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| 1.
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Nakahashi, Takuya ; Tada, Hayato ; Sakata, Kenji ; Nomura, Akihiro ; Ohira, Miho ; Mori, Mika ; Takamura, Masayuki ; Hayashi, Kenshi ; Yamagishi, Masakazu ; Kawashiri, Masa-aki ; 多田, 隼人 ; 坂田, 憲治 ; 野村, 章洋 ; 大平, 美穂 ; 森, 三佳 ; 高村, 雅之 ; 林, 研至 ; 山岸, 正和 ; 川尻, 剛照
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金沢大学附属病院循環器内科<br />Aim: To assess whether combining measurements obtained from carotid ultrasonography in addition to th
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e age, creatinine, and ejection fraction (ACEF) score would improve the predictive ability of outcome in patients with acute coronary syndrome (ACS).\nMethods: We examined 264 patients with ACS (194 men; mean age: 68±11 years) who underwent percutaneous coronary intervention. The carotid plaque score (cPS) and intima–media thickness (cIMT) were determined by carotid ultrasonography. The modified ACEF score was calculated using the following formula: (age/left ventricular ejection fraction) ＋1 point for every 10 mL/min reduction in creatinine clearance below 60 mL/min per 1.73 m2. The endpoint of this study was major adverse cardiovascular and cerebrovascular events (MACEs), defined as all-cause death, myocardial infarction, stoke, and target vessel revascularization.\nResults: During the median 4-year follow-up, there were 121 incidents of MACEs. Multivariate Cox proportional hazard regression analysis revealed that cPS ≥9.8 (hazard ratio [HR], 1.52; 95% confidence interval [CI], 1.01–2.31) and ACEF score ≥1.20 (HR, 1.62; 95% CI, 1.11–2.39) were significantly associated with MACEs, whereas cIMT was not. When the new combined risk score was calculated by multiplying the cPS by the modified ACEF score, the freedom from MACEs at 5 years was 71% and 31% for the lower and higher scores, respectively (p＜0.001). The area under the receiver-operating characteristic curve for MACEs for the ACEF score, cPS, and combined risk score were 0.65, 0.66, and 0.71, respectively (p＜0.05).\nConclusion: The cPS offers an incremental predictive value when combined to the simple ACEF score in ACS.<br />This article distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.
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Nomura, Akihiro ; Tada, Hayato ; Nohara, Atsushi ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; 野村, 章洋 ; 多田, 隼人 ; 野原, 淳 ; 川尻, 剛照 ; 山岸, 正和
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金沢大学附属病院先端医療開発センター<br />Aim: Sitosterolemia is an extremely rare, autosomal recessive disease characterized by high plas
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ma cholesterols and plant sterols because of increased absorption of dietary cholesterols and sterols from the intestine, and decreased excretion from biliary tract. Previous study indicated that sitosterolemic patients might be vulnerable to post-prandial hyperlipidemia, including high remnant-like lipoprotein particles (RLP) level. Here we evaluate whether a loading dietary fat increases a post-prandial RLP cholesterol level in sitosterolemic patients compared to heterozygous familial hypercholesterolemic patients (FH).\nMethods: We recruit total of 20 patients: 5 patients with homozygous sitosterolemia, 5 patients with heterozygous sitosterolemia, and 10 patients with heterozygous FH as controls from May 2015 to March 2018 at Kanazawa University Hospital, Japan. All patients receive Oral Fat Tolerance Test (OFTT) cream (50 g/body surface area square meter, orally only once, and the cream includes 34% of fat, 74 mg of cholesterol, and rich in palmitic and oleic acids. The primary endpoint is the change of a RLP cholesterol level after OFTT cream loading between sitosterolemia and FH. We measure them at baseline, and 2, 4, and 6 hours after the oral fat loading.\nResults: This is the first study to evaluate whether sitosterolemia patients have a higher post-prandial RLP cholesterol level compared to heterozygous FH patients.\nConclusion: The result may become an additional evidence to restrict dietary cholesterols for sitosterolemia. This study is registered at University Hospital Medical Information Network (UMIN) Clinical Trials Registry (UMIN ID: UMIN000020330).<br />This article distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.
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Tada, Hayato ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Yasuda, Kenji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 小林, 淳二 ; 馬淵, 宏 ; 山岸, 正和 ; 林, 研至
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金沢大学附属病院循環器内科<br />Aim: The Japan Atherosclerosis Society (JAS) guidelines for the prevention of atherosclerotic disease
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s 2012 (JAS2012) proposed lipid management targets; however, less data is available regarding the attainment rates of each target in community-based settings. Therefore, we assessed the attainment rates of lipid management targets among subjects who underwent Japanese specific health checkups.\nMethods: A total of 85,716 subjects (male=29,282, 34.2%) aged 40–74 years who underwent specific health checkups from 2012 to 2014 in Kanazawa city, Japan, were included in this study. We evaluated the attainment rates of the lipid management targets according to the JAS2012 guideline and investigated the clinical characteristics of the subjects without achieving the targets.\nResults: The target for LDL cholesterol (LDL-C) was the least attained in all risk categories, 89, 72, 50, and 34% for category I, II, III, and secondary prevention, respectively, in 2014. In addition, these rates inversely correlated with the grade of risk categories (p-value for trends ＜0.001). Attainment rate of the LDL-C target in the suspected chronic kidney disease (CKD) group was significantly lower than in the groups with diabetes, stroke, or absolute risk in category III (49.2, 60.3, 63.5, 54.4%, respectively, p-value ＜0.001 for each). Moreover, the attainment rate of the LDL-C target was significantly lower in subjects that did not receive lipid-lowering therapy than in those who received it in the secondary prevention (27.7 and 40.6%, respectively, p-value ＜0.001).\nConclusions: Lipid management is inadequate in community-based settings, particularly, in subjects with CKD and secondary prevention.<br />This article distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.
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Tada, Hayato ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; 多田, 隼人 ; 川尻, 剛照 ; 山岸, 正和
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金沢大学附属病院循環器内科<br />We have learned that low-density lipoprotein (LDL) cholesterol is the cause of atherosclerosis from v
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arious aspects, including a single case with familial hypercholesterolemia, other cases with different types of Mendelian dyslipidemias, large-scale randomized controlled trials using LDL cholesterol lowering therapies, and Mendelian randomization studies using common as well as rare variants associated with LDL cholesterol levels. There is no doubt that determinations of genotypes in lipid-associated genes have contributed not only to the genetic diagnosis for Mendelian dyslipidemias but also to the discoveries of novel therapeutic targets. Furthermore, recent studies have shown that such genetic information could provide useful clues for the risk prediction as well as risk stratification in general and in particular population. We provide the current understanding of genetic analyses relating to plasma lipids and coronary artery disease.<br />This article distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.
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Sakamoto, Aiji ; Sugamoto, Yuka ; Tokunaga, Y. ; Yoshimuta, Tsuyoshi ; Hayashi, Kenshi ; Konno, Tetsuo ; Kawashiri, Masa-aki ; Takeda, Yoshiyu ; Yamagishi, Masakazu ; 林, 研至 ; 今野, 哲雄 ; 川尻, 剛照 ; 武田, 仁勇 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Ephrin B1 and its cognate receptor, Eph receptor B2, key regulators of embryogenesis, are expressed
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in human atherosclerotic plaque and inhibit adult human monocyte chemotaxis. Few data exist, however, regarding the gene expression profiles of the ephrin (EFN) and Eph receptor (EPH) family of genes in atherosclerosis-related human cells. Gene expression profiles were determined of all 21 members of this gene family in atherosclerosis-related cells by reverse transcription-polymerase chain reaction analysis. The following 17 members were detected in adult human peripheral blood monocytes: EFNA1 and EFNA3 - EFNA5 (coding for ephrins A1 and A3 - A5); EPHA1, EPHA2, EPHA4 - EPHA6 and EPHA8 (coding for Eph receptors A1, A2, A4 - A6 and A8); EFNB1 and EFNB2 (coding for ephrins B1 and B2); and EPHB1 - EPHB4 and EPHB6 (coding for Eph receptors B1 - B4 and B6). THP-1 monocytic cells, Jurkat T cells and adult arterial endothelial cells also expressed multiple EFN and EPH genes. These results indicate that a wide variety of ephrins and Eph receptors might affect monocyte chemotaxis, contributing to the development of atherosclerosis. Their pathological significance requires further study. © 2011 Field House Publishing LLP.
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Tada, Hayato ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; 多田, 隼人 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 小林, 淳二 ; 馬渕, 宏 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Autosomal recessive hypercholesterolemia (ARH) is an extremely rare inherited disorder, the cause of
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which is mutations in the low-density lipoprotein (LDL) receptor adaptor protein 1 (LDLRAP1) gene. Only 36 families with 14 different mutations have been reported in the literature to date. The clinical phenotype of ARH is milder than that of homozygous familial hypercholesterolemia (FH) caused by LDL receptor gene mutations. Recently, the lipoprotein metabolism of ARH was investigated in both humans and mice by several investigators, including ourselves. Based on these findings the preserved clearance of LDL receptor-dependent very-LDL (VLDL) may be a possible mechanism underlying the responsiveness to statins and the milder phenotype of ARH. Although ARH has been described as being “recessive,” several studies, including ours, have indicated that a heterozygous carrier status of the LDLRAP1 gene is associated with mild hypercholesterolemia and exacerbates the phenotype of FH resulting from LDL receptor gene mutations. This review summarizes current understanding regarding ARH and its causative gene, LDLRAP1, and attempts to provide new insight into novel pharmacological targets for treating dyslipidemic patients. © Journal of Atherosclerosis and Thrombosis. All right received.<br />出版者照会後に全文公開
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Tada, Hayato ; Nohara, Atsushi ; Kawashiri, Masa-aki ; Inazu, Akihiro ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; 多田, 隼人 ; 野原, 淳 ; 川尻, 剛照 ; 稲津, 明広 ; 馬渕, 宏 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />We herein report a case of marked transient hypercholesterolemia in a man receiving low-dose mitotan
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e as adjuvant chemotherapy for adrenocortical carcinoma.A 58-year-old man without any clinical symptoms or history of hypercholesterolemia was admitted to our hospital to treat an adrenocortical carcinoma detected on general screening using computed tomography. He reported no chest symptom and did not exhibit any established risk factors for coronary artery disease, such as diabetes, obesity, hypertension or relevant family history, with the exception of current smoking, on admission. A stress electrocardiogram showed negative findings. The left adrenal tumor as well as left kidney, spleen and distal portion of the pancreas were subsequently resected using radical surgery. The histopathological findings confirmed the preoperative diagnosis of adrenocortical carcinoma. After the operation, treatment with low-dose mitotane (1g/day) was introduced as adjuvant chemotherapy. Interestingly, the patient developed marked hyper-LDL cholesterolemia at a level equivalent to that of familial hypercholesterolemia (LDL cholesterol level ~ 300 mg/ dL) following the introduction of mitotane, without evidence of primary or secondary hypercholesterolemia due to other causes. A coronary angiogram performed to assess the new-onset angina revealed three-vessel disease, which was later revascularized via percutaneous coronary intervention eight months after the start of mitotane therapy. The cholesterol level normalized with the suspension of mitotane. This case suggests that mitotane can cause severe hypercholesterolemia, potentially resulting in coronary atherosclerosis. © 2014, Japan Atherosclerosis Society. All rights reserved.<br />出版者照会後に全文公開
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Tada, Hayato ; Kawashiri, Masa-aki ; Konno, Tetsuo ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 今野, 哲雄 ; 山岸, 正和 ; 林, 研至
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金沢大学医薬保健研究域医学系<br />Blood lipid levels are highly heritable and modifiable risk factors for coronary artery disease (CAD
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), and are the leading cause of death worldwide. These facts have motivated human genetic association studies that have the substantial potential to define the risk factors that are causal and to identify pathways and therapeutic targets for lipids and CAD. The success of the HapMap project that provided an extensive catalog of human genetic variations and the development of microarray based genotyping chips (typically containing variations with allele frequencies ＞5%) facilitated common variant association study (CVAS; formerly termed genomewide association study, GWAS) identifying disease-associated variants in a genome-wide manner. To date, 157 loci associated with blood lipids and 46 loci with CAD have been successfully identified, accounting for approximately 12%– 14% of heritability for lipids and 10% of heritability for CAD. However, there is yet a major challenge termed “missing heritability problem,” namely the observation that loci detected by CVAS explain only a small fraction of the inferred genetic variations. To explain such missing portions, focuses in genetic association studies have shifted from common to rare variants. However, it is challenging to apply rare variant association study (RVAS) in an unbiased manner because such variants typically lack the sufficient number to be identified statistically. In this review, we provide a current understanding of the genetic architecture mostly derived from CVAS, and several updates on the progress and limitations of RVAS for lipids and CAD. © 2016, Japan Atherosclerosis Society. All rights reserved.<br />出版者照会後に全文公開
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Tsuji, Shigetsugu ; Nohara, Atsushi ; Hayashi, Yoshiaki ; Yoshida, Isao ; Oka, Rie ; Moriuchi, Tadashi ; Higashita, Tomomi ; Miyamoto, Susumu ; Suzuki, Ayako ; Okada, Toshihide ; Yamagishi, Masakazu ; 野原, 淳 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Aim: The role of gastrectomy in glycemic control has been established in the current era of bariatri
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c surgery for obesity. Gastrectomy in obese patients is associated with increased levels of high-density lipoprotein cholesterol (HDL-C). However, limited data on the effects of gastrectomy in nonobese patients are available. We herein investigated the long-term plasma lipid changes in nonobese patients who had undergone gastrectomy. Methods: Patients were enrolled as part of routine healthcare examinations from 1984 to 2003. Preoperative and postoperative data from patients who had undergone curative gastrectomy were analyzed for up to 10 years postoperatively. Three age- and sex-matched controls were assigned to each case. Results: Sixty-four nonobese patients without diabetes mellitus or a history of having taken lipidlowering drugs who underwent curative gastrectomy during the study period were enrolled (60 subtotal gastrectomies, four total gastrectomies). The median follow-up period was 7.6 years. The mean body mass index was 9.6% lower one year after gastrectomy (p<0.01), then plateaued with a slight recovery. Intriguingly, the preoperative HDL-C level was 21% higher one year after gastrectomy (p<0.01), increased by another 30% six years after gastrectomy and remained at this level for the rest of the follow-up period. No significant changes in the HDL-C level were observed in the controls. The degree of HDL-C elevation was consistently significant, irrespective of the baseline triglyceride level, HDL-C level or body weight. Conclusions: Gastrectomy in nonobese patients was associated with consistent and distinct longterm HDL-C elevations and body mass index reductions. © 2015 Japan Atherosclerosis Society.<br />出版者照会後に全文公開
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Uchiyama, K. ; Ino, H. ; Hayashi, Kenshi ; Fujioka, K. ; Takabatake, S. ; Yokawa, J. ; Namura, M. ; Mizuno S. ; Tatami, R. ; Kanaya, H. ; Nitta, Y. ; Michishita, I. ; Hirase, H. ; Ueda, K. ; Aoyama, T. ; Okeie, K. ; Haraki, T. ; Mori, K. ; Araki, T. ; Minamoto, M. ; Oiwake, H. ; Konno, Tetsuo ; Sakata, Kenji ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; 林, 研至 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Percutaneous coronary intervention (PCI) using a drug-eluting stent (DES) leads to less re-stenosis
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than PCI using a bare metal stent (BMS), however there is still controversy whether use of a DES for severe coronary disease leads to an acceptable outcome in patients with diabetes mellitus (DM). In this study 8159 lesions were treated in 6739 patients (mean age 68.9 years) with coronary artery disease. Use of a DES significantly decreased the re-stenosis rate compared with BMS in both DM (9.6% versus 21.3%) and non-DM (9.5% versus 17.1%) patients. The re-stenosis rate was significantly higher in DM than in non-DM patients in the BMS group but not in the DES group. There was no statistically significant difference in event-free survival after stenting of patients with left main coronary artery (LMCA) disease between the BMS and DES groups. It was concluded that, compared with BMS, DES reduced re-stenosis in patients with DM, however, we advise careful treatment after using DES for severe coronary disease, including LMCA lesions, in patients with DM. © 2011 Field House Publishing LLP.
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Nitta, Y. ; Yamamoto, R. ; Yamaguchi, Y. ; Katsuda, S. ; Kaku, B. ; Taguchi, T. ; Takabatake, S. ; Nakahama, K. ; Yamagishi, Masakazu ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Calcium channel blockers (CCBs) can prevent cardiovascular events in patients with coronary artery d
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isease (CAD). This study looked retrospectively at the prognosis of CAD in hypertensive patients with CAD who had undergone a coronary angiograph, had been given a CCB (benidipine [n = 66], amlodipine [n = 45], or long-acting nifedipine [n = 31]) on hospital discharge and were then followed up for a mean ± SD of 5.2 ± 2.9 years. Systolic/diastolic blood pressure for all 142 patients decreased significantly from a mean ± SD of 137 ± 20/74 ± 15 mmHg to 129 ± 20/71 ± 12 mmHg. Major adverse cardiovascular events (MACE) occurred in 15 patients. Chronic kidney disease (CKD) was a significant risk factor for MACE (hazard ratio 2.35, 95%confidence intervals 1.45, 3.80). Benidipine was superior to nifedipine in preventing MACE in patients both with and without CKD. In conclusion, benidipine and amlodipine reduced the frequency of MACE in hypertensive patients with CAD, particularly in those with complicating CKD. © 2010 Field House Publishing LLP.
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Oka, Rie ; Yamada, Takayoshi ; Nakanishi, Chiaki ; Konno, Tetsuo ; Kawashiri, Masa-aki ; Hayashi, Kenshi ; Nohara, Atsushi ; Inazu, Akihiro ; Yamagishi, Masakazu ; 大家, 理恵 ; 八木, 邦公 ; 今野, 哲雄 ; 川尻, 剛照 ; 林, 研至 ; 野原, 淳 ; 稲津, 明広 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Aim: The commonly observed relationship between increased visceral adiposity and metabolic abnormali
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ties may be partly mediated by a concomitant increase in liver fat content. We evaluated the independent association between the level of alanine aminotransferase (ALT) as a surrogate marker of the liver fat content and the incidence of metabolic abnormalities after adjusting for the amount of visceral adipose tissue (AT). Methods: The subjects included 1,118 Japanese individuals (44% women) who underwent computed tomography to assess the amount of visceral AT on medical checkups. Cross-sectional associations between the serum ALT, visceral AT and metabolic risk factors were examined. Results: The ALT level and visceral AT were found to show a significant correlation (r =0.41 in men and r =0.36 in women, p<0.001). In a multivariable linear regression analysis, the ALT level and visceral AT were found to be independently associated with blood pressure in men and triglycerides and 2-hour post-challenge glucose in both genders (p<0.01), whereas only visceral AT was found to be associated with HDL-cholesterol (p<0.01). When the participants were classified into four subgroups based on the 75th percentiles of ALT and visceral AT, the low-ALT/high-visceral AT group, but not the high-ALT/low-visceral AT group, had a significantly higher odds ratio for low HDL-cholesterol among both genders (p<0.05) and for hypertriglyceridemia in men only (p<0.05). Meanwhile, the high-ALT/low-visceral AT group, but not the low-ALT/high-visceral AT group, had a significantly higher odds ratio for IGT among women (p<0.05). Conclusions: Although the ALT level and visceral AT were found to be independently associated with most metabolic risk factors, visceral AT had a dominant association with dyslipidemia in both genders, while the ALT level appeared to have a closer association with IGT in women.<br />出版者照会後に全文公開
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Tada, Hayato ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; 多田, 隼人 ; 川尻, 剛照 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />出版者照会後に全文公開
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Fujino, Noboru ; Yoshimuta, Tsuyoshi ; Ichida, Fukiko ; Kinugawa, Koichiro ; Usuda, Kazuo ; Kitayama, Michihiko ; Ino, Hidekazu ; Kuroda, Shigetoshi ; Tada, Hiroshi ; Mizuno, Sumio ; Hayashi, Kenshi ; Takemura, Hirofumi ; Yamagishi, Masakazu ; 藤野, 陽 ; 吉牟田, 剛 ; 林, 研至 ; 竹村, 博文 ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />The 81st Annual Scientific Meeting of the Japanese Circulation Society was held in Kanazawa, Japan,
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on March 17-19, 2017 under a miraculously clear sky. The frontlines of healthcare and medicine are dramatically changing. Thus, “Cardiovascular Medicine for Next Generation” was chosen as the main theme of this meeting. The program was constructed around major identified issues, including renewal of our understanding of basic cardiovascular medicine, translational research, and preventive molecular medicine, all of which are anticipated to transcend the medical field over the next generation. Despite the provincial location, 15,672 participants, including more than 400 from overseas countries, attended the 3-day meeting, and there were in-depth discussions in the various sessions. In particular, to our great pleasure, Her Imperial Highness Princess Takamado kindly attended the opening ceremony and extended congratulations to us. The meeting successfully completed and we sincerely appreciate the great cooperation and support from all affiliates. © 2017 Circulation Journal. All rights reserved.<br />出版者照会後に全文公開
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Nomura, Akihiro ; Konno, Tetsuo ; Fujita, Takashi ; Tanaka, Yoshihiro ; Nagata, Yoji ; Tsuda, Toyonobu ; Hodatsu, Akihiko ; Sakata, Kenji ; Nakamura, Hiroyuki ; Kawashiri, Masa-aki ; Fujino, Noboru ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 今野, 哲雄 ; 坂田, 憲治 ; 川尻, 剛照 ; 藤野, 陽 ; 山岸, 正和 ; 林, 研至
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金沢大学医薬保健研究域医学系<br />Background: Although fragmented QRS complex (frag-QRS) reflecting intra-ventricular conduction delay
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has been shown to be a prognostic marker for cardiac events, few data exist regarding the impact of frag-QRS on cardiac events in hypertrophic cardiomyopathy (HCM).Methods and Results: Ninety-four HCM patients (56 male; mean age, 58}17 years) were retrospectively investigated. Frag-QRS was defined as the presence of various RsR’ patterns in at least 2 contiguous ECG leads. Major arrhythmic events (MAE) were defined as sudden cardiac death, and combined sustained ventricular tachycardia/ventricular fibrillation. New-onset atrial fibrillation (AF) was diagnosed based on ECG during provisional or routine medical examination. Heart failure (HF) with hospitalization was defined as hospital admission due to subjective or objective symptoms. Frag-QRS was detected in 31 patients (33%). TNNI3 was the most frequent disease-causing gene. Median follow-up was 4.6 years. The 4-year cumulative survival rates of cardiac death, MAE, new-onset AF and HF with hospitalization were 97.6%, 94.6%, 87.5% and 89.3%, respectively. On multivariate analysis, frag-QRS was significantly associated with HF with hospitalization (adjusted hazard ratios [95% confidence intervals]: 5.4 [1.2–36], P=0.03). Moreover, HF-free survival was significantly lower in the frag-QRS (+) group compared to the frag-QRS (–) group (79.0% vs. 95.1%, P=0.03).Conclusions: Frag-QRS is associated with HF with hospitalization in HCM patients who had a unique distribution of gene mutations. © 2014, The Japanese Circulation Society<br />出版者照会後に全文公開
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Takashima, Hiroaki ; Ozaki, Yukio ; Morimoto, Takeshi ; Kimura, Takeshi ; Hiro, Takafumi ; Miyauchi, Katsumi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Daida, Hiroyuki ; Mizuno, Tomofumi ; Asai, Kenji ; Kuroda, Yasuo ; Kosaka, Takashi ; Kuhara, Yasushi ; Kurita, Akiyoshi ; Maeda, Kazuyuki ; Amano, Tetsuya ; Matsuzaki, Masunori ; 山岸, 正和
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金沢大学医薬保健研究域医学系<br />Background: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndr
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ome) trial showed that intensive statin therapy could induce significant coronary plaque regression in acute coronary syndrome (ACS). We evaluated the impact of metabolic syndrome (MetS) and its components on coronary plaque regression in the JAPAN-ACS patients. Methods and Results: Serial intravascular ultrasound measurements over 8-12 months were performed in 242 ACS patients receiving pitavastatin or atorvastatin. Patients were divided into groups according to the presence of MetS or the number of MetS components. Although the percent change in plaque volume (%PV) was not significantly different between the MetS (n=119) and non-MetS (n=123) groups (P=0.50), it was significantly associated with an increasing number of MetS components (component 0: -24.0%, n=7; components 1: -20.8%, n=31; components 2: -16.1%, n=69; components 3: -18.7%, n=83; components 4: -13.5%, n=52; P=0.037 for trend). The percent change in body mass index (%BMI) significantly correlated with %PV (r=0.15, P=0.021), especially in the MetS components 4 group (r=0.35, P=0.017). In addition, %BMI was an independent predictor of plaque regression after adjustment for the changes of low- and high-density lipoprotein cholesterol, triglycerides and HbA1c. Conclusions: The clustering of MetS components, but not the presence of MetS itself, could attenuate coronary plaque regression during intensive statin therapy in ACS patients. Therefore, to achieve a greater degree of plaque regression, it is necessary to treat to each MetS component and use lifestyle modification.<br />出版者照会後に全文公開
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Nakanishi, Chiaki ; Nagaya, Noritoshi ; Ohnishi, Shunsuke ; Yamahara, Kenichi ; Takabatake, Shu ; Konno, Tetsuo ; Hayashi, Kenshi ; Kawashiri, Masa-aki ; Tsubokawa, Toshinari ; Yamagishi, Masakazu ; 中西, 千明 ; 今野, 哲雄 ; 林, 研至 ; 川尻, 剛照 ; 山岸, 正和
概要:
金沢大学医薬保健研究域医学系<br />Background: Mesenchymal stem cells (MSC) are multipotent and reside in bone marrow (BM), adipose tis
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sue and many other tissues. However, the molecular foundations underlying the differences in proliferation, differentiation potential and paracrine effects between adipose tissue-derived MSC (ASC) and BM-derived MSC (BM-MSC) are not well-known. Therefore, we investigated differences in the gene and secretory protein expressions of the 2 types of MSC. Methods and Results: ASC and BM-MSC were obtained from subcutaneous adipose tissue and BM of adult Lewis rats. ASC proliferated as rapidly as BM-MSC, and had expanded 200-fold in approximately 2 weeks. On microarray analysis of 31,099 genes, 571 (1.8%) were more highly (>3-fold) expressed in ASC, and a number of these genes were associated with mitosis and immune response. On the other hand, 571 genes (1.8%) were more highly expressed in BM-MSC, and some of these genes were associated with organ development and morphogenesis. In secretory protein analysis, ASC secreted significantly larger amounts of growth factor and inflammatory cytokines, such as vascular endothelial growth factor, hepatocyte growth factor and interleukin 6, whereas BM-MSC secreted significantly larger amounts of stromal-derived factor-1α. Conclusions: There are significant differences between ASC and BM-MSC in the cytokine secretome, which may provide clues to the molecule mechanisms associated with tissue regeneration and alternative cell sources.<br />出版者照会後に全文公開
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| 18.
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Funada, Akira ; Konno, Tetsuo ; Fujino, Noboru ; Muramoto, Akihiko ; Hayashi, Kenshi ; Tsubokawa, Toshinari ; Sakata, Kenji ; Kawashiri, Masa-aki ; Takeda, Yoshiyu ; Ino, Hidekazu ; Yamagishi, Masakazu ; 舟田, 晃 ; 今野, 哲雄 ; 藤野, 陽 ; 林, 研至 ; 坂田, 憲治 ; 川尻, 剛照 ; 武田, 仁勇 ; 井野, 秀一 ; 山岸, 正和
概要:
金沢大学医薬保健研究域医学系<br />Background: Although the renin - angiotensin system (RAS) can affect the development of left ventric
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ular (LV) hypertrophy, few data exist regarding the relationships between RAS polymorphisms and alteration of LV function. The effect of RAS polymorphisms on LV function in genotyped hypertrophic cardiomyopathy (HCM) was examined in the present study. Methods and Results: The study group comprised 126 carriers with sarcomere gene mutations from 49 HCM families (64 males, mean age 51±21 years). LV morphology and function were evaluated by echocardiography. In angiotensin-converting enzyme (ACE) insertion/deletion (I/D), the D allele (n=81) exhibited significantly larger LV end-systolic dimension (LVDs) (32±11 mm) and lower ejection fraction (56±15%) than those with the II genotype (28±7 mm and 62±12%, respectively, P<0.05; n=45). Although angiotensin II type 1 receptor (AT1-R) A/C1166 polymorphism did not affect echocardiographic parameters, the presence of the ACE D allele with the AT1-R C1166 allele (n=9) was associated with larger LVDs (37±17 mm) and lower ejection fraction (48±20%) compared with other genotypes (30±9 mm and 58±14%, respectively, P<0.05; n=117). Under these conditions, severe LV hypertrophy was frequently associated with LV wall thinning. Conclusions: The presence of both the ACE D and AT1-R C1166 allele is associated with LV dilation with systolic dysfunction in genotyped HCM. In addition to the severity of LV hypertrophy, screening for these RAS polymorphisms could contribute to further risk stratification of patients with HCM, although other genetic polymorphisms should be further examined.<br />出版者照会後に全文公開
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| 19.
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Fukushima, Yoshifumi ; Daida, Hiroyuki ; Morimoto, Takeshi ; Kasai, Takatoshi ; Miyauchi, Katsumi ; Yamagishi, Sho-ichi ; Takeuchi, Masayoshi ; Hiro, Takafumi ; Kimura, Takeshi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Ozaki, Yukio ; Matsuzaki, Masunori ; JAPAN-ACS Investigators ; 山岸, 正和
概要:
金沢大学医薬保健研究域医学系<br />Background: The Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome (JAPAN-
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ACS) trial demonstrated that early aggressive statin therapy in patients with ACS significantly reduces plaque volume (PV). Advanced glycation end products (AGEs) and the receptors of AGEs (RAGE) may lead to angiopathy in diabetes mellitus (DM) and may affect on the development of coronary PV. The present sub-study of JAPAN-ACS investigates the association between AGEs and RAGE, and PV.Methods: Intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) was undertaken, followed by the initiation of statin treatment (either 4 mg/day of pitavastatin or 20 mg/day of atorvastatin), in patients with ACS. In the 208 JAPAN-ACS subjects, PV using IVUS in non-culprit segment > 5 mm proximal or distal to the culprit lesion and, serum levels of AGEs and soluble RAGE (sRAGE) were measured at baseline and 8-12 months after PCI.Results: At baseline, no differences in the levels of either AGEs or sRAGE were found between patients with DM and those without DM. The levels of AGEs decreased significantly with statin therapy from 8.6 ± 2.2 to 8.0 ± 2.1 U/ml (p < 0.001), whereas the levels of sRAGE did not change. There were no significant correlations between changes in PV and the changes in levels of AGEs as well as sRAGE. However, high baseline AGEs levels were significantly associated with plaque progression (odds ratio, 1.21; 95% confidence interval, 1.01 - 1.48; p = 0.044) even after adjusting for DM in multivariate logistic regression models.Conclusions: High baseline AGEs levels were associated with plaque progression in the JAPAN-ACS trial. This relationship was independent of DM. These findings suggest AGEs may be related to long-term glucose control and other oxidative stresses in ACS.Trial registration: NCT00242944. © 2013 Fukushima et al.; licensee BioMed Central Ltd.
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| 20.
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Mizushima, Ichiro ; Inoue, Dai ; Yamamoto, Motohisa ; Yamada, Kazunori ; Saeki, Takako ; Ubara, Yoshifumi ; Matsui, Shoko ; Masaki, Yasufumi ; Wada, Takashi ; Kasashima, Satomi ; Harada, Kenichi ; Takahashi, Hiroki ; Notohara, Kenji ; Nakanuma, Yasuni ; Umehara, Hisanori ; Yamagishi, Masakazu ; Kawano, Mitsuhiro ; 水島, 伊知郎 ; 井上, 大 ; 山田, 和徳 ; 和田, 隆志 ; 笠島, 里美 ; 原田, 憲一 ; 中沼, 安二 ; 梅原, 久範 ; 山岸, 正和 ; 川野, 充弘
概要:
金沢大学医薬保健研究域医学系<br />Introduction: Immunoglobulin G4 (IgG4)-related aortitis/periaortitis and periarteritis are vascular
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manifestations of IgG4-related disease. In this disease, the affected aneurysmal lesion has been suspected to be at risk of rupture. In this study, we aimed to clarify the clinical course after corticosteroid therapy in IgG4-related aortitis/periaortitis and periarteritis.Methods: We retrospectively evaluated clinical features, including laboratory data, imaging findings and the course after corticosteroid therapy, in 40 patients diagnosed with IgG4-related aortitis/periaortitis and periarteritis on the basis of periaortic/periarterial radiological findings, satisfaction of the comprehensive diagnostic criteria or each organ-specific diagnostic criteria, and exclusion of other diseases. Results: The patients were mainly elderly, with an average age of 66.4 years and with a marked male predominance and extensive other organ involvement. Subjective symptoms were scanty, and only a small proportion had elevated serum C-reactive protein levels. The affected aorta/artery were the abdominal aortas or the iliac arteries in most cases. Thirty-six patients were treated with prednisolone, and the periaortic/periarterial lesions improved in most of them during the follow-up period. Two (50.0%) of four patients with luminal dilatation of the affected lesions before corticosteroid therapy had exacerbations of luminal dilatation after therapy, whereas none of the twenty-six patients without it had a new appearance of luminal dilatation after therapy. Conclusions: The results of this retrospective multicenter study highlight three important points: (1) the possibility of latent existence and progression of periaortic/periarterial lesions, (2) the efficacy of corticosteroid therapy in preventing new aneurysm formation in patients without luminal dilatation of periaortic/periarterial lesions and (3) the possibility that a small proportion of patients may actually develop luminal dilatation of periaortic/periarterial lesions in IgG4-related aortitis/periaortitis and periarteritis. A larger-scale prospective study is required to confirm the efficacy and safety of corticosteroid therapy in patients with versus those without luminal dilatation and to devise a more useful and safe treatment strategy, including administration of other immunosuppressants. © 2014 Mizushima et al.; licensee BioMed Central Ltd.
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| 21.
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Konno, Tetsuo ; Hayashi, Kenshi ; Fujino, Noboru ; Nagata, Yoji ; Hodatsu, Akihiko ; Masuta, Eiichi ; Sakata, Kenji ; Nakamura, Hiroyuki ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; 今野, 哲雄 ; 林, 研至 ; 藤野, 陽 ; 永田, 庸二 ; 寳達, 明彦 ; 坂田, 憲治 ; 中村, 裕之 ; 川尻, 剛照 ; 山岸, 正和
概要:
金沢大学医薬保健研究域医学系<br />Background: Myocardial scarring can be assessed by cardiac magnetic resonance imaging with late gado
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linium enhancement and by endomyocardial biopsy. However, accuracy of late gadolinium enhancement for predicting microscopic myocardial scarring in biopsied specimens remains unknown in hypertrophic cardiomyopathy. We investigated whether late gadolinium enhancement in the whole heart reflects microscopic myocardial scarring in the small biopsied specimens in hypertrophic cardiomyopathy. Methods and Results: Twenty-one consecutive patients with hypertrophic cardiomyopathy who were examined both by cardiac magnetic resonance imaging and by endomyocardial biopsy were retrospectively studied. The right interventricular septum was the target site for endomyocardial biopsy in all patients. Late gadolinium enhancement in the ventricular septum had an excellent sensitivity (100%) with a low specificity (40%) for predicting microscopic myocardial scarring in biopsied specimens. The sensitivity of late gadolinium enhancement in the whole heart remained 100% with a specificity of 27% for predicting microscopic myocardial scarring in biopsied specimens. Quantitative assessments of fibrosis revealed that the extent of late gadolinium enhancement in the whole heart was the only independent variable related to the microscopic collagen fraction in biopsied specimens (β = 0.59, 95% confident interval: 0.15-1.0, p = 0.012). Conclusions: Although there was a compromise in the specificity, the sensitivity of late gadolinium enhancement was excellent for prediction of microscopic myocardial scarring in hypertrophic cardiomyopathy. Moreover, the severity of late gadolinium enhancement was independently associated with the quantitative collagen fraction in biopsied specimens in hypertrophic cardiomyopathy. These findings indicate that late gadolinium enhancement can reflect both the presence and the extent of microscopic myocardial scarring in the small biopsied specimens in hypertrophic cardiomyopathy. © 2014 Konno et al.
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| 22.
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Kometani, Mitsuhiro ; Yoneda, Takashi ; Demura, Masashi ; Koide, Hiroshi ; Nishimoto, Koshiro ; Mukai, Kuniaki ; Gomez-Sanchez, Celso E. ; Akagi, Tadayuki ; Yokota, Takashi ; Horike, Shin-ichi ; Karashima, Shigehiro ; Miyamori, Isamu ; Yamagishi, Masakazu ; Takeda, Yoshiyu ; 米田, 隆 ; 赤木, 紀之 ; 横田, 崇 ; 堀家, 慎一 ; 唐島, 成宙 ; 宮森, 勇 ; 山岸, 正和 ; 武田, 仁勇
概要:
金沢大学医薬保健研究域医学系<br />Adrenocortical hormone excess, due to primary aldosteronism (PA) or hypercortisolemia, causes hypert
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ension and cardiovascular complications. In PA, hypomethylation of aldosterone synthase (CYP11B2) is associated with aldosterone overproduction. However, in hypercortisolemia, the role of DNA methylation of 11β-hydroxylase (CYP11B1), which catalyzes cortisol biosynthesis and is highly homologous to CYP11B2, is unclear. The aims of our study were to determine whether the CYP11B1 expression was regulated through DNA methylation in hypercortisolemia with cortisol-producing adenoma (CPA), and to investigate a possible relationship between DNA methylation and somatic mutations identified in CPA. Methylation analysis showed that the CYP11B1 promoter was significantly less methylated in CPA than in adjacent unaffected adrenal tissue and white blood cells. Furthermore, in CPA with somatic mutations in either the catalytic subunit of protein kinase A (PRKACA) or the guanine nucleotide-binding protein subunit alpha (GNAS) gene, the CYP11B1 promoter was significantly hypomethylated. In addition, DNA methylation reduced CYP11B1 promoter activity using a reporter assay. Our study results suggest that DNA methylation at the CYP11B1 promoter plays a role in the regulation of CYP11B1 expression and cortisol production in CPA, and that somatic mutations associated with CPA reduce DNA methylation at the CYP11B1 promoter. © 2017 The Author(s).
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| 23.
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Tagawa, Shotoku ; Nakanishi, Chiaki ; Mori, Masayuki ; Yoshimuta, Tsuyoshi ; Yoshida, Shohei ; Shimojima, Masaya ; Yokawa, Junichiro ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 田川, 庄督 ; 中西, 千明 ; 吉牟田, 剛 ; 吉田, 昌平 ; 川尻, 剛照 ; 山岸, 正和 ; 林, 研至
概要:
金沢大学医薬保健研究域医学系<br />The clinical implications of early and late endothelial progenitor cells (EPCs) in coronary artery d
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isease (CAD) remain unclear. We investigated endothelial dysfunction in CAD by simultaneously examining early and late EPC colony formation and gene expression of specific surface markers in EPCs. EPCs were extracted from a total of 83 subjects with (n=47) and without (n=36) CAD. Early and late EPC colonies were formed from mononuclear cells extracted from peripheral blood. We found that fewer early EPC colonies were produced in the CAD group (7.2 ± 3.l/well) than those in the control group (12.4 ± 1.4/well, p<0.05), and more late EPC colonies were produced in the CAD group (0.8 ± 0.2/well) than those in the control group (0.25 ± 0.02/well, p<0.05). In the CAD group, the relative expression of CD31 and KDR of early and late EPCs was lower than in the control group. These results demonstrate that CAD patients could have increased late EPC density and that early and late EPCs in CAD patients exhibited immature endothelial characteristics. We suggest that changes in EPC colony count and gene expression of endothelial markers may have relation with development of CAD. © 2015 Shotoku Tagawa et al.
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24. Trajectories of Postload Plasma Glucose in the Development of Type 2 Diabetes in Japanese Adults
Oka, Rie ; Shibata, Kyoko ; Sakurai, Masaru ; Kometani, Mitsuhiro ; Yamagishi, Masakazu ; Yoshimura, Kenichi ; Yoneda, Takashi ; 大家, 理恵 ; 柴田, 恭子 ; 櫻井, 勝 ; 米谷, 充弘 ; 山岸, 正和 ; 吉村, 健一 ; 米田, 隆
概要:
金沢大学附属病院研修医・専門医総合教育センター<br />We aimed to clarify how the trajectories of 1-hour postload plasma glucose (PG) and 2-hour
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PG were different in the development of type 2 diabetes. Using data of repeated health checkups in Japanese workers from April 2006 to March 2016, longitudinal changes of fasting, 1-hour, and 2-hour PG on the oral glucose tolerance test were analyzed with a linear mixed effects model. Of the 1464 nondiabetic subjects at baseline, 112 subjects progressed to type 2 diabetes during the observation period (progressors). In progressors, 1-hour PG and 2-hour PG showed gradual increases with slopes of 1.33 ± 0.2 and 0.58 ± 0.2 mg/dL/year, respectively, followed by a steep increase by which they attained diabetes. Until immediately before the diabetes transition, age- and sex-adjusted mean level of 2-hour PG was 149 ± 2.7 mg/dL, 34 ± 2.7 (30%) higher compared to nonprogressors, while that of 1-hour PG was 206 ± 4.1 mg/dL, 60 ± 4.3 mg/dL (41%) higher compared to nonprogressors. In conclusion, diabetes transition was preceded by a mild elevation of 2-hour PG for several years or more. The elevation in 1-hour PG was larger than that of 2-hour PG until immediately before the transition to diabetes. © 2017 Rie Oka et al.<br />Embargo Period 12 months
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| 25.
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Al Mahmuda, Naila ; Yokoyama, Shigeru ; Huang, Jian-Jun ; Liu, Li ; Munesue, Toshio ; Nakatani, Hideo ; Hayashi, Kenshi ; Yagi, Kunimasa ; Yamagishi, Masakazu ; Higashida, Haruhiro
概要:
Autism Spectrum Disorder (ASD) is a group of neurodevelopmental disorders with complex genetic etiology. Recent studies
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have indicated that children with ASD may have altered folate or methionine metabolism, suggesting that the folate-methionine cycle may play a key role in the etiology of ASD. SLC19A1, also referred to as reduced folate carrier 1 (RFC1), is a member of the solute carrier group of transporters and is one of the key enzymes in the folate metabolism pathway. Findings from multiple genomic screens suggest the presence of an autism susceptibility locus on chromosome 21q22.3, which includes SLC19A1. Therefore, we performed a case-control study in a Japanese population. In this study, DNA samples obtained from 147 ASD patients at the Kanazawa University Hospital in Japan and 150 unrelated healthy Japanese volunteers were examined by the sequence-specific primer-polymerase chain reaction method pooled with fluorescence correlation spectroscopy. p < 0.05 was considered to represent a statistically significant outcome. Of 13 single nucleotide polymorphisms (SNPs) examined, a significant p-value was obtained for AA genotype of one SNP (rs1023159, OR = 0.39, 95% CI = 0.16-0.91, p = 0.0394; Fisher’s exact test). Despite some conflicting results, our findings supported a role for the polymorphism rs1023159 of the SLC19A1 gene, alone or in combination, as a risk factor for ASD. However, the findings were not consistent after multiple testing corrections. In conclusion, although our results supported a role of the SLC19A1 gene in the etiology of ASD, it was not a significant risk factor for the ASD samples analyzed in this study. © 2016 by the authors; licensee MDPI, Basel, Switzerland.
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| 26.
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Munesue, Toshio ; Yokoyama, Shigeru ; Nakamura, Kazuhiko ; Anitha, Ayyappan ; Yamada, Kazuo ; Hayashi, Kenshi ; Asaka, Tomoya ; Liu, Hong-Xiang ; Jin, Duo ; Koizumi, Keita ; Islam, Mohammad Saharul ; Huang, Jian-Jun ; Ma, Wen-Jie ; Kim, Uh-Hyun ; Kim, Sun-Jun ; Park, Keunwan ; Kim, Dongsup ; Kikuchi, Mitsuru ; Ono, Yasuki ; Nakatani, Hideo ; Suda, Shiro ; Miyachi, Taishi ; Hirai, Hirokazu ; Salmina, Alla ; Pichugina, Yu A. ; Soumarokov, Andrei A. ; Takei, Nori ; Mori, Norio ; Tsujii, Masatsugu ; Sugiyama, Toshiro ; Yagi, Kunimasa ; Yamagishi, Masakazu ; Sasaki, Tsukasa ; Yamasue, Hidenori ; Kato, Nobumasa ; Hashimoto, Ryota ; Taniike, Masako ; Hayashi, Yutaka ; Hamada, Jun-ichiro ; Suzuki, Shioto ; Ooi, Akishi ; Noda, Mami ; Kamiyama, Yuko ; Kido, Mizuho A. ; Lopatina, Olga ; Hashii, Minako ; Amina, Sarwat ; Malavasi, Fabio ; Huang, Eric J. ; Zhang, Jiasheng ; Shimizu, Nobuaki ; Yoshikawa, Takeo ; Matsushima, Akihiro ; Minabe, Yoshio ; Higashida, Haruhiro
概要:
金沢大学医薬保健研究域医学系<br />The neurobiological basis of autism spectrum disorder (ASD) remains poorly understood. Given the rol
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e of CD38 in social recognition through oxytocin (OT) release, we hypothesized that CD38 may play a role in the etiology of ASD. Here, we first examined the immunohistochemical expression of CD38 in the hypothalamus of post-mortem brains of non-ASD subjects and found that CD38 was colocalized with OT in secretory neurons. In studies of the association between CD38 and autism, we analyzed 10 single nucleotide polymorphisms (SNPs) and mutations of CD38 by re-sequencing DNAs mainly from a case-control study in Japan, and Caucasian cases mainly recruited to the Autism Genetic Resource Exchange (AGRE). The SNPs of CD38, rs6449197 (p< 0.040) and rs3796863 (p< 0.005) showed significant associations with a subset of ASD (IQ > 70; designated as high-functioning autism (HFA)) in the U.S. 104 AGRE family trios, but not with Japanese 188 HFA subjects. A mutation that caused tryptophan to replace arginine at amino acid residue 140 (R140W; (rs1800561, 4693C>T)) was found in 0.6-4.6% of the Japanese population and was associated with ASD in the smaller case-control study. The SNP was clustered in pedigrees in which the fathers and brothers of T-allele-carrier probands had ASD or ASD traits. In this cohort OT plasma levels were lower in subjects with the T allele than in those without. One proband with the T allele who was taking nasal OT spray showed relief of symptoms. The two variant CD38 poloymorphysms tested may be of interest with regard of the pathophysiology of ASD. © 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society.
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| 27.
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Yoshimuta, Tsuyoshi ; Yokoyama, Hiroyuki ; Okajima, Toshiya ; Yamagishi, Masakazu ; Nonogi, Hiroshi
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金沢大学医薬保健研究域医学系
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Demura, Masashi ; Demura, Yoshiki ; Ameshima, Shingo ; Ishizaki, Takeshi ; Sasaki, Masato ; Miyamori, Isamu ; Yamagishi, Masakazu ; Takeda, Yoshiyu ; Bulun, Serdar E.
概要:
金沢大学医薬保健研究域医学系<br />In humans, aromatase (CYP19) gene expression is regulated via alternative promoters. Activation of e
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ach promoter gives rise to a CYP19 mRNA species with a unique 5′-untranslated region. Inhibition of aromatase has been reported to downregulate lung tumor growth. The genetic basis for CYP19 gene expression and aromatase activity in lung cancer remains poorly understood. We analyzed tissues from 15 patients with non-small cell lung cancer (NSCLC) to evaluate CYP19 promoter usage and promoter-specific aromatase mRNA levels in NSCLC tumor tissues and adjacent non-malignant tissues. CYP19 promoter usage was determined by multiplex RT-PCR and aromatase mRNA levels were measured with real-time RT-PCR. In non-malignant tissues, aromatase mRNA was primarily derived from activation of CYP19 promoter I.4. Although promoter I.4 usage was also dominant in tumor tissues, I.4 activation was significantly lower compared with adjacent non-malignant tissues. Activity of promoters I.3, I.1 and I.7 was significantly higher in tumor tissues compared with non-malignant tissues. In 4 of 15 cases of non-small cell lung cancer, switching from CYP19 promoter I.4 to the alternative promoters II, I.1 or I.7 was observed. In 9 cases, there were significantly higher levels of aromatase mRNA in lung tumor tissues compared with adjacent non-malignant tissues. These findings suggest aberrant activation of alternative CYP19 promoters that may lead to upregulation of local aromatase expression in some cases of NSCLC. Further studies are needed to examine the impact of alternative CYP19 promoter usage on local estrogen levels and lung tumor growth. © 2011 Elsevier Ireland Ltd. All rights reserved.
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| 29.
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Mabuchi, Hiroshi ; Nohara, Atsushi ; Noguchi, Tohru ; Kobayashi, Junji ; Kawashiri, Masaaki ; Tada, Hayato ; Nakanishi, Chiaki ; Mori, Mika ; Yamagishi, Masakazu ; Inazu, Akihiro ; Koizumi, Junji ; Hokuriku FH Study Group
概要:
金沢大学医学系研究科<br />Aim: Familial hypercholesterolemia (FH) is caused by mutations of FH genes, i.e. LDL-receptor (LDLR), PC
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SK9 and apolipoprotein B (ApoB) gene. We evaluated the usefulness of DNA analysis for the diagnosis of homozygous FH (homo-FH), and studied the frequency of FH in the Hokuriku district of Japan. Methods: Twenty-five homo-FH patients were recruited. LDLR mutations were identified using the Invader assay method. Mutations in PCSK9 were detected by PCR-SSCP followed by direct sequence analysis. Results: We confirmed 15 true homozygotes and 10 compound heterozygotes for LDLR mutations. Three types of double heterozygotes for LDLR and PCSK9 were found. No FH patients due to ApoB mutations were found. The incidences of homo-FH and hetero-FH in the Hokuriku district were 1/171,167 and 1/208, respectively. Conclusions: Our observations underlined the value of FH gene analysis in diagnosing homo-FH and confirmed extraordinarily high frequency of FH in the Hokuriku district of Japan. © 2010 Elsevier Ireland Ltd.
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Oka, Rie ; Kobayashi, Junji ; Inazu, Akihiro ; Yagi, Kunimasa ; Miyamoto, Susumu ; Sakurai, Masaru ; Nakamura, Koshi ; Miura, Katsuyuki ; Nakagawa, Hideaki ; Yamagishi, Masakazu
概要:
金沢大学大学院医学系研究科<br />北陸中央病院内科<br />We investigated the relative impacts of visceral adiposity and insulin resistance on th
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e metabolic risk profile in middle-aged Japanese men. A cross-sectional study was conducted in 636 nondiabetic Japanese men with a mean age of 51.6 years. Visceral adipose tissue (AT) was assessed using computed tomography, and insulin resistance was determined by the homeostasis model assessment of insulin resistance (HOMA-IR). Metabolic risk factors were diagnosed according to the National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome criteria: (1) hypertriglyceridemia, (2) low high-density lipoprotein cholesterol, (3) hypertension, (4) impaired fasting glucose, and (5) impaired glucose tolerance. Visceral AT and HOMA-IR were significantly and positively correlated with each other (r = 0.41, P < .001). Using the 75th percentile value as a cut point, those with isolated large visceral AT showed significantly greater odds ratios for each of the 5 risk factors measured except impaired fasting glucose, whereas those with isolated high HOMA-IR showed significantly greater odds ratios for each of the 5 risk factors except hypertriglyceridemia and impaired glucose tolerance, compared with the control group. The combined group (increased visceral AT and HOMA-IR) had the highest odds ratios for all studied risk factors. On logistic regression analysis using visceral AT and HOMA-IR as continuous independent variables, they were each independently associated with most of the metabolic risk factors and their clustering. In conclusion, neither visceral AT nor HOMA-IR stands out as the sole driving force of the risk profile; each makes a significant contribution to metabolic abnormalities in Japanese men. © 2010 Elsevier Inc. All rights reserved.
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Zoshima, Takeshi ; Matsumura, Masami ; Suzuki, Yasunori ; Kakuchi, Yasushi ; Mizushima, Ichiro ; Fujii, Hiroshi ; Yamada, Kazunori ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
概要:
We describe a patient with refractory cutaneous polyarteritis nodosa (CPAN) with hepatitis B virus (HBV) carrier status
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who was successfully treated with tumor necrosis factor alpha (TNF-α) blockade, using etanercept, and we review 5 similar cases. We administered etanercept because of the occurrence of repeated flares despite aggressive therapy. C-reactive protein normalization; prednisolone dose-sparing; and absence of any adverse events, including HBV reactivation with nucleotide analogue administration, or renal dysfunction, have been achieved for 8 months. TNF-α blockade should be considered for intractable CPAN. © 2012 Japan College of Rheumatology.<br />In Press → 出版者照会後に全文を公開.
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Noguchi, Tohru ; Kobayashi, Junji ; Yagi, Kunimasa ; Nohara, Atsushi ; Yamaaki, Naoto ; Sugihara, Masako ; Ito, Naoko ; Oka, Rie ; Kawashiri, Masaaki ; Tada, Hayato ; Takata, Mutsuko ; Inazu, Akihiro ; Yamagishi, Masakazu ; Mabuchi, Hiroshi
概要:
金沢大学医学系研究科<br />Background: Bezafibrate and fenofibrate show different binding properties against peroxisome proliferato
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r-activated receptor subtypes, which could cause different clinical effects on circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) levels and on various metabolic markers. Methods: An open, randomized, four-phased crossover study using 400 mg of bezafibrate or 200 mg of fenofibrate was performed. Study subjects were 14 dyslipidemia with impaired glucose tolerance or type 2 diabetes mellitus (61 ± 16 years, body mass index (BMI) 26 ± 3 kg/m2, total cholesterol (TC) 219 ± 53 mg/dL, triglyceride (TG) 183 ± 83 mg/dL, high-density lipoprotein-cholesterol (HDL-C) 46 ± 8 mg/dL, fasting plasma glucose 133 ± 31 mg/dL and HbA1c 6.2 ± 0.8%). Subjects were given either bezafibrate or fenofibrate for 8 weeks, discontinued for 4 weeks and then switched to the other fibrate for 8 weeks. Circulating PCSK9 levels and other metabolic parameters, including adiponectin, leptin and urine 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured at 0, 8, 12 and 20 weeks. Results: Plasma PCSK9 concentrations were significantly increased (+39.7% for bezafibrate and +66.8% for fenofibrate, p < 0.001) in all patients except for one subject when treated with bezafibrate. Both bezafibrate and fenofibrate caused reductions in TG (-38.3%, p < 0.001 vs. -32.9%, p < 0.01) and increases in HDL-C (+18.0%, p < 0.001 vs. +11.7%, p < 0.001). Fenofibrate significantly reduced serum cholesterol levels (TC, -11.2%, p < 0.01; non-HDL-C, -17.3%, p < 0.01; apolipoprotein B, -15.1%, p < 0.01), whereas bezafibrate significantly improved glucose tolerance (insulin, -17.0%, p < 0.05) and metabolic markers (γ-GTP, -38.9%, p < 0.01; adiponectin, +15.4%, p < 0.05; urine 8-OHdG/Cre, -9.5%, p < 0.05). Conclusion: Both bezafibrate and fenofibrate increased plasma PCSK9 concentrations. The addition of a PCSK9 inhibitor to each fibrate therapy may achieve beneficial cholesterol lowering along with desirable effects of respective fibrates. © 2011 Elsevier Ireland Ltd. All rights reserved.
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| 33.
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Zoshima, Takeshi ; Matsumura, Masami ; Suzuki, Yasunori ; Kakuchi, Yasushi ; Mizushima, Ichiro ; Fujii, Hiroshi ; Yamada, Kazunori ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
概要:
We describe a patient with refractory cutaneous polyarteritis nodosa (CPAN) with hepatitis B virus (HBV) carrier status
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who was successfully treated with tumor necrosis factor alpha (TNF-α) blockade, using etanercept, and we review 5 similar cases. We administered etanercept because of the occurrence of repeated flares despite aggressive therapy. C-reactive protein normalization; prednisolone dose-sparing; and absence of any adverse events, including HBV reactivation with nucleotide analogue administration, or renal dysfunction, have been achieved for 8 months. TNF-α blockade should be considered for intractable CPAN. © 2012 Japan College of Rheumatology.<br />This is the pre-peer reviewed version of the following article: http://informahealthcare.com/doi/abs/10.3109/s10165-012-0732-8, which has been published in final form at http://dspace.lib.kanazawa-u.ac.jp/dspace/handle/2297/36280 .
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| 34.
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Demura, Masashi ; Wang, Fen ; Yoneda, Takashi ; Karashima, Shigehiro ; Mori, Shunsuke ; Oe, Masashi ; Kometani, Mitsuhiro ; Sawamura, Toshitaka ; Cheng, Yuan ; Maeda, Yuji ; Namiki, Mikio ; Ino, Hidekazu ; Fujino, Noboru ; Uchiyama, Katsuharu ; Tsubokawa, Toshinari ; Yamagishi, Masakazu ; Nakamura, Yasuhiro ; Ono, Katsuhiko ; Sasano, Hironobu ; Demura, Yoshiki ; Takeda, Yoshiyu
概要:
金沢大学医薬保健研究域医学系<br />Objective: Nuclear receptors are involved in a wide variety of functions, including aldosteronogenes
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is. Nuclear receptor families NR4A [nerve growth factor-induced clone B (NGFIB), Nur-related factor 1 (NURR1) and neuron-derived orphan receptor 1 (NOR1)] and NR2F [chicken ovalbumin upstream promoter-transcription factor 1 (COUP-TFI), COUP-TFII and NR2F6) activate, whereas NR5A1 [steroidogenic factor 1 (SF1)] represses CYP11B2 (aldosterone synthase) gene transcription. The present study was undertaken to elucidate the mechanism of differential regulation of nuclear receptors between cardiovascular and adrenal tissues. Methods: We collected tissues of artery (n = 9), cardiomyopathy muscle (n = 9), heart muscle (noncardiomyopathy) (n = 6), adrenal gland (n = 9) and aldosterone-producing adenoma (APA) (n = 9). 5′-rapid amplification of cDNA ends (RACE) identified transcription start sites. Multiplex reverse-transcription PCR (RT-PCR) determined use of alternative noncoding exons 1 (ANEs). Results: In adrenocortical H295R cells, angiotensin II, KCl or cAMP, all stimulated CYP11B2 transcription and NR4A was upregulated, whereas NR2F and NR5A1 were downregulated. 5′-RACE and RT-PCR revealed four ANEs of NGFIB (NR4A1), three of NURR1 (NR4A2), two of NOR1 (NR4A3) and two of SF1 (NR5A1) in cardiovascular and adrenal tissues. Quantitative multiplex RT-PCR showed NR4A and NR5A1 differentially employed multiple ANEs in a tissue-specific manner. The use of ANEs of NGFIB and NURR1 was significantly different between APA and artery. Changes in use of ANEs of NGFIB and NOR1 were observed between cardiomyopathy and noncardiomyopathy. The NR4A mRNA levels in artery were high compared with cardiac and adrenal tissues, whereas the NR5A1 mRNA level in adrenal tissues was extremely high compared with cardiovascular tissues. Conclusion: NR4A and NR5A1 genes are complex in terms of alternative promoter use. The use of ANEs may be associated with the pathophysiology of the heart and adrenal gland. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.
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| 35.
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Moriuchi, Tadashi ; Oka, Rie ; Yagi, Kunimasa ; Miyamoto, Susumu ; Nomura, Hideki ; Yamagishi, Masakazu ; Mabuchi, Hiroshi ; Kobayashi, Junji ; Koizumi, Junji
概要:
Objective High-normal, the intermediate category between normal fasting glucose (NFG) and impaired fasting glucose (IFG)
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, was introduced in the criteria of the disordered glucose metabolism in 2008. The aim of this study was to investigate the risk for future incidence of type 2 diabetes of the subjects with high-normal and to examine how other metabolic variables could be useful for their risk stratification. Methods A historical cohort study was conducted from 2001 to 2008, inclusive, in 4,165 non-diabetic employees at public schools (2,229 men and 1,936 women; age 45.8±5.9 years, range 25-55 years). They were classified at baseline as NFG with fasting plasma glucose (FPG)<100 mg/dL, high-normal with FPG 100-109 mg/dL, and IFG with FPG 110-125 mg/dL. The incidence of type 2 diabetes (defined either by FPG 126 mg/dL or by receiving treatments) was measured. Results The cumulative incidence during a mean follow-up of 5.1 years were 16/3,364 (0.5%), 40/613 (6.5%), and 53/188 (28.2%) in subjects with NFG, high-normal, and IFG, respectively. Multivariate-adjusted odds ratios for the incidence were still significant both in high-normal and IFG compared to NFG. Body mass index (BMI) and alanine aminotransaminase (ALT) were associated with the incidence of type 2 diabetes independently of FPG categories (p<0.05). Conclusion The future incidence of type 2 diabetes in subjects with high-normal was significantly higher than in those with NFG in this population. BMI and ALT can improve risk stratification in high-normal subjects. © 2010 The Japanese Society of Internal Medicine.
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| 36.
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Matsumura, Masami ; Ito, Kiyoaki ; Kawamura, Rika ; Fujii, Hiroshi ; Inoue, Ryo ; Yamada, Kazunori ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
概要:
A 53-year-old woman with systemic lupus erythematosus presented with a 3-day history of fever and coughing. Diagnosis of
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pneumococcal bronchitis was made based on symptoms and positivity of pneumococcal urinary antigen test. On day 3, severe low back pain acutely occurred. Pneumococcal vertebral osteomyelitis and psoas abscess was diagnosed 17 days later by yield of penicillin-susceptible S. pneumoniae strain in blood cultures and drainage fluid. Although pneumococcal urinary antigen test is a useful tool for the diagnosis of pneumococcal pneumonia, we should consider the possibility of pneumococcal infections other than pneumonia or overwhelming bacteremia in immunosuppressive patients when urinary antigen test is positive © 2011 The Japanese Society of Internal Medicine.
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| 37.
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Matsumura, Masami ; Kawamura, Rika ; Inoue, Ryo ; Kawano, Mitsuhiro ; Yamagishi, Masakazu
概要:
金沢大学医薬保健研究域医学系医学教育研究センター<br />Cryptococcal meningitis is a recognized complication of systemic lupus erythematosus (SLE)
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, with high mortality rates, particularly in those treated with immunosuppressive agents. We describe a patient diagnosed simultaneously with cryptococcal meningoencephalitis and SLE and reviewed four similar cases reported in the literature. In our case, profound low CD4 lymphocyte count and low complement levels were observed. The patient was treated with prednisolone, fluconazole, and 5-flucytosine and evinced good clinical improvement. This case suggests that intrinsic immunological abnormality related to SLE predisposed to opportunistic infections. © 2010 Japan College of Rheumatology.
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| 38.
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Gamou, Tadatsugu ; Sakata, Kenji ; Tada, Hayato ; Konno, Tetsuo ; Hayashi, Kenshi ; Ino, Hidekazu ; Yamagishi, Masakazu ; Kawashiri, Masa-aki ; on behalf of the MILLION Study Group ; 坂田, 憲治 ; 多田, 隼人 ; 今野, 哲雄 ; 林, 研至 ; 井野, 秀一 ; 山岸, 正和 ; 川尻, 剛照
概要:
Background:The MILLION study, a prospective randomized multicenter study, revealed that lipid and blood pressure (BP)-lo
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wering therapy resulted in regression of coronary plaque as determined by intravascular ultrasound (IVUS). In the present study we performed additional analysis to investigate the associated factors with regression of coronary plaque. Methods and Results:We investigated serial 3D IVUS images from 68 patients in the MILLION study. Standard IVUS parameters were assessed at both baseline and follow-up (18–24 months). Volumetric data were standardized by length as normalized volume. In patients with plaque regression (n=52), plaque volumenormalizedsignificantly decreased from 64.8 to 55.8 mm3(P<0.0001) and vessel volumenormalizedsignificantly decreased from 135.0 to 127.5 mm3(P=0.0008). There was no difference in lumen volumenormalizedfrom 70.1 to 71.8 mm3(P=0.27). There were no correlations between % changes in vessel volume and cholesterol or BP. On the other hand, negative correlations between % change in vessel volume and vessel volumenormalizedat baseline (r=−0.352, P=0.009) or plaque volumenormalizedat baseline (r=−0.336, P=0.01) were observed. Conclusions:The current data demonstrated that in patients with plaque regression treated by aggressive lipid and BP-lowering therapy, the plaque regression was derived from reverse vessel remodeling determined by vessel volume and plaque burden at baseline irrespective of decreases in lipids and BP.<br />出版者照会後に全文公開
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| 39.
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Araki, Daisuke ; Fujii, Hiroshi ; Matsumura, Masami ; Yamagishi, Masakazu ; Yachie, Akihiro ; Kawano, Mitsuhiro
概要:
Hemophagocytic syndrome (HPS) is a severe, potentially life-threatening disorder characterized by an excessive activatio
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n of macrophages, such as may occur in the setting of lupus. A 62-year-old Japanese woman treated with etanercept for rheumatoid arthritis developed persistent fever, cytopenia, coagulopathy, and hyperferritinemia. Simultaneously, lupus-like features including pleuritis, hypocomplementemia, and positive autoantibodies were observed. She was diagnosed with HPS related to etanercept-induced lupus, and underwent immunosuppressive therapy with successful recovery. To our knowledge, this is the first case of etanercept-induced lupus accompanied by HPS. This case suggests that HPS should be considered as a complication during TNF-α inhibitor therapy.
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| 40.
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Funada, Akira ; Masuta, Eiichi ; Fujino, Noboru ; Hayashi, Kenshi ; Ino, Hidekazu ; Kita, Yoshihito ; Ikeda, Hiroko ; Fujii, Takahiko ; Nakanuma, Yasuni ; Yamagishi, Masakazu
概要:
Hypertrophic cardiomyopathy (HCM) is associated with gene mutations that encode sarcomeric proteins. However, the relationship between genotype and histopathologic fndings is unclear. We report on two autopsy cases with advanced
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HCM associated with deletion of lysine 183 mutation in the cardiac troponin I gene. One case, a 74-year-old female exhibited dilated cardiomyopathy-like features. Transmural scarring was diffuse and circumferential, involving the whole left ventricle, especially the ventricular septum which was replaced with extensive fbrosis and showed marked wall thinning. The other case, a 92-year-old male revealed typical HCM fndings. Patchy scars which corresponded to replacement fbrosis were found extending from the septum to the anterior wall. These two autopsy cases indicate the clinical heterogeneity of HCM even within the same disease-causing mutation and suggest that the degree and extent of fbrosis determine differences in the clinical manifestations of HCM. This is the frst autopsy report that demonstrates identical sarcomeric gene mutations causing different clinical manifestations and histologic fndings. The fndings suggest that additional genetic or environmental factors infuence the phenotypic expressions and clinical courses of HCM caused by genetic mutation of sarcomeric proteins.
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| 41.
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Matsumura, Masami ; Suzuki, Yasunori ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
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| 42.
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Matsumura, Masami ; Suzuki, Yasunori ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
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| 43.
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Yaegashi, Takanori ; Furusho, Hiroshi ; Chikata, Akio ; Usui, Soichiro ; Kaneko, Shuichi ; Yamagishi, Masakazu ; Takamura, Masayuki
概要:
Introduction. Right ventricular septal pacing is thought to be better than right ventricular apical pacing for shortenin
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g the QRS duration and for preserving left ventricular function. However, right ventricular septal pacing may not be effective in all cases. In this case report, we present a rare case in which right ventricular septal pacing induced thoroughly separated right and left ventricular excitation despite the presence of a relatively narrow QRS wave during atrium-only pacing. Case presentation. We report a case of 63-year-old Japanese man with cardiomyopathy with an implantable cardioverter defibrillator placement for ventricular tachycardia. Three years after implantation, he developed second-degree atrio-ventricular block. Therefore, atrio-ventricular sequential pacing was started; then his heart failure was much worsened. His electrocardiogram showed a dissociated biphasic QRS wave during right ventricular high-septal pacing, despite the presence of a non-fragmented QRS morphology during atrium-only pacing. An activation map during right ventricular high-septal pacing showed that right ventricular conduction started at the pacing site and ended at the right ventricular basal inferior site. Subsequently after a 10ms interval, left ventricular conduction started at the left ventricular posteroseptum and ended at the left ventricular lateral wall. These data indicate that during right ventricular high-septal pacing, the first component of the QRS wave supposedly reflects only right ventricular excitation and the second component only left ventricular excitation. Also due to the intracardiac electrograms, it was assumed that this phenomenon was caused by transversely limited severe transseptal conduction disturbance. Conclusion: It should be noted that even ventricular septal pacing could evoke harmful interventricular dyssynchrony due to transversely limited severe septal conduction disturbance, despite the presence of a relatively narrow QRS wave. © 2014 Yaegashi et al.; licensee BioMed Central Ltd.
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| 44.
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Karashima, Shigehiro ; Yoneda, Takashi ; Kometani, Mitsuhiro ; Ohe, Masashi ; Mori, Shunsuke ; Sawamura, Toshitaka ; Furukawa, Kenji ; Seta, Takashi ; Yamagishi, Masakazu ; Takeda, Yoshiyu
概要:
The mineralocorticoid receptor (MR) is expressed in the kidneys and in adipose tissue, and primary aldosteronism (PA) is
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associated with metabolic syndrome. This study assessed the effects of MR blockade by eplerenone (EPL) and spironolactone (SPL) on blood pressure (BP) and metabolic factors in patients with PA. Fifty-four patients with PA were treated with one of two MRAs, EPL (25-100 mg daily, n=27) or SPL (12.5-100 mg daily, n=27) for 12 months. Visceral (VAT) and subcutaneous adipose tissue were quantified using CT and FatScan imaging analysis software. Body mass index, homeostasis model assessment-insulin resistance (HOMA-IR), serum creatinine, potassium and lipids, urinary albumin excretion (UAE) and plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were measured before and after treatment. EPL and SPL decreased BP and increased serum potassium levels to similar degrees. PAC and PRA did not differ between the two groups. Although treatment with the MRAs did not change HOMA-IR or serum lipids, they significantly decreased UAE and VAT (P<0.05). These results suggest that EPL and SPL are effective and safe for the treatment of PA. The long-term metabolic and renal effects of these MRAs should be further investigated. © 2016 The Japanese Society of Hypertension. All rights reserved.<br />Embargo Period 6 months
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| 45.
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Konno, Tetsuo ; Hayashi, Kenshi ; Fujino, Noboru ; Yamagishi, Masakazu
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| 46.
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Onoe, Tamehito ; Yamada, Kazunori ; Mizushima, Ichiro ; Ito, Kiyoaki ; Kawakami, Takahiro ; Daimon, Shoichiro ; Muramoto, Hiroaki ; Konoshita, Tadashi ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
概要:
Background: Uromodulin kidney disease (UKD) is an inherited kidney disease caused by a uromodulin (UMOD) gene mutation.
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The UMOD gene encodes the Tamm-Horsfall protein (THP), which is the most abundant protein in healthy human urine. Because of its rarity, the incidence of UKD has not been fully elucidated. The purpose of the present study is to clarify the frequency of UKD among patients who underwent renal biopsy. Methods: Immunostaining for THP was performed for patients <50 years of age with renal insufficiency and hyperuricemia without overt urinalysis abnormality from renal biopsy databases. Serum and urinary THP concentrations were evaluated in available individuals. Results: Fifteen patients were selected for immunostaining from a total of 3787 patients. In three independent patients, abnormal THP accumulation in renal tubular cells was observed. A novel missense A247P UMOD mutation was detected in two of the three patients, including one having a typical family history of familial juvenile hyperuricemic nephropathy. Serum and urinary THP concentrations of all available patients withUMODA247P mutationwere significantly lower than those of controls. Conclusions: In the present study, UKDwas detected in <1 in 1000 subjects who underwent renal biopsies. However, in subjects meeting all of the above criteria, abnormal THP accumulation was detected in 20% (3/15), suggesting that renal biopsy with immunostaining for THP is a good tool for diagnosing UKD. Also, lowserum THP concentration detected in the present subjects might be a good diagnostic marker or important in understanding the pathogenesis of UKD. © The Author 2015.<br />Publisher's version/PDF on institutional repository or centrally organised repositories
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| 47.
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Yoshimitsu, Masashi ; Sawada, Takeshi ; Kobayashi, Takeshi ; Yamagishi, Masakazu
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| 48.
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Hiro, Takafumi ; Kimura, Takeshi ; Morimoto, Takeshi ; Miyauchi, Katsumi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Ozaki, Yukio ; Kimura, Kazuo ; Saito, Satoshi ; Yamaguchi, Tetsu ; Daida, Hiroyuki ; Matsuzaki, Masunori ; The JAPAN-ACS Investigators ; 山岸, 正和
概要:
Background: The Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome (JAPAN-ACS) trial has found
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that early aggressive statin therapy in patients with acute coronary syndrome (ACS) significantly reduces the plaque volume (PV) of non-culprit coronary lesions. The purpose of the present study was to evaluate clinical factors that have an impact on plaque regression using statin therapy. Methods and Results: Serial intravascular ultrasound observations over 8-12 months were performed in 252 ACS patients receiving pitavastatin or atorvastatin. Linear regression analysis identified the presence of diabetes mellitus (DM) and PV at baseline as inhibiting factors, and serum remnant-like particle-cholesterol level at baseline as a significant factor significantly affecting the degree of plaque regression. Significant correlation between % change of PV and low-density lipoprotein cholesterol (LDL-C) level was found in patients with DM (n=73, P<0.05, r=0.4), whereas there was no significant correlation between the 2 parameters in patients without DM (n=178). Conclusions: The regression of coronary plaque induced by statin therapy after ACS was weaker in diabetic patients than their counterparts. Moreover, vigorous reduction of the LDL-C levels might induce a greater degree of plaque regression in ACS patients with DM. (Circ J 2010; 74: 1165 - 1174)<br />出版者照会後に全文公開
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| 49.
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Yoshimuta, Tsuyoshi ; Yokoyama, Hiroyuki ; Okajima, Toshiya ; Tanaka, Hiroshi ; Toyoda, Kazunori ; Nagatsuka, Kazuyuki ; Higashi, Masahiro ; Hayashi, Kenshi ; Kawashiri, Masa-aki ; Yasuda, Satoshi ; Yamagishi, Masakazu ; 林, 研至 ; 川尻, 剛照 ; 山岸, 正和
概要:
Background:Plasma d-dimer is known to be a useful clinical marker of thrombogenic status, and d-dimer is used as a diagn
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ostic marker for acute aortic dissection (AAD). Little is known, however, regarding the clinical value of d-dimer for diagnosis of asymptomatic AAD in patients with ischemic stroke. We investigated whether d-dimer could be used for early diagnosis of AAD with isolated neurological symptoms in ischemic stroke patients.Methods and Results:We evaluated a total of 1,236 consecutive patients with symptomatic ischemic stroke without chest or back pain who underwent either head computed tomography or magnetic resonance imaging. d-dimer was measured within 24 h after onset. There were 9 patients with Stanford type A AAD and they had significantly higher d-dimer than the patients without AAD (mean, 46.47±54.48 μg/ml; range, 6.9–167.1 μg/ml vs. 2.33±3.58 μg/ml, 0.3–57.9 μg/ml, P<0.001). When a cut-off of 6.9 μg/ml was adopted for d-dimer on the basis of receiver operating characteristics analysis, the sensitivity and specificity for AAD were 100% and 94.8%, respectively, while the positive and negative predictive values were 14.7% and 100%, respectively.Conclusions:d-dimer might be a useful marker for the early diagnosis of AAD with isolated neurological symptoms in ischemic stroke patients. Whole-body contrast-enhanced computed tomography should be performed in ischemic stroke patients who have high d-dimer. (Circ J 2015; 79: 1841–1845)<br />出版者照会後に全文公開
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| 50.
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Miyauchi, Katsumi ; Daida, Hiroyuki ; Morimoto, Takeshi ; Hiro, Takafumi ; Kimura, Takeshi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Ozaki, Yukio ; Kadota, Kazushige ; Kimura, Kazuo ; Hirayama, Atsushi ; Kimura, Kazumi ; Hasegawa, Yasuhiro ; Uchiyama, Shinichiro ; Matsuzaki, Masunori ; for the JAPAN-ACS Investigators
概要:
Background: The JAPAN-ACS study demonstrated that statins significantly reduced coronary plaque volume in patients with
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acute coronary syndrome (ACS). The clinical implications of plaque regression for clinical outcomes in ACS patients has not been established. The Extended JAPAN-ACS study was conducted to evaluate the relationship between coronary plaque regression and long-term clinical outcome, and to explore the factors associated with cardiovascular events. Methods and Results: Patients with intravascular ultrasound (IVUS) data at both enrollment and follow-up in the JAPAN-ACS study were enrolled and observed for at least 3 years. Patients were divided into lesser and greater coronary plaque regression groups. The primary endpoint was defined as a composite of the following events: cardiovascular death, nonfatal myocardial infarction, nonfatal cerebral infarction, and unstable angina. The median value of the percent change in plaque volume, 18.0%, was used as a cutoff point. There were 4 primary events (3.4%) in the lesser regression group, and 2 events (1.7%) in the greater regression group (P=0.4). Cumulative secondary cardiovascular events did not differ between the 2 groups. Multivariate analysis identified the high-density lipoprotein cholesterol (HDL-C) at baseline and the % change of the external elastic membrane volume as independent risk factors of cardiovascular events. Conclusions: Coronary plaque regression induced by an intensive statin regimen did not predict future cardiovascular events in ACS patients. Rather, the baseline HDL-C level and reverse vessel remodeling might serve as predictors for cardiovascular events. (Circ J 2012; 76: 825-832)<br />出版者照会後に全文公開
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| 51.
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Tada, Hayato ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 山岸, 正和 ; 林, 研至
概要:
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| 52.
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Mizushima, Ichiro ; Yamamot, Motohisa ; Inoue, Dai ; Nishi, Shinichi ; Taniguchi, Yoshinori ; Ubara, Yoshifumi ; Matsui, Shoko ; Yasuno, Tetsuhiko ; Nakashima, Hitoshi ; Takahashi, Hiroki ; Yamada, Kazunori ; Nomura, Hideki ; Yamagishi, Masakazu ; Saito, Takao ; Kawano, Mitsuhiro
概要:
Background: In immunoglobulin G4-related kidney disease (IgG4-RKD), focal or diffuse renal cortical atrophy is often obs
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erved in the clinical course after glucocorticoid therapy. This study aimed to clarify the factors related to renal atrophy after glucocorticoid therapy in IgG4-RKD. Methods: We retrospectively evaluated clinical features including laboratory data and computed tomography (CT) findings before and after glucocorticoid therapy in 23 patients diagnosed with IgG4-RKD, all of whom were followed up for more than 24 months. Results: Seventeen patients were men, and six were women (average age 62.0 years). Average follow-up period was 54.9 months. The average estimated glomerular filtration rate (eGFR) at diagnosis was 81.7 mL/min/1.73 m2. All patients had had multiple low-density lesions on contrast-enhanced CT before glucocorticoid therapy, and showed disappearance or reduction of these lesions after it. Pre-treatment eGFR and serum IgE level in 11 patients in whom renal cortical atrophy developed 24 months after the start of glucocorticoid therapy were significantly different from those in 12 patients in whom no obvious atrophy was found at that time (68.9 ± 30.1 vs 93.5 ± 14.1 mL/min/1.73 m2, P = 0.036, and 587 ± 254 vs 284 ± 263 IU/mL, P = 0.008, respectively). Pre-treatment eGFR and serum IgE level were also significant risk factors for renal atrophy development 24 months after the start of therapy with an odds ratio of 0.520 (per 10 mL/min/1.73 m2, 95% confidence interval (CI) 0.273-0.993, P = 0.048) and 1.090 (per 10 IU/mL, 95% CI: 1.013-1.174, P = 0.022), respectively, in age-adjusted, sex-adjusted, serum IgG4 level-adjusted logistic regression analysis. Receiver operating characteristic curve analysis showed that eGFR of less than 71.0 mL/min/1.73 m2 and serum IgE of more than 436.5 IU/mL were the most appropriate cutoffs and yielded sensitivity of 63.6% and specificity of 100%, and sensitivity of 90.9% and specificity of 75.0%, respectively, in predicting renal atrophy development. Conclusions: This study suggests that pre-treatment renal insufficiency and serum IgE elevation predict renal atrophy development after glucocorticoid therapy in IgG4-RKD. © 2016 The Author(s).
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| 53.
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Oe, Kotaro ; Araki, Tsutomu ; Nakashima, Akikatsu ; Sato, Katsuaki ; Konno, Tetsuo ; Yamagishi, Masakazu
概要:
A 73-year-old man was admitted to our hospital because of bilateral foot pain. He was treated with thrombolysis for cere
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bral infarction about 5 months ago. Anticoagulants had not been used because of hemorrhagic infarction. The pulses of bilateral pedal arteries were palpable, but cyanosis was present in the bilateral toes. Laboratory data indicated azotemia and eosinophilia. Magnetic resonance imaging revealed multiple plaques of the thoracic and abdominal aorta, one of which was ulcerated. Skin biopsy proved the diagnosis of cholesterol crystal embolism (CCE). Because no invasive vascular procedure was performed, we assumed that CCE in this patient was related to thrombolysis. We should be cautious for late onset of CCE after thrombolysis. © 2010 The Japanese Society of Internal Medicine.
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Nozue, Tsuyoshi ; Higashikata, Toshinori ; Inazu, Akihiro ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Kobayashi, Junji ; Koizumi, Junji ; Yamagishi, Masakazu ; Mabuchi, Hiroshi
概要:
Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive sterol storage disease caused by a mutated sterol 27-
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hydroxylase (CYP27A1) gene. We analyzed the CYP27A1 gene in two Japanese CTX patients. The CYP27A1 gene was amplified by PCR and screened by PCR-SSCP. The nucleotide sequence was analyzed to confirm mutations. Case 1 was a compound heterozygote for Arg104Gln in exon 2 and Arg441Gln in exon 8. To our knowledge, this is the first report in which the Arg104Gln mutation is identified in CTX patients. Probably case 2 would be a compound heterozygote for Arg441Trp in exon 8 and a mutation that was not identified. © 2010 The Japanese Society of Internal Medicine.
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| 55.
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Tanaka, Yoshihiro ; Sakata, Kenji ; Waseda, Yohei ; Fujimura, Takashi ; Yamada, Keisuke ; Oyama, Takeru ; Kawashiri, Masa-aki ; Yamagishi, Masakazu
概要:
A 79-year-old man with diabetes and partial gastrectomy visited our hospital due to gradually worsening epigastric pain
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on exertion. Unstable angina was suspected and coronary angiography was performed, which revealed severe stenosis of the left ascending artery. Despite successful intervention, the pain persisted. A careful physical examination finally revealed the point of tenderness on the xiphoid process, and the patient was diagnosed with xiphodynia. The severe epigastric pain resolved immediately after xiphoidectomy. This case demonstrates that symptoms of xiphodynia may mimic those of various types of disorders, such as angina, and that careful palpation is warranted during routine physical examinations. © 2015 The Japanese Society of Internal Medicine.
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| 56.
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Funada, Akira ; Goto, Yoshikazu ; Tada, Hayato ; Teramoto, Ryota ; Shimojima, Masaya ; Hayashi, Kenshi ; Yamagishi, Masakazu ; 舟田 , 晃 ; 後藤, 由和 ; 多田, 隼人 ; 寺本, 了太 ; 下島, 正也 ; 林, 研至 ; 山岸, 正和
概要:
Background:The appropriate duration of prehospital cardiopulmonary resuscitation (CPR)administered by emergency medical
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service (EMS) providers for patients with out-of-hospital cardiac arrest (OHCA) necessary to achieve 1-month survival with favorable neurological outcome (Cerebral Performance Category 1 or 2, CPC 1–2) is unclear and could differ by age. Methods and Results:We analyzed the records of 35,709 adult OHCA patients with return of spontaneous circulation (ROSC) before hospital arrival in a prospectively recorded Japanese registry between 2011 and 2014. The CPR duration was defined as the time from CPR initiation by EMS providers to prehospital ROSC. The rate of 1-month CPC 1–2 was 21.4% (7,650/35,709). The CPR duration was independently and inversely associated with 1-month CPC 1–2 (adjusted odds ratio, 0.93 per 1-min increment; 95% confidence interval, 0.93–0.94). The CPR duration increased with age (P<0.001). However, the CPR duration beyond which the proportion of OHCA patients with 1-month CPC 1–2 decreased to <1% declined with age: 28 min for patients aged 18–64 years, 25 min for 65–74 years, 23 min for 75–84 years, 20 min for 85–94 years, and 18 min for ≥95 years. Conclusions:In patients who achieved prehospital ROSC after OHCA, the duration of CPR administered by EMS providers necessary to achieve 1-month CPC 1–2 varied by age.<br />出版者照会後に全文公開
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| 57.
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Kometani, Mitsuhiro ; Yoneda, Takashi ; Demura, Masashi ; Karashima, Shigehiro ; Mori, Shunsuke ; Oe, Masashi ; Sawamura, Toshitaka ; Okuda, Rika ; Yamagishi, Masakazu ; Takeda, Yoshiyu
概要:
Primary aldosteronism (PA) is a major cause of secondary hypertension, divided into two subtypes: unilateral and bilater
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al. Unilateral PA (u-PA) is surgically-curable. Medical treatment with mineralocorticoid receptors antagonists is recommended as a second-line treatment when the patients are not candidate for surgical treatment. The present case was a 39-year-old woman with u-PA, who had refused surgery, had suffered from adverse effects of medical treatment. She was treated with transcatheter adrenal arterial embolization (TAAE). Her blood pressure had been well controlled without progression of cardiorenovascular damage for 12 years. TAAE can be the third treatment option for u-PA patients. © 2016 The Japanese Society of Internal Medicine.
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| 58.
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Demura, Masashi ; Yoneda, Takashi ; Karashima, Shigehiro ; Higashikata, Toshinori ; Mabuchi, Hiroshi ; Kawano, Mitsuhiro ; Yamagishi, Masakazu ; Takeda, Yoshiyu
概要:
Introduction: The combination of a pituitary prolactinoma and an aldosterone-producing adrenal adenoma is extremely rare. To the best of our knowledge, double endocrine tumors in association with heart-hand syndrome have
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not previously been reported. Case Presentation: A 21-year-old Japanese woman presented with galactorrhea and decreased visual acuity.A large pituitary adenoma with an increased level of serum prolactin was apparent by computed tomography. She additionally showed mild hypertension (136/90mmHg)accompanied by hypokalemia. The plasma aldosterone concentration was increased. Computed tomography showed a mass in the right adrenal gland. No other tumors were found despite extensive imaging studies. Physical and radiographic examinations showed skeletal malformations of the hands and feet, including hypoplasia of the first digit in all four limbs. An atrial septal defect was demonstrated by echocardiography. Similar digital and cardiac abnormalities were detected in our patient's father, and a clinical diagnosis ofhereditary heart-hand syndrome was made. Conclusion: No established heart-hand syndrome was wholly compatible with the family's phenotype. Her father had no obvious endocrine tumors, implying that the parent of transmission determined variable phenotypic expression of the disease: heart-hand syndrome with multiple endocrine tumors from the paternal transmission or no endocrine tumor from the maternal transmission. This suggests that the gene or genes responsible for the disease may be under tissue-specific imprinting control.
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| 59.
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Oe, Kotaro ; Araki, Tsutomu ; Konno, Tetsuo ; Ino, Hidekazu ; Yamagishi, Masakazu
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| 60.
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Sugihara, Masako ; Oka, Rie ; Sakurai, Masaru ; Nakamura, Koshi ; Moriuchi, Tadashi ; Miyamoto, Susumu ; Takeda, Yoshiyu ; Yagi, Kunimasa ; Yamagishi, Masakazu
概要:
Objective Early studies have indicated that body fat shifts from peripheral stores to central stores with aging. The obj
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ective of this study was to investigate age-related changes in abdominal fat distribution of Japanese men and women of the general population over a wide range of body mass indices (BMI). Methods A total of 2,220 non-diabetic, apparently healthy Japanese adults (1,240 men and 980 women; age range 40-69 years) were included in the study sample. All subjects underwent a CT scan at the level of the umbilicus, and the areas of visceral adipose tissue (AT) and subcutaneous AT were quantified. Results When the subjects were stratified by BMI into 18.5-23.0 kg/m2, 23.0-27.5 kg/m2, and 27.5 kg/m2 or higher, visceral AT was positively correlated with age in all of the BMI strata in both genders (p<0.01). In contrast, subcutaneous AT was negatively correlated with age in men with BMIs in excess of 23.0 kg/m2 (p< 0.01) and not at all in women. The mean levels of subcutaneous AT were over 2-fold greater than visceral AT in women aged 60-69 years in any BMI stratum. Conclusion In Japanese men and women, visceral AT was increased with age in all BMI strata in both genders, whereas subcutaneous AT was decreased with age in men with BMIs in excess of 23.0 kg/m2 and not at all in women. Even with these age-related changes in abdominal fat distribution, women retained the subcutaneous-dominant type of fat distribution up to 70 years. © 2011 The Japanese Society of Internal Medicine.
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| 61.
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Narumi, Kenta ; Kondoh, Atsushi ; Udagawa, Takeshi ; Hara, Hidehiko ; Goto, Naoko ; Ikarashi, Yoshinori ; Ohnami, Shumpei ; Okada, Toshihide ; Yamagishi, Masakazu ; Yoshida, Teruhiko ; Aoki, Kazunori
概要:
Type I interferon (IFN) protein is a cytokine with pleiotropic biological functions that include induction of apoptosis,
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inhibition of angiogenesis, and immunomodulation. We have demonstrated that intratumoral injection of an IFN-α-expressing adenovirus effectively induces cell death of cancer cells and elicits a systemic tumor-specific immunity in several animal models. On the other hand, reports demonstrated that an elevation of IFN in the serum following an intramuscular delivery of a vector is able to activate antitumor immunity. In this study, we compared the intratumoral and systemic routes of IFN gene transfer with regard to the effect and safety of the treatment. Intratumoral injection of an IFN-α adenovirus effectively activated tumor-responsive lymphocytes and caused tumor suppression not only in the gene-transduced tumors but also in distant tumors, which was more effective than the intravenous administration of the same vector. The expression of co-stimulatory molecules on CD11c+ cells isolated from regional lymph nodes was enhanced by IFN gene transfer into the tumors. Systemic toxicity such as an elevation of hepatic enzymes was much lower in mice treated by intratumoral gene transfer than in those treated by systemic gene transfer. Our data suggest that the intratumoral route of the IFN vector is superior to intravenous administration, due to the effective induction of antitumor immunity and the lower toxicity. © 2010 Japanese Cancer Association.
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| 62.
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Sakamoto, Aiji ; Kawashiri, Masaaki ; Ishibashi-Ueda, Hatsue ; Sugamoto, Yuka ; Yoshimuta, Tsuyoshi ; Higashikata, Takeo ; Ogino, Hitoshi ; Tada, Hayato ; Konno, Tetsuo ; Hayashi, Kenshi ; Yamagishi, Masakazu
概要:
We examined the expression of ephrin-B1 and its cognate receptor EphB2, key regulators of angiogenesis and embryogenesis
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, in human abdominal aortic aneurysm (AAA) and analyzed their functional roles in cell migration. From 10 patients (9 males and 1 female; age, 68.5 ± 2.4) who underwent vascular surgery for AAA, we obtained AAA and adjacent control tissues. Using real-time RT-PCR, we analyzed expression of ephrin-B1 and EphB2. We also histologically localized these molecules in AAA tissues. Finally, effects of ephrin-B1 and EphB2 on inflammatory cell chemotaxis were examined by cell migration assay. Expression levels of ephrin-B1 (0.410 ± 0.046 versus 1.198 ± 0.252, P = 0.027) and EphB2 (0.764 ± 0.212 versus 1.272 ± 0.137, P = 0.594) were higher in AAA than normal control. Both ephrin-B1 and EphB2 were expressed in macrophages, T lymphocytes, and endothelial cells within AAA. In chemotaxis assay, ephrin-B1 and EphB2 inhibited mononuclear-cell chemotaxis induced by stromal derived factor-1 down to 54.7 ± 12.7 (P = 0.01) and 50.7 ± 13.1 (P = 0.01), respectively. These data suggest that ephrin-B1 and EphB2 might be functional in human adult inflammatory cells and involved in the pathogenesis of AAA, although specific roles of these molecules should further be sought. © 2012 Aiji Sakamoto et al.
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| 63.
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Shimojima, Masaya ; Kawashiri, Masa-aki ; Nitta, Yutaka ; Yoshida, Taiji ; Katsuda, Shouji ; Kaku, Bunji ; Taguchi, Tomio ; Hasegawa, Akira ; Konno, Tetsuo ; Hayashi, Kenshi ; Yamagishi, Masakazu
概要:
Although intensive lipid lowering by statins can enhance plaque stability, few data exist regarding how early statins ch
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ange plaque composition and morphology in clinical setting. Therefore, to examine early changes in plaque composition and morphology by intensive lipid lowering with statins, we evaluate coronary plaques from acute coronary syndrome (ACS) before and 3 weeks after lipid lowering by coronary CT angiography. We enrolled 110 patients with suspected ACS and underwent coronary CT. We defined plaque as unstable when CT number of plaque< 50HU and remodeling index (lesion diameter/reference diameter) >1.10. Rosuvastatin (5 mg/day) or atorvastatin (20 mg/day) were introduced to reduce low density lipoprotein cholesterol (LDL-C). Then, CT was again performed by the same condition 3 weeks after lipid lowering therapy. Total 10 patients (8 men, mean age 72.0 years), in whom informed consent regarding serial CT examination was obtained, were analyzed. Among them, 4 patients who denied to have intensive lipid lowering were served as controls. In remaining 6 patients, LDL-C reduced from 129.5±26.9 mg/dl to 68.5±11.1 mg/dl after statin treatment. Under these conditions, CT number of the targeted plaque significantly increased from 16.0±15.9 to 50.8±35.0 HU (p<0.05) and remodeling index decreased from 1.22±0.11 to 1.11±0.06 (p<0.05), although these values substantially unchanged in controls. These results demonstrate that MDCT-determined plaque composition as well as volume could be changed within 3 weeks after intensive lipid lowering. This may explain acute effects of statins in treatment of acute coronary syndrome.
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| 64.
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Daida, Hiroyuki ; Takayama, Tadateru ; Hiro, Takafumi ; Yamagishi, Masakazu ; Hirayama, Atsushi ; Saito, Satoshi ; Yamaguchi, Tetsu
概要:
Background: The incidence of cardiac events is higher in patients with diabetes than in people without diabetes. The Cor
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onary Atherosclerosis Study Measuring Effects of Rosuvastatin Using Intravascular Ultrasound in Japanese Subjects (COSMOS) demonstrated significant plaque regression in Japanese patients with chronic coronary disease after 76 weeks of rosuvastatin (2.5 mg once daily, up-titrated to a maximum of 20 mg/day to achieve LDL cholesterol <80 mg/dl).Methods: In this subanalysis of COSMOS, we examined the association between HbA1c and plaque regression in 40 patients with HbA1c ≥6.5% (high group) and 86 patients with HbA1c <6.5% (low group).Results: In multivariate analyses, HbA1c and plaque volume at baseline were major determinants of plaque regression. LDL cholesterol decreased by 37% and 39% in the high and low groups, respectively, while HDL cholesterol increased by 16% and 22%, respectively. The reduction in plaque volume was significantly (p = 0.04) greater in the low group (from 71.0 ± 39.9 to 64.7 ± 34.7 mm3) than in the high group (from 74.3 ± 34.2 to 71.4 ± 32.3 mm3). Vessel volume increased in the high group but not in the low group (change from baseline: +4.2% vs -0.8%, p = 0.02). Change in plaque volume was significantly correlated with baseline HbA1c.Conclusions: Despite similar improvements in lipid levels, plaque regression was less pronounced in patients with high HbA1c levels compared with those with low levels. Tight glucose control during statin therapy may enhance plaque regression in patients with stable coronary disease.Trial registration: ClinicalTrials.gov, Identifier NCT00329160. © 2012 Daida et al.; licensee BioMed Central Ltd.
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| 65.
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Tada, Hayato ; Kobayashi, Junji ; Kawashiri, Masa-aki ; Miyashita, Kazuya ; Nohara, Atsushi ; Inazu, Akihiro ; Nakajima, Katsuyuki ; Mabuchi, Hiroshi ; Yamagishi, Masakazu
概要:
Background: This study was performed to compare the effects of three different lipid-lowering therapies (statins, ezetim
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ibe, and colestimide) on lipoprotein lipase and endothelial lipase masses in pre-heparin plasma (pre-heparin LPL and EL mass, respectively) from patients with familial hypercholesterolemia (FH). FH is usually treated by coadministration of these three drugs. Methods: The pre-heparin LPL and EL masses were measured in fresh frozen plasma drawn and stored at various time points during coadministration of the three drugs from patients with heterozygous FH harboring a single mutation in the LDL receptor (n = 16, mean age 63 years). The patients were randomly divided into two groups based on the timing when ezetimibe was added. Results: Plasma LPL mass concentration was significantly reduced by rosuvastatin at 20 mg/day (median = 87.4 [IQR: 71.4-124.7] to 67.5 [IQR: 62.1-114.3] ng/ml, P < 0.05). In contrast, ezetimibe at 10 mg/day as well as colestimide at 3.62 g/day did not alter its level substantially (median = 67.5 [IQR: 62.1-114.3] to 70.2 [IQR: 58.3-106.2], and to 74.9 [IQR: 55.6-101.3] ng/ml, respectively) in the group starting with rosuvastatin followed by the addition of ezetimibe and colestimide. On the other hand, the magnitude in LPL mass reduction was lower in the group starting with ezetimibe at 10 mg/day before reaching the maximum dose of 20 mg/day of rosuvastatin. Plasma EL mass concentration was significantly increased by rosuvastatin at 20 mg/day (median = 278.8 [IQR: 186.7-288.7] to 297.0 [IQR: 266.2-300.2] ng/ml, P < 0.05), whereas other drugs did not significantly alter its level. Conclusion: The effects on changes of LPL and EL mass differed depending on the lipid-lowering therapy, which may impact the prevention of atherosclerosis differently. © 2016 Tada et al.
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| 66.
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Mori, Kiyoo ; Yamada, Kazunori ; Konno, Tetsuo ; Inoue, Dai ; Uno, Yoshihide ; Watanabe, Michio ; Okuda, Miho ; Oe, Kotaro ; Kawano, Mitsuhiro ; Yamagishi, Masakazu
概要:
We herein report the case of a 65-year-old man with pericardial involvement associated with autoimmune pancreatitis. Che
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st CT imaging showed pericardial thickening. The patient responded to corticosteroid therapy, and the pericardial thickening resolved. Multiple organs are involved in immunoglobulin G4 (IgG4)- related disease (IgG4-RD); however, only a few cases of IgG4-related chronic constrictive pericarditis have been reported. To our knowledge, this is the first reported case of IgG4-RD with pericardial involvement at an early stage. This case indicates that recognizing pericardial complications in autoimmune pancreatitis is important and that CT imaging may be useful for obtaining the diagnosis and providing follow-up of pericardial lesions in cases of IgG4-RD. © 2015 The Japanese Society of Internal Medicine.
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| 67.
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Yamaaki, Naoto ; Yagi, Kunimasa ; Kobayashi, Junji ; Nohara, Atsushi ; Ito, Naoko ; Asano, Akimichi ; Nakano, Kaoru ; Liu, Jianhui ; Okamoto, Takuya ; Mori, Yukiko ; Ohbatake, Azusa ; Okazaki, Satoko ; Takeda, Yoshiyu ; Yamagishi, Masakazu
概要:
Background. Although retinol-binding protein 4 (RBP4) associates with insulin resistance and remnant-like particles trig
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lyceride (RLP-TG) elevated in the insulin resistant state, few data exist regarding the relationship between RBP4 and RLP-TG. Subjects and Methods. The study included 92 Japanese type 2 diabetic mellitus (T2DM) male patients (age 60.5 ± 13.6 years, body mass index (BMI) 24.7 ± 4.1 kg/m2, waist circumference (WC) 88.4 ± 10.7 cm, and HbA1c (NGSP) 7.2 ± 1.9 %). Patients on medications affecting insulin sensitivity, including fibrates, biguanides, and thiazolidinedione, were excluded. Visceral fat area (VFA) and subcutaneous fat area (SFA) were measured by computed tomography. Results. RBP4 levels showed a significant positive correlation with RLP-TG (r = 0.2544 and P = 0.0056), TG (r = 0.1852 and P = 0.041), RLP-TG/TG (r = 0.23765 and P = 0.0241), and age (r = - 0.2082 and P = 0.0219), although there was no significant correlation with VFA, SFA, adiponectin levels, or homeostasis model of assessment insulin resistance (HOMA-R). Multiple regression analysis revealed that RBP4 was an independent determinant of RLP-TG (P = 0.0193) but was not a determinant of TG. Conclusions. RBP4 correlates positively with serum RLP-TG independent of fat accumulation in T2DM. RBP4 may regulate remnant metabolism independent of glycemic control in T2DM. © 2013 Naoto Yamaaki et al.
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| 68.
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Fukushima, Yoshifumi ; Daida, Hiroyuki ; Morimoto, Takeshi ; Kasai, Takatoshi ; Miyauchi, Katsumi ; Yamagishi, Sho-ichi ; Takeuchi, Masayoshi ; Hiro, Takafumi ; Kimura, Takeshi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Ozaki, Yukio ; Matsuzaki, Masunori
概要:
Background: The Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome (JAPAN-ACS) trial demonstra
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ted that early aggressive statin therapy in patients with ACS significantly reduces plaque volume (PV). Advanced glycation end products (AGEs) and the receptors of AGEs (RAGE) may lead to angiopathy in diabetes mellitus (DM) and may affect on the development of coronary PV. The present sub-study of JAPAN-ACS investigates the association between AGEs and RAGE, and PV.Methods: Intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) was undertaken, followed by the initiation of statin treatment (either 4 mg/day of pitavastatin or 20 mg/day of atorvastatin), in patients with ACS. In the 208 JAPAN-ACS subjects, PV using IVUS in non-culprit segment > 5 mm proximal or distal to the culprit lesion and, serum levels of AGEs and soluble RAGE (sRAGE) were measured at baseline and 8-12 months after PCI.Results: At baseline, no differences in the levels of either AGEs or sRAGE were found between patients with DM and those without DM. The levels of AGEs decreased significantly with statin therapy from 8.6 ± 2.2 to 8.0 ± 2.1 U/ml (p < 0.001), whereas the levels of sRAGE did not change. There were no significant correlations between changes in PV and the changes in levels of AGEs as well as sRAGE. However, high baseline AGEs levels were significantly associated with plaque progression (odds ratio, 1.21; 95% confidence interval, 1.01 - 1.48; p = 0.044) even after adjusting for DM in multivariate logistic regression models.Conclusions: High baseline AGEs levels were associated with plaque progression in the JAPAN-ACS trial. This relationship was independent of DM. These findings suggest AGEs may be related to long-term glucose control and other oxidative stresses in ACS.Trial registration: NCT00242944. © 2013 Fukushima et al.; licensee BioMed Central Ltd.
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| 69.
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Onoe, Tamehito ; Konoshita, Tadashi ; Tsuneyama, Koichi ; Hamano, Ryoko ; Mizushima, Ichiro ; Kakuchi, Yasushi ; Yamada, Kazunori ; Hayashi, Kenshi ; Kuroda, Masahiro ; Kagitani, Satoshi ; Nomura, Hideki ; Yamagishi, Masakazu ; Kawano, Mitsuhiro
概要:
Background: Situs inversus is a rare complication of cystic kidney diseases. Only three genes, INVS (NPHP2), NPHP3 and PKD2 have been proved to be responsible for some cases, while the responsible genes in many others are still
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unknown. Case Reports: Here we report two male patients with situs inversus combined with cystic kidney disease without any family history of polycystic kidney disease. Their renal function was normal in childhood but culminated in end stage renal disease in middle age. No pathogenic mutations were found in mutation analysis of INVS, IFT88, PKD2, UMOD or NPHP3 in them. Conclusions: Past reported cases of situs inversus and cystic kidney diseases were divided into three groups, i.e., gestational lethal renal dysplasia group, infantile or juvenile nephronophthisis group and polycystic kidney disease group. The present patients are different from each of these groups. Moreover, the renal lesions of the present two cases are quite different from each other, with one showing mildly atrophic kidneys with small numbers of cysts and the other an enlarged polycystic kidney disease, suggesting very heterogeneous entities.
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| 70.
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Chujo, Daisuke ; Foucat, Emile ; Takita, Morihito ; Itoh, Takeshi ; Sugimoto, Koji ; Shimoda, Masayuki ; Yagi, Kunimasa ; Yamagishi, Masakazu ; Tamura, Yoshiko ; Yu, Liping ; Naziruddin, Bashoo ; Levy, Marlon F. ; Ueno, Hideki ; Matsumoto, Shinichi
概要:
Islet transplantation is one of the most promising therapies for type 1 diabetes (T1D). A major issue in islet transplan
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tation is the loss of graft function at late phase. Several studies suggested the involvement of islet-specific T-cells in such islet graft dysfunction. In this study, we investigated the breadth and type of glutamic acid decarboxylase 65 (GAD65)-specific T-cells in T1D patients after allogeneic islet transplantation. Peripheral blood mononuclear cells (PBMCs) were obtained from islet-transplanted T1D patients during insulin-independent period and cultured for 7 days with pools of GAD65 overlapping peptides in the presence of IL-2. Cytokine secretion profiles of peptide-reactive T-cells were analyzed after a short-term restimulation with the same peptides by a multiplex bead-based cytokine assay and by an intracytoplasmic cytokine detection assay. Robust GAD65-specific CD4(+) and CD8(+) T-cell responses were detected in patients who eventually developed chronic graft dysfunction. Multiple GAD65 peptides were found to induce specific T-cell responses in these patients, indicating that the repertoire of GAD65-specific T-cells was broad. Furthermore, GAD65-specific CD4(+) T-cells were composed of heterogeneous populations, which differentially expressed cytokines including IFN-γ and type 2 cytokines, but not IL-10. In contrast, patients who showed only marginal GAD65-specific T-cell responses maintained substantially longer graft survival and insulin independence. In conclusion, our study suggests that the emergence of islet-specific T-cells precedes the development of chronic graft dysfunction in islet-transplanted patients. Thus, our observations support the hypothesis that these islet-specific T-cells contribute to the development of chronic islet graft dysfunction.
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| 71.
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Ma, Wen-Jie ; Hashii, Minako ; Munesue, Toshio ; Hayashi, Kenshi ; Yagi, Kunimasa ; Yamagishi, Masakazu
概要:
Background: The human oxytocin receptor (hOXTR) is implicated in the etiology of autism spectrum disorders (ASDs) and is
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a potential target for therapeutic intervention. Several studies have reported single-nucleotide polymorphisms (SNPs) of the OXTR gene associated with ASDs. These SNPs, however, reside outside the protein-coding region. Not much is known about genetic variations that cause amino acid substitutions that alter receptor functions. Methods. Variations in the OXTR gene were analyzed in 132 ASD patients at Kanazawa University Hospital in Japan and 248 unrelated healthy Japanese volunteers by re-sequencing and real-time polymerase chain reaction-based genotyping. Functional changes in variant OXTRs were assessed by radioligand binding assay and measurements of intracellular free calcium concentrations ([Ca§ssup§2+§esup§]§ssub§i§esub§) and inositol 1,4,5-trisphosphate (IP§ssub§3§esub§) levels. Results: Six subjects (4.5%) in the ASD group and two in the control group (0.8%) were identified as heterozygotes carrying the R376G variation (rs35062132; c.1126C>G); one individual from the ASD group (0.8%) and three members of the control group (1.2%) were found to be carrying R376C (c.1126C>T). The C/G genotype significantly correlated with an increased risk of ASDs (odds ratio (OR) = 5.83; 95% confidence interval (CI) = 1.16 to 29.33; P = 0.024, Fisher's exact test). Consistently, the G allele showed a correlation with an increased likelihood of ASDs (OR = 5.73; 95% CI = 1.15 to 28.61; P = 0.024, Fisher's exact test). The frequencies of the C/T genotype and the T allele in the ASD and control groups did not differ significantly. We also examined changes in agonist-induced cellular responses mediated by the variant receptors hOXTR-376G and hOXTR-376C. OXT-induced receptor internalization and recycling were faster in hOXTR-376G-expressing HEK-293 cells than in cells expressing hOXTR-376R or hOXTR-376C. In addition, the elevation in [Ca§ssup§2+§esup§]§ssub§i§esub§ and IP§ssub§3§esub§ formation decreased in the cells expressing hOXTR-376G and hOXTR-376C tagged with enhanced green fluorescent protein (EGFP), in comparison with the cells expressing the common-type hOXTR-376R tagged with EGFP. Conclusions: These results suggest that the rare genetic variation rs35062132 might contribute to the pathogenesis of ASDs, and could provide a molecular basis of individual differences in OXTR-mediated modulation of social behavior. © 2013 Ma et al.; licensee BioMed Central Ltd.
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| 72.
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Shimojima, Masaya ; Yuasa, Shinsuke ; Motoda, Chikaaki ; Yozu, Gakuto ; Nagai, Toshihiro ; Ito, Shogo ; Lachmann, Mark ; Kashimura, Shin ; Takei, Makoto ; Kusumoto, Dai ; Kunitomi, Akira ; Hayashiji, Nozomi ; Seki, Tomohisa ; Tohyama, Shugo ; Hashimoto, Hisayuki ; Kodaira, Masaki ; Egashira, Toru ; Hayashi, Kenshi ; Nakanishi, Chiaki ; Sakata, Kenji ; Yamagishi, Masakazu ; Fukuda, Keiichi
概要:
Alteration of the nuclear Ca2+ transient is an early event in cardiac remodeling. Regulation of the nuclear Ca2+ transie
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nt is partly independent of the cytosolic Ca2+ transient in cardiomyocytes. One nuclear membrane protein, emerin, is encoded by EMD, and an EMD mutation causes Emery-Dreifuss muscular dystrophy (EDMD). It remains unclear whether emerin is involved in nuclear Ca2+ homeostasis. The aim of this study is to elucidate the role of emerin in rat cardiomyocytes by means of hypertrophic stimuli and in EDMD induced pluripotent stem (iPS) cell-derived cardiomyocytes in terms of nuclear structure and the Ca2+ transient. The cardiac hypertrophic stimuli increased the nuclear area, decreased nuclear invagination, and increased the half-decay time of the nuclear Ca2+ transient in cardiomyocytes. Emd knockdown cardiomyocytes showed similar properties after hypertrophic stimuli. The EDMD-iPS cell-derived cardiomyocytes showed increased nuclear area, decreased nuclear invagination, and increased half-decay time of the nuclear Ca2+ transient. An autopsied heart from a patient with EDMD also showed increased nuclear area and decreased nuclear invagination. These data suggest that Emerin plays a crucial role in nuclear structure and in the nuclear Ca2+ transient. Thus, emerin and the nuclear Ca2+ transient are possible therapeutic targets in heart failure and EDMD. © The Author(s) 2017.
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| 73.
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Oe, Kotaro ; Araki, Tsutomu ; Hayashi, Kenshi ; Yamagishi, Masakazu
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| 74.
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Naito, Ryo ; Miyauchi, Katsumi ; Daida, Hiroyuki ; Morimoto, Takeshi ; Hiro, Takafumi ; Kimura, Takeshi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Ozaki, Yukio ; Matsuzaki, Masunori ; for the aJAPAN-ACS Investigators ; 山岸, 正和
概要:
Aim: Diabetic patients with coronary artery disease have a high incidence of cardiovascular events, which was associated
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with increased coronary plaque volume. Low-density lipoprotein cholesterol (LDL-C) and blood pressure (BP) play pivotal roles in the progression of coronary plaque. Several trials have shown that intervention for a single risk factor reduced the development of coronary plaque progression. However, it remained uncertain whether total risk management for LDL-C, BP, and glycosylated Hb (HbA1c) has a beneficial effect on coronary plaque volume in diabetic patients. Methods: This study was a sub-study of the JAPAN-ACS that was a prospective, randomized, open-label trial that evaluated the impact of intensive lipid-lowering therapy on coronary plaque volume in patients with acute coronary syndrome (ACS). Among a total of 252 patients, 73 diabetic patients were analyzed. We examined the impact of total risk management (LDL-C ＜80 mg/dL, systolic BP ＜130 mmHg, and HbA1c ＜6.5%) on changes in coronary plaque volume. The patients were divided into four groups according to the number of risk factors that achieved the target value. Results: Baseline characteristics were similar among the groups. The degree of coronary plaque regression was greater in patients who achieved total risk management. The number of risk factors that achieved the target level was associated with the extent of the coronary plaque volume reduction in a dose-dependent manner. Conclusion: Total risk management that focused on LDL-C, BP, and HbA1c had a beneficial impact on the coronary plaque regression in diabetic patients with ACS.<br />出版者照会後に全文公開
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| 75.
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Arai, Hidenori ; Hiro, Takafumi ; Kimura, Takeshi ; Morimoto, Takeshi ; Miyauchi, Katsumi ; Nakagawa, Yoshihisa ; Yamagishi, Masakazu ; Ozaki, Yukio ; Kimura, Kazuo ; Saito, Satoshi ; Yamaguchi, Tetsu ; Daida, Hiroyuki ; Matsuzaki, Masunori ; 山岸, 正和
概要:
Aim: We have shown that aggressive lipid lowering by pitavastatin and atorvastatin results in marked regression of ather
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osclerotic coronary lesions after acute coronary syndrome (ACS). The purpose of this study was to address the association of lipid levels after statin therapy with regression of atherosclerotic coronary lesions and major cardiovascular events in patients after ACS. Methods: JAPAN-ACS is a prospective, randomized open-label study performed at 33 centers in Japan. Patients with ACS undergoing intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) were randomly assigned to receive either 4 mg/day pitavastatin or 20 mg/day atorvastatin within 72 hours after PCI. IVUS image was obtained in 251 patients, including 73 diabetic patients. Lipid profiles at the end of the study were divided into quartiles and the association with the percent change in non-culprit coronary plaque volume (PV) was assessed in total and diabetic patients. We also studied whether baseline and follow-up levels of HDL-cholesterol are associated with restenosis after PCI. Results: Decreasing LDL-cholesterol, non-HDL-cholesterol, LDL-C/HDL-C ratio, apolipoprotein B quartiles were associated with a progressively smaller plaque burden in total and diabetic patients. In diabetic patients, further reduction of these parameters was associated with a significantly greater reduction in PV. We also found that patients with lower HDL-cholesterol had a significantly higher incidence of target lesion revascularization. Conclusions: Early intensive statin therapy in patients after ACS results in remarkable regression of coronary PV. Diabetic patients can have a benefit with more intensive therapy to achieve a lower target level in Japanese.<br />出版者照会後に全文公開
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| 76.
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Heart Care Network Groups. ; Yamagishi, Masakazu ; 山岸, 正和
概要:
Aims: In Japan, it is believed that guidelines for lifestyle-related disease are used in routine clinical practice, howe
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ver, there are few reports on the actual rate of healthcare conducted in accordance with these guidelines by general practitioners and on their usefulness in preventing cardiovascular events. Therefore, the Heart Care Network (HCN) groups were organized mainly by general practitioners treating lifestyle diseases in 62 areas of Japan. Methods: The HCN has collected data on lifestyle diseases in high-risk patients in routine practices and investigated management conditions, guideline target achievement rates and medication. Additionally, the incidence of cardiovascular events was assessed. Results: We analyzed 14,064 cases. The lipid profile, blood pressure, glycemic control were significantly improved over the 3 years. The incidence of cardiovascular events were significantly reduced by the achievement of target LDL cholesterol, systolic blood pressure and hemoglobin A1c and even after adjustment for age, gender, history of myocardial infarction, the reduction of these lifestylerelated parameters remains significant. Conclusion: These results revealed the current trends in the healthcare activities of general practitioners, the management conditions for lifestyle diseases in CHD high-risk patients and their effects on reducing cardiovascular events.<br />出版者照会後に全文公開
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| 77.
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Tada, Hayato ; Kawashiri, Masa-aki ; Yoshida, Taiji ; Teramoto, Ryota ; Nohara, Atsushi ; Konno, Tetsuo ; Inazu, Akihiro ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 寺本, 了太 ; 野原, 淳 ; 稲津, 明広 ; 馬渕, 宏 ; 山岸, 正和 ; 林, 研至
概要:
Background:It has been shown that serum lipoprotein(a) [Lp(a)] is elevated in familial hypercholesterolemia (FH) with mu
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tation(s) of the LDL receptor (LDLR) gene. However, few data exist regarding Lp(a) levels in FH with gain-of-function mutations of the PCSK9 gene.Methods and Results:We evaluated 42 mutation-determined heterozygous FH patients with aPCSK9gain-of-function mutation (FH-PCSK9, mean age 52, mean LDL-C 235 mg/dl), 198 mutation-determined heterozygous FH patients with aLDLRmutation (FH-LDLR, mean age 44, mean LDL-C 217 mg/dl), and 4,015 controls (CONTROL, mean age 56, mean LDL-C 109 mg/dl). We assessed their Lp(a), total cholesterol, triglycerides, HDL-C, LDL-C, use of statins, presence of hypertension, diabetes, chronic kidney disease, smoking, body mass index (BMI) and coronary artery disease (CAD). Multiple regression analysis showed that HDL-C, use of statins, presence of hypertension, smoking, BMI, and Lp(a) were independently associated with the presence of CAD. Under these conditions, the serum levels of Lp(a) in patients with FH were significantly higher than those of the CONTROL group regardless of their causative genes, among the groups propensity score-matched (median Lp(a) 12.6 mg/dl [IQR:9.4–33.9], 21.1 mg/dl [IQR:11.7–34.9], and 5.0 mg/dl [IQR:2.7–8.1] in the FH-LDLR, FH-PCSK9, and CONTROL groups, respectively, P=0.002 for FH-LDLR vs. CONTROL, P=0.002 for FH-PCSK9 vs. CONTROL).Conclusions:These data demonstrate that serum Lp(a) is elevated in patients with FH caused by PCSK9 gain-of-function mutations to the same level as that in FH caused by LDLR mutations. (Circ J 2016; 80: 512–518)<br />出版者照会後に全文公開
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| 78.
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Kawashiri, Masa-aki ; Tada, Hayato ; Yamagishi, Masakazu ; 川尻, 剛照 ; 多田, 隼人 ; 山岸, 正和
概要:
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| 79.
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Tada, Hayato ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; 多田, 隼人 ; 川尻, 剛照 ; 山岸, 正和
概要:
We have learned that low-density lipoprotein (LDL) cholesterol is the cause of atherosclerosis from various aspects, inc
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luding a single case with familial hypercholesterolemia, other cases with different types of Mendelian dyslipidemias, large-scale randomized controlled trials using LDL cholesterol lowering therapies, and Mendelian randomization studies using common as well as rare variants associated with LDL cholesterol levels. There is no doubt that determinations of genotypes in lipid-associated genes have contributed not only to the genetic diagnosis for Mendelian dyslipidemias but also to the discoveries of novel therapeutic targets. Furthermore, recent studies have shown that such genetic information could provide useful clues for the risk prediction as well as risk stratification in general and in particular population. We provide the current understanding of genetic analyses relating to plasma lipids and coronary artery disease.<br />出版者照会後に全文公開
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| 80.
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Tada, Hayato ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Yasuda, Kenji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 小林, 淳二 ; 馬渕, 宏 ; 山岸, 正和 ; 林, 研至
概要:
Aim: The Japan Atherosclerosis Society (JAS) guidelines for the prevention of atherosclerotic diseases 2012 (JAS2012) pr
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oposed lipid management targets; however, less data is available regarding the attainment rates of each target in community-based settings. Therefore, we assessed the attainment rates of lipid management targets among subjects who underwent Japanese specific health checkups. Methods: A total of 85,716 subjects (male=29,282, 34.2%) aged 40–74 years who underwent specific health checkups from 2012 to 2014 in Kanazawa city, Japan, were included in this study. We evaluated the attainment rates of the lipid management targets according to the JAS2012 guideline and investigated the clinical characteristics of the subjects without achieving the targets. Results: The target for LDL cholesterol (LDL-C) was the least attained in all risk categories, 89, 72, 50, and 34% for category I, II, III, and secondary prevention, respectively, in 2014. In addition, these rates inversely correlated with the grade of risk categories (p-value for trends ＜0.001). Attainment rate of the LDL-C target in the suspected chronic kidney disease (CKD) group was significantly lower than in the groups with diabetes, stroke, or absolute risk in category III (49.2, 60.3, 63.5, 54.4%, respectively, p-value ＜0.001 for each). Moreover, the attainment rate of the LDL-C target was significantly lower in subjects that did not receive lipid-lowering therapy than in those who received it in the secondary prevention (27.7 and 40.6%, respectively, p-value ＜0.001). Conclusions: Lipid management is inadequate in community-based settings, particularly, in subjects with CKD and secondary prevention.<br />出版者照会後に全文公開
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| 81.
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Oka, Rie ; Yagi, Kunimasa ; Sakurai, Masaru ; Nakamura, Koshi ; Nagasawa, Shin-ya ; Miyamoto, Susumu ; Nohara, Atsushi ; Kawashiri, Masa-aki ; Hayashi, Kenshi ; Takeda, Yoshiyu ; Yamagishi, Masakazu ; 八木, 邦公 ; 櫻井, 勝 ; 中村, 幸志 ; 野原, 淳 ; 川尻, 剛照 ; 林, 研至 ; 武田, 仁勇 ; 山岸, 正和
概要:
Aim: The enlargement of visceral adipose tissue (VAT) is considered to mediate the close relationship between obesity an
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d insulin resistance. We aimed to determine whether a stronger association of VAT compared to subcutaneous adipose tissue (SAT) with insulin resistance could be confirmed and generalized in non-diabetic Japanese men and women. Methods: Participants were 912 non-diabetic Japanese (636 men and 276 women, mean age 52.4±7.0 years, and mean BMI 24.9±3.1 kg/m2). VAT and SAT were measured through the use of computed tomography scanning. Homeostatic model for the assessment of insulin resistance (HOMA-IR) and Matsuda insulin sensitivity index (ISI) were calculated based on results from the oral glucose tolerance test. Results: For both genders, subjects in higher tertiles of SAT as well as VAT showed significantly higher levels of HOMA-IR and lower levels of Matsuda ISI (p<0.001). In multiple regression analyses with VAT and SAT included in the model, only VAT, but not SAT, was independently associated with Matsuda ISI in women (p<0.001), whereas both SAT and VAT were independently associated with HOMA-IR and with Matsuda ISI in men (p<0.001). When VAT and waist circumference were jointly included in the model, only VAT, but not waist circumference, was independently associated with Matsuda ISI in women (p<0.001) but not in men. Conclusion: VAT had a stronger association with insulin resistance than SAT or waist circumference in women but not in men. BMI showed a comparable association with insulin resistance to VAT in this population.<br />出版者照会後に全文公開
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| 82.
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Tada, Hayato ; Kawashiri, Masa-aki ; Okada, Hirofumi ; Endo, Saori ; Toyoshima, Yuka ; Konno, Tetsuo ; Nohara, Atsushi ; Inazu, Akihiro ; Takao, Akira ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 今野, 哲雄 ; 野原, 淳 ; 稲津, 明広 ; 馬渕, 宏 ; 山岸, 正和 ; 林, 研至
概要:
Whole exome sequencing (WES) technologies have accelerated genetic studies of Mendelian disorders, yielding approximatel
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y 30% diagnostic success. We encountered a 13-year-old Japanese female initially diagnosed with familial hypercholesterolemia on the basis of clinical manifestations of severe hypercholesterolemia (initial LDL cholesterol=609 mg/dl at the age of one) and systemic intertriginous xanthomas with histories of recurrent self-limiting episodes of fever and arthritis. Both her phenotypes seemed to co-segregate in a recessive manner. We performed WES on this patient, who was considered a proband. Among 206,430 variants found in this individual, we found 18,220 nonsense, missense, or splice site variants, of which 3,087 were rare (minor allele frequency ≤ 0.01 or not reported) in 1000 Genome (Asian population). Filtering by assuming a recessive pattern of inheritance with the use of an in silico annotation prediction tool, we successfully narrowed down the candidates to the compound heterozygous mutations in the ABCG5 gene (c.1256G＞A or p.Arg419His/c.1763-1G＞A [splice acceptor site]) and to the double-compound heterozygous mutations in the MEFV gene (c.329T＞C/C or p.Leu110Pro/c.442G＞C/C or p.Glu148Val). The patient was genetically diagnosed with sitosterolemia and familial Mediterranean fever using WES for the first time. Such a comprehensive approach is useful for identifying causative mutations for multiple unrelated inheritable diseases.<br />出版者照会後に全文公開
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| 83.
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Teramoto, Ryota ; Sakata, Kenji ; Miwa, Kenji ; Matsubara, Takao ; Yasuda, Toshihiko ; Inoue, Masaru ; Okada, Hirofumi ; Kanaya, Honin ; Kawashiri, Masa-aki ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 寺本, 了太 ; 坂田, 憲治 ; 川尻, 剛照 ; 山岸, 正和 ; 林, 研至
概要:
Aim: Although distal embolization during percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI)
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deteriorates cardiac function, whether distal protection (DP) can improve prognosis is still controversial. We investigated whether a filter-type DP device, Filtrap®, could improve long-term outcomes after PCI for AMI. Method: We studied 164 patients (130 men, mean age: 65.7 years) who underwent PCI. Patients were divided into two groups based on the use of Filtrap®. The occurrence of congestive heart failure (CHF) and major adverse cardiac events (MACE) defined as cardiac death, recurrent AMI, and target vessel revascularization were compared. Result: Between DP (n=53, 41 men, mean age: 65.5 years) and non-DP (n=111, 89 men, mean age: 65.8 years) groups, although there was significantly greater plaque area in the DP group than in the non-DP group, there were no significant differences in coronary reperfusion flow after PCI. Interestingly, patients with CHF in the non-DP group exhibited a higher CK level than those in the DP group. During a 2-year follow-up period, cumulative CHF was significantly lower in the DP group than in the non-DP group (log-rank p=0.018), and there was no significant difference in the MACE rate (log-rank p=0.238). The use of DP device could not predict MACE, but could predict CHF by multivariate analysis (odds ratio=0.099, 95% CI: 0.02–0.42, p=0.005). Conclusion: These results demonstrate that favorable clinical outcomes could be achieved by the filter-type DP device in AMI, particularly in patients with CHF.<br />出版者照会後に全文公開
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| 84.
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Okazaki-Sakai, Satoko ; Yoshimoto, Sachiko ; Yagi, Kunimasa ; Wakasugi, Takanobu ; Takeda, Yoshiyu ; Yamagishi, Masakazu
概要:
A 62-year-old woman complained of repeated hypoglycemic events. A 75g oral glucose tolerance test (75 gOGTT) showed a ma
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rked increase in the plasma insulin level and impaired glucose tolerance. The patient exhibited a high titer of plasma anti-insulin autoantibodies. Her diagnosis was insulin autoimmune syndrome (IAS). Following the cessation of loxoprofen-sodium (LOXs), she experienced no further hypoglycemic episodes. However, the hypoglycemic attacks recurred following the accidental readministration of LOXs in an adhesive skin patch. Considering the changes in the titer of anti-insulin autoantibodies, the repeated 75 gOGTT and the repeated Scatchard analysis, we determined LOXs to be the cause of the IAS and evaluated the characteristics of the autoantibodies. © 2013 by The Japanese Society of Internal Medicine.
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| 85.
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Ohtani, Rumiko ; Inazu, Akihiro ; Noji, Yoshihiro ; Wakasugi, Takanobu ; Miwa, Kenji ; Tada, Hayato ; Kawashiri, Masa-aki ; Noguchi, Tohru ; Nohara, Atsushi ; Kobayashi, Junji ; Koizumi, Junji ; Yamagishi, Masakazu ; Mabuchi, Hiroshi
概要:
Thesis of Ohtani, Rumiko / 大谷 留珠子 博士学位論文(金沢大学 / 大学院医薬保健学総合研究科)<br />Background: The half of hyperalphalipoproteinemia (H
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ALP) in Japan is caused by CETP gene mutations. Other than two prevalent mutations (D442G and Intron 14 splicing donor site +. 1G>A), some rare CETP mutations are found in Japanese HALP subjects. Methods: CETP gene analysis of genomic DNA from subjects was performed by restriction fragment length polymorphism (RFLP) and sequencing analysis. Mutations which were suspected to cause a splicing defect or a protein secretion defect were investigated in COS-1 cells transfected with a CETP minigene construct or a cDNA expression vector. Results: Each of three subjects was identified as a carrier of CETP gene mutation of a compound heterozygote of c.653_654delGGinsAAAC and Intron 14 splicing donor site +. 1G>A, a heterozygote of c.658G>A or a homozygote of L261R. The c.658G>A mutation was located at the last nucleotide of exon 7, and it was confirmed to cause splicing abnormality revealed by the CETP minigene analysis. The L261R CETP was not secreted to conditioned media of the cells. Conclusions: Three novel CETP gene mutations are responsible for HALP by CETP deficiency. It is predicted that there are more rare CETP gene mutations in Japanese, and these multiple rare mutations alone or a combination with each of prevalent mutations is responsible for mild-to-moderate or marked HALP, respectively. © 2011 Elsevier B.V.
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| 86.
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Kaneko, Yoshibumi ; Miyajima, Hiroaki ; Piperno, Alberto ; Tomosugi, Naohisa ; Hayashi, Hisao ; Morotomi, Natsuko ; Tsuchida, Ken-ichi ; Ikeda, Takaaki ; Ishikawa, Akihisa ; Ota, Yusuke ; Wakusawa, Shinya ; Yoshioka, Kentaro ; Kono, Satoshi ; Pelucchi, Sara ; Hattori, Ai ; Tatsumi, Yasuaki ; Okada, Toshihide ; Yamagishi, Masakazu
概要:
石川県立中央病院<br />金沢大学医薬保健研究域医学系<br />Iron overload syndromes include a wide spectrum of genetic and acquired conditions. Re
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cent studies suggest suppressed hepcidin synthesis in the liver to be the molecular basis of hemochromatosis. However, a liver with acquired iron overload synthesizes an adequate amount of hepcidin. Thus, hepcidin could function as a biochemical marker for differential diagnosis of iron overload syndromes. Methods We measured serum iron parameters and hepcidin- 25 levels followed by sequencing HFE, HJV, HAMP, TFR2, and SLC40A1 genes in 13 Japanese patients with iron overload syndromes. In addition, we performed direct measurement of serum hepcidin-25 levels using liquid chromatography-tandem mass spectrometry in 3 Japanese patients with aceruloplasminemia and 4 Italians with HFE hemochromatosis. Results One patient with HJV hemochromatosis, 2 with TFR2 hemochromatosis, and 3 with ferroportin disease were found among the 13 Japanese patients. The remaining 7 Japanese patients showed no evidence for genetic basis of iron overload syndrome. As far as the serum hepcidin-25 was concerned, seven patients with hemochromatosis and 3 with aceruloplasminemia showed markedly decreased serum hepcidin-25 levels. In contrast, 3 patients with ferroportin disease and 7 with secondary iron overload syndromes showed serum hepcidin levels parallel to their hyperferritinemia. Patients with iron overload syndromes were divided into 2 phenotypes presenting as low and high hepcidinemia. These were then associated with their genotypes. Conclusion Determining serum hepcidin-25 levels may aid differential diagnosis of iron overload syndromes prior to genetic analysis. © Springer 2010.
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| 87.
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Matsuo, Shinro ; Nakajima, Kenichi ; Kinuya, Seigo ; Yamagishi, Masakazu
概要:
Objective: Takotsubo cardiomyopathy is a cardiac syndrome with an acute onset defined by chest symptoms and ST segment e
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levation on electrocardiograms. Takotsubo cardiomyopathy is sometimes misdiagnosed as acute myocardial infarction (AMI). Therefore a non-invasive diagnostic method is needed to be established for setting up appropriate strategies. The purpose of this study was to detect myocardial metabolic abnormalities and to determine the diagnostic usefulness of 123I-beta-methy-iodophenyl pentadecanoic acid (123I-BMIPP) imaging in patients with takotsubo cardiomyopathy. Methods and results: We examined 16 patients with takotsubo cardiomyopathy and 12 with AMI in the left anterior descending artery. All patients were studied with resting 123I-BMIPP imaging. Total defect score (TDS) of 123I-BMIPP and perfusion were semi-quantitatively determined with single-photon emission computed tomography (SPECT) imaging using a 17-segment 5-point model. TDS of 123I-BMIPP were 4.8 ± 2.7 in patients with Takotsubo cardiomyopathy and 22.4 ± 10.7 in AMI. The ratio of summed BMIPP defect score of non-apical to apical segments in Takotsubo cardiomyopathy was smaller than that of the patients with AMI (0.1 ± 0.1 vs. 1.1 ± 0.7, p < 0.0001), indicating that 123I-BMIPP abnormalities were exclusively observed the in apical area. The ratio of summed perfusion defect scores of non-apical to apical segments in takotsubo cardiomyopathy did not differ significantly from that of AMI (0.52 ± 0.6 vs. 0.57 ± 0.3, p = NS). Summed BMIPP defect score in the apical area of takotsubo cardiomyopathy was larger than that of perfusion defect score (3.9 ± 2.7 vs. 1.8 ± 1.8, p = 0.04). Conclusion: Impaired metabolic metabolism exclusively in the apical region was observed by 123I-BMIPP SPECT images in takotsubo cardiomyopathy. These typical metabolic SPECT features of the disease can be utilized on differential diagnosis of takotsubo cardiomyopathy. © 2013.<br />This is the author's version of a work accepted for publication by Japanese College of Cardiology. Changes resulting from the publishing process, including peer review, editing, corrections, structural formatting and other quality control mechanisms, may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. The definitive version has been published in Journal of Cardiology, 64 (1), pp. 49-56,2014 July, 10.1016/j.jjcc.2013.10.019
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| 88.
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Yamamoto, Ryusuke ; Tada, Hayato ; Tsubokawa, Toshinari ; Konno, Tetsuo ; Hayashi, Kenshi ; Saito, Takekatsu ; Kawashiri, Masa-aki ; Ohta, Kunio ; Yachie, Akihiro ; Yamagishi, Masakazu
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| 89.
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Kakuchi, Yasushi ; Yamada, Kazunori ; Suzuki, Yasunori ; Ito, Naoko ; Yagi, Kunimasa ; Matsumura, Masami ; Yamagishi, Masakazu ; Umehara, Hisanori ; Zen, Yoh ; Hasegawa, Minoru ; Takehara, Kazuhiko ; Kawano, Mitsuhiro
概要:
We describe a 60-year-old man with IgG4-related chronic sclerosing dacryoadenitis and sialoadenitis associated with lymp
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hoplasmacytic and eosinophilic infiltration in erythematous nodules. Physical examination revealed left eye extrusion and small itchy nodules on the scalp and neck. The serum IgG level was 1,570 mg/dL, IgG4 463 mg/dL (29.5%), and IgE 4,554 IU/mL. Lacrimal gland biopsy disclosed prominent infiltrates of IgG4-positive plasma cells and scattered eosinophilic infiltrates with fibrosis, consistent with IgG4-related disease. A skin biopsy of a cutaneous nodule demonstrated that the infiltrated plasma cells around arterioles or venules in the deep dermis and subcutaneous fat tissue were strongly positive for IgG4. Although the swollen lacrimal and parotid gland and itchy subcutaneous erythematous nodules improved rapidly with oral prednisolone at a dose of 20 mg per day, the skin, lacrimal, and parotid lesions deteriorated simultaneously during steroid tapering and improved after increasing the dosage. As skin lesions are easy to biopsy, further study of the skin manifestations of IgG4-related disease will be important in further clarifying the clinical spectrum, pathophysiology and response to therapy of this disorder. © 2011 The Japanese Society of Internal Medicine.
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| 90.
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Tada, Hayato ; Tsubokawa, Toshinari ; Konno, Tetsuo ; Hayashi, Kenshi ; Uchiyama, Katsuharu ; Kawashiri, Masa-aki ; Tomita, Shigeyuki ; Ino, Hidekazu ; Watanabe, Go ; Yamagishi, Masakazu
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| 91.
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Tada, Hayato ; Kawashiri, Masa-aki ; Ohtani, Rumiko ; Noguchi, Tohru ; Nakanishi, Chiaki ; Konno, Tetsuo ; Hayashia, Kenshi ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu
概要:
Background: Autosomal recessive hypercholesterolemia (ARH) is an extremely rare inherited hypercholesterolemia, the caus
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e of which is mutations in low-density lipoprotein (LDL) receptor adaptor protein 1 (LDLRAP1) gene. Methods: A total of 146 heterozygous familial hypercholesterolemic (FH) patients with a mutation in LDLR gene were screened for genes encoding proprotein convertase subtilisin/kexin type 9 (PCSK9) and LDLRAP1. Results: Among the 146 subjects, we identified a 79-year-old Japanese female with double mutations in LDLR gene (c.2431A > T) and LDLRAP1 gene (c.606dup). Two other relatives with double mutations in those genes in her family were also identified. Although the proband exhibited massive Achilles tendon xanthoma and coronary and aortic valvular disease, serum LDL-C level of subjects with double mutations was similar with that of subjects with single LDLR mutation (284.0 ± 43.5 versus 265.1 ± 57.4 mg/dl). Conclusion: Additional mutation in LDLRAP1 may account for severer phenotype in terms of xanthoma and atherosclerotic cardiovascular disease in FH patients. © 2011 Elsevier Ireland Ltd. All rights reserved.
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| 92.
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Tada, Hayato ; Tsubokawa, Toshinari ; Konno, Tetsuo ; Hayashi, Kenshi ; Uchiyama, Katsuharu ; Kawashiri, Masa-aki ; Tomita, Shigeyuki ; Ino, Hidekazu ; Watanabe, Go ; Yamagishi, Masakazu
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| 93.
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Tada, Hayato ; Kawashiri, Masa-aki ; Ohtani, Rumiko ; Noguchi, Tohru ; Nakanishi, Chiaki ; Konno, Tetsuo ; Hayashi, Kenshi ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu
概要:
Background: Autosomal recessive hypercholesterolemia (ARH) is an extremely rare inherited hypercholesterolemia, the caus
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e of which is mutations in low-density lipoprotein (LDL) receptor adaptor protein 1 (LDLRAP1) gene. Methods: A total of 146 heterozygous familial hypercholesterolemic (FH) patients with a mutation in LDLR gene were screened for genes encoding proprotein convertase subtilisin/kexin type 9 (PCSK9) and LDLRAP1. Results: Among the 146 subjects, we identified a 79-year-old Japanese female with double mutations in LDLR gene (c.2431A > T) and LDLRAP1 gene (c.606dup). Two other relatives with double mutations in those genes in her family were also identified. Although the proband exhibited massive Achilles tendon xanthoma and coronary and aortic valvular disease, serum LDL-C level of subjects with double mutations was similar with that of subjects with single LDLR mutation (284.0 ± 43.5 versus 265.1 ± 57.4. mg/dl). Conclusion: Additional mutation in LDLRAP1 may account for severer phenotype in terms of xanthoma and atherosclerotic cardiovascular disease in FH patients. © 2011 Elsevier Ireland Ltd.
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| 94.
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Tada, Hayato ; Konno, Tetsuo ; Aizu, Motohiko ; Yokawa, Junichiro ; Tsubokawa, Toshinari ; Fujii, Hiroshi ; Hayashi, Kenshi ; Uchiyama, Katsuharu ; Matsumura, Masami ; Kawano, Mitsuhiro ; Kawashiri, Masa-aki ; Yamagishi, Masakazu
概要:
We report a case with pulmonary veno-occlusive disease (PVOD) associated with systemic sclerosis which exhibits strong r
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esistance to pulmonary vasodilator. A 55-year-old female with severe pulmonary hypertension was admitted to our hospital to be introduced to epoprostenol infusion therapy. She was diagnosed as having pulmonary arterial hypertension (PAH) associated with systemic sclerosis at the age of 51. Several aggressive treatments with pulmonary vasodilators, including oral prostaglandin, endothelin receptor antagonists, and phosphodiesterase 5 inhibitors, failed to improve her symptoms. We introduced continuous intravenous epoprostenol therapy from 2 μg/kg/min for her. However, pulmonary edema appeared and worsened in a dose-dependent manner. We made a diagnosis of PVOD clinically at that time. Thereafter, pulmonary edema gradually disappeared consistent with the reduction of the dose of epoprostenol infusion. She died of renal failure and infection 4 months after the introduction of epoprostenol infusion therapy. A histological examination revealed severe stenosis and occlusions of pulmonary veins as well as pulmonary arteries over a wide area. We suggest that prevalence of veno-occlusive type of disease could be one of the major mechanisms of less responsive or even refractory to pulmonary vasodilator therapies in patients with PAH associated with connective tissue disease. © 2011 Japanese College of Cardiology.
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| 95.
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Tada, Hayato ; Kawashiri, Masa-aki ; Ohtani, Rumiko ; Noguchi, Tohru ; Nakanishi, Chiaki ; Konno, Tetsuo ; Hayashi, Kenshi ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu
概要:
Background: Autosomal recessive hypercholesterolemia (ARH) is an extremely rare inherited hypercholesterolemia, the caus
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e of which is mutations in low-density lipoprotein (LDL) receptor adaptor protein 1 (LDLRAP1) gene. Methods: A total of 146 heterozygous familial hypercholesterolemic (FH) patients with a mutation in LDLR gene were screened for genes encoding proprotein convertase subtilisin/kexin type 9 (PCSK9) and LDLRAP1. Results: Among the 146 subjects, we identified a 79-year-old Japanese female with double mutations in LDLR gene (c.2431A > T) and LDLRAP1 gene (c.606dup). Two other relatives with double mutations in those genes in her family were also identified. Although the proband exhibited massive Achilles tendon xanthoma and coronary and aortic valvular disease, serum LDL-C level of subjects with double mutations was similar with that of subjects with single LDLR mutation (284.0 ± 43.5 versus 265.1 ± 57.4. mg/dl). Conclusion: Additional mutation in LDLRAP1 may account for severer phenotype in terms of xanthoma and atherosclerotic cardiovascular disease in FH patients. © 2011 Elsevier Ireland Ltd.
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| 96.
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Tada, Hayato ; Konno, Tetsuo ; Aizu, Motohiko ; Yokawa, Junichiro ; Tsubokawa, Toshinari ; Fujii, Hiroshi ; Hayashi, Kenshi ; Uchiyama, Katsuharu ; Matsumura, Masami ; Kawano, Mitsuhiro ; Kawashiri, Masa-aki ; Yamagishi, Masakazu
概要:
We report a case with pulmonary veno-occlusive disease (PVOD) associated with systemic sclerosis which exhibits strong r
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esistance to pulmonary vasodilator.A 55-year-old female with severe pulmonary hypertension was admitted to our hospital to be introduced to epoprostenol infusion therapy. She was diagnosed as having pulmonary arterial hypertension (PAH) associated with systemic sclerosis at the age of 51. Several aggressive treatments with pulmonary vasodilators, including oral prostaglandin, endothelin receptor antagonists, and phosphodiesterase 5 inhibitors, failed to improve her symptoms. We introduced continuous intravenous epoprostenol therapy from 2. μg/kg/min for her. However, pulmonary edema appeared and worsened in a dose-dependent manner. We made a diagnosis of PVOD clinically at that time. Thereafter, pulmonary edema gradually disappeared consistent with the reduction of the dose of epoprostenol infusion. She died of renal failure and infection 4. months after the introduction of epoprostenol infusion therapy. A histological examination revealed severe stenosis and occlusions of pulmonary veins as well as pulmonary arteries over a wide area. We suggest that prevalence of veno-occlusive type of disease could be one of the major mechanisms of less responsive or even refractory to pulmonary vasodilator therapies in patients with PAH associated with connective tissue disease. © 2011 Japanese College of Cardiology.
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| 97.
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Sakamoto, Aiji ; Kawashiri, Masaaki ; Ishibashi-Ueda, Hatsue ; Sugamoto, Yuka ; Yoshimuta, Tsuyoshi ; Higashikata, Takeo ; Ogino, Hitoshi ; Tada, Hayato ; Konno, Tetsuo ; Hayashi, Kenshi ; Yamagishi, Masakazu
概要:
We examined the expression of ephrin-B1 and its cognate receptor EphB2, key regulators of angiogenesis and embryogenesis
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, in human abdominal aortic aneurysm (AAA) and analyzed their functional roles in cell migration. From 10 patients (9 males and 1 female; age, 68.5 ± 2.4) who underwent vascular surgery for AAA, we obtained AAA and adjacent control tissues. Using real-time RT-PCR, we analyzed expression of ephrin-B1 and EphB2. We also histologically localized these molecules in AAA tissues. Finally, effects of ephrin-B1 and EphB2 on inflammatory cell chemotaxis were examined by cell migration assay. Expression levels of ephrin-B1 (0.410 ± 0.046 versus 1.198 ± 0.252, P = 0.027) and EphB2 (0.764 ± 0.212 versus 1.272 ± 0.137, P = 0.594) were higher in AAA than normal control. Both ephrin-B1 and EphB2 were expressed in macrophages, T lymphocytes, and endothelial cells within AAA. In chemotaxis assay, ephrin-B1 and EphB2 inhibited mononuclear-cell chemotaxis induced by stromal derived factor-1 down to 54.7 ± 12.7 (P = 0.01) and 50.7 ± 13.1 (P = 0.01), respectively. These data suggest that ephrin-B1 and EphB2 might be functional in human adult inflammatory cells and involved in the pathogenesis of AAA, although specific roles of these molecules should further be sought. © 2012 Aiji Sakamoto et al.
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| 98.
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Funada, Akira ; Goto, Yoshikazu ; Maeda, Tetsuo ; Teramoto, Ryota ; Hayashi, Kenshi ; Yamagishi, Masakazu
概要:
Background:There is sparse data regarding the survival and neurological outcome of elderly patients with out-of-hospital
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cardiac arrest (OHCA).Methods and Results:OHCA patients (334,730) aged ≥75 years were analyzed using a nationwide, prospective, population-based Japanese OHCA database from 2008 to 2012. The overall 1-month survival with favorable neurological outcome (Cerebral Performance Category Scale, category 1 or 2; CPC 1-2) rate was 0.88%. During the study period, the annual 1-month CPC 1-2 rate in whole OHCA significantly improved (0.73% to 0.96%, P for trend <0.001). In particular, outcomes of OHCA patients aged 75 to 84 years and those aged 85 to 94 years significantly improved (0.98% to 1.28%, P for trend=0.01; 0.46% to 0.70%, P for trend <0.001, respectively). However, in OHCA patients aged ≥95 years, the outcomes did not improve. Multivariate logistic regression analysis indicated that younger age, shockable first documented rhythm, witnessed arrest, earlier emergency medical service (EMS) response time, and cardiac etiology were significantly associated with the 1-month CPC 1-2. Under these conditions, elderly OHCA patients who had cardiac etiology, shockable rhythm and had a witnessed arrest had acceptable 1-month CPC1-2 rate; 7.98% in cases where OHCA was witnessed by family, 15.2% by non-family, and 25.6% by EMS.Conclusions:The annual 1-month CPC 1-2 rate after OHCA among elderly patients significantly improved, and the resuscitation of elderly patients in a selected population is not futile.
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| 99.
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Tada, Hayato ; Kawashiri, Masa-aki ; Okada, Hirofumi ; Teramoto, Ryota ; Konno, Tetsuo ; Yoshimuta, Tsuyoshi ; Sakata, Kenji ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; Hayashi, Kenshi
概要:
The aims of this study were (1) to determine whether the accumulation of coronary plaque burden assessed with coronary c
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omputed tomography angiography (CCTA) can predict future events and (2) to estimate the onset and progression of coronary atherosclerosis in patients with familial hypercholesterolemia (FH). Consecutive 101 Japanese patients with heterozygous FH (men= 52, mean age 56 ± 16years, mean low-density lipoprotein cholesterol 264 ± 58mg/dl) who underwent 64-detector row CCTA without known coronary artery disease were retrospectively evaluated by assigning a score (0 to 5) to each of 17 coronary artery segments according to the Society of Cardiovascular Computed Tomography guidelines. Those scores were summed and subsequently natural log transformed. The periods to major adverse cardiac events (MACE) were estimated using multivariable Cox proportional hazards models. During the follow-up period (median 941days), 21 MACE had occurred. Receiver operating characteristic curve analyses identified a plaque burden score of 3.35 (raw score 28.5) as the optimal cutoff for predicting a worse prognosis. Multivariate Coxregression analysis identified the presence of a plaque score ≥3.35 as a significant independent predictor of MACE (hazard ratio= 3.65; 95% confidence interval 1.32 to 25.84, p<0.05). The regression equations were Y= 0.68. X- 15.6 (r= 0.54, p <0.05) in male and Y= 0.74. X- 24.8 (r= 0.69, p <0.05) in female patients with heterozygous FH. In conclusion, coronary plaque burden identified in a noninvasive, quantitative manner was significantly associated with future coronary events in Japanese patients with heterozygous FH and that coronary atherosclerosis may start to develop, on average, at age 23 and 34years in male and female patients with heterozygous FH, respectively.
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| 100.
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Yoshida, Shohei ; Tada, Hayato ; Yamagishi, Masakazu
概要:
発行後1年より全文公開
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