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N Iwai

Publications and source records attributed to N Iwai.

At least 91 records · Page 5Linked to original sources
PubMed1998

[I/D polymorphism of angiotensin converting enzyme gene and myocardial infarction].

The DD genotype of angiotensin converting enzyme gene has been reported to be a risk factor for myocardial infarction. However, this association has not been confirmed in some study populations. We hypothesized that the discrepancies between these studies may be due to variations in the definition of ischemic heart diseases. According to the genotype of the ACE gene, we analyzed the profiles of 320 patients who underwent coronary angiography for suspected ischemic heart disease. We found that the II genotype of the ACE gene was associated with a longer period of time between the first anginal pain and the onset of myocardial infarction. Because higher ACE has been reported to be associated with higher plasminogen activator inhibitor-1 activity, our observation suggests that the genotype of the ACE gene is a marker of fibrinolytic activity.

Aged↗
PubMed1997

Myoepithelial hamartoma of the ileum causing intussusception in an infant

Intussusception is a relatively common pediatric gastrointestinal emergency, although the etiology in most cases remains unknown. In a small number of cases the lead point is a tumor or tumor-like lesion of the small bowel. We report an unusual case of a myoepithelial hamartoma of the ileum causing an intussusception in a 4-month-old boy. This is the second such report in the literature.

Journal Article↗
PubMed1997

Genetic analysis of renin gene expression in the central nervous system of spontaneously hypertensive rats.

Renin expression in the central nervous system in spontaneously hypertensive rats (SHR) has been reported to be higher than that in age-matched Wistar-Kyoto (WKY) rats. In the present study, we examined the mechanisms of enhancement of renin mRNA concentration in the brainstem of SHR using F2 hybrid rats derived from cross-breeding SHR with WKY. The SHR allele of the renin gene was significantly associated with higher brain renin mRNA concentration in both 10- and 24-week-old F2 populations. However, neither the genotype of the renin gene nor the brain renin mRNA concentration was associated with blood pressure or urinary volume. Thus, the higher renin mRNA concentration in the brainstem of SHR was indicated to be genetically determined by the genotype of the renin gene. Further study is required to clarify the pathophysiological meaning of this increased renin expression in the brain of SHR.

Aldosterone↗
PubMed1997

Rat chromosome 1: regional localization of seven genes (Slc9a3, Srd5a1, Esr, Tcp1, Grik5, Tnnt3, Jak2) and anchoring of the genetic linkage map to the cytogenetic map.

Seven genes were regionally localized on rat Chromosome (Chr) 1, from 1p11 to 1q42, and two of these genes were also included in a linkage map. This mapping work integrates the genetic linkage map and the cytogenetic map, and allows us to orient the linkage map with respect to the centromere, and to deduce the approximate position of the centromere in the linkage map. These mapping data also indicate that the Slc9a3 gene, encoding the Na+/H+ exchanger 3, is an unlikely candidate for the blood pressure loci assigned to rat Chr 1. These new localizations expand comparative mapping between rat Chr 1 and mouse or human chromosomes.

Animals↗
PubMed1997

Myoepithelial hamartoma of the ileum causing intussusception in an infant.

Intussusception is a relatively common pediatric gastrointestinal emergency, although the etiology in most cases remains unknown. In a small number of cases the lead point is a tumor or tumor-like lesion of the small bowel. We report an unusual case of a myoepithelial hamartoma of the ileum causing an intussusception in a 4-month-old boy. This is the second such report in the literature.

Diagnosis, Differential↗
PubMed1997

Is a new biofeedback therapy effective for fecal incontinence in patients who have anorectal malformations?

PURPOSE: The authors devised computerized equipment for use in the biofeedback therapy in the management of fecal continence after surgery for anorectal malformations. METHODS: The therapy was used for two to eight sessions in 14 children (11 who had high-type anomalies and three who had intermediate-type anomalies). The ages ranged 5 to 14 years. A control group of 17 children, aged 5 to 11 years, who had encopresis, was also treated with the same biofeedback therapy. RESULTS: Clinical improvement was noted in 5 of the 14 (36%) children who had fecal incontinence, and in 15 of the 17 children (88%) who had encopresis. Both in patients who had fecal incontinence and in those who had encopresis, anal resting pressures were not affected by biofeedback therapy. Furthermore, the anal resting pressure in children who had fecal incontinence was significantly lower than that in children who had encopresis. However, anorectal manometry showed that the biofeedback therapy improved voluntary sphincter function and rectal sensation in both groups. CONCLUSION: Biofeedback therapy appears to be effective in most children who have encopresis whose sphincter function is intact, and in some children who have fecal incontinence after surgery for anorectal malformations.

Adolescent↗
PubMed1997

Germline mutation of the RET proto-oncogene in children with total intestinal aganglionosis.

To clarify the pathogenesis of total intestinal aganglionosis, an extremely severe from of neural crest-derived cell migration disorder of the gut, the authors studied possible germline mutations of the RET proto-oncogene (10q11.2) in five pedigrees at high risk for congenital aganglionosis. All five patients analyzed were boys, and one had a family history of Hirschsprung's disease. Genomic DNA was extracted from lymphoblastoid cell lines established from patients and their relatives. Polymerase chain reaction (PCR) products, which were amplified using specific primers (RET; exon 1 approximately 20), were electrophoresed to analyze the single-strand conformational polymorphism (SSCP) patterns. DNA sequences were determined in pedigrees showing abnormal SSCP bands. Among the five patients, three germline mutations were found in the receptor tyrosine kinase domain (exon 15; codons 884, 897, and 904). Amino acid substitutions of the Ret protein were predicted based on the mutated nucleotide changes. Phenotypic variations of congenital aganglionosis may depend on the RET mutation pattern and other genetic or environmental determinants. In our series of patients, male sexuality and germline mutation of the RET tyrosine kinase domain were the most likely factors contributing to this form of Hirschsprung's disease.

Child↗
PubMed1997

A comparison of anal endosonography with electromyography and manometry in high and intermediate anorectal anomalies.

Anal endosonography, electromyography (EMG) of the external anal sphincter (EAS), and manometry of the internal anal sphincter (IAS) were performed in 15 patients with anorectal anomalies (10 with high and five with intermediate anomalies), ranging in age from 8 to 18 years. The anal endosonographic findings were compared with those for the EMG of the EAS and manometry of the IAS. An image including the hyperechoic band that corresponds to the EAS was obtained in all 15 patients. However, the distribution of EAS image was inadequate in high anomalies. In four patients who showed in Kelly score of 5 or 6, good visualization of the EAS was obtained in both anal endosonography and EMG. An Image including the hypoechoic band that corresponds to the IAS was obtained in five patients with high anomalies and in one with intermediate anomalies. Therefore, even in patients with anomalies, at these levels the IAS could be ultrasonically detected. However, only one of these six patients exhibited an anorectal reflex. These results indicate that, for the EAS, the findings of anal endosonography correspond well with those of EMG, but that for the IAS, they do not correspond with those of manometry. At the time of surgery for anorectal anomalies care should taken to preserve the IAS, which can be detected by anal endosonography even in patients with high or intermediate anomalies.

Adolescent↗
PubMed1997

Association analyses of S(A) gene variant in essential hypertensives.

A gene designated S(A) has been implicated in hypertension (HT) in rat genetic models and Japanese HT patients. However, a linkage study in whites was negative. Because of the limitations of genetic analyses, confirmation in different settings is imperative. Therefore, we conducted a cross-sectional case-control study involving 106 HT and 96 normotensive (NT) white subjects. A polymerase chain reaction technique was developed for PstI restriction fragment length polymorphism (RFLP) determination. We could find no association of this RFLP with HT (frequency of minor allele, A2 = 0.11 in HTs v 0.07 in NTs). However, A2 displayed an association with increase in body mass index in HTs: for a body mass index mean of 26 kg/m2 or more, A2 = 0.17 compared to 0.06 for body mass index of less than 26 kg/m2 (chi2 = 6.4, P = .01; odd ratio 3.4, 95% confidence interval 1.2 to 10.0); for a body mass index of 28 kg/m2 or more, A2 = 0.20 (chi2 = 10.4, P = .001; odds ratio 4.0, 95% confidence interval 1.5 to 10.5). Furthermore, A2 tracked significantly with elevation in body mass index in the HTs (F = 4.8, P = .01 by one-way ANOVA). In conclusion, we could find no association of S(A) genotype with HT, but obtained preliminary evidence for a possible association with variation in body mass index in a severely affected HT group with a strong family history of HT.

Alleles↗
PubMed1997

Relationship between the response to the angiotensin converting enzyme inhibitor imidapril and the angiotensin converting enzyme genotype.

Insertion (I)/deletion (D) polymorphism of the angiotensin converting enzyme (ACE) gene has been reported to be involved in various cardiovascular diseases. We investigated prospectively whether the response to the ACE inhibitor imidapril varied according to the ACE genotype or plasma ACE activity in Japanese hypertensive patients. The study population consisted of 57 hypertensive patients. After a 4-week observation period, imidapril was administered at a dose of 5 mg/day and blood pressure was measured every 2 weeks for 6 weeks. The plasma ACE activity in patients with the DD or ID genotype was significantly higher than that in patients with the II genotype. Neither the reduction nor the percent reduction in systolic blood pressure was significantly different between patients with either the DD or ID genotype and patients with the II genotype (DD or ID v II, 18.8 +/- 2.4 v 20.2 +/- 3.3 mm Hg; P = NS, 10.9 +/- 1.4 v 11.7 +/- 1.9%; P = NS, respectively). However, both the reduction and the percent reduction in diastolic blood pressure tended to be higher in patients with the II genotype (DD or ID v II, 7.9 +/- 1.2 v 12.4 +/- 2.2 mm Hg; P = .0669, 8.1 +/- 1.2 v 12.4 +/- 2.2%; P = .0569, respectively). The reduction in diastolic blood pressure was inversely correlated with plasma ACE activity (r = 0.301, P = .0253). In conclusion, the response to imidapril in hypertensive patients is determined at least in part by the ACE genotype.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Results of a modified Duhamel Operation for Hirschsprung's disease using the GIA stapler.

Thirty-six patients with Hirschsprung's disease underwent surgery using modified Duhamel operation with the GIA (gastrointestinal autosuture) stapler over a 12-year period at our institution. We now present our experience from the perspective of postoperative complications and anorectal function. Postoperative complications included minimal anal bleeding due to the GIA stapler in 2 patients, and mild enterocolitis in 6 patients. Severe complications such as anastomotic leakage or stricture were not observed in our series. Overall, postoperative anorectal function was good in patients without Down's syndrome or cerebral palsy. Follow-up of our patients showed that a good quality of life was achieved during childhood. We conclude, therefore, that the modified Duhamel operation, with the use of the GIA stapler, is a safe and easy procedure for correction of Hirschsprung's disease.

Child, Preschool↗
PubMed1997

Enhancement of neutrophil infiltration in the corpus after failure of Helicobacter pylori eradication.

Neutrophil accumulation plays an important role in Helicobacter pylori-associated gastric mucosal injury. In this study, the mucosal content of myeloperoxidase (MPO), which is a measure of neutrophil accumulation and interleukin-8 (IL-8) was assayed and changes in MPO and IL-8 content were determined before and after H. pylori eradication therapy. Thirty-seven H. pylori-positive patients (11DU/26GU) underwent H. pylori eradication therapy with lansoprazole (30 mg/day, 6 weeks) and amoxicillin (2 g/day, 2 weeks), followed by famotidine (20 mg/day, 8 weeks). H. pylori-infection status was evaluated by routine endoscopic examinations (culture, CLO, histology). Immediately and 8 weeks after cessation of the anti-H. pylori therapy, these tests were repeated. Intragastric urease activity was estimated by delta 13CO2, which was obtained by the [13C]urea breath test (UBT). Mucosal samples were taken and tissue MPO and IL-8 contents were assayed by EIA and ELISA, respectively. Histologic examination was also performed. Among the 37 patients, 21 cases of H. pylori infection were eradicated (56.8%). Intragastric urease activity was dramatically reduced immediately after the anti-H. pylori therapy, whereas, it was re-elevated 8 weeks later in the relapsed cases. Antral MPO content was decreased in the eradicated and relapsed cases. MPO in the corpus was also decreased in the eradicated cases. Nevertheless, it was enhanced (3.5-fold) in the relapsed cases at 8 weeks after therapy. Changes in mucosal IL-8 content were similar to those of MPO. In eradicated cases, neutrophil infiltration is improved in both the antrum and corpus. However failure of eradication therapy results in the enhancement of neutrophil accumulation in the corpus. Further study is necessary to clarify the mechanism of neutrophil accumulation after therapy for H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Sodium intake regulates renin gene expression differently in the hypothalamus and kidney of rats.

OBJECTIVE: To elucidate the different effects of sodium intake on renin messenger RNA (mRNA) in the hypothalamus and the kidney and to investigate the role of hypothalamic renin in sodium-induced hypertension. DESIGN AND METHODS: We investigated the expression of the renin gene in the hypothalamus and the kidney of rats with altered sodium intake and those administered either deoxycorticosterone acetate (DOCA) or sodium. Diets containing a high (8% NaCl), normal (2% NaCl), or low (0.2% NaCl) amount of sodium were administered to 12-week-old male Wistar rats for 10 days or 8 weeks before the rats were killed. Male Wistar rats administered either DOCA or 1% NaCl were killed 2 weeks (during the prehypertensive stage) or 6 weeks (during the hypertensive stage) after the start of treatment. The hypothalamus and kidneys were excised for extraction of total RNA. Competitive polymerase chain reaction of renin mRNA and deletion-mutated renin RNA was performed, and the renin mRNA concentration was calculated. RESULTS: A high sodium intake for 10 days increased the renin mRNA in the hypothalamus; the hypothalamic renin mRNA had not been suppressed after 8 weeks of a high sodium intake despite the lowering in renal renin mRNA. Renin mRNA levels in the hypothalamus were not suppressed either in the prehypertensive or in the hypertensive stage in rats treated with DOCA or sodium, or both, although the renal renin mRNA was reduced in rats administered DOCA or sodium, or both, compared with that in sham-treated control rats, during both stages. CONCLUSIONS: The expression of the renin gene is regulated differently in the rat hypothalamus from that in the kidney. The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension.

Animals↗
PubMed1997

Expression of angiotensin converting enzyme and chymase in human atria.

BACKGROUND: A cardiac angiotensin II-generating system has been suspected to be involved in various cardiac pathological conditions. Both angiotensin converting enzyme and human chymase can convert angiotensin I to angiotensin II. OBJECTIVE: To clarify the relative contributions of these two enzymatic pathways to angiotensin II generation in vivo. METHODS: We assessed the expression levels of messenger RNA (mRNA) for collagen type I alpha, transforming growth factor-beta(1), brain natriuretic peptide, angiotensin converting enzyme and chymase in right atrial appendages by competitive polymerase chain reaction and Northern blot analyses. Correlations among the concentrations of these mRNA were analysed to obtain insight that might be important in understanding the formation of angiotensin II in atrial tissue. RESULTS: The collagen type I alpha and brain natriuretic peptide mRNA concentrations were correlated significantly to the mean pulmonary arterial pressure. Multivariate regression analysis revealed that the collagen type I alpha mRNA concentration could be explained in terms of the brain natriuretic peptide (P = 0.0005) and angiotensin converting enzyme (P = 0.0084) mRNA concentrations (r = 0.598, P < 0.0001). The chymase mRNA concentration had no significant correlation to the collagen type I alpha mRNA concentration. Moreover, multiple regression analysis revealed that the transforming growth factor-beta(1) mRNA concentration could be explained in terms of the angiotensin converting enzyme mRNA concentration alone (r = 0.424, P = 0.014). CONCLUSIONS: The present results suggest that the level of angiotensin converting enzyme affects the tissue angiotensin II level in human atria; however, we could obtain no evidence that chymase is important in determining the tissue angiotensin II level.

Adolescent↗
PubMed1997

Effect of genotype on the angiotensin-converting enzyme mRNA level in human atria.

1. To clarify the mechanism of the association between I/D polymorphism of the angiotensin-converting enzyme (ACE) gene and various cardiovascular disease, ACE mRNA levels in human atrial appendages were assessed in relation to the genotype of the ACE gene. 2. Angiotensin-converting enzyme mRNA levels were positively correlated with age and tended to show a positive correlation with mean pulmonary pressure (mPA). Multiple regression analysis indicated that age and mPA, but not the genotype of the ACE gene, were predictors of ACE mRNA levels in human atrial appendages. 3. The present study indicates that I/D polymorphism of the ACE gene is not simply reflected in ACE mRNA levels and that further study is needed to determine the mechanism of the association between this polymorphism and various cardiovascular diseases.

Adolescent↗
PubMed1997

Differential regulation of natriuretic peptide genes in infarcted rat hearts.

1. We investigated the regulation of the atrial natriuretic peptide and brain natriuretic peptide genes in a rat model of myocardial infarction induced by isoproterenol (IP rat) and in a rat model of cardiac hypertrophy induced by aorto-caval shunt (AC shunt rat). 2. Brain natriuretic peptide (BNP) mRNA levels in atria were significantly higher in IP rats than in controls at 18 h after the administration of isoproterenol, but not significant increases were observed in atrial natriuretic peptide (ANP) mRNA expression levels at any time point examined. In the ventricles, the BNP mRNA levels peaked at 18 h after isoproterenol administration, whereas ANP mRNA levels gradually increased until 3 days after isoproterenol administration. 3. The BNP mRNA levels in both atria and ventricles were significantly increased at 1 day after the introduction of aorto-caval shunt, while the ANP mRNA levels were not. 4. Plasma BNP levels were closely correlated with left ventricular weight per bodyweight, in both IP rats and AC shunt rats. 5. These results suggest the differential regulation of ANP and BNP genes in both the atria and ventricles in these two pathological models.

Animals↗