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

 965
  • Yu Yoshiki, Yukio Ozaki, Mitsuru Abe, Tevfik F Ismail, Hiroshi Takahashi, Masaharu Akao, Hideki Kawai, Takashi Muramatsu, Masahide Harada, Masaya Ohta, Yosuke Hashimoto, Yuichiro Shiki, Masayuki Koshikawa, Keiichi Miyajima, Hidemaro Takatsu, Yudai Niwa, Naoyuki Kawashima, Reina Ozaki, Naotake Tsuboi, Satoshi Iimuro, Hiroshi Iwata, Ichiro Sakuma, Yoshihisa Nakagawa, Kiyoshi Hibi, Takafumi Hiro, Yoshihiro Fukumoto, Seiji Hokimoto, Katsumi Miyauchi, Hisao Ogawa, Hiroyuki Daida, Hiroaki Shimokawa, Hideo Izawa, Takeshi Kimura, Ryozo Nagai
    Journal of the American Heart Association 14(2) e034627 2025年1月21日  
    BACKGROUND: The effect of worsening renal function and baseline chronic kidney disease (CKD) on outcomes in patients with chronic coronary syndrome in the setting of optimal medical therapy remains unknown. METHODS AND RESULTS: The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease) study is a prospective, multicenter, randomized trial of high-dose (pitavastatin 4 mg/day) or low-dose (pitavastatin 1 mg/day) statin therapy in 12 118 patients with chronic coronary syndrome. The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, stroke, or unstable angina requiring hospitalization (major adverse cardiac and cerebral events [MACCE]). CKD was defined as an estimated glomerular filtration rate [eGFR] <60 mL/min per 1.73 m2. WRF was defined as a decrease in eGFR ≥20% in the initial year; borderline renal function was an annual decrease of 0%<eGFR<20%, and stable renal function was no decrease. Of 12 118 patients, 4340 had baseline CKD and 7778 did not. The rate of MACCE at 5 years was significantly lower in those without (5.5%) versus with CKD (9.5%) (P<0.0001). After excluding 1247 patients who had MACCE, were censored, or missing eGFR within 1 year, 10 871 patients were included. Of these, 3885 were baseline CKD and the remaining 6986 did not have baseline CKD. Of the 10 871 patients, 577 patients had WRF, 6014 patients showed borderline renal function, and the remaining 4280 patients maintained stable renal function. In patients with CKD, WRF was an independent predictor for MACCE at 4 years as compared with stable renal function (hazard ratio [HR]: 1.67; [95% CI, 1.03-2.73; P=0.039]). In patients without CKD, borderline renal function was a significant predictor for MACCE at 4 years compared with stable renal function (HR: 1.40 [95% CI, 1.03-1.91; P=0.032]). CONCLUSIONS: Baseline CKD was an independent predictor for MACCE in patients with CCS. WRF was a significant predictor for MACCE in patients with CKD. Because borderline renal function was an independent predictor for MACCE even in patients without CKD, mild-to-moderate annual declines of eGFR should be carefully monitored (NCT01042730). REGISTRATION: URL: https://www.clinicaltrials.gov; Unique Identifier: NCT01042730.
  • Kosuke Nagaoka, Natsuka Kimura, Satoru Inoda, Takuya Takayama, Yusuke Arai, Yasuo Yanagi, Takashi Shimada, Ryozo Nagai, Hidenori Takahashi, Kenichi Aizawa
    International Journal of Molecular Sciences 26(2) 556-556 2025年1月10日  査読有り
  • 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 &amp; 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.
  • 西田 翔, 石間 環, 木村 夏花, 岩見 大基, 永井 良三, 今井 靖, 相澤 健一
    移植 59(総会臨時) 292-292 2024年9月  

MISC

 1923
  • T Utsugi, T Kanda, Kobayashi, I, T Uchiyama, H Ito, Y Ohyama, S Tomono, S Kawazu, R Nagai
    DIABETOLOGIA 42 A103-A103 1999年8月  
  • S Hiroi, H Harada, H Nishi, M Satoh, R Nagai, A Kimura
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 261(2) 332-339 1999年8月  
    To reveal genetic risk factors of nonfamilial idiopathic cardiomyopathy (IDC) in Japanese, polymorphisms in the SOD2 and HLA-DRB1 genes were investigated in 86 patients and 380 healthy controls. There was a significant excess of homozygotes for the V allele [Val versus Ala (A allele), a polymorphism in the leader peptide of manganese superoxide dismutase at position 16] of the SOD2 gene in the patients compared with the controls (87.2% versus 74.7%, odds ratio = 2.30, p = 0.013, pc &lt; 0.03), and a significant increase in the frequency of HLA-DRB1*1401 in the patients was confirmed (14.0% vs 4.5%, odds ratio = 3.46, p = 0.001, pc &lt; 0.03). A two-locus analysis suggested that these two genetic markers (SOD2-VV genotype and DRB1*1401) may play a synergistic role in controlling the susceptibility to nonfamilial IDC. In addition, processing efficiency of Val-type SOD2 leader peptide in the presence of mitochondria was significantly lower than that of the Ala-type by 11 +/- 4%, suggesting that this lower processing efficiency was in part an underlying mechanism of the association between the SOD2-VV genotype and nonfamilial IDC. (C) 1999 Academic Press.
  • S Watanabe, A Osa, T Sekine, NS Ishioka, M Koizumi, T Kojima, A Hasegawa, M Yoshii, E Okamoto, K Aoyagi, A Miyajima, R Nagai
    APPLIED RADIATION AND ISOTOPES 51(2) 197-202 1999年8月  
    A coronary stent was made radioactive by implantation of Xe-133 ions for the purpose of suppressing the renarrowing of the part of blood vessel in which the stent is implanted. Electrons of relatively low energies emitted in the decay of Xe-133 may give an antiproliferative effect of ionizing radiation to the intimal cells within a limited range of 1 mm. A Xe-133(+) beam accelerated at 40 or 60 keV was directed to several stainless steel stents mounted on a target-holder table that could revolve and move up and down to distribute the Xe-133(+) ions within a stent as well as among the stents. The radioactive stents produced contained up to 100 kBq of Xe-133 and were implanted into the abdominal aortas of rabbits. Neointimal thickening was analyzed by histomorphometry for samples taken 4 weeks after stent implantation. The results indicate that the radioactive stents have a potential to suppress neointimal hyperplasia in rabbits. (C) 1999 Elsevier Science Ltd. All rights reserved.
  • H Sakamoto, T Sakamaki, T Kanda, M Kurabayashi, R Nagai, J Fujii
    Angiology 50(8) 683-7 1999年8月  査読有り
    Loculation of a pleural effusion within an interlobar fissure as a result of congestive heart failure is a well-known entity. It has been termed "vanishing" or "phantom" tumor because its roentgenographic appearance simulates a pulmonary tumor and resolves with treatment of the congestive heart failure. The authors describe an 89-year-old man with a loculated pericardial effusion on the left cardiac border on chest roentgenogram. This was initially thought to represent an occult metastatic malignancy; however, its etiology became obvious when it disappeared with therapy of heart failure. Loculated pericardial effusion should be included in the differential diagnosis of roentgenographic densities in the chest when seen on the left cardiac border.
  • S Saito, R Aikawa, I Shiojima, R Nagai, Y Yazaki, I Komuro
    FEBS letters 456(1) 103-7 1999年7月30日  査読有り
    We here examined the role of the interleukin-6 (IL-6) family of cytokines in endothelin-1 (ET-1)-induced hypertrophic responses using cultured cardiac myocytes of neonatal rats. ET-1 induced expression of IL-6 and leukemia inhibitory factor (LIF) genes. ET-1-induced LIF gene expression was abolished by inhibition of protein kinase C activity. ET-1 activated the promoter of atrial natriuretic peptide and beta-type myosin heavy chain genes through the tyrosine kinase pathway and IL-6 receptor gp130. These results suggest that the IL-6 family of cytokines mediates ET-1-induced expression of some fetal genes in cardiac myocytes.
  • N Watanabe, M Kurabayashi, Y Shimomura, K Kawai-Kowase, Y Hoshino, I Manabe, M Watanabe, M Aikawa, M Kuro-o, T Suzuki, Y Yazaki, R Nagai
    Circulation research 85(2) 182-91 1999年7月23日  査読有り
    We have recently characterized the promoter region of the rabbit embryonic smooth muscle myosin heavy chain (SMemb/NMHC-B) gene and identified the 15-bp sequence, designated SE1, located at -105 from the transcriptional start site as an important regulatory element for its transcriptional activity in a smooth muscle cell (SMC) line. In this study, we attempted to isolate cDNA clones encoding for the transcription factors that control the expression of the SMemb gene through binding to this cis-regulatory element. We screened a lambdagt11 cDNA library prepared from C2/2 cells, a rabbit-derived SMC line, by using a radiolabeled concatenated oligonucleotide containing SE1 as a probe. Sequence analysis revealed that one of the cDNA clones corresponds to the rabbit homologue of basic transcriptional element binding protein-2 (BTEB2), which has previously been identified as one of the Krüppel-like transcription factor. Gel mobility shift assays and antibody supershift analyses with nuclear extracts from C2/2 cells indicate that BTEB2 is a major component of nuclear factor:SE1 complexes. Furthermore, a glutathione S-transferase-BTEB2 fusion protein binds to the SE1 in a sequence-specific manner. In support of the functionality of BTEB2 binding, basal promoter activity and BTEB2-induced transcriptional activation were markedly attenuated by the disruption of the SE1. In adult rabbit tissues, BTEB2 mRNA was most highly expressed in intestine, urinary bladder, and uterus. BTEB2 mRNA levels were downregulated in rabbit aorta during normal development. Moreover, immunohistochemical analysis indicated a marked induction of BTEB2 protein in the neointimal SMC after balloon injury in rat aorta. These results suggest that BTEB2 mediates the transcriptional regulation of the SMemb/NMHC-B gene and possibly plays a role in regulating gene expression during phenotypic modulation of vascular SMC.
  • H Kurihara, Y Kurihara, R Nagai, Y Yazaki
    Cellular and molecular biology (Noisy-le-Grand, France) 45(5) 639-51 1999年7月  査読有り
    A series of gene targeting research have revealed novel roles of endothelins (ETs), peptides with potent vasoconstrictive and proliferative activities, in neural crest development in mammals. The phenotype of mice lacking the ET-1/ET-A receptor-mediated signalling affects cranial/cardiac neural crest-derived structures including the branchial arches and great vessels, and is highly similar to a set of the phenotypes of the avian neural crest ablation model. In contrast, mice lacking the ET-3/ET-B receptor-mediated signalling have defects in enteric neurons and melanocytes derived from trunk/vagal neural crest, resulting in megacolon and coat color spotting. Thus, both distinct pathways of the ET system seem to participate in the normal development of different neural crest lineages. Moreover, mutations in the human ET-3 and ET-B receptor genes have been identified in patients with Hirschsprung disease. As for the mechanisms involving the ET system in neural crest development, HANDs and Goosecoid, transcriptional factors essential for embryogenesis, have been suggested as key molecules downstream to the ET-mediated signalling in cranial/cardiac neural crest.
  • H Sumino, K Satö, T Sakamaki, T Kanda, T Nakamura, T Takahashi, H Sakamoto, I Kobayashi, R Nagai
    Journal of human hypertension 13(7) 437-42 1999年7月  査読有り
    OBJECTIVE: To examine the influence of systemic nitric oxide (NO) synthesis on blood pressure in patients with chronic renal failure undergoing haemodialysis, since nitric oxides are susceptible to renal excretion or are dialysed, a different indicator that is unaffected by renal function, such as the level of exhaled NO was evaluated. We examined the levels of the endogenous NO before and after a haemodialysis session. DESIGN AND METHODS: We evaluated the serum concentrations of nitrite/nitrate and the rate of nitric oxide release into exhaled air in 10 patients with hypertension who were receiving maintenance haemodialysis. RESULTS: The serum concentrations of nitrite/nitrate before haemodialysis were significantly higher than those in 10 normal controls (183 +/- 151 microM vs 42 +/- 17 microM, P < 0.05). These levels decreased significantly by the end of haemodialysis (42 +/- 26 microM). Because the amount of nitric oxide in the deepest expirate correlated well with the duration of exhalation, we were able to derive the rate of release of NO. The rate of NO release was 0.034 +/- 0.012 nmol/sec before haemodialysis, similar to that in normal controls (0.031 +/- 0.013nmol/sec). The rate was significantly reduced after dialysis (0.023 +/- 0.010 nmol/sec) (P < 0.05). The mean pre-dialysis mean blood pressure (109 +/- 11 mm Hg) and the post-dialysis blood pressure (106 +/- 9 mm Hg) were the same. CONCLUSIONS: These data indicate that NO production does not appear to have a critical role in control of arterial blood pressure across haemodialysis in patients with chronic renal failure.
  • N Koitabashi, T Utsugi, R Seki, E Okamoto, Y Sando, Y Kaneko, R Nagai
    JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 63(7) 572-575 1999年7月  
    A 23-year-old woman with heterozygous Fabry's disease who had acroparesthesia was admitted to hospital for precise examination of the disease before childbearing. She had no cardiac-related symptoms and no abnormality on physical examination. The alpha-galactosidase A activity in her leukocytes was present, but lower than normal. However, the endomyocardial biopsy showed specific changes for Fabry's disease. As Fabry's disease is a ran X-linked recessive inborn error of glycosphingolipid metabolism, heterozygous females are usually asymptomatic, but rarely can be affected as severely as hemizygous males. This is an isolated case of heterozygous Fabry's disease in a female in whom cardiac involvement was detected by endomyocardial biopsy, although she had no cardiac abnormality on physiological examinations. In conclusion, endomyocardial biopsy is useful for evaluation of the cardiac involvement of Fabry's disease even in an asymptomatic case.
  • A Yoshida, T Kanda, H Sakamoto, H Masuda, T Iwasaki, T Nakajima, I Kobayashi, R Nagai
    Angiology 50(7) 607-11 1999年7月  査読有り
    The authors report a rare case of a malignant hemangioendothelioma (MH) originating in the pericardium. In this case, a metastatic skin lesion was found first, and subsequently the existence of a primary cardiac lesion was confirmed. Generally, primary cardiac tumors grow slowly, and the prognosis of MH is relatively good. In this case, however, the patient died suddenly during the creation of a pericardial window for drainage. An autopsy showed that the MH originated from a pericardial lesion in the right atrium.
  • J Kiraku, T Nakamura, T Sugiyama, N Takahashi, M Kuro-o, J Fujii, R Nagai
    Japanese journal of pharmacology 80(2) 181-3 1999年6月  
    We studied the role of nitric oxide (NO) synthesis in amelioration of blood pressure elevation during dietary salt loading in transgenic mice overexpressing sodium proton exchanger. Systolic blood pressure rose after starting salt loading only in the high-salt group of transgenic mice. However, this elevation of blood pressure was not continued. Urinary excretion of inorganic nitrite and nitrate in the high-salt group of transgenic mice was significantly higher than in the high-salt group of control mice. These results suggest that increased NO synthesis in response to salt loading is one of the anti-hypertensive mechanisms in transgenic mice overexpressing sodium proton exchanger.
  • T Yokoyama, K Sekiguchi, T Tanaka, K Tomaru, M Arai, T Suzuki, R Nagai
    The American journal of physiology 276(6) H1968-76-H1976 1999年6月  査読有り
    To determine whether ANG II as well as mechanical stress affect the production of tumor necrosis factor (TNF) in the heart, neonatal rat cardiac myocytes and fibroblasts were cultured separately and treated for 6 h with ANG II, lipopolysaccharide (LPS), or cyclic mechanical stretch. LPS induced the production of TNF in cardiac myocytes and fibroblasts. However, TNF synthesis in fibroblasts was 20- to 40-fold higher than in myocytes. ANG II (>/=10(-8) M) and mechanical stretch stimulated the production of TNF in cardiac fibroblasts but not in myocytes. Furthermore, both ANG II and LPS increased the expression of TNF-alpha mRNA in cardiac fibroblasts. Isoproterenol inhibited both LPS- and ANG II-induced production of TNF in cardiac fibroblasts with increasing intracellular cAMP level. Moreover, both isoproterenol and dibutyryl cAMP inhibited LPS-induced TNF-alpha mRNA expression. Thus activation of the renin-angiotensin system, as well as mechanical stress, can stimulate production of TNF in cardiac fibroblasts. Furthermore, beta-adrenergic receptors may be responsible for the regulation of TNF synthesis at the transcriptional level by elevating intracellular cAMP.
  • Y Ito, S Imai, G Ui, M Nakano, K Imai, H Kamiyama, F Naganuma, K Matsui, N Ohashi, R Nagai
    EUROPEAN JOURNAL OF PHARMACOLOGY 374(3) 355-366 1999年6月  
    Na+-H+ exchange inhibitors may reduce myocardial damage after reperfusion. However, their effects on microvascular deterioration are not known. We examined the potency of a novel Na+-H+ exchange inhibitor, SM-30550 [ N-(Aminoiminomethyl)-1,4-dimethyl-1H-indole-2-carboxamide methanesulfonate], and its effects on microvascular damage after reperfusion. In an in vitro study. the Na+-H+ exchange inhibiting activity of SM-20550 was about 10 times greater than that of ethylisopropyl amiloride. In in vivo experiments, we occluded the left circumflex coronary artery in 29 dogs for 2 h and then reperfused for 5 h. SM-20550 was administered either before ischemia (n = 11) or before reperfusion (n = 7). Another 11 dogs served as controls. We found that SM-20550 not only improved coronary vasodilator responses to acetylcholine and adenosine after reperfusion, but also reduced infarct size (P &lt; 0.01). Intramyocardial bleeding, which should reflect microvascular damage, was not found in dogs with SM-20550 treatment. Infarct size was correlated inversely with collateral blood flow in control (both, P &lt; 0.01) but not in SM-20550-treated animals. Furthermore, SM-20550 significantly suppressed ventricular fibrillation during both ischemia and reperfusion. These results suggest that protective effects of Na+-H+ exchange inhibitors on reperfused myocardium are due at least in part to microvascular protection. (C) 1999 Elsevier Science B.V. All rights reserved.
  • 斎藤 勇一郎, 黒尾 誠, 鍋島 陽一, 永井 良三
    脈管学 : 日本脈管学会機関誌 : the journal of Japanese College of Angiology 39(5) 237-241 1999年5月25日  
  • A Kojima, K Kaneda, M Ueda, A Maki, A Takabayashi, S Fukushima, H Sakurai, R Nagai, Matsui-Yuasa, I
    VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY 434(5) 413-422 1999年5月  
    We examined the expression of smooth muscle cytoskeleton in spindle-shaped cells in the capsule of hepatocellular carcinoma (HCC) and the septa of liver cirrhosis (LC). Serial sections of livers resected from 11 patients were stained with monoclonal antibodies against vimentin, desmin, smooth muscle actin (1A4, HHF35, CGA7) and smooth muscle myosin heavy chain isoforms (SM1, SM2). Capsular spindle-shaped cells exhibited a cytoskeletal feature indicative of intermediately differentiated smooth muscle cells. Computer-assisted morphometry revealed that the proportions of 1A4-, HHF35-, CGA7- and SM1- positive areas to vimentin-positive area were 88.0+/-11.0%, 50.8+/-17.4%, 25.3+/-16.4% and 19.4+/-12.4% (n=11) in main rumours and 86.6+/-9.4%, 50.9+/-18.7%, 21.1+/-12.3% and 17.6+/-9.7% (n=12) in daughter rumours, indicating that spindle-shaped cells are heterogeneous in cytoskeletal expression. Septal spindle-shaped cells in LC lacked the cytoskeletal proteins specific to differentiated smooth muscle cells (CGA7, SM1, SM2 and desmin). Electron microscopically, capsular spindle-shaped cells contained more microfilaments and less rough endoplasmic reticulum than do septal cells. Intermediately differentiated smooth muscle cells are induced in the capsule of HCC but not in the septa of LC, suggesting a role for stromal interaction by tumour cells in the induction of smooth muscle cells.
  • 永井 良三
    東京女子医科大学雑誌 69(4) 164-169 1999年4月25日  
    It has been well recognized that patients with major coronary risk factors develop atherosclerosis in a higher frequency, but there are many atherosclerotic patients without these risk factors, suggesting the presence of other unknown risk factors regulating development of atherosclerosis. It has been known that the most important risk factor for atherosclerosis is "aging" to whatever extent the major risk factors are involved in atherogenesis. We recently identified the klotho gene as a possible regulator of human aging process. Because endothelial function is impaired in aged subjects, it is plausible to hypothesize that klotho may protect against endothelial dysfunction. Therefore, we decided to examine whether the klotho-deficient mice have endothelial dysfunction. We first found that the klotho gene product itself or its metabolites protect against endothelial dysfunction as a humoral factor because endothelium-dependent arterial dilatation was impaired in the klotho-deficient heterozygous mouse, which was improved by establishing parabiosis with a wildtype mouse but not with a heterozygous mouse. Reduced expression of the klotho gene seems to be a risk factor of arterial diseases because heterozygous mouse with apparently normal histology of the arterial wall developed hypertension with high-salt drinking water and atherosclerosis with high cholesterol diet. We also have shown that in animal models of hypertension, kidney diseases, hyperlipidemia and diabetes, all of which are known as an important risk factor for atherosclerosis, klotho gene expression was reduced in kidney. It is noteworthy that endothelial dysfunction observed in a rat model of hyperlipidemia and hyperglycemia (OLETF rat) could be improved by angiotensin converting enzyme inhibitor, which is accompanied by increased klotho gene expression in kidney. Our results suggest that klotho gene expression is regulated by local or systemic stress against kidney or the vascular wall.
  • 永井 良三, 倉林 正彦, 眞鍋 一郎, 黒尾 誠, 鍋島 陽一
    日本医師会雑誌 121(7) 1048-1051 1999年4月  
  • M Tanehata, H Adachi, S Oshima, K Taniguchi, H Itoh, A Hasegawa, R Nagai
    JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 63(4) 274-277 1999年4月  
    The significance of the time from anaerobic threshold to respiratory compensation point (RCP-AT time) in patients with chronic heart failure was investigated. Thirty-seven patients with chronic heart failure (New York Heart Association class II or III) were enroled into the study. Cardiopulmonary exercise testing was performed using breath-by-breath gas sampling. A bicycle ergometer was used, and incremental exercise testing was carried out. Anaerobic threshold, respiratory compensation point (RCP), and the slope of oxygen uptake ((V) over dot O-2) as a function of work rate (Delta(V) over dot O2/Delta WR) were measured. A positive correlation (r=0.53) between RCP-AT time and Delta(V) over dot O2/Delta WR was found. RCP-AT time was corrected for the whole exercise period (ramp exercise-RCP point), and the correlation between corrected RCP-AT time and Delta(V) over dot O2/Delta WR was still present (r=0.46). There was no correlation between RCP-AT time and anaerobic threshold. These findings suggest that RCP-AT time is a new parameter that reflects the rate of the aerobic and anaerobic metabolism after AT.
  • H Sakamoto, T Sakamaki, T Tani, Y Sugai, T Nakamura, Z Ono, T Kanda, M Kurabayashi, R Nagai
    Archives of physical medicine and rehabilitation 80(4) 470-2 1999年4月  査読有り
    The excessive pressor response triggered in patients by an alerting reaction to a doctor's presence has been termed the "white coat effect." A 68-year-old man with verbal apraxia after multiple lacunar infarctions was referred to the hospital for speech rehabilitation. He experienced difficulty in talking with the speech therapist during therapy sessions but not when talking with his friends or family. Because the therapist's presence was stressful to the patient, it was considered that his anxiety might produce an excessive increase in blood pressure. Blood pressure monitoring was performed during 2 separate days of speech therapies consisting of two sessions each. In one session, therapy was directed by the therapist; in the other, therapy was self-directed. The therapist-directed approach substantially increased both systolic and diastolic blood pressures, whereas the self-directed therapy slightly increased only systolic pressure. It was concluded that the excessive pressor response seen in this patient during therapist-directed speech therapy resulted from the white coat effect induced by the therapist's presence.
  • 田中 亨, 倉林 正彦, 相原 康, 永井 良三
    Japanese circulation journal 63(1) 173-173 1999年3月1日  
  • 森本 達也, 長谷川 浩二, 垣田 剛, 鏑木 敏志, 篠山 重威, 倉林 正彦, 永井 良三
    Japanese circulation journal 63(1) 168-168 1999年3月1日  
  • 瀬田 享博, 倉林 正彦, 相原 康, 都丸 浩一, 関口 賢一, 永井 良三
    Japanese circulation journal 63(1) 657-657 1999年3月1日  
  • 武田 真一, 倉林 正彦, 相原 康, 都丸 浩一, 田中 亨, 永井 良三, 真鍋 一郎, 久留 一郎, 重政 千秋
    Japanese circulation journal 63(1) 656-656 1999年3月1日  
  • 阿久澤 暢洋, 倉林 正彦, 坂本 浩之助, 永井 良三
    Japanese circulation journal 63(1) 655-655 1999年3月1日  
  • 持田 学, 小野 善平, 角野 博之, 斎藤 勇一郎, 坂本 浩之助, 倉品 年成, 中村 哲也, 永井 良三, 酒巻 哲夫
    Japanese circulation journal 63(1) 651-651 1999年3月1日  
  • 佐藤 真人, 倉林 正彦, 田中 亨, 前野 敏孝, 内山 強, 永井 良三
    Japanese circulation journal 63(1) 654-654 1999年3月1日  
  • 都丸 造一, 相原 康, 関口 賢一, 倉林 正彦, 新井 昌史, 永井 良三
    Japanese circulation journal 63(1) 656-656 1999年3月1日  
  • 大山 裕子, 倉林 正彦, 関口 賢一, 大山 良雄, 小和瀬 桂子, 下村 幸生, 永井 良三
    Japanese circulation journal 63(1) 654-654 1999年3月1日  
  • 内山 強, 倉林 正彦, 大山 良雄, 宇都木 敏浩, 阿久澤 暢洋, 関口 賢一, 相原 康, 武田 真一, 田中 亨, 河津 捷二, 永井 良三, 伴野 祥一
    Japanese circulation journal 63(1) 297-297 1999年3月1日  
  • 田中 亨, 倉林 正彦, 金井 宏義, 永井 良三
    Japanese circulation journal 63(1) 302-302 1999年3月1日  
  • 相原 康, 倉林 正彦, 関口 賢一, 都丸 浩一, 新井 昌史, 永井 良三
    Japanese circulation journal 63(1) 460-460 1999年3月1日  
  • 斉藤 勇一郎, 中村 哲也, 相澤 宏樹, 大山 良雄, 小野 善平, 相原 康, 倉林 正彦, 永井 良三, 鍋島 陽一, 増田 浩明, 黒尾 誠
    Japanese circulation journal 63(1) 476-476 1999年3月1日  
  • 武田 真一, 倉林 正彦, 相原 康, 都丸 浩一, 田中 亨, 金井 宏義, 永井 良三, 真鍋 一郎, 久留 一郎, 重政 千秋
    Japanese circulation journal 63(1) 252-252 1999年3月1日  
  • 都丸 浩一, 相原 康, 関口 賢一, 倉林 正彦, 新井 昌史, 永井 良三
    Japanese circulation journal 63(1) 252-252 1999年3月1日  
  • 滝沢 敬子, 新井 昌史, 倉林 正彦, 永井 良三
    Japanese circulation journal 63(1) 249-249 1999年3月1日  
  • 神田 享勉, 田中 亨, 関口 賢一, 瀬田 享博, 横山 知行, 永井 良三
    Japanese circulation journal 63(1) 348-348 1999年3月1日  
  • 大山 裕子, 倉林 正彦, 阿久澤 暢洋, 関口 賢一, 永井 良三
    Japanese circulation journal 63(1) 344-344 1999年3月1日  
  • 和田 久泰, 斉藤 邦明, 清島 満, 鷹津 久登, 藤原 久義, 神田 享勉, 永井 良三
    Japanese circulation journal 63(1) 349-349 1999年3月1日  
  • 相原 康, 倉林 正彦, 田中 亨, 斉藤 勇一郎, 中村 哲也, 神田 享勉, 永井 良三
    Japanese circulation journal 63(1) 313-313 1999年3月1日  
  • 小室 一成, 永井 良三
    Japanese circulation journal 63(1) 88-88 1999年3月1日  
  • 斎藤 勇一郎, 中村 哲也, 相澤 宏樹, 松村 穣, 大山 良雄, 倉林 正彦, 永井 良三, 鍋島 陽一, 増田 浩明, 黒尾 誠
    Japanese circulation journal 63(1) 72-72 1999年3月1日  
  • 関口 賢一, 横山 知行, 倉林 正彦, 都丸 浩一, 田中 亨, 新井 昌史, 神田 亨勉, 永井 良三
    Japanese circulation journal 63(1) 426-426 1999年3月1日  
  • 田中 亨, 倉林 正彦, 金井 宏義, 永井 良三
    Japanese circulation journal 63(1) 378-378 1999年3月1日  
  • 小和瀬 桂子, 倉林 正彦, 大山 良雄, 相原 康, 田中 亨, 永井 良三
    Japanese circulation journal 63(1) 183-183 1999年3月1日  
  • 斉藤 勇一郎, 中村 哲也, 相澤 宏樹, 金井 宏義, 武田 真一, 大山 良雄, 倉品 年成, 松村 穣, 倉林 正彦, 永井 良三, 鍋島 陽一, 増田 浩明, 黒尾 誠
    Japanese circulation journal 63(1) 204-204 1999年3月1日  
  • 相澤 宏樹, 中村 哲也, 斉藤 勇一郎, 松村 穣, 大山 良雄, 倉林 正彦, 長谷川 昭, 永井 良三, 鍋島 陽一, 増田 浩明, 黒尾 誠
    Japanese circulation journal 63(1) 187-187 1999年3月1日  
  • 金井 宏義, 倉林 正彦, 田中 亨, 相原 康, 武田 真一, 永井 良三, 川畑 正博, 宮園 浩平
    Japanese circulation journal 63(1) 183-183 1999年3月1日  
  • 渡邊 直, 倉林 正彦, 関口 賢一, 内山 強, 永井 良三
    Japanese circulation journal 63(1) 182-182 1999年3月1日  
  • Arai Masashi, Takizawa Takako, Tomaru Koichi, Kurabayashi Masahiko, Nagai Ryozo
    Japanese circulation journal 63(1) 105-105 1999年3月1日  
  • Kowase Keiko, Kurabayashi Masahiko, Ohyama Yoshio, Aihara Yasushi, Tanaka Toru, Uchiyama Tsuyoshi, Akuzawa Nobuhiro, Tomaru Koichi, Sekiguchi Kenichi, Sakamoto Hironosuke, Nagai Ryozo
    Japanese circulation journal 63(1) 105-105 1999年3月1日  

書籍等出版物

 21

共同研究・競争的資金等の研究課題

 91