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H Nishio

Publications and source records attributed to H Nishio.

At least 19 recordsLinked to original sources
PubMed2007

Intrahepatic cholangiojejunostomy following hepatobiliary resection.

BACKGROUND: Although intrahepatic cholangiojejunostomy is technically difficult, with recent improvements in surgery it should be possible to perform the anastomosis safely. The aim of this study was to evaluate the incidence of anastomotic leak after intrahepatic cholangiojejunostomy and to identify risk factors for such leakage. METHODS: Intrahepatic cholangiojejunostomy was performed in 423 patients undergoing hepatobiliary resection between January 1991 and December 2005. Anastomotic leak was proven radiographically by leakage from the anastomosis of contrast medium introduced via a biliary drainage tube placed during surgery. RESULTS: Anastomotic leak occurred in 27 patients (6.4 per cent), and was not related to the number of bile ducts reconstructed. The leak rate decreased significantly from 9.5 per cent (19 of 199) in the first 10 years to 3.6 per cent (eight of 224) in the last 5 years. Anastomotic leak was often followed by infections such as wound infection, intra-abdominal abscess and bacteraemia. Multivariable analysis identified age and intraoperative blood loss as independent risk factors for anastomotic leak. All leaks were treated by maintaining a prophylactically placed drain near the cholangiojejunostomy; neither repeat laparotomy nor percutaneous transhepatic biliary drainage was required. CONCLUSION: Although demanding, intrahepatic cholangiojejunostomy can be performed successfully with a relatively low failure rate. Routine use of prophylactic drains and anastomotic stenting allows safe management of anastomotic leak with conservative therapy.

Aged↗
PubMed2006

Isolation and characterization of mammalian D-aspartyl endopeptidase.

The accumulation of D-isomers of aspartic acid (D-Asp) in proteins during aging has been implicated in the pathogenesis of Alzheimer's disease (AD), cataracts and arteriosclerosis. Here, we identified a specific lactacystin-sensitive endopeptidase that cleaves the D-Asp-containing protein and named it D-aspartyl endopeptidase (DAEP). DAEP has a multi-complex structure (MW: 600 kDa) and is localized in the inner mitochondrial membrane. However, DAEP activity was not detected in E. coli, S. cerevisiae, and C. elegans. A specific inhibitor for DAEP, i-DAEP: (benzoyl-L-Arg-L-His-[D-Asp]-CH(2)Cl; MW: 563.01), was newly synthesized and inhibited DAEP activity (IC(50), 3 microM), a factor of ten greater than lactacystin on DAEP. On the other hand, i-DAEP did not inhibit either the 20S or 26S proteasome. And we identified succinate dehydrogenase and glutamate dehydrogenase 1 as components of DAEP by affinity label using biotinylated i-DAEP. In the long life span of mammals, DAEP may serve as a scavenger against accumulation of racemized proteins in aging. Insights into DAEP will provide the foundation for developing treatments of diseases, such as AD, in which accumulation of D-Asp-containing proteins are implicated.

Acetylcysteine↗
PubMed2006

E-cadherin is a novel transcriptional target of the KLF6 tumor suppressor.

The tumor suppressor KLF6 is a member of the Krüppel-like family of transcription factors, which has been implicated in the pathogenesis of several human carcinomas. Uncovering the transcriptional targets relevant for its tumorigenic properties, including cellular proliferation and invasion, will be essential to understanding possible mechanisms by which KLF6 and its antagonistic splice form, KLF6-SV1, regulate this development. To begin defining possible metastatic-related pathways, we analysed the effect of KLF6 dysregulation on a recognized suppressor of cellular invasion, E-cadherin. Targeted KLF6 reduction in an ovarian cancer cell line, SKOV-3, resulted in a 50% reduction of E-cadherin expression (P<0.01) and conversely, KLF6-SV1 silencing upregulated E-cadherin approximately fivefold (P<0.0001). These changes resulted from KLF6 directly transactivating the E-cadherin promoter as demonstrated by luciferase promoter assay and chromatin immunoprecipitation (ChIP). KLF6-mediated changes in E-cadherin levels were accompanied by downstream changes in both the subcellular localization of beta-catenin and c-myc expression levels. Moreover, and consistent with these experimental findings, patient-derived epithelial ovarian tumors with low KLF6 and high KLF6-SV1 expression ratios had significantly decreased E-cadherin expression (P<0.0001). These combined findings highlight the E-cadherin pathway as a novel and functionally important mediator by which changes in KLF6 and KLF6-SV1 can directly alter ovarian tumor invasion and metastasis.

3' Untranslated Regions↗
PubMed2006

Effects of perinatal stress on the anxiety-related behavior of the adolescence mouse.

We evaluated the effects of sound noise or forced swim stress applied to pregnant mice or to neonatal mice on the anxiety-related behavior using the elevated plus-maze test performed during the age of 5 weeks. The forced swim stress applied at the late gestation period, days 10-18 of pregnancy, caused a significant reduction of the body weight gain of the dams. However, the anxiety-related behavior of the male and female offspring were not affected by the antenatal stress treatment. When the forced swim stress was applied to the neonatal mice during the late lactation period, 14-18 days after birth, the male mice showed an elevated level of anxiolytic behavior accompanying the reduction of the emotion-related motor activity. The anxiety-related behavior of the female mice was not affected by the stress treatment. Furthermore, we applied the sound noise or forced swim stress to the neonatal mice immediately after the weaning, 21-25 days after birth. The stress applied after the weaning period had no effect on the anxiety-related behavior. These results suggested that the stress applied during the lactation period, but not that during the antenatal period, nor after the weaning period, might have gender-dependently reduced the anxiety level of the male mouse. It was shown that the effects of perinatal stress on the anxiety-related behavior of the adolescent mouse varied according to the period of application and gender. The hypothesis that gender-dependent abnormalities in neurodevelopment might be caused by the excess stress applied to the breast-fed infant is of importance in elucidating the relationship between the psychoneurotic disorder in childhood and the environment stress of the breast-fed infant.

Age Factors↗
PubMed2005

Effects of (Z)-3-hexenol, a major component of green odor, on anxiety-related behavior of the mouse in an elevated plus-maze test and biogenic amines and their metabolites in the brain.

In the present study, the effect of (Z)-3-hexenol, one of the main constituent of green odor, on the anxiety-related behavior of mouse and the content of 5-hydroxytryptamine (5-HT), dopamine and their metabolites in the brain were investigated. Evaluation of anxiety-related animal behavior was performed by measuring the percent of time spent on the open arms and the percent of open-arm entries as conventional anxiety indices. The number of times displaying risk-assessment from a closed arm was also measured as an ethological anxiety index. Diazepam, an anxiolytic agent, enhanced the percent of time spent on the open arms and the percent of open-arm entries. The number of times displaying risk-assessment was not affected by diazepam in the present study. The percent of time on the open arms were depressed, and the number of times displaying risk-assessment were stimulated by 1-(3-trifluoromethylphenyl)piperazine (TFMPP), indicating that TFMPP acts as an anxiogenic agent. (Z)-3-Hexenol revealed anxiolytic activity and increased the percent of time spent on the open arms and decreased the number of times displaying risk-assessment. In the neurochemical study, diazepam had no effect on the content of 5-HT and its metabolite in the brain cortex or hippocampus. On the other hand, TFMPP inhibited the 5-HT turnover rate accompanied by the elevation of the 5-HT content and reduction of the 5-HIAA content in the brain cortex and hippocampus. (Z)-3-Hexenol significantly increased the 5-HT content without affecting the 5-HIAA content or the 5-HT turnover rate in the brain cortex or hippocampus. Changes in serotonergic activity in the cortex and hippocampus were suggested to be involved in the anxiolytic effect of (Z)-3-hexenol observed in the elevated plus-maze test.

Animals↗
PubMed2005

Evidence for involvement of p59fyn in fasting-induced thymic involution.

p59fyn, a member of the src-family protein tyrosine kinase, is expressed abundantly in thymus. We examined the possible involvement of p59fyn in thymic involution induced by a fasting stress in Fyn-/- mice. An acute 48 h fast resulted in severe atrophy of the thymus and a marked decrease of the total thymocyte number with depletion of the CD4+CD8+[double positive (DP)] population in Fyn+/+ (control) mice. A remarkable increase in terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling-positive signals was detected in the fasted group of control mice. However, these findings were not observed in Fyn-/- mice. Interestingly, MRL/MPJ-lpr/lpr, a Fas-deficient model animal, also showed no significant decrease of DP cell numbers in the fasted group. p59fyn is known to interact with Fas signalling, and these findings suggest that p59fyn is involved in fasting-induced thymic involution, raising the possibility that Fas/p59fyn-mediated signalling may, at least partially, be associated with the phenomenon.

Animals↗
PubMed2005

[Successful resection of left ventricular myxoma in a toddler; report of a case].

A 4-year-old girl was found to have large left ventricular myxoma without any tumor-related symptoms. She underwent an urgent surgery and the myxoma was successfully removed through a left ventriculectomy. Great care was taken to prevent tumor-embolization during surgery, and to resect the endocardium attaching directly to the tumor. Future surveillance of this case warrants our operative technique described in this report.

Cardiac Surgical Procedures↗
PubMed2004

Dual role of endogenous nitric oxide in development of dextran sodium sulfate-induced colitis in rats.

The role of nitric oxide (NO) in the etiology of ulcerative colitis is controversial with reports of the improvement and aggravation of colonic lesions by inducible NO synthase (iNOS) inhibitors. In the present study, we compared the effect of the selective iNOS inhibitor aminoguanidine and the nonselective NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) on a dextran sulfate sodium (DSS)-induced model of colitis in rats. Experimental colitis was induced by a 3% DSS-solution added to drinking water for 7 days. Aminoguanidine (5 approximately 20 mg/kg) and L-NAME (10 mg/kg) were administered p.o. twice daily for the first 3 days, the last 3 days or all 6 days of DSS treatment. Body weight and severity of colitis (diarrhea, bloody feces) were observed over a period of 7 days. DSS treatment resulted in severe colonic lesions, accompanied by diarrhea, bloody feces, decrease of body weight and colon shortening. All of the parameters investigated improved significantly with aminoguanidine treatment at 20 mg/kg for 6 days or the last 3 days of DSS-treatment, but L-NAME did not significantly affect the colitis during these periods. When L-NAME or aminoguanidine was given in the first 3 days of DSS treatment, the colonic lesions were slightly aggravated by L-NAME but not affected by aminoguanidine. The expression of iNOS mRNA was observed from the 3(rd) day of DSS treatment. These results suggested that endogenous NO exerts a biphasic influence on DSS-induced colitis, depending on the NOS isoenzyme; a beneficial effect of NO derived from constitutive NOS and a detrimental effect of NO produced by iNOS in the development of colitis.

Animals↗
PubMed2004

Analysis of the survival motor neuron and neuronal apoptosis inhibitory protein genes in Malay patients with Spinal Muscular Atrophy.

In Malaysia, Spinal Muscular Atrophy (SMA) is diagnosed based on clinical observation with or without muscle biopsy. Molecular analyses of the SMA-related genes have not been available so far. In this preliminary study, we searched for homozygous deletion of Survival Motor Neuron (SMN1) and Neuronal Apoptosis Inhibitory Protein (NAIP) genes in Malay patients with SMA and found homozygous deletion of SMN1 exon 7 and 8 in all the patients while homozygous deletion of NAIP exon 5 was detected in only our type 1 patients but not in the type 3 patient. To the best of our knowledge, these are the first SMA cases diagnosed at the molecular level in Malaysia.

Cyclic AMP Response Element-Binding Protein↗
PubMed2001

Molecular cloning and characterization of a KRAB-containing zinc finger protein, ZNF317, and its isoforms.

To identify zinc finger genes in human primary cultured erythroid progenitor cells, RT-PCR was performed using primers specific for the conserved sequence in zinc finger domains of mouse Friend of GATA-1. We identified a novel Krüppel-associated box (KRAB) zinc finger gene, ZNF317. Evaluation of full-length cDNA obtained by RACE showed that it encoded a protein composed of 13 Krüppel-like zinc fingers and a KRAB domain. RT-PCR analysis revealed four alternatively splicing products (ZNF317-1 through ZNF317-4). The ZNF317 gene has seven exons and is located in human chromosome 19p13. Northern analysis revealed that ZNF317-1 and ZNF317-2 transcripts were ubiquitously expressed, whereas ZNF317-3 and ZNF317-4 transcripts were detected only in lymphocytes, spleen, and lung. Competitive RT-PCR analysis showed that the expression of ZNF317 mRNA significantly decreased during erythroid maturation. In lymphocytes, ZNF317 expression was reduced in response to mitogenic stimulation. We propose that ZNF317 may play an important role in erythroid maturation and lymphoid proliferation.

Alternative Splicing↗
PubMed2001

Possible role of orexin A in nonadrenergic, noncholinergic inhibitory response of muscle of the mouse small intestine.

The effect of a novel peptide, orexin A, on longitudinal muscle of ICR mouse small intestine was examined in vitro. Exogenous orexin A induced a transient contraction in duodenal, jejunal and ileal segments. Atropine and tetrodotoxin completely inhibited the contractions. Contraction of longitudinal muscle of jejunal segments induced by electrical field stimulation was still observed after the jejunal segment had been desensitized to orexin A, suggesting that orexin A is not a final neurotransmitter to induce the contraction. On the other hand, in the presence of atropine and guanethidine, orexin A induced a transient gradual relaxation in duodenal, jejunal and ileal segments. Electrical field stimulation also induced significant relaxation of the muscle in jejunal segments. The electrical field stimulation-induced relaxation was inhibited by 55% after the desensitization of the segments to orexin A. Although the electrical field stimulation-induced relaxation was inhibited by 47% by a nitric oxide synthesis inhibitor, NG-nitro-L-arginine (L-NOARG), orexin desensitization did not affect the relaxation which persisted after L-NOARG treatment. The exogenous orexin A-induced relaxation was completely inhibited by L-NOARG. The results suggest that orexin A partially mediates nonadrenergic, noncholinergic (NANC) relaxation via activation of nitrergic neurones in longitudinal muscle of ICR mouse small intestine.

Animals↗
PubMed2001

Clinical features and skewed X-chromosome inactivation in female carriers of X-linked recessive spinal and bulbar muscular atrophy.

In X-linked recessive disorders, a few female gene carriers become symptomatic. Recent evidence implicates skewed X-chromosome inactivation in such female carriers. We studied the clinical features of eight female gene carriers of X-linked recessive spinal and bulbar muscular atrophy (SBMA), and evaluated the relationship between phenotype and genotype from the viewpoint of X-chromosome inactivation. Seven of eight cases were symptomatic, showing mild muscle weakness, frequent muscle cramps, slight elevation of the serum creatinine kinase level, or neurogenic changes on the electromyogram. Only one carrier was asymptomatic clinically. For the estimation of X-chromosome inactivation, the methylation status of the androgen receptor (AR) gene was determined by polymerase chain reaction-based assay. Highly skewed inactivation of the affected AR gene was found in the asymptomatic carrier, while symptomatic carriers had a random or lower inactivation pattern of the affected AR gene. These findings suggest that most female carriers of SBMA show some clinical abnormalities, and highly skewed inactivation of the affected X-chromosome seems to closely relate with escape of the manifestation in female carriers of SBMA.

Adult↗
PubMed2001

Polymorphisms of renin-angiotensin system genes in childhood IgA nephropathy.

We investigated whether polymorphisms of the renin-angiotensin system genes are involved in IgA nephropathy in Japanese children. We identified the M235T polymorphism of the angiotensinogen (AGT) gene, the I/D polymorphisms of the angiotensin-converting enzyme (ACE) gene, and the A1166C polymorphism of the angiotensin II type 1 receptor gene in 95 Japanese children with IgA nephropathy and 99 healthy Japanese adults. There were no differences in the genotype and allele frequencies of these genes between patients with IgA nephropathy and controls. Urinary protein excretion at the time of biopsy was significantly greater in patients with the TT genotype of the AGT gene than in those with the MM/MT genotypes of the AGT gene (1.32 +/- 1.42 versus 0.75 +/- 0.78 g/day; P = 0.01) and in patients with the ID/DD genotypes of the ACE gene than in those with the II genotype of the ACE gene (1.45 +/- 1.50 versus 0.63 +/- 0.56 g/day; P = 0.001). Thus, the TT genotype of the AGT gene and the ID/DD genotype of the ACE gene are associated with increased severity of proteinuria, suggesting that AGT and ACE gene polymorphisms may play a significant role in the progression of IgA nephropathy in Japanese children.

Adolescent↗
PubMed2001

Prenatal stress and postnatal development of neonatal rats--sex-dependent effects on emotional behavior and learning ability of neonatal rats.

Maternal sound stress (800 Hz; 77 dB, every other minute for 15 min/day, from day 10 to 18 of gestation), combined with forced swimming stress (15 min/day), was found to cause potentiation of sound-induced loss of locomotor activity, referred to as emotional behavior, of male offspring, but not that of female offspring, at 4 weeks of age. Maternal stress also caused an increase in the total number of errors by male, but not female offspring in the water-maze test at 6 weeks of age. These effects of stress on emotional behavior and learning behavior were abolished when dams were pretreated with buspirone (30 min before the stress, from day 8 to 18 of gestation). Thus, prenatal stress might have sex-dependent effects on emotional behavior and learning ability of neonatal rats.

Acoustic Stimulation↗
PubMed2001

Immunohistochemical study of the phosphorylated and activated form of c-Jun NH2-terminal kinase in human aorta.

c-Jun NH2-terminal kinase is a key enzyme mediating the cellular response to a variety of extracellular stimuli. In the present study, we performed immunohistochemical studies of the expression of the phosphorylated form of the kinase in 51 human aortas of various ages. The phosphorylated kinase immunoreactivity was strongly detected in vascular smooth muscle cells of the medial vessel layer of atherosclerotic lesions from adults. Immunoreactivity was also strongly detected in similar cells of the intima. On the other hand, immunoreactive phosphorylated kinase was only weakly defected in the medial vascular smooth muscle cells of non-atherosclerotic lesions from adults. We also investigated the expression of the phosphorylated kinase in infant aortas. In contrast to its weak immunoreactivity in adult non-atherosclerotic lesions, the kinase immunoreactivity was detected in high amounts in vascular smooth muscle cells of non-atherosclerotic lesions from infants. Thus, the abundant expression of the phosphorylated kinase in these cells in atherosclerotic lesions of adults and non-atherosclerotic lesions of infants suggests that the activation of c-Jun NH2-terminal kinase may be an important element initiating the proliferation of vascular smooth muscle cells during atherogenesis and aortic development.

Adult↗
PubMed2001

Immunolocalisation of the janus kinases (JAK)--signal transducers and activators of transcription (STAT) pathway in human epidermis.

The janus kinases (JAK) and signal transducers and activators of the transcription (STAT) pathway have been shown to be activated by a number of cytokines or growth factors and to play significant roles in the differentiation of various cell types. In the present study, we investigated the distribution of the JAK-STAT pathway using immunohistochemistry in the human epidermis. Each element of the pathway showed abundant and differential expression in the epidermis. The differential distribution of the elements was most strikingly observed in the horny keratinised cell and granular layers of the epidermis. JAK2, JAK3, STAT1 and STAT5 were expressed in high amounts, and JAK1, TYK2, STAT2, STAT3, STAT4 and STAT6 to a much lesser extent in the horny cell layer. JAK3, TYK2, STAT2, STAT3, STAT4 and STAT6 were more abundantly expressed in the granular layer than the lower layers of the epidermis. JAK1, STAT1 and STAT5 were expressed at almost the same levels in the various layers of the epidermis. These results show that elements of the JAK-STAT pathway are abundantly and differentially expressed in the epidermis. It is suggested that each element of the pathway may play a role at a distinct stage of keratinocyte differentiation.

Adult↗
PubMed2001

Possible involvement of Fyn kinase in ethanol-stimulated Cas tyrosine phosphorylation in rat cerebellum and cerebral cortex.

In the present study, we have investigated the effect of intraperitoneal injection of ethanol (3.5 g/kg) on tyrosine phosphorylation in rat brain. Immunoblot analysis using an antiphosphotyrosine antibody revealed that a 130-kDa protein band was detected in the brain extract in response to ethanol administration. This ethanol-stimulated tyrosine phosphorylation of the 130-kDa protein was found in the brain but not in the heart, liver or thymus. The 130-kDa phosphotyrosine-containing protein was identified by immunoprecipitation to be Cas, a crk-associated src substrate. This ethanol-stimulated tyrosine phosphorylation of Cas was observed most prominently in the cerebellum and the cerebral cortex. We further examined the possible involvement of Fyn kinase in ethanol-stimulated Cas tyrosine phosphorylation. Immunecomplex kinase assay showed that Fyn was activated in the cerebellum and cerebral cortex of ethanol-administered rats. Immunoprecipitation experiments also showed that Fyn was co-immunoprecipitated with an anti-Cas antibody in these regions from ethanol-administered rats. Furthermore, exogenous Fyn was shown to phosphorylate Cas from cerebellum and cerebral cortex in vitro. These findings indicate that ethanol stimulates tyrosine phosphorylation of Cas in rat cerebellum and cerebral cortex, and that Fyn may be involved in the process.

Animals↗