cerebral arteries, and the incidence of vasa vasorum related to severity of atherosclerosis. The development of vasa vasorum in the tunica media may reflect some pathological changes of cerebral arteries.

Adolescent↗