Biomedical subjects

N Yoshida

Publications and source records attributed to N Yoshida.

At least 253 records · Page 14Linked to original sources

PubMed1997

Cerebral angioplasty in a patient with vascular dementia.

A 66-year-old man with a history of previous transient ischemic attacks had progressive memory and gait disturbance caused by severe stenoses of both the internal carotid arteries and vertebral arteries. The patient underwent percutaneous transluminal angioplasty of the vertebral arteries and endarterectomy of the internal carotid arteries with satisfactory results. On admission, the patient was alert, but disoriented to time and place. He exhibited mild motor weakness in both legs. Neuropsychological tests revealed remarkable intellectual deterioration and he required maximum support to perform activities of daily living. Higher cortical function and the ability to perform activities of daily living improved remarkably after the angioplasty. Angioplasty is an alternative therapy to reverse functional deficits in patients with cerebrovascular hemodynamic compromise.

Aged↗

PubMed1997

Methylprednisolone inhibits neutrophil-endothelial cell interactions induced by interleukin-1beta under flow conditions.

The effects of methylprednisolone (m-PSL) on IL-1beta-induced neutrophil-endothelial cell interactions, which are normally mediated by increased expression of both intercellular adhesion molecule-1 (ICAM-1) and E-selectin on endothelial cells, were examined using an in vitro flow system. Human neutrophilic polymorphonuclear leukocytes (PMN) were perfused at a shear stress of 1 dyne/cm2 on human umbilical vein endothelial cells (HUVEC) pretreated with IL-1beta (20 U/mL) for 4 hours. Many PMN adhered to IL-1-stimulated HUVEC and then migrated beneath endothelial cell monolayers. Treatment of HUVEC with m-PSL inhibited adherence and migration of PMN in a dose dependent manner. M-PSL also inhibited IL-1beta-induced upregulation of E-selectin and ICAM-1 on HUVEC in a dose dependent manner. These results suggest that m-PSL works as an anti-inflammatory agent through inhibiting PMN-endothelial cell interactions.

Adult↗

PubMed1997

Quantification of singlet oxygen from hematoporphyrin derivative by electron spin resonance.

The mechanism of the generation and the quantitative analysis of singlet oxygen (1O2) formed by the exposure of a hematoporphyrin derivative (HpD) to light was re-evaluated by electron spin resonance (ESR) combined with 2,2,6,6,-tetramethyl-4-piperidine (TMPD). The change from TMPD to 2,2,6,6,-tetramethyl-4-piperidine-N-oxide (TAN) has been reported to depend on singlet oxygen. However, we confirmed that this reagent also react with superoxide anion (O2-) and hydroxyl radicals (OH). Therefore, the reactions between TMPD and 1O2, O2- and OH were re-examined using a kinetic approach. We found that the generation of TAN was proportional to the concentration of TMPD and HpD, as well as to the duration and strength of the illumination. The generation of TAN was not inhibited by dimethyl-sulfoxide (DMSO) or superoxide dismutase (SOD). The reaction rate between TMPD and 1O2 was determined to be 5.0 x 10(-7) M min-1. The generation of 1O2 from HpD was 2.7 x 10(-7) M min-1 under our conditions. The competitive reaction observed between 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and TMPD for O2- or OH shows that TMPD reacts with both forms of active oxygen, but gave no ESR signal. The second-order reaction rate constant of TMPD between O2- and OH was calculated as 73 M-1 s-1 and 1.5 x 10(9) M-1 s-1, respectively. The photochemical generation of 1O2 from methylene blue, another sensitizer, was also demonstrated by this method. These results show that ESR signal of TAN can be used for the highly selective monitoring of 1O2.

Cyclic N-Oxides↗

PubMed1997

Removal of sialic acid from mucin-like surface molecules of Trypanosoma cruzi metacyclic trypomastigotes enhances parasite-host cell interaction.

The 35/50 kDa mucin-like surface glycoprotein (gp35/50) of Trypanosoma cruzi metacyclic trypomastigotes has been implicated in mammalian cell invasion. In this study we investigated whether the sialyl residues of gp35/50 are required for interaction of parasites with target cells. After treatment with bacterial neuraminidase, the metacyclic forms (G strain) remained reactive with the monoclonal antibody (mAb) 10D8 but lost their reactivity with mAb 3C9, that recognizes sialic acid-containing epitopes on gp35/50, and entered HeLa cells in significantly higher numbers as compared to untreated controls. Resialylation of gp35/50, by incubation of parasites with T. cruzi trans-sialidase and sialyl lactose, restored the reactivity with mAb 3C9 as well as the affinity for sialic acid specific lectin. Accordingly, the rate of invasion of resialylated parasites was reduced to levels similar to those observed before desialylation. Purified G strain gp35/50, desialylated by neuraminidase treatment, bound to HeLa cells more than its sialylated counterpart. The Ca2+ signaling activity, which has been associated with cell invasion, was also determined by measuring the cytosolic Ca2+ concentration ([Ca2+]i), in HeLa cells upon interaction with sonicated extracts from untreated or neuraminidase-treated parasites, or with purified gp35/50 in its sialylated or desialylated form. Consistent with the results of cell invasion assay, the desialylated parasite preparations, as well as the sialic acid free gp35/50, induced an average elevation in [Ca2+]i significantly higher than that triggered by untreated controls. None of these effects, namely the increase in infectivity and Ca2+ signaling activity, was observed with neuraminidase-treated CL strain metacyclic trypomastigotes, which express a variant form of sialic acid gp35/50 molecule that is not recognized by mAb 10D8 and apparently is not involved in target cell invasion.

Animals↗

PubMed1997

Free radical-scavenging activity of Crassostera gigas extract (JCOE).

In the present study, we evaluate the free radical-scavenging activity of JCOE (Japan clinic oyster extract), a powder extracted from Crassostera gigas by a spin-trapping method using electron paramagnetic resonance (EPR), and also estimate the protective effect against gastric mucosal cell injury induced by hydrogen peroxide. The EPR study demonstrated that JCOE directly scavenged superoxide radical as well as hydroxyl radical in a concentration-dependent manner. After exposure to hydrogen peroxide for 4 h in Hank's balanced buffered solution, cell viability of rat gastric mucosal cells (RGM-1) was measured by modified MTT assay. Hydrogen peroxide-induced injury was not reversed by 1-h preincubation with 100 to 1,000 micrograms/mL JCOE solution which has high reactivity to hydroxyl radicals, indicating that the active ingredients, including taurine of JCOE on scavenging action of hydroxyl radical, did not penetrate cell membranes easily. Twenty-four hour pretreatment with the JCOE solution significantly reversed the decrease in cell viability induced by hydrogen peroxide, indicating the possibility that JCOE solution may stimulate the endogenous eliminating system against hydrogen peroxide.

Animals↗

PubMed1997

Effects of rebamipide, a novel anti-ulcer agent, on gastric mucosal injury induced by platelet-activating factor in rats.

We examined the role of gastric mucosal blood flow, lipid peroxidation, and neutrophil accumulation mediated by platelet-activating factor in the protective effect of rebamipide against gastric mucosal injury in rats. The intravenous injection of platelet-activating factor induced hyperemia and hemorrhagic erosions in rat stomachs. Rebamipide did not affect the decrease in the gastric mucosal blood flow induced by platelet-activating factor. The increase in gastric injury score after platelet-activating factor injection and the increase in thiobarbituric acid-reactive substances were significantly inhibited by the administration of rebamipide. The gastric injury score was closely correlated with the accumulation of lipid peroxides. Tissue-associated myeloperoxidase activity in the gastric mucosa significantly increased after platelet activating factor injection; this increase was not influenced by rebamipide treatment. The protective effect of rebamipide against the platelet-activiting factor-induced gastric mucosal injury may be due to direct inhibition of lipid peroxidation or scavenging of oxygen radicals that initiate lipid peroxidation.

Alanine↗

PubMed1997

Intercellular adhesion molecule-1 and CD18 are involved in neutrophil adhesion and its cytotoxicity to cultured sinusoidal endothelial cells in rats.

The expression of several adhesion molecules is increased on the hepatic sinusoidal endothelial cells (SECs) in various liver diseases. The objective of this study is to assess the roles of intercellular adhesion molecule 1 (ICAM-1) and of CD18 in the interaction between the neutrophils (polymorphonuclear leukocytes [PMNs]) and SECs and in the injury to SECs mediated by PMNs. Rat PMNs was perfused on SECs stimulated with tumor necrosis factor alpha (TNF-alpha) using an in vitro flow system. The number of adhered PMNs to SECs and that of PMNs migrated under SECs was counted and the effects of anti-ICAM-1, anti-CD18, and dexamethasone were studied. We also define the effect of these antibodies on the SEC injury mediated by PMNs stimulated with phorbol 12-myristate 13-acetate (PMA) or N-formyl-methionyl-leucyl-phenylalanine (fMLP). TNF-alpha significantly increased the adhesion of PMNs to SECs (322 +/- 26 cells/mm2) compared with controls (194 +/- 22 cells/mm2). Anti-ICAM-1 and anti-CD18 significantly inhibited the adhesion of PMNs (131 +/- 10 and 51 +/- 30 cells/mm2, respectively). These antibodies also decreased the migration rate of PMNs (6.0% and 7.9%, respectively) compared with controls (migration rate, 21.2%). The SEC injury induced by PMA- and fMLP-activated PMNs was prevented by anti-ICAM-1 and anti-CD18. The adhesion of PMNs induced by TNF-alpha was inhibited by the treatment with dexamethasone (160 +/- 20 cells/mm2) via a down-regulation of ICAM-1 expression on SECs. The interactions between ICAM-1 and CD18 appeared to be important in the adhesion and the migration of PMNs to SECs. The injury to SECs was induced by the close interaction between the activated PMNs and SECs mediated via ICAM-1 and CD18.

Animals↗

PubMed1997

Monochloramine-induced cell growth inhibition and apoptosis in a rat gastric mucosal cell line.

Recent studies have indicated that monochloramine (NH2Cl), a reaction product of NH3 and hypochlorous acid, is involved in the pathogenesis of Helicobacter pylori-associated gastric mucosal damage, but how NH2Cl contributes to lesions is unclear. In the present study, the effects of NH2Cl on mucosal cell growth and the cell cycle were evaluated in vitro using a normal rat gastric mucosal cell line RGM-1. Cell viability was assessed by the Trypan Blue dye exclusion test and cell cycle patterns were determined by DNA labeling with propidium iodide and flow cytometric quantification. NH2Cl inhibited the growth of RGM-1 cells in a concentration-dependent manner. Exposure of cells to NH2Cl caused a time- and dose-dependent loss of G1-phase cells with accumulation of G2/M-phase cells, and produced a fraction of subdiploid cells with oligonucleosomal DNA degradation characteristic of apoptosis. NH2Cl-induced apoptosis was confirmed by fluorescent microscopy with Hoechst 33342 and propidium iodide. These results suggest that NH2Cl inhibits gastric mucosal cell growth and induces apoptosis in RGM-1 cells, events that may be important in gastric mucosal damage or atrophy induced by H. pylori infection.

Animals↗

PubMed1997

Interactions of neutrophils and endothelial cells under low flow conditions in vitro.

The interactions of polymorphonuclear leukocytes (PMN) and endothelial cells are modulated by adhesion molecules, inflammatory cytokines, and shear stress. We investigated the changes in PMN-endothelial cell interactions induced by interleukin (IL)-1 beta under low flow conditions. PMN were isolated from the venous blood of healthy adults, and endothelial cells were obtained from human umbilical veins. The number of PMN that adhered to the endothelial cells monolayer that was treated with IL-1 increased significantly at shear stresses from .5 to 4.0 dyn/cm2 as compared with untreated endothelial cells. Anti-intercellular adhesion molecule (ICAM)-1 monoclonal antibody (mAb), anti-E-selectin mAb, and anti-CD18 mAb each significantly inhibited the increase in PMN adherence induced by IL-1 at a low shear stress (1.0 dyn/cm2). Anti-CD18 mAb significantly reduced the number of PMN that migrated through the endothelial monolayer by blocking the adherence of PMN to the luminal surface of the endothelial cells, as well as their transendothelial migration. In contrast, anti-ICAM-1 and anti-E-selectin mAb each reduced the number of PMN that migrated by reducing the number of PMN that adhered to the luminal surface without significantly influencing the percent of the adherent PMN that had migrated. Although anti-L-selectin mAb reduced the adherence and migration of PMN, these effects were not statistically significant. These results indicated that under low flow conditions, as well as in the nonflow state, PMN-endothelial cell interactions were elicited via CD11/CD18 and ICAM-1 without the involvement of selectins.

Adult↗

PubMed1997

A case of X-linked alpha-thalassemia/mental retardation syndrome: analysis of hemoglobin by an automated glycated hemoglobin analyzer.

A 5-year-old male patient with X-linked alpha-thalassemia/mental retardation syndrome is reported. He showed multiple minor anomalies including characteristic facial abnormalities, alpha-thalassemia, severe mental retardation, and hypogonadism. Analysis of his hemoglobin by high performance liquid chromatography using an automated glycated hemoglobin analyzer revealed an abnormal peak. Identification of an abnormal peak by an automated glycated hemoglobin analyzer will aid in the diagnosis of patients with X-linked alpha-thalassemia/mental retardation syndrome.

Abnormalities, Multiple↗

PubMed1997

[An autopsy case of chronic granulomatous disease diagnosed by biopsy].

This report concerns a male patient aged 25 years, diagnosed at the age of 12 years as suffering from chronic granulomatous disease. This patient had p47-phox deficiency. He was admitted to this hospital because of fever and dyspnea accompanied by right spontaneous pneumothorax. He failed to respond to medical treatment. He died from respiratory failure four months after admission. Autopsy demonstrated pigmented lipid histiocytes characteristic of CGD. These characteristic pigmented cells were distributed in the spleen, liver, lymph nodes and in the small intestine. As for the nature of the pigment, lipofuschin-like compound were identified. Granulomatous component was seen in the mucosa of the stomach obtained by operation. The presence and characteristic distribution of such pigmented macrophages in tissue in young adults may suggest the diagnosis of CGD.

Adult↗

PubMed1997

Effect of Z-103 on TNB-induced colitis in rats.

Z-103 is a chelate compound consisting of zinc ion and L-carnosine. In this study, we investigated the protective effect of Z-103 against colonic damage induced by 2,4,6-trinitrobenzene sulfonic acid (TNB) in rats. Colonic inflammation was induced by administering TNB dissolved in 50% ethanol (120 mg/ml) in male Wistar rats (total volume of 0.25 ml per rat) following a 48-hour fast. After the administration of TNB, Z-103 was given at a dose of 30 mg/kg per rat for 1 week. A second group of rats received sulfasalazine (SASP) at 300 mg/kg and a third group of rats received 30 mg/kg of ZnSO4 for 1 week. Colonic inflammation was assessed 1 week following TNB administration. Both macro- and microscopic evaluation showed that the inflammatory responses induced by TNB were reduced by treatment with Z-103, SASP and ZnSO4. The score (graded from 0 to 5 according to the macroscopic lesions) and colonic wet weight (distal 8 cm of the colon) were significantly decreased by treatment with Z-103, SASP and ZnSO4. The increase in thiobarbituric acid-reactive substances in the colonic mucosa following TNB administration were inhibited in the Z-103 and SASP groups. These results suggest that Z-103 is as effective against TNB-induced colitis as SASP.

Animals↗

PubMed1997

Essential roles of the winged helix transcription factor MFH-1 in aortic arch patterning and skeletogenesis.

Mesenchyme Fork Head-1 (MFH-1) is a forkhead (also called winged helix) transcription factor defined by a common 100-amino acid DNA-binding domain. MFH-1 is expressed in non-notochordal mesoderm in the prospective trunk region and in cephalic neural-crest and cephalic mesoderm-derived mesenchymal cells in the prechordal region of early embryos. Subsequently, strong expression is localized in developing cartilaginous tissues, kidney and dorsal aortas. To investigate the developmental roles of MFH-1 during embryogenesis, mice lacking the MFH-1 locus were generated by targeted mutagenesis. MFH-1-deficient mice died embryonically and perinatally, and exhibited interrupted aortic arch and skeletal defects in the neurocranium and the vertebral column. Interruption of the aortic arch seen in the mutant mice was the same as in human congenital anomalies. These results suggest that MFH-1 has indispensable roles during the extensive remodeling of the aortic arch in neural-crest-derived cells and in skeletogenesis in cells derived from the neural crest and the mesoderm.

Animals↗

PubMed1997

Mutations within the reactive-site region of human pancreatic secretory trypsin inhibitor confer alpha-thrombin and factor Xa inhibitory activities.

Mutations were introduced into the reactive-site region of human pancreatic secretory trypsin inhibitor (PSTI) to produce thrombin and/or factor Xa inhibitors. All of five mutants showed trypsin inhibitory activity as strong as wild-type PSTI. Moreover, the Arg (P1), Pro-Arg (P2-P1), and Pro-Arg-Ile-Tyr-Asn (P2-P1-P1'-P2'-P3') (bold letters indicated replaced amino acids compared to the wild type) mutants had additional inhibitory activities toward factor Xa, both thrombin and factor Xa, and thrombin, respectively, at 1 x 10(-5) M.

Antithrombins↗

PubMed1997

Effect of the histamine H2-receptor antagonist (+/-)-(E)-1-[2-hydroxy-2-(4-hydroxyphenyl)ethyl]-3'-[2-[[[5-methylamino ) methyl-2-furyl] methyl]thio]ethyl]-2"-(methylsulfonyl)guanidine on acute gastric mucosal injury in rats and its free-radical scavenging activities.

The protective effect of T-593 ((+/-)-(E)-1-[2-hydroxy-2-(4-hydroxyphenyl)ethyl]-3'-[2-[[[5-(methylamino) methyl-2-furyl]methyl]thio]ethyl]-2"-(methylsulfonyl)guanidine, CAS 140695-21-2), a new histamine H2-receptor antagonist, was investigated in rats with acute gastric mucosal injury. An ischemic injury followed by reperfusion was produced by applying a small vascular clamp to the celiac artery for 30 min and then removing it for 60 min. T-593 significantly reduced the area of the lesion in the stomach in a dose-dependent manner, and doses of 0.3 and 3.0 mg/kg inhibited the increase of lipid peroxides in the gastric mucosa after ischemia-reperfusion. A spin-trapping method using 5,5-dimethyl-1-pyrroline-N-oxide showed that T-593 scavenged hydroxyl radicals generated by the hydrogen peroxide-ferrous iron sulfate system. T-593 also significantly inhibited the increase of lipid peroxides induced by free-radical initiators in gastric mucosal homogenates. Thus, the protective effect of T-593 against acute gastric mucosal injury induced by ischemia and followed by reperfusion may result, in part, from its antioxidant properties.

Animals↗

PubMed1997

[Western blot analysis of anti-M2 antibodies in anti-mitochondrial antibody-negative primary biliary cirrhosis].

One variety of anti-mitochondrial antibody(AMA) is characteristically found in sera from patients with primary biliary cirrhosis(PBC). The major target antigens of this type of AMA are M2s. It is well known, however, that AMA-negative PBC also exists. An alternative disease concept, called autoimmune cholangiopathy, recently has been advocated. This new concept is defined by the following criteria: 1)the failure to detect AMA and anti-M2, 2)the detection of a diffuse type of anti-nuclear antibody and anti-smooth muscle antibody, 3)pathological findings compatible with PBC, and 4)the effectiveness of prednisolone. However, the difference between AMA-negative PBC and autoimmune cholangiopathy is controversial. Therefore, we analyzed antibodies to four major M2 proteins with Western blotting in 34 cases of immunofluorescent AMA-negative PBC. In 31(91.2%) of these 34 AMA-negative sera, antibodies to at least one of these four major M2 proteins was detected. In serum samples from 34 control patients with AMA-positive PBC, antibodies to at least one of these four proteins were detected in all cases. In addition, we studied the frequency of cases which satisfied the serological criteria of autoimmune cholangiopathy. In only one(0.7%) of 141 cases was the serological criteria met. We conclude that to clarify the serological differences between autoimmune cholangiopathy and AMA-negative PBC, the analysis of M2 proteins by Western blotting is essential.

Adult↗

PubMed1997

Comparison of effect of mosapride citrate and existing 5-HT4 receptor agonists on gastrointestinal motility in vivo and in vitro.

Mosapride citrate is a new gastroprokinetic agent that enhances the upper GI motility by stimulating 5-hydroxytryptamine4 (5-HT4) receptors. The purpose of this study was to compare the effects of mosapride and the existing 5-HT4 receptor agonists on GI motility in conscious dogs and on various 5-HT4 receptor-mediated responses in vitro. In conscious dogs with force transducers implanted, mosapride (0.3-3 mg/kg i.v.) stimulated the antral motility without affecting the colonic motility. However, cisapride, zacopride and BIMU 8 (0. 1-1 mg/kg i.v.) stimulated both antral and colonic motility. The enhanced GI motility induced by mosapride or cisapride was antagonized by pretreatment with GR113808 (1 mg/kg bolus i.v., thereafter 1 mg/kg/hr infusion), a selective 5-HT4 receptor antagonist. In the receptor binding studies, mosapride inhibited [3H]-GR113808 binding to 5-HT4 receptor sites of guinea pig striatum with an IC50 value of 113 nM. In addition, mosapride caused relaxation of the carbachol-precontracted rat esophagus, enhanced the electrically evoked contractions of guinea pig ileum and evoked the contractions of guinea pig distal colon with EC50 values of 208, 73, and 3029 nM, respectively; this indicates that mosapride has a low affinity for colon than for the rest of the GI tract. In contrast, cisapride, zacopride or BIMU 8 had similar potencies in all preparations examined. In conclusion, these studies indicate that mosapride selectively stimulates upper GI motility in vivo and in vitro. These results also suggest heterogeneity of 5-HT4 receptors in the GI tract.

Animals↗

PubMed1996

Primary structures of fungal fructosyl amino acid oxidases and their application to the measurement of glycated proteins.

Fructosyl amino acid oxidase (FAOD), which is active toward model compounds of the glycated proteins in blood, N epsilon-fructosyl N sigma-Z-lysine and N-fructosyl valine, was purified to homogeneity from Aspergillus terreus GP1. Though the enzyme did not use glycated proteins directly as its substrate, it used glycated human serum albumin (HSA) when HSA was treated with a protease. Linear relationships between both the concentration and the increase in absorbance and the glycation rate of glycated HSA and the increase in absorbance were observed. cDNAs coding for FAODs were cloned from cDNA libraries of A. terreus GP1 and Penicillium janthinellum AKU 3413. The coding region for both fungal FAODs consisted of 1314 bp encoding 437 amino acids. The sequence of a dinucleotide-binding motif, GXGXXG, was in the deduced N-terminal region and a similar sequence to that the active site of bacterial sarcosine oxidases was found near the C-terminal region of FAOD. The of C-terminal tripeptides SKL and AKL of FAODs from A. terreus and P. janthinellum, respectively, represent typical peroxisomal-targeting signals. Finally, FAOD protein was produced in Escherichia coli transformants in an active form, and at the same level as in the original fungi.

Amino Acid Oxidoreductases↗