研究者業績

永井 良三

ナガイ リョウゾウ  (Ryozo Nagai)

基本情報

所属
自治医科大学 自治医科大学 学長
学位
博士(医学)

J-GLOBAL ID
200901024033893870
researchmap会員ID
1000190318

受賞

 7

論文

 955
  • Yasuhiro Hitomi, Yasushi Imai, Masanari Kuwabara, Yusuke Oba, Tomoyuki Kabutoya, Kazuomi Kario, Hisaki Makimoto, Takahide Kohro, Eiichi Shiraki, Naoyuki Akashi, Hideo Fujita, Tetsuya Matoba, Yoshihiro Miyamoto, Arihiro Kiyosue, Kenichi Tsujita, Masaharu Nakayama, Ryozo Nagai
    IJC Heart & Vasculature 54 101507-101507 2024年10月  
  • Yusuke Oba, Tomoyuki Kabutoya, Takahide Kohro, Yasushi Imai, Kazuomi Kario, Hisahiko Sato, Kotaro Nochioka, Masaharu Nakayama, Naoyuki Akashi, Hideo Fujita, Yoshiko Mizuno, Arihiro Kiyosue, Takamasa Iwai, Yoshihiro Miyamoto, Yasuhiro Nakano, Masanobu Ishii, Taishi Nakamura, Kenichi Tsujita, Tetsuya Matoba, Ryozo Nagai
    Hypertension research : official journal of the Japanese Society of Hypertension 2024年9月19日  
    The Japanese Society of Hypertension have established a blood pressure (BP) target of 130/80 mmHg for patients with coronary artery disease (CAD). We evaluated the data of 8793 CAD patients in the Clinical Deep Data Accumulation System database who underwent cardiac catheterization at six university hospitals and the National Cerebral and Cardiovascular Center (average age 70 ± 11 years, 78% male, 43% with acute coronary syndrome [ACS]). Patients were divided into two groups based on whether or not they achieved the guideline-recommended BP of <130/80 mmHg. We analyzed the relationship between BP classification and major adverse cardiac and cerebral event (MACCE) separately in two groups: those with ACS and those with chronic coronary syndrome (CCS). During an average follow-up period of 33 months, 710 MACCEs occurred. A BP below 130/80 mmHg was associated with fewer MACCEs in both the overall (hazard ratio [HR] 0.83, 95% confidence interval [CI] 0.70-1.00, p = 0.048) and the ACS group (HR 0.67, 95%CI 0.51-0.88, p = 0.003). In particular, stroke events were also lower among those with a BP below 130/80 mmHg in both the overall (HR 0.69, 95%CI 0.53-0.90, p = 0.006) and ACS groups (HR 0.44, 95%CI 0.30-0.67, p < 0.001). In conclusion, the achievement of BP guidelines was associated with improved outcomes in CAD patients, particularly in reducing stroke risk among those with ACS.
  • So Ikebe, Masanobu Ishii, Yasuhiro Otsuka, Taishi Nakamura, Kenichi Tsujita, Tetsuya Matoba, Takahide Kohro, Yusuke Oba, Tomoyuki Kabutoya, Yasushi Imai, Kazuomi Kario, Arihiro Kiyosue, Yoshiko Mizuno, Kotaro Nochioka, Masaharu Nakayama, Takamasa Iwai, Yoshihiro Miyamoto, Hisahiko Sato, Naoyuki Akashi, Hideo Fujita, Ryozo Nagai
    International Journal of Cardiology: Cardiovascular Risk and Prevention 22 2024年9月  
    The authors regret that the original version of the article incorrectly stated the study period as “April 2014 to March 2020" in both the Abstract and the Methods section. The correct study period should have been “April 2013 to March 2019". The authors would like to apologise for any inconvenience caused.
  • Hiroshi Iwata, Katsumi Miyauchi, Ryo Naito, Satoshi Iimuro, Yukio Ozaki, Ichiro Sakuma, Yoshihisa Nakagawa, Kiyoshi Hibi, Takefui Hiro, Yoshihiro Fukumoto, Seiji Hokimoto, Yasushi Saito, Hisao Ogawa, Hiroaki Shimokawa, Hiroyuki Daida, Takeshi Kimura, Ryozo Nagai
    JACC: Advances 3(7) 2024年7月  
    Background: The prognostic implications of persistent low-grade inflammation in patients with chronic coronary syndrome (CCS) are underexplored. The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy with Pitavastatin in Coronary Artery Disease) study demonstrated the benefit of higher intensity pitavastatin in Japanese patients with CCS. Objectives: This prespecified subanalysis of the REAL-CAD study aimed to assess the prognostic effect of the persistent low-grade inflammation represented by high-sensitivity C-reactive protein (hs-CRP) in CCS patients. Methods: The present analysis involved patients without events until 6 months after randomization and whose hs-CRP levels were available at baseline and 6 months (n = 10,460). The primary endpoint was the composite of cardiovascular mortality, myocardial infarction, stroke, and unstable angina hospitalization. Landmark analyses evaluated the prognostic impact of continuous inflammation in 4 groups based on the median levels of hs-CRP (0.5 mg/L for both) at baseline and 6 months. The 4 groups included patient with persistently low, elevated (increased), reduced, and persistently high hs-CRP. Results: Adjusted Cox proportional hazard analyses demonstrated an increased risk of the primary endpoint in the group with persistently high hs-CRP when compared to the group with persistently low hs-CRP as a reference (adjusted HR: 1.48, 95% CI: 1.18-1.89; P = 0.001), but with a similar risk in the group with elevated (HR: 1.07, 95% CI: 0.77-1.49, P = 0.68) and reduced (HR: 0.92; 95% CI: 0.66-1.27; P = 0.60) hs-CRP. Conclusions: The study shows that persistent low-grade inflammation is associated with poor outcomes and underscores the need to address residual inflammatory risk in CCS patients. (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease [REAL-CAD]; NCT01042730)
  • Hiroshi Iwata, Katsumi Miyauchi, Ryo Naito, Satoshi Iimuro, Yukio Ozaki, Ichiro Sakuma, Yoshihisa Nakagawa, Kiyoshi Hibi, Takefui Hiro, Yoshihiro Fukumoto, Seiji Hokimoto, Yasushi Saito, Hisao Ogawa, Hiroaki Shimokawa, Hiroyuki Daida, Takeshi Kimura, Ryozo Nagai
    JACC. Advances 3(7) 100996-100996 2024年7月  
    BACKGROUND: The prognostic implications of persistent low-grade inflammation in patients with chronic coronary syndrome (CCS) are underexplored. The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy with Pitavastatin in Coronary Artery Disease) study demonstrated the benefit of higher intensity pitavastatin in Japanese patients with CCS. OBJECTIVES: This prespecified subanalysis of the REAL-CAD study aimed to assess the prognostic effect of the persistent low-grade inflammation represented by high-sensitivity C-reactive protein (hs-CRP) in CCS patients. METHODS: The present analysis involved patients without events until 6 months after randomization and whose hs-CRP levels were available at baseline and 6 months (n = 10,460). The primary endpoint was the composite of cardiovascular mortality, myocardial infarction, stroke, and unstable angina hospitalization. Landmark analyses evaluated the prognostic impact of continuous inflammation in 4 groups based on the median levels of hs-CRP (0.5 mg/L for both) at baseline and 6 months. The 4 groups included patient with persistently low, elevated (increased), reduced, and persistently high hs-CRP. RESULTS: Adjusted Cox proportional hazard analyses demonstrated an increased risk of the primary endpoint in the group with persistently high hs-CRP when compared to the group with persistently low hs-CRP as a reference (adjusted HR: 1.48, 95% CI: 1.18-1.89; P = 0.001), but with a similar risk in the group with elevated (HR: 1.07, 95% CI: 0.77-1.49, P = 0.68) and reduced (HR: 0.92; 95% CI: 0.66-1.27; P = 0.60) hs-CRP. CONCLUSIONS: The study shows that persistent low-grade inflammation is associated with poor outcomes and underscores the need to address residual inflammatory risk in CCS patients. (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease [REAL-CAD]; NCT01042730).

MISC

 1913
  • K Moriguchi, H Rakugi, A Moriguchi, J Higaki, R Nagal, S Nagata, T Ogihara
    JOURNAL OF HYPERTENSION 16 S181-S181 1998年6月  
  • Y Saito, T Nakamura, H Sumino, J Hoshino, T Kurashina, Z Ono, R Nagai
    JOURNAL OF HYPERTENSION 16 S133-S133 1998年6月  
  • J Hoshino, T Nakamura, Y Saito, H Sumino, T Kurashina, Z Ono, R Nagai
    JOURNAL OF HYPERTENSION 16 S85-S85 1998年6月  
  • T Kurashina, T Nakamura, Y Saito, J Hoshino, H Sumino, H Sakamoto, R Nagai
    JOURNAL OF HYPERTENSION 16 S134-S134 1998年6月  
  • N Mise, K Kimura, N Suzuki, K Miyashita, R Nagai, A Goto, M Omata
    JOURNAL OF HYPERTENSION 16 S125-S125 1998年6月  
  • Ohyabu, I, T Takasaki, S Akiba, S Nomura, N Enokizono, Y Sagara, J Hiroi, R Nagai, H Yoshida
    PATHOLOGY INTERNATIONAL 48(6) 433-439 1998年6月  
    The expression of myosin in normal and diseased mammary glands of 199 Japanese women was evaluated immunohistochemically by the avidin-biotin peroxidase complex method using antibodies to three human smooth muscle myosin heavy chain isoforms derived from the vascular smooth muscle: myosin SM1 is expressed consistently from fetal stage to adulthood, myosin SM2 appears only in well-differentiated smooth muscle after birth, and myosin SMemb is more abundant in embryonic aortas. SM1 was expressed in myoepithelial cells of normal mammary glands and fibrocystic diseases and in myoepithelial-like tumor cells in the basal layer of fibroadenomas and phyllodes tumors. SM2 was expressed only in the myoepithelial cells of mammary glands in breastfeeding women. SMemb was expressed more intensely in the cytoplasm of luminal epithelial cells in larger fibroadenomas (P &lt; 0.01), or in the cytoplasm of carcinoma cells in invasive ductal carcinomas with metastasized lymph nodes (P &lt; 0.001) and in those of higher histological grade (P &lt; 0.0001), Multivariate logistic analysis showed a significant correlation only between the expression of SMemb and histological grade (P &lt; 0.0001), which is a prognostic factor of mammary carcinomas. These findings suggested the possible prognostic value of SMemb.
  • M Inoue, T Kanda, M Arai, B M McManus, T Suzuki, I Kobayashi, R Nagai
    Research communications in molecular pathology and pharmacology 100(3) 327-38 1998年6月  査読有り
    We evaluated the effects of myocardial infarction (MI) on the hemodynamics and the expression of atrial natriuretic peptide (ANP) mRNA in rats with streptozotocin-induced diabetes. Eight weeks after streptozotocin injection, the diabetic rats and age-matched nondiabetic controls underwent coronary artery ligation. One week later, the left ventricular end-diastolic pressure, systolic blood pressure, infarct size, and serum ANP levels did not differ significantly between the diabetic and nondiabetic rats. Compared with control animals without MI, the atrial ANP/beta-actin mRNA ratio in rats with MI was increased to 195% in diabetic animals and 213% in nondiabetic animals. In the left ventricle, however, the ANP/beta-actin mRNA ratio in diabetic animals with MI was increased to only 131% compared with control animals, whereas the corresponding increase in nondiabetic animals was 240% (p<0.05). Thus, the modulation of ANP mRNA expression after MI was impaired in the left ventricle, but not in the atria, of diabetic rats. A reduced myocardial expression of ANP could increase the morbidity and mortality associated with cardiovascular disorders in patients with diabetes.
  • T Iwami, T Nakamura, N Niwamae, T Yamagishi, T Utsugi, R Nagai
    INTERNAL MEDICINE 37(6) 528-533 1998年6月  
    A 68-year-old woman was referred for evaluation of an incidentally discovered left adrenal mass, Her chief complaint was body weight loss, She showed no symptoms or signs suggestive of Cushing's syndrome. The circadian rhythm of blood pressure was also normal. Hormonal assessment revealed an abnormal diurnal variation in serum cortisol levels, suppressed baseline plasma adrenocorticotrophic hormone, and nonsuppression of serum and urinary cortisol with the dexamethasone suppression test. Adrenal scintigraphy with I-131-6-beta-iodomethyl-norcholesterol showed uptake on the left adrenal and inhibition of the contralateral adrenal gland. She was diagnosed as pre-clinical Cushing's syndrome. Due to the lack of clinical symptoms and the risks of surgery, we emphasize the importance of careful assessment of the cortisol metabolism and scintigraphic scanning under dexamethasone suppression to avoid post-surgical Addisonian crisis.
  • N Akuzawa, T Nakamura, T Kurashina, Y Saito, J Hoshino, H Sakamoto, H Sumino, Z Ono, R Nagai
    American journal of hypertension 11(6 Pt 1) 697-707 1998年6月  査読有り
    We investigated the ability of the angiotensin converting enzyme (ACE) inhibitor imidapril hydrochloride, and of the calcium channel blocker amlodipine besilate, to prevent nephrosclerosis and left ventricular hypertrophy (LVH) in rats with hypertension induced by chronic inhibition of nitric oxide (NO). Male Wistar rats were given distilled water (control), NG-nitro-L-arginine methyl ester (L-NAME) 500 mg/L, L-NAME plus imidapril 10 mg/L or 100 mg/L, or L-NAME plus amlodipine 50 mg/L or 100 mg/L in the drinking water (n = 10-12). We then collected 24-h urine samples at 2, 4, and 6 weeks, obtained blood samples at 6 weeks, and histologically examined the kidney and heart. L-NAME markedly reduced the levels of NO metabolites in serum and urine while increasing the tail-cuff blood pressure, the urinary albumin level (1.90 +/- 0.65 v 0.05 +/- 0.02 mg/day/100 g in control), and the area of the left ventricular wall (83.3 +/- 3.0 v 69.8 +/- 1.8 mm2 in control). Nephrosclerosis and myocardial interstitial fibrosis were documented histologically. The plasma renin activity was significantly higher in rats treated with L-NAME than in the control rats. The concomitant administration of imidapril (10 mg/L) with L-NAME completely normalized the tail-cuff pressure, the LVH (70.8 +/- 1.8 mm2), the albuminuria (0.05 +/- 0.01 mg/day/100 g), and the histologic changes. Amlodipine (50 mg/L) also ameliorated the L-NAME-induced effects, but to a lesser extent. Thus, the chronic inhibition of NO synthesis in rats produced nephrosclerosis and LVH that were effectively prevented by giving imidapril at a dose lower than that of amlodipine. We conclude that ACE inhibitors can prevent nephrosclerosis and LVH even in the presence of a reduction in NO production, implying that in rats the inhibition of the renin-angiotensin system is more effective than the blockade of calcium channels in preventing hypertensive tissue injury.
  • H Bai, R Morishita, Kida, I, T Yamakawa, W Zhang, M Aoki, H Matsushita, A Noda, R Nagai, Y Kaneda, J Higaki, T Ogihara, Y Sawa, H Matsuda
    GENE THERAPY 5(6) 761-769 1998年6月  
    The senescent cell-derived inhibitor (sdi)-1 (p21) protein has been identified as a downstream mediator of the tumor suppressor p53 in the cell cycle regulation. In this study, we focused on the function of sdi-1 gene in inhibiting vascular smooth cell (VSMC) proliferation after vein grafting in a rabbit model. To test the hypothesis, we transfected human sdi-1 gene by an intra-operative approach. Accompanied by markedly increased sdi-1 protein, the significant increase in PCNA-stained VSMCs in vein grafts was inhibited by transfection of sdi-1 gene. Moreover, at 2 weeks after transfection, transfer of sdi-1 gene resulted in a significant inhibition in neointimal formation, compared with control vector. Of importance, immunohistological studies determining the expression pattern of myosin heavy isoforms, adult type specific SM2 and embryonic specific SMemb/NMHC-B, demonstrated expression of the adult phenotype of VSMCs in the neointima of sdi-1 gene-1 transfected Vein grafts at 2 weeks after the operation, while the neointima was predominantly composed of embryonic phenotype of VSMCs in the control grafts. Overall, these results demonstrate that a single intraluminal incubation of human sdi-1 gene can result in a significant inhibition of neointimal formation after vein grafting, associated with phenotypic change of VSMCs from neonatal to adult type in a rabbit model. Inhibition of hyperplasia in a graft model by transfection of sdi-1 gene may be due to the change in VSMC phenotype from neonatal to adult, in addition to the inhibition of VSMC growth.
  • R Nagai, H Sano, K Matsumoto, Y Jinnouchi, H Suzuki, T Kodama, S Horiuchi
    DIABETES 47 A23-A23 1998年5月  
  • T Uchiyama, S Jikawazu, T Ohno, S Tomono, T Utsugi, N Kato, A Tsuchida, Y Ohyama, R Nagai, T Tanabe, M Yabuuchi
    DIABETES 47 A153-A153 1998年5月  
  • T Utsugi, T Kanda, Kobayashi, I, T Uchiyama, Y Ohyama, N Katoh, S Tsuchida, S Tomono, S Kawazu, R Nagai
    DIABETES 47 A201-A201 1998年5月  
  • A Miyajima, T Toyama, T Hatori, Y Aihara, T Iwasaki, A Hasegawa, R Nagai, T Suzuki, T Inoue, K Endo, H Hoshizaki, S Ohshima, K Taniguchi
    JOURNAL OF NUCLEAR MEDICINE 39(5) 153P-153P 1998年5月  
  • Y Ohyama, T Utsugi, T Ohno, T Uchiyama, H Ito, SI Tomono, M Kuro-O, R Nagai
    DIABETES 47 A393-A393 1998年5月  
  • H Sato, W Okumura, T Toyama, T Iwasaki, T Suzuki, R Nagai, T Inoue, K Endo, N Kanazawa
    JOURNAL OF NUCLEAR MEDICINE 39(5) 152P-152P 1998年5月  
  • A Matsumori, N Ohashi, K Hasegawa, S Sasayama, T Eto, T Imaizumi, T Izumi, K Kawamura, M Kawana, A Kimura, A Kitabatake, M Matsuzaki, R Nagai, H Tanaka, M Hiroe, M Hori, H Inoko, Y Seko, M Sekiguchi, K Shimotohno, Y Sugishita, N Takeda, K Takihara, M Tanaka, T Tokuhisa, T Toyo-oka, M Yokoyama
    JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 62(5) 389-391 1998年5月  
    As a collaborative research project of the Committees for the Study of Idiopathic Cardiomyopathy, a questionnaire was sent out to 19 medical institutions in Japan in order to examine the possible association between hepatitis C virus (HCV) infection and cardiomyopathies. Hepatitis C virus antibody was found in 74 of 697 patients (10.6%) with hypertrophic cardiomyopathy (mean age, 57.7 years) and in 42 of 663 patients (6.3%) with dilated cardiomyopathy (mean age, 56.5 years); these prevalences were significantly higher than that found in volunteer blood donors in Japan (2.4%, 50-59 pears of age, each p&lt;0.0001). The prevalence was significantly higher in patients suffering from hypertrophic cardiomyopathy as opposed to those with dilated cardiomyopathy (p&lt;0.01). The presence of HCV antibody was detected in 650 of 11,967 patients (5.4%) patients seeking care in 5 academic hospitals. Various cardiac abnormalities were found among these patients, arrhythmias being the most frequent. These observations suggest that HCV infection is an important cause of a variety of otherwise unexplained heart diseases.
  • T Takahashi, T Kanda, H Sumino, M Inoue, K Sato, T Sakamaki, I Kobayashi, A Iwamoto, R Nagai
    Research in experimental medicine. Zeitschrift fur die gesamte experimentelle Medizin einschliesslich experimenteller Chirurgie 197(6) 319-28 1998年4月  査読有り
    We evaluated the effects of oral administration of E4021 (100 mg/kg/day), a type V phosphodiesterase inhibitor, on immunoreactivities of endothelin-1, endothelin receptors, and nitric oxide synthases in pulmonary arteries in a rat model of pulmonary hypertension. Immunoreactivities of endothelin-1 and endothelial nitric oxide synthase were observed significantly less frequently, together with significant reduction of right ventricular overload and medial thickening in rats treated with E4021 than in the control with monocrotaline on day 28. The levels of plasma endothelin-1 and serum nitrite and nitrate were significantly lower in rats that received E4021 than in the control with monocrotaline. Oral administration of E4021 modulates endogenous immunoreactivities of endothelin-1 and endothelial nitric oxide synthase with the improvement or right ventricular overload and medial thickening.
  • T Itoh, T Tanaka, R Nagai, T Kamiya, T Sawayama, T Nakayama, H Tomoike, H Sakurada, Y Yazaki, Y Nakamura
    Human genetics 102(4) 435-9 1998年4月  査読有り
    Familial long QT syndrome (LQTS) is characterized by prolonged ventricular repolarization. Clinical symptoms include recurrent syncopal attacks, and sudden death may occur as a result of ventricular tachyarrhythmias. Three genes responsible for this syndrome (KVLQT1, HERG, and SCN5A) have been identified so far, and mutations have been reported on the basis of partially characterized genomic organization. To optimize the search for HERG mutations, we have determined the genomic structure of HERG and investigated mutations in LQTS families. Human genomic clones containing the HERG gene were isolated from a human genomic library by using reverse-transcribed polymerase chain reaction (RT-PCR) products from this gene as probes. We determined exon/intron boundaries and flanking intronic sequences by using primers synthesized on the basis of the HERG cDNA sequence available in the DNA database. HERG was shown to consist of 15 exons spanning approximately 19 kb on chromosome 7q35. Subsequently, we synthesized oligonucleotide primers to cover the entire coding region and searched for mutations in 36 Japanese LQTS families. When genomic DNA from each proband was examined by the PCR/single-strand conformation polymorphism technique followed by direct DNA sequencing, five novel mutations were detected. Each mutation was present in affected relatives of the respective proband. This work should increase the efficiency of screening mutations associated with HERG.
  • 永井 良三, 星野 洋一
    臨床病理 46(3) 249-257 1998年3月25日  
  • 杉山 大介, 中村 哲也, 岩崎 勉, 大山 良雄, 高間 典明, 山岸 高弘, 永井 良三
    Japanese circulation journal 61 815-815 1998年3月20日  
  • 金子 克己, 間仁田 守, 岩崎 俊弥, 安藤 達夫, 久保田 幸夫, 加地 辰美, 永井 良三
    Japanese circulation journal 61 816-816 1998年3月20日  
  • 庭前 野菊, 金古 善明, 谷口 靖広, 間仁田 守, 伊藤 敏夫, 山岸 高宏, 天野 晶夫, 永井 良三
    Japanese circulation journal 61 804-804 1998年3月20日  
  • T Yamazaki, I Komuro, S Kudoh, Y Zou, R Nagai, R Aikawa, H Uozumi, Y Yazaki
    Circulation research 82(4) 430-7 1998年3月9日  査読有り
    We have previously reported that stretching of cardiomyocytes activates the phosphorylation cascade of protein kinases, including Raf-1 kinase and mitogen-activated protein (MAP) kinases, followed by an increase in protein synthesis partly through enhanced secretion of angiotensin II and endothelin-1. Membrane proteins, such as ion channels and exchangers, have been postulated to first receive extracellular stimuli and evoke intracellular signals. The present study was performed to determine whether mechanosensitive ion channels and exchangers are involved in stretch-induced hypertrophic responses. Neonatal rat cardiomyocytes cultured on expandable silicone dishes were stretched after pretreatment with a specific inhibitor of stretch-sensitive cation channels (gadolinium and streptomycin), of ATP-sensitive K+ channels (glibenclamide), of hyperpolarization-activated inward channels (CsCl), or of the Na+-H+ exchanger (HOE 694). Pretreatment with gadolinium, streptomycin, glibenclamide, and CsCl did not show any inhibitory effects on MAP kinase activation by mechanical stretch. HOE 694, however, markedly attenuated stretch-induced activation of Raf-1 kinase and MAP kinases by approximately 50% and 60%, respectively, and attenuated stretch-induced increase in phenylalanine incorporation into proteins. In contrast, HOE 694 did not inhibit angiotensin II-and endothelin-1-induced Raf-1 kinase and MAP kinase activation. These results suggest that among many mechanosensitive ion channels and exchangers, the Na+-H+ exchanger plays a critical role in mechanical stress-induced cardiomyocyte hypertrophy.
  • H Nagaoka, T Iizuka, S Kubota, M Inoue, E Yamaguchi, T Suzuki, R Nagai
    Japanese circulation journal 62(3) 160-6 1998年3月  査読有り
    To evaluate the clinical significance of reversible perfusion defects that were observed soon after the successful deployment of a coronary stent, 47 patients underwent thallium-201 myocardial scintigraphy and radionuclide angiography in conjunction with adenosine-induced coronary hyperemia before and after complete revascularization. Coronary angiography showed a significant decrease in the percent diameter stenosis (from 87+/-11% before stenting to -1+/-5% after stenting, p<0.01) with no major dissection, residual stenosis, or intra-stent formation of thrombus. Even after the angiographically successful procedure, reversible perfusion defects were present in 17 (36%) of the 47 patients, none of whom showed any wall motion abnormalities during the infusion of adenosine. Disease duration was significantly longer and collateral vessels were more common in the patients with than in those without thallium redistribution, whereas the other clinical, pre- and post-stent angiographic and hemodynamic factors were similar. In conclusion, reversible perfusion defects without wall motion abnormalities were demonstrated during the infusion of adenosine in approximately one-third of patients soon after coronary stenting, and were not consistently related to acute unfavorable outcomes of stent placement.
  • T Shiraki-Iida, H Aizawa, Y Matsumura, S Sekine, A Iida, H Anazawa, R Nagai, M Kuro-o, Y Nabeshima
    FEBS LETTERS 424(1-2) 6-10 1998年3月  
    We previously established a novel mouse model for human aging and identified the genetic foundation responsible for it. A defect in expression of a novel gene, termed klotho (kl), leads to a syndrome resembling human aging in mice. The kl gene encodes a single-pass membrane protein whose extracellular domain carries homology to beta-glucosidases. In this report, we present the entire mouse kl gene organization. The mouse kl gene spans about 50 kilobases and consists of five exons. The promoter region lacks a TATA-box and contains four potential binding sites for SP1. We further show that two kl gene transcripts encoding membrane or secreted protein are generated through alternative transcriptional termination. These findings provide fundamental information for further study of the kl gene which may regulate aging in Five. (C) 1998 Federation of European Biochemical Societies.
  • N Mise, K Kimura, R Nagai, S Ohba, N Suzuki, K Miyashita, A Tojo, A Goto, M Omata
    NEPHRON 78(3) 284-289 1998年3月  
    To characterize the phenotypic alteration in mesangial cells in human glomerulonephritis, we investigated the expression of nonmuscle-type myosin heavy chain, SMemb, and alpha-smooth muscle actin (alpha-SM actin) in IgA nephropathy. The expression of SMemb and alpha-SM actin was examined by immunohistochemistry in biopsy specimens from 45 patients with IgA nephropathy. We examined a total of 489 glomeruli representing all patients enrolled, and found that mesangial expression of SMemb and alpha-SM actin was associated with mesangial proliferation. Only mesangial expression of SMemb showed a significant relationship with mesangial matrix accumulation. Semiquantitative evaluation using composite expression scores showed that the expression of SMemb was elevated in the patients with poor renal prognosis. The expression of alpha-SM actin showed no significant relationship with renal prognosis. These results suggest that mesangial expression of SMemb is an important factor in the progression of IgA nephropathy, and that SMemb and alpha-SM actin are associated with the activation of mesangial cells by different mechanisms.
  • 相原 康, 倉林 正彦, 田中 享, 都丸 浩一, 新井 昌史, 大山 良雄, 相澤 宏樹, 関口 賢一, 内山 強, 小和瀬 桂子, 阿久澤 暢洋, 永井 良三
    Japanese circulation journal 62 567-567 1998年2月28日  
  • 坂本 浩之助, 倉林 正彦, 星野 洋一, 神田 享勉, 永井 良三, 澤田 芳枝, 酒巻 哲夫, 土屋 陽子, 前田 雅弘, 清藤 勉
    Japanese circulation journal 62 238-238 1998年2月28日  
  • 喜楽 順一, 宮 芳紀, 長谷川 修一, 中野 正幸, 神田 享勉, 今井 進, 永井 良三
    Japanese circulation journal 62 244-244 1998年2月28日  
  • 直田 匡彦, 外山 卓二, 小板橋 紀通, 中津川 昌利, 富田 智之, 夛田 浩, 川上 武, 磯部 直樹, 櫻井 繁樹, 安達 仁, 内藤 滋人, 野上 昭彦, 星崎 洋, 大島 茂, 谷口 興一, 永井 良三
    Japanese circulation journal 62 235-235 1998年2月28日  
  • 関口 賢一, 倉林 正彦, 横山 知行, 都丸 浩一, 新井 昌史, 大山 良雄, 相原 康, 相澤 宏樹, 田中 亨, 内山 強, 小和瀬 桂子, 阿久澤 暢洋, 神田 享勉, 永井 良三
    Japanese circulation journal 62 243-243 1998年2月28日  
  • 関口 賢一, 田中 亨, 横山 知行, 新井 昌史, 神田 享勉, 鈴木 忠, 倉林 正彦, 永井 良三
    Japanese circulation journal 62 225-225 1998年2月28日  
  • 大山 良雄, 倉林 正彦, 坂本 浩之助, 星野 洋一, 相原 康, 都丸 浩一, 内山 強, 阿久澤 暢洋, 小和瀬 桂子, 田中 亨, 関口 賢一, 永井 良三, 黒尾 誠, 下村 行生, 真鍋 一郎
    Japanese circulation journal 62 288-288 1998年2月28日  
  • 斉藤 勇一郎, 中村 哲也, 角野 博之, 星野 仁, 倉品 年成, 小野 善平, 永井 良三
    Japanese circulation journal 62 422-422 1998年2月28日  
  • 斉藤 勇一郎, 中村 哲也, 山岸 高宏, 相澤 宏樹, 角野 博之, 星野 仁, 大山 良雄, 倉品 年成, 小野 善平, 倉林 正彦, 永井 良三, 黒尾 誠
    Japanese circulation journal 62 139-139 1998年2月28日  
  • 都丸 浩一, 倉林 正彦, 新井 昌史, 横山 知行, 大山 良雄, 相澤 宏樹, 相原 康, 関口 賢一, 田中 亨, 内山 強, 小和瀬 桂子, 阿久澤 暢洋, 永井 良三
    Japanese circulation journal 62 519-519 1998年2月28日  
  • 阿久澤 暢洋, 倉林 正彦, 坂本 浩之助, 大山 良雄, 相澤 宏樹, 相原 康, 田中 亨, 小和瀬 桂子, 内山 強, 永井 良三
    Japanese circulation journal 62 534-534 1998年2月28日  
  • 田中 亨, 神田 享勉, 関口 賢一, 坂本 浩之助, 横山 知行, 倉林 正彦, 永井 良三
    Japanese circulation journal 62 517-517 1998年2月28日  
  • 田中 亨, 倉林 正彦, 相原 康, 小和瀬 桂子, 阿久澤 暢洋, 内山 強, 都丸 浩一, 関口 賢一, 相澤 宏樹, 大山 良雄, 永井 良三
    Japanese circulation journal 62 315-315 1998年2月28日  
  • 増田 浩明, 松村 穣, 黒尾 誠, 相澤 宏樹, 永井 良三, 荒川 絵美, 鍋島 陽一
    Japanese circulation journal 62 317-317 1998年2月28日  
  • 松村 穣, 増田 浩明, 鍋島 陽一, 黒尾 誠, 相澤 宏樹, 永井 良三, 飯田 卓子, 荒川 絵美
    Japanese circulation journal 62 317-317 1998年2月28日  
  • 飯田 卓子, 荒川 絵美, 相澤 宏樹, 永井 良三, 松村 穣, 増田 浩明, 鍋島 陽一, 黒尾 誠
    Japanese circulation journal 62 317-317 1998年2月28日  
  • 大山 良雄, 相澤 宏樹, 相原 康, 倉林 正彦, 永井 良三, 増田 浩明, 松村 穣, 黒尾 誠, 鍋島 陽一
    Japanese circulation journal 62 314-314 1998年2月28日  
  • 外山 卓二, 星崎 洋, 磯部 直樹, 小板橋 紀通, 直田 匡彦, 中津川 昌利, 富田 智之, 川上 武, 堀江 康人, 夛田 浩, 櫻井 繁樹, 安達 仁, 内藤 滋人, 野上 昭彦, 大島 茂, 谷口 興一, 永井 良三
    Japanese circulation journal 62 261-261 1998年2月28日  
  • 坂本 浩之助, 中村 哲也, 阿久澤 暢洋, 角野 博之, 斉藤 勇一郎, 倉品 年成, 小野 善平, 永井 良三
    Japanese circulation journal 62 283-283 1998年2月28日  
  • 中村 哲也, 相澤 宏樹, 大山 良雄, 斉藤 勇一郎, 倉品 年成, 角野 博之, 星野 仁, 倉林 正彦, 永井 良三, 黒尾 誠, 松村 穣, 増田 浩明, 鍋島 陽一
    Japanese circulation journal 62 282-282 1998年2月28日  
  • 小和瀬 桂子, 倉林 正彦, 坂本 浩之助, 星野 洋一, 大山 良雄, 相澤 宏樹, 相原 康, 田中 亨, 内山 強, 阿久澤 暢洋, 都丸 浩一, 関口 賢一, 永井 良三, 神田 享勉
    Japanese circulation journal 62 370-370 1998年2月28日  
  • 都丸 浩一, 倉林 正彦, 新井 昌史, 大山 良雄, 相澤 宏樹, 関口 賢一, 相原 康, 田中 亨, 横山 知行, 永井 良三
    Japanese circulation journal 62 366-366 1998年2月28日  
  • 新井 昌史, 関口 賢一, 都丸 浩一, 滝沢 敬子, 横山 知行, 倉林 正彦, 永井 良三
    Japanese circulation journal 62 379-379 1998年2月28日  

書籍等出版物

 21

共同研究・競争的資金等の研究課題

 91