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1. Efficacy and Safety of Adding Empagliflozin to Liraglutide on Renal Function in Patients with Advanced-Stage Type 2 Diabetic Kidney Disease: A Randomized Controlled Trial

Author

Sunagawa K, Hirai K, Sunagawa S, Kamiya N, Komesu I, Sunagawa Y, Sunagawa H, Nakachi K, Hirai A, Ookawara S, and Morishita Y

Subjects
empagliflozin, sodium-glucose co-transporter 2 inhibitor, liraglutide, glucagon-like peptide-1 receptor agonist, diabetic kidney disease, diabetic nephropathy, Specialties of internal medicine, RC581-951
Abstract

Kae Sunagawa,1,2 Keiji Hirai,3 Sumito Sunagawa,1,2 Norifumi Kamiya,1 Isao Komesu,1 Yusako Sunagawa,1 Hiroshi Sunagawa,1 Ken Nakachi,4 Aizan Hirai,5 Susumu Ookawara,3 Yoshiyuki Morishita3 1Sunagawa Medical Clinic, Okinawa, Japan; 2Division of Endocrinology, Diabetes and Metabolism, Hematology, and Rheumatology, University of the Ryukyus, Okinawa, Japan; 3Division of Nephrology, Saitama Medical Center, Jichi Medical University, Saitama, Japan; 4Department of Internal Medicine, Shonan Hospital, Okinawa, Japan; 5Department of Internal Medicine, Chiba Cerebral and Cardiovascular Center, Chiba, JapanCorrespondence: Keiji Hirai, Division of Nephrology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University, 1-847 Amanuma-cho, Saitama-shi, Saitama-ken, 330-8503, Japan, Tel +81 48 647 2111, Fax +81 48 647 6831, Email keijihirai@kfy.biglobe.ne.jpPurpose: The aim of this study was to investigate the additional effects of empagliflozin on liraglutide in patients with advanced-stage type 2 diabetic kidney disease.Patients and Methods: Forty-one patients were randomly assigned (1:1) to treatment with liraglutide alone during the first 6 months and subsequent treatment with liraglutide plus empagliflozin during the next 6 months (liraglutide plus empagliflozin group) (n = 20) or treatment with liraglutide alone for 12 months (liraglutide group) (n = 21). Liraglutide was administered subcutaneously once daily at a starting dose of 0.3 mg/day and up-titrated weekly by 0.3 mg to a maximum dose of 0.9 mg/day. Empagliflozin was administered orally at a dose of 10 mg once daily. The primary outcome was the change in renal function (estimated glomerular filtration rate) during the latter 6 months. Secondary outcomes were changes in body weight, systolic blood pressure, hemoglobin, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, uric acid, blood glucose, hemoglobin A1c, and urine protein creatinine ratio during the latter 6 months.Results: Empagliflozin significantly increased the hemoglobin concentration (from 12.9 ± 1.9 to 13.7 ± 1.9 g/dL; p< 0.05) and decreased body weight (from 66.1 ± 12.9 to 64.5 ± 12.6 kg; p< 0.05). No significant differences were observed between the groups for estimated glomerular filtration rate, systolic blood pressure, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, uric acid, blood glucose, hemoglobin A1c, and urine protein creatinine ratio.Conclusion: Empagliflozin increased hemoglobin concentration and decreased body weight in patients with advanced-stage type 2 diabetic kidney disease who received liraglutide. However, empagliflozin did not provide short-term benefits with regard to renal function decline, urinary protein excretion, or glycemic control in these patients.Keywords: empagliflozin, sodium-glucose co-transporter 2 inhibitor, liraglutide, glucagon-like peptide-1 receptor agonist, diabetic kidney disease, diabetic nephropathy

Published
2024

2. Sex-specific relevance of diabetes to occlusive vascular and other mortality: a collaborative meta-analysis of individual data from 980 793 adults from 68 prospective studies

Author

Gnatiuc, L, Herrington, WG, Halsey, J, Tuomilehto, J, Fang, X, Kim, HC, De Bacquer, D, Dobson, AJ, Criqui, MH, Jacobs, DR, Jr, Leon, DA, Peters, SAE, Ueshima, H, Sherliker, P, Peto, R, Collins, R, Huxley, RR, Emberson, JR, Woodward, M, Lewington, S, Aoki, N, Arima, H, Arnesen, E, Aromaa, A, Assmann, G, Bachman, DL, Baigent, C, Bartholomew, H, Benetos, A, Bengtsson, C, Bennett, D, Björkelund, C, Blackburn, H, Bonaa, K, Boyle, E, Broadhurst, R, Carstensen, J, Chambless, L, Chen, Z, Chew, SK, Clarke, R, Cox, C, Curb, JD, D'Agostino, R, Date, C, Davey Smith, G, De Backer, G, Dhaliwal, SS, Duan, XF, Ducimetiere, P, Duffy, S, Eliassen, H, Elwood, P, Empana, J, Garcia-Palmieri, MH, Gazes, P, Giles, GG, Gillis, C, Goldbourt, U, Gu, DF, Guasch-Ferre, M, Guize, L, Haheim, L, Hart, C, Hashimoto, S, Hashimoto, T, Heng, D, Hjermann, I, Ho, SC, Hobbs, M, Hole, D, Holme, I, Horibe, H, Hozawa, A, Hu, F, Hughes, K, Iida, M, Imai, K, Imai, Y, Iso, H, Jackson, R, Jamrozik, K, Jee, SH, Jensen, G, Jiang, CQ, Johansen, NB, Jorgensen, T, Jousilahti, P, Kagaya, M, Keil, J, Keller, J, Kim, IS, Kita, Y, Kitamura, A, Kiyohara, Y, Knekt, P, Knuiman, M, Kornitzer, M, Kromhout, D, Kronmal, R, Lam, TH, Law, M, Lee, J, Leren, P, Levy, D, Li, YH, Lissner, L, Luepker, R, Luszcz, M, MacMahon, S, Maegawa, H, Marmot, M, Matsutani, Y, Meade, T, Morris, J, Morris, R, Murayama, T, Naito, Y, Nakachi, K, Nakamura, M, Nakayama, T, Neaton, J, Nietert, PJ, Nishimoto, Y, Norton, R, Nozaki, A, Ohkubo, T, Okayama, A, Pan, WH, Puska, P, Qizilbash, N, Reunanen, A, Rimm, E, Rodgers, A, Saitoh, S, Sakata, K, Sato, S, Schnohr, P, Schulte, H, Selmer, R, Sharp, D, Shifu, X, Shimamoto, K, Shipley, M, Silbershatz, H, Sorlie, p, Sritara, P, Suh, I, Sutherland, SE, Sweetnam, P, Tamakoshi, A, Tanaka, H, Thomsen, T, Tominaga, S, Tomita, M, Törnberg, S, Tunstall-Pedoe, H, Tverdal, A, Vartiainen, E, Wald, N, Wannamethee, SG, Welborn, TA, Whincup, P, Whitlock, G, Willett, W, Woo, J, Wu, ZL, Yao, SX, Yarnell, J, Yokoyama, T, Yoshiike, N, and Zhang, XH

Published
2018
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4. COTI-2, A Novel Thiosemicarbazone Derivative, Exhibits Antitumor Activity in HNSCC through p53-dependent and -independent Mechanisms

Author

Jeffrey N. Myers, Xiayu Rao, Meng Gao, Mei Zhao, Zhiyi Liu, Noriaki Tanaka, Hideaki Takahashi, Jing Wang, Steven J. Frank, Abdullah A. Osman, Li Wang, Walter N. Hittelman, Antje Lindemann, Gordon B. Mills, Tseng-Cheng Chen, Ameeta A. Patel, Lin Tang, Natalie L. Silver, Nakachi K Maduka, and WeiWei Liu

Subjects
DNA Replication, Thiosemicarbazones, 0301 basic medicine, Cancer Research, Transcription, Genetic, DNA damage, Antineoplastic Agents, Apoptosis, Article, Mice, 03 medical and health sciences, 0302 clinical medicine, stomatognathic system, Stress, Physiological, In vivo, Cell Line, Tumor, medicine, Animals, Humans, neoplasms, Cellular Senescence, PI3K/AKT/mTOR pathway, Cell Proliferation, Cisplatin, Squamous Cell Carcinoma of Head and Neck, Chemistry, Gene Expression Profiling, Cell Cycle, Cell cycle, medicine.disease, Xenograft Model Antitumor Assays, Head and neck squamous-cell carcinoma, Disease Models, Animal, stomatognathic diseases, 030104 developmental biology, Oncology, 030220 oncology & carcinogenesis, Cancer cell, Cancer research, Tumor Suppressor Protein p53, DNA Damage, Protein Binding, Signal Transduction, medicine.drug
Abstract

Purpose: TP53 mutations are highly prevalent in head and neck squamous cell carcinoma (HNSCC) and associated with increased resistance to conventional treatment primarily consisting of chemotherapy and radiation. Restoration of wild-type p53 function in TP53-mutant cancer cells represents an attractive therapeutic approach and has been explored in recent years. In this study, the efficacy of a putative p53 reactivator called COTI-2 was evaluated in HNSCC cell lines with different TP53 status. Experimental Design: Clonogenic survival assays and an orthotopic mouse model of oral cancer were used to examine in vitro and in vivo sensitivity of HNSCC cell lines with either wild-type, null, or mutant TP53 to COTI-2 alone, and in combination with cisplatin and/or radiation. Western blotting, cell cycle, live-cell imaging, RNA sequencing, reverse-phase protein array, chromatin immunoprecipitation, and apoptosis analyses were performed to dissect molecular mechanisms. Results: COTI-2 decreased clonogenic survival of HNSCC cells and potentiated response to cisplatin and/or radiation in vitro and in vivo irrespective of TP53 status. Mechanistically, COTI-2 normalized wild-type p53 target gene expression and restored DNA-binding properties to the p53-mutant protein in HNSCC. In addition, COTI-2 induced DNA damage and replication stress responses leading to apoptosis and/or senescence. Furthermore, COTI-2 lead to activation of AMPK and inhibition of the mTOR pathways in vitro in HNSCC cells. Conclusions: COTI-2 inhibits tumor growth in vitro and in vivo in HNSCC likely through p53-dependent and p53-independent mechanisms. Combination of COTI-2 with cisplatin or radiation may be highly relevant in treating patients with HNSCC harboring TP53 mutations.

Published
2019
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13. COTI-2, A Novel Thiosemicarbazone Derivative, Exhibits Antitumor Activity in HNSCC through p53-dependent and -independent Mechanisms

Author

Lindemann, Antje, primary, Patel, Ameeta A., additional, Silver, Natalie L., additional, Tang, Lin, additional, Liu, Zhiyi, additional, Wang, Li, additional, Tanaka, Noriaki, additional, Rao, Xiayu, additional, Takahashi, Hideaki, additional, Maduka, Nakachi K., additional, Zhao, Mei, additional, Chen, Tseng-Cheng, additional, Liu, WeiWei, additional, Gao, Meng, additional, Wang, Jing, additional, Frank, Steven J., additional, Hittelman, Walter N., additional, Mills, Gordon B., additional, Myers, Jeffrey N., additional, and Osman, Abdullah A., additional

Published
2019
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16. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies

Author

Whitlock, Gary, Lewington, Sarah, Sherliker, Paul, Clarke, Robert, Emberson, Jonathan, Halsey, Jim, Qizilbash, Nawab, Collins, Rory, Peto, Richard, Lewington, S, MacMahon, S, Peto, R, Aromaa, A, Baigent, C, Carstensen, J, Chen, Z, Clarke, R, Collins, R, Duffy, S, Kromhout, D, Neaton, J, Qizilbash, N, Rodgers, A, Tominaga, S, Toernberg, S, Tunstall-Pedoe, H, Whitlock, G, Chambless, L, De Backer, G, De Bacquer, D, Kornitzer, M, Whincup, P, Wannamethee, SG, Morris, R, Wald, N, Morris, J, Law, M, Knuiman, M, Bartholomew, H, Smith, G Davey, Sweetnam, P, Elwood, P, Yarnell, J, Kronmal, R, Sutherland, S, Keil, J, Jensen, G, Schnohr, P, Hames, C, Tyroler, A, Knekt, P, Reunanen, A, Tuomilehto, J, Jousilahti, P, VArtiainen, E, Puska, P, Kuznetsova, Tatiana, Richart, Tom, Staessen, Jan A, Thijs, Lutgarde, Jorgensen, T, Thomsen, T, Sharp, D, Curb, JD, Iso, H, Sato, S, Kitamura, A, Naito, Y, Benetos, A, Guize, L, Goldbourt, U, Tomita, M, Nishimoto, Y, Murayama, T, Criqui, M, Davis, C, Hart, C, Hole, D, Gillis, C, Jacobs, D, Blackburn, H, Luepker, R, Eberly, L, Cox, C, Levy, D, D'Agostino, R, Silbershatz, H, Tverdal, A, Selmer, R, Meade, T, Garrow, K, Cooper, J, Speizer, F, Stampfer, M, Menotti, A, Spagnolo, A, Tsuji, I, Imai, Y, Ohkubo, T, Hisamichi, S, Haheim, L, Holme, I, Hjermann, I, Leren, P, Ducimetiere, P, Empana, J, Jamrozik, K, Broadhurst, R, Assmann, G, Schulte, H, Bengtsson, C, Bjoerkelund, C, Lissner, L, Sorlie, P, Garcia-Palmieri, M, Barrett-Conner, E, Langer, R, Nakachi, K, Imai, K, Fang, X, Buzina, R, Nissinen, A, Aravanis, C, Dontas, A, Kafatos, A, Adachi, H, Toshima, H, Imaizumi, T, Nedeljkovic, S, Ostojic, M, CHen, Z, Nakayama, T, Yoshiike, N, Yokoyama, T, Date, C, Tanaka, H, Keller, J, Bonaa, K, Arnesen, E, Rimm, E, Gaziano, M, Buring, JE, Hennekens, C, Tornberg, S, Shipley, M, Leon, D, Marmot, M, Emberson, J, Halsey, J, Palmer, A, Parish, S, and Sherliker, P

Subjects
Male, obesity, Nutrition and Disease, Respiratory Tract Diseases, Myocardial Ischemia, individual data, 030204 cardiovascular system & hematology, Overweight, Body Mass Index, 0302 clinical medicine, blood-pressure, Cause of Death, Voeding en Ziekte, Medicine, Prospective Studies, 030212 general & internal medicine, Prospective cohort study, risk, Cause of death, Aged, 80 and over, Hazard ratio, Articles, General Medicine, Middle Aged, 3. Good health, Stroke, Female, medicine.symptom, Adult, medicine.medical_specialty, Waist, abdominal adiposity, united-states, 03 medical and health sciences, vascular mortality, Internal medicine, Humans, korean men, Mortality, Aged, VLAG, business.industry, Anthropometry, medicine.disease, Obesity, Surgery, randomized-trials, coronary-heart-disease, business, Body mass index
Abstract

Summary Background The main associations of body-mass index (BMI) with overall and cause-specific mortality can best be assessed by long-term prospective follow-up of large numbers of people. The Prospective Studies Collaboration aimed to investigate these associations by sharing data from many studies. Methods Collaborative analyses were undertaken of baseline BMI versus mortality in 57 prospective studies with 894 576 participants, mostly in western Europe and North America (61% [n=541 452] male, mean recruitment age 46 [SD 11] years, median recruitment year 1979 [IQR 1975–85], mean BMI 25 [SD 4] kg/m2). The analyses were adjusted for age, sex, smoking status, and study. To limit reverse causality, the first 5 years of follow-up were excluded, leaving 66 552 deaths of known cause during a mean of 8 (SD 6) further years of follow-up (mean age at death 67 [SD 10] years): 30 416 vascular; 2070 diabetic, renal or hepatic; 22 592 neoplastic; 3770 respiratory; 7704 other. Findings In both sexes, mortality was lowest at about 22·5–25 kg/m2. Above this range, positive associations were recorded for several specific causes and inverse associations for none, the absolute excess risks for higher BMI and smoking were roughly additive, and each 5 kg/m2 higher BMI was on average associated with about 30% higher overall mortality (hazard ratio per 5 kg/m2 [HR] 1·29 [95% CI 1·27–1·32]): 40% for vascular mortality (HR 1·41 [1·37–1·45]); 60–120% for diabetic, renal, and hepatic mortality (HRs 2·16 [1·89–2·46], 1·59 [1·27–1·99], and 1·82 [1·59–2·09], respectively); 10% for neoplastic mortality (HR 1·10 [1·06–1·15]); and 20% for respiratory and for all other mortality (HRs 1·20 [1·07–1·34] and 1·20 [1·16–1·25], respectively). Below the range 22·5–25 kg/m2, BMI was associated inversely with overall mortality, mainly because of strong inverse associations with respiratory disease and lung cancer. These inverse associations were much stronger for smokers than for non-smokers, despite cigarette consumption per smoker varying little with BMI. Interpretation Although other anthropometric measures (eg, waist circumference, waist-to-hip ratio) could well add extra information to BMI, and BMI to them, BMI is in itself a strong predictor of overall mortality both above and below the apparent optimum of about 22·5–25 kg/m2. The progressive excess mortality above this range is due mainly to vascular disease and is probably largely causal. At 30–35 kg/m2, median survival is reduced by 2–4 years; at 40–45 kg/m2, it is reduced by 8–10 years (which is comparable with the effects of smoking). The definite excess mortality below 22·5 kg/m2 is due mainly to smoking-related diseases, and is not fully explained. Funding UK Medical Research Council, British Heart Foundation, Cancer Research UK, EU BIOMED programme, US National Institute on Aging, and Clinical Trial Service Unit (Oxford, UK).

Published
2009
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20. Metabolic mediators of the effects of body-mass index, overweight, and obesity on coronary heart disease and stroke: A pooled analysis of 97 prospective cohorts with 1·8 million participants

Author

Lu, Y. Hajifathalian, K. Ezzati, M. Woodward, M. Rimm, E.B. Danaei, G. Selmer, R. Strand, B.H. Dobson, A. Hozawa, A. Nozaki, A. Okayama, A. Rodgers, A. Tamakoshi, A. Zhou, B.F. Zhou, B. Yao, C.H. Jiang, C.Q. Gu, D.F. Heng, D. Giles, G.G. Shan, G.L. Whitlock, G. Arima, H. Kim, H.C. Christensen, H. Horibe, H. Maegawa, H. Tanaka, H. Ueshima, H. Zhang, H.Y. Kim, I.S. Suh, I. Fuh, J.L. Lee, J. Woo, J. Xie, J.X. Zhou, J. Hughes, K. Jamrozik, K. Nakachi, K. Sakata, K. Shimamoto, K. Chen, L.Q. Liu, L.S. Hobbs, M. Iida, M. Kagaya, M. Divitini, M.L. Luszcz, M. Nakamura, M. Huang, M.S. Knuiman, M.W. Aoki, N. Norman, P. Sritara, P. Yang, Q.D. Broadhurst, R. Huxley, R. Jackson, R. Norton, R. Ameratunga, S. Ho, S.C. Li, S.C. Jee, S.H. Chew, S.K. Macmahon, S. Choudhury, S.R. Saitoh, S. Yao, S.X. Welborn, T.A. Lam, T.H. Hashimoto, T. Ohkubo, T. Pan, W.-H. Duan, X.F. Fang, X. Wu, X.G. Fang, X.H. Yu, X.H. Li, Y.H. He, Y. Imai, Y. Kita, Y. Kiyohara, Y. Matsutani, Y. Hong, Z. Wu, Z.L. Chen, Z.M. Wu, Z.S. Tang, Z. Li, Z.Z. Parker, E.D. Pereira, M.A. Stevens, J. Panagiotakos, D.B. Pitsavos, C. Attia, J.R. D’este, C.A. Zhang, X. Clays, E. De Bacquer, D.A.O. Van Herck, K. Morrison, H.I. Wang, F. Chuang, S.-Y. Yeh, W.-T. Chen, Z. Smith, M.C. Zhou, M. Wang, W. Zhang, X.-T. Zhao, D. Vollset, S.E. Fuchs, S.C. Fuchs, F.D. Moreira, L.B. Dontas, I.A. Dontas, C.A. Kafatos, A.G. Moschandreas, J. Lanti, M. Menotti, A. Kromhout, D. Jensen, M.K. Overvad, K. Tjonneland, A. Klotsche, J. Wittchen, H.-U. Fischer, S. Hanefeld, M. Schwanebeck, U. Simons, L.A. Simons, J. Bender, R. Matthies, S. Nissinen, A. Tolonen, H.K. Tuomilehto, J. Chaturvedi, N. Fuller, J.H. Soedamah-Muthu, S.S. Kotseva, K. Wood, D.A. Bots, M.L. Moons, K.G.M. Heliovaara, M. Knekt, P.B. Rissanen, H. Ferrie, J.E. Shipley, M.J. Smith, G.D. Johansson, S. Lappas, G. Rosengren, A. Sham, A. Yu, R.H.Y. Hata, J. Ninomiya, T. Hoshide, S. Kario, K. Rastenyte, D. Tamosiunas, A. de Simone, G. Devereux, R.B. Gerdts, E. Colquhoun, D.M. Keech, A.C. Kirby, A.C. Mizuno, K. Nakamura, H. Uchiyama, S. Bassett, J.K. Hodge, A.M. Wilhelmsen, L. Dhaliwal, S.S. Nakamura, Y. Kadota, A. Okamura, T. Sandvei, M.S. Vatten, L.J. Vik, A. Morkedal, B. Romundstad, P.R. Elkind, M.S.V. Gardener, H. Sacco, R.L. Mignano, A. Novo, S. Rizzo, M. Assmann, G. Schulte, H. Lissner, L. Skoog, I. Sundh, V. Marin, A. Medrano, M.J. Hofman, A. Kuningas, M. Stricker, B.H. van der Graaf, Y. Visseren, F.L.J. Lee, J.J.M. Bemelmans, W. de Groot, L.C.P.G.M. de Hollander, E.L. Adachi, H. Hirai, Y. Azizi, F. Hadaegh, F. Khalili, D. Mathiesen, E.B. Njolstad, I. Wilsgaard, T. Can, G. Onat, A. Arnlov, J. Sundstrom, J. Blackburn, H.W. Jacobs, D.R. Averna, M.R. Cefalu, A.B. Noto, D. Concin, H. Nagel, G. Ulmer, H. Krasnow, R.E. Swan, G.E. Kivimaki, M. David Batty, G. Milic, N. Ostojic, M.C. Parapid, B. Geleijnse, J.M. Waterham, E. Feskens, E.J. The Global Burden of Metabolic Risk Factors for Chronic Diseases Collaboration (BMI Mediated Effects)

Abstract

Background Body-mass index (BMI) and diabetes have increased worldwide, whereas global average blood pressure and cholesterol have decreased or remained unchanged in the past three decades. We quantified how much of the effects of BMI on coronary heart disease and stroke are mediated through blood pressure, cholesterol, and glucose, and how much is independent of these factors. Methods We pooled data from 97 prospective cohort studies that collectively enrolled 1·8 million participants between 1948 and 2005, and that included 57 161 coronary heart disease and 31 093 stroke events. For each cohort we excluded participants who were younger than 18 years, had a BMI of lower than 20 kg/m2, or who had a history of coronary heart disease or stroke. We estimated the hazard ratio (HR) of BMI on coronary heart disease and stroke with and without adjustment for all possible combinations of blood pressure, cholesterol, and glucose. We pooled HRs with a random-effects model and calculated the attenuation of excess risk after adjustment for mediators. Findings The HR for each 5 kg/m2 higher BMI was 1·27 (95% CI 1·23-1·31) for coronary heart disease and 1·18 (1·14-1·22) for stroke after adjustment for confounders. Additional adjustment for the three metabolic risk factors reduced the HRs to 1·15 (1·12-1·18) for coronary heart disease and 1·04 (1·01-1·08) for stroke, suggesting that 46% (95% CI 42-50) of the excess risk of BMI for coronary heart disease and 76% (65-91) for stroke is mediated by these factors. Blood pressure was the most important mediator, accounting for 31% (28-35) of the excess risk for coronary heart disease and 65% (56-75) for stroke. The percentage excess risks mediated by these three mediators did not differ significantly between Asian and western cohorts (North America, western Europe, Australia, and New Zealand). Both overweight (BMI ≥25 to

Published
2014

21. Metabolic mediators of the effects of body-mass index, overweight, and obesity on coronary heart disease and stroke: A pooled analysis of 97 prospective cohorts with 1·8 million participants

Author

Lu, Y. Hajifathalian, K. Ezzati, M. Woodward, M. Rimm, E.B. Danaei, G. Selmer, R. Strand, B.H. Dobson, A. Hozawa, A. Nozaki, A. Okayama, A. Rodgers, A. Tamakoshi, A. Zhou, B.F. Zhou, B. Yao, C.H. Jiang, C.Q. Gu, D.F. Heng, D. Giles, G.G. Shan, G.L. Whitlock, G. Arima, H. Kim, H.C. Christensen, H. Horibe, H. Maegawa, H. Tanaka, H. Ueshima, H. Zhang, H.Y. Kim, I.S. Suh, I. Fuh, J.L. Lee, J. Woo, J. Xie, J.X. Zhou, J. Hughes, K. Jamrozik, K. Nakachi, K. Sakata, K. Shimamoto, K. Chen, L.Q. Liu, L.S. Hobbs, M. Iida, M. Kagaya, M. Divitini, M.L. Luszcz, M. Nakamura, M. Huang, M.S. Knuiman, M.W. Aoki, N. Norman, P. Sritara, P. Yang, Q.D. Broadhurst, R. Huxley, R. Jackson, R. Norton, R. Ameratunga, S. Ho, S.C. Li, S.C. Jee, S.H. Chew, S.K. Macmahon, S. Choudhury, S.R. Saitoh, S. Yao, S.X. Welborn, T.A. Lam, T.H. Hashimoto, T. Ohkubo, T. Pan, W.-H. Duan, X.F. Fang, X. Wu, X.G. Fang, X.H. Yu, X.H. Li, Y.H. He, Y. Imai, Y. Kita, Y. Kiyohara, Y. Matsutani, Y. Hong, Z. Wu, Z.L. Chen, Z.M. Wu, Z.S. Tang, Z. Li, Z.Z. Parker, E.D. Pereira, M.A. Stevens, J. Panagiotakos, D.B. Pitsavos, C. Attia, J.R. D’este, C.A. Zhang, X. Clays, E. De Bacquer, D.A.O. Van Herck, K. Morrison, H.I. Wang, F. Chuang, S.-Y. Yeh, W.-T. Chen, Z. Smith, M.C. Zhou, M. Wang, W. Zhang, X.-T. Zhao, D. Vollset, S.E. Fuchs, S.C. Fuchs, F.D. Moreira, L.B. Dontas, I.A. Dontas, C.A. Kafatos, A.G. Moschandreas, J. Lanti, M. Menotti, A. Kromhout, D. Jensen, M.K. Overvad, K. Tjonneland, A. Klotsche, J. Wittchen, H.-U. Fischer, S. Hanefeld, M. Schwanebeck, U. Simons, L.A. Simons, J. Bender, R. Matthies, S. Nissinen, A. Tolonen, H.K. Tuomilehto, J. Chaturvedi, N. Fuller, J.H. Soedamah-Muthu, S.S. Kotseva, K. Wood, D.A. Bots, M.L. Moons, K.G.M. Heliovaara, M. Knekt, P.B. Rissanen, H. Ferrie, J.E. Shipley, M.J. Smith, G.D. Johansson, S. Lappas, G. Rosengren, A. Sham, A. Yu, R.H.Y. Hata, J. Ninomiya, T. Hoshide, S. Kario, K. Rastenyte, D. Tamosiunas, A. de Simone, G. Devereux, R.B. Gerdts, E. Colquhoun, D.M. Keech, A.C. K and Lu, Y. Hajifathalian, K. Ezzati, M. Woodward, M. Rimm, E.B. Danaei, G. Selmer, R. Strand, B.H. Dobson, A. Hozawa, A. Nozaki, A. Okayama, A. Rodgers, A. Tamakoshi, A. Zhou, B.F. Zhou, B. Yao, C.H. Jiang, C.Q. Gu, D.F. Heng, D. Giles, G.G. Shan, G.L. Whitlock, G. Arima, H. Kim, H.C. Christensen, H. Horibe, H. Maegawa, H. Tanaka, H. Ueshima, H. Zhang, H.Y. Kim, I.S. Suh, I. Fuh, J.L. Lee, J. Woo, J. Xie, J.X. Zhou, J. Hughes, K. Jamrozik, K. Nakachi, K. Sakata, K. Shimamoto, K. Chen, L.Q. Liu, L.S. Hobbs, M. Iida, M. Kagaya, M. Divitini, M.L. Luszcz, M. Nakamura, M. Huang, M.S. Knuiman, M.W. Aoki, N. Norman, P. Sritara, P. Yang, Q.D. Broadhurst, R. Huxley, R. Jackson, R. Norton, R. Ameratunga, S. Ho, S.C. Li, S.C. Jee, S.H. Chew, S.K. Macmahon, S. Choudhury, S.R. Saitoh, S. Yao, S.X. Welborn, T.A. Lam, T.H. Hashimoto, T. Ohkubo, T. Pan, W.-H. Duan, X.F. Fang, X. Wu, X.G. Fang, X.H. Yu, X.H. Li, Y.H. He, Y. Imai, Y. Kita, Y. Kiyohara, Y. Matsutani, Y. Hong, Z. Wu, Z.L. Chen, Z.M. Wu, Z.S. Tang, Z. Li, Z.Z. Parker, E.D. Pereira, M.A. Stevens, J. Panagiotakos, D.B. Pitsavos, C. Attia, J.R. D’este, C.A. Zhang, X. Clays, E. De Bacquer, D.A.O. Van Herck, K. Morrison, H.I. Wang, F. Chuang, S.-Y. Yeh, W.-T. Chen, Z. Smith, M.C. Zhou, M. Wang, W. Zhang, X.-T. Zhao, D. Vollset, S.E. Fuchs, S.C. Fuchs, F.D. Moreira, L.B. Dontas, I.A. Dontas, C.A. Kafatos, A.G. Moschandreas, J. Lanti, M. Menotti, A. Kromhout, D. Jensen, M.K. Overvad, K. Tjonneland, A. Klotsche, J. Wittchen, H.-U. Fischer, S. Hanefeld, M. Schwanebeck, U. Simons, L.A. Simons, J. Bender, R. Matthies, S. Nissinen, A. Tolonen, H.K. Tuomilehto, J. Chaturvedi, N. Fuller, J.H. Soedamah-Muthu, S.S. Kotseva, K. Wood, D.A. Bots, M.L. Moons, K.G.M. Heliovaara, M. Knekt, P.B. Rissanen, H. Ferrie, J.E. Shipley, M.J. Smith, G.D. Johansson, S. Lappas, G. Rosengren, A. Sham, A. Yu, R.H.Y. Hata, J. Ninomiya, T. Hoshide, S. Kario, K. Rastenyte, D. Tamosiunas, A. de Simone, G. Devereux, R.B. Gerdts, E. Colquhoun, D.M. Keech, A.C. K

Abstract

Background Body-mass index (BMI) and diabetes have increased worldwide, whereas global average blood pressure and cholesterol have decreased or remained unchanged in the past three decades. We quantified how much of the effects of BMI on coronary heart disease and stroke are mediated through blood pressure, cholesterol, and glucose, and how much is independent of these factors. Methods We pooled data from 97 prospective cohort studies that collectively enrolled 1·8 million participants between 1948 and 2005, and that included 57 161 coronary heart disease and 31 093 stroke events. For each cohort we excluded participants who were younger than 18 years, had a BMI of lower than 20 kg/m2, or who had a history of coronary heart disease or stroke. We estimated the hazard ratio (HR) of BMI on coronary heart disease and stroke with and without adjustment for all possible combinations of blood pressure, cholesterol, and glucose. We pooled HRs with a random-effects model and calculated the attenuation of excess risk after adjustment for mediators. Findings The HR for each 5 kg/m2 higher BMI was 1·27 (95% CI 1·23-1·31) for coronary heart disease and 1·18 (1·14-1·22) for stroke after adjustment for confounders. Additional adjustment for the three metabolic risk factors reduced the HRs to 1·15 (1·12-1·18) for coronary heart disease and 1·04 (1·01-1·08) for stroke, suggesting that 46% (95% CI 42-50) of the excess risk of BMI for coronary heart disease and 76% (65-91) for stroke is mediated by these factors. Blood pressure was the most important mediator, accounting for 31% (28-35) of the excess risk for coronary heart disease and 65% (56-75) for stroke. The percentage excess risks mediated by these three mediators did not differ significantly between Asian and western cohorts (North America, western Europe, Australia, and New Zealand). Both overweight (BMI ≥25 to <30 kg/m2) and obesity (BMI ≥30 kg/m2) were associated with a significantly increased risk of coronary heart disea

Published
2014

22. A comparison of risk factors for mortality from heart failure in Asian and non-Asian populations: An overview of individual participant data from 32 prospective cohorts from the Asia-Pacific Region

Author

Huxley, RR, Barzi, F, Woo, J, Giles, G, Lam, TH, Rahimi, K, Konety, S, Ohkubo, T, Jee, SH, Fang, X, Woodward, M ; https://orcid.org/0000-0001-9800-5296, Okayama, A, Ueshima, H, Maegawa, H, Nakamura, M, Aoki, N, Wu, ZS, Yao, CH, Luszcz, M, Welborn, TA, Tang, Z, Liu, LS, Xie, JX, Norton, R ; https://orcid.org/0000-0002-3988-315X, Ameratunga, S, MacMahon, S ; https://orcid.org/0000-0003-2064-7699, Whitlock, G, Knuiman, MW, Christensen, H, Wu, XG, Zhou, J, Yu, XH, Tamakoshi, A, Pan, WH, Wu, ZL, Chen, LQ, Shan, GL, Sritara, P, Gu, DF, Duan, XF, G.Whitlock, Jackson, R, Li, YH, Jiang, CQ, Kiyohara, Y, Arima, H, Iida, M, Ho, SC, Hong, Z, Huang, MS, Zhou, B, Fuh, JL, Kita, Y, Choudhury, SR, Suh, I, Kim, IS, Hashimoto, T, Sakata, K, Dobson, A, Imai, Y, Hozawa, A, the late, KJ, Hobbs, M, Broadhurst, R, Nakachi, K, Fang, XH, Li, SC, Yang, QD, Chen, ZM, Tanaka, H, Nozaki, A, Horibe, H, Matsutani, Y, Kagaya, M, Hughes, K, Lee, J, Heng, D, Chew, SK, Zhou, BF, Zhang, HY, Shimamoto, K, Saitoh, S, Li, ZZ, Norman, P, Jamrozik, K, He, Y, Yao, SX, Huxley, RR, Barzi, F, Woo, J, Giles, G, Lam, TH, Rahimi, K, Konety, S, Ohkubo, T, Jee, SH, Fang, X, Woodward, M ; https://orcid.org/0000-0001-9800-5296, Okayama, A, Ueshima, H, Maegawa, H, Nakamura, M, Aoki, N, Wu, ZS, Yao, CH, Luszcz, M, Welborn, TA, Tang, Z, Liu, LS, Xie, JX, Norton, R ; https://orcid.org/0000-0002-3988-315X, Ameratunga, S, MacMahon, S ; https://orcid.org/0000-0003-2064-7699, Whitlock, G, Knuiman, MW, Christensen, H, Wu, XG, Zhou, J, Yu, XH, Tamakoshi, A, Pan, WH, Wu, ZL, Chen, LQ, Shan, GL, Sritara, P, Gu, DF, Duan, XF, G.Whitlock, Jackson, R, Li, YH, Jiang, CQ, Kiyohara, Y, Arima, H, Iida, M, Ho, SC, Hong, Z, Huang, MS, Zhou, B, Fuh, JL, Kita, Y, Choudhury, SR, Suh, I, Kim, IS, Hashimoto, T, Sakata, K, Dobson, A, Imai, Y, Hozawa, A, the late, KJ, Hobbs, M, Broadhurst, R, Nakachi, K, Fang, XH, Li, SC, Yang, QD, Chen, ZM, Tanaka, H, Nozaki, A, Horibe, H, Matsutani, Y, Kagaya, M, Hughes, K, Lee, J, Heng, D, Chew, SK, Zhou, BF, Zhang, HY, Shimamoto, K, Saitoh, S, Li, ZZ, Norman, P, Jamrozik, K, He, Y, and Yao, SX

Abstract

Background: Most of what is known regarding the epidemiology of mortality from heart failure (HF) comes from studies within Western populations with few data available from the Asia-Pacific region where the burden of heart failure is increasing.Methods: Individual level data from 543694 (85% Asian; 36% female) participants from 32 cohorts in the Asia Pacific Cohort Studies Collaboration were included in the analysis. Adjusted hazard ratios (HR) and 95% confidence intervals (CI) for mortality from HF were estimated separately for Asians and non-Asians for a quintet of cardiovascular risk factors: systolic blood pressure, diabetes, body mass index, cigarette smoking and total cholesterol. All analyses were stratified by sex and study.Results: During 3,793,229 person years of follow-up there were 614 HF deaths (80% Asian). The positive associations between elevated blood pressure, obesity, and cigarette smoking were consistent for Asians and non-Asians. There was evidence to indicate that diabetes was a weaker risk factor for death from HF for Asians compared with non-Asians: HR 1.26 (95% CI: 0.74-2.13) versus 3.04 (95% CI 1.76-5.25) respectively; p for interaction = 0.022. Additional adjustment for covariates did not materially change the overall associations. There was no good evidence to indicate that total cholesterol was a risk factor for HF mortality in either population.Conclusions: Most traditional cardiovascular risk factors including elevated blood pressure, obesity and cigarette smoking appear to operate similarly to increase the risk of death from HF in Asians and non-Asians populations alike. © 2014 Huxley et al.; licensee BioMed Central Ltd.

Published
2014

23. A comparison of risk factors for mortality from heart failure in Asian and non-Asian populations: An overview of individual participant data from 32 prospective cohorts from the Asia-Pacific Region

Author

Huxley, Rachel, Barzi, F., Woo, J., Giles, G., Lam, T., Rahimi, K., Konety, S., Ohkubo, T., Jee, S., Fang, X., Woodward, M., Okayama, A., Ueshima, H., Maegawa, H., Nakamura, M., Aoki, N., Wu, Z., Yao, C., Luszcz, M., Welborn, T., Tang, Z., Liu, L., Xie, J., Norton, R., Ameratunga, S., MacMahon, S., Whitlock, G., Knuiman, M., Christensen, H., Wu, X., Zhou, J., Yu, X., Tamakoshi, A., Pan, W., Chen, L., Shan, G., Sritara, P., Gu, D., Duan, X., Jackson, R., Li, Y., Jiang, C., Kiyohara, Y., Arima, H., Iida, M., Ho, S., Hong, Z., Huang, M., Zhou, B., Fuh, J., Kita, Y., Choudhury, S., Suh, I., Kim, I., Hashimoto, T., Sakata, K., Dobson, A., Imai, Y., Hozawa, A., the late, K., Hobbs, M., Broadhurst, R., Nakachi, K., Li, S., Yang, Q., Chen, Z., Tanaka, H., Nozaki, A., Horibe, H., Matsutani, Y., Kagaya, M., Hughes, K., Lee, J., Heng, D., Chew, S., Zhang, H., Shimamoto, K., Saitoh, S., Li, Z., Norman, P., Jamrozik, K., He, Y., Huxley, Rachel, Barzi, F., Woo, J., Giles, G., Lam, T., Rahimi, K., Konety, S., Ohkubo, T., Jee, S., Fang, X., Woodward, M., Okayama, A., Ueshima, H., Maegawa, H., Nakamura, M., Aoki, N., Wu, Z., Yao, C., Luszcz, M., Welborn, T., Tang, Z., Liu, L., Xie, J., Norton, R., Ameratunga, S., MacMahon, S., Whitlock, G., Knuiman, M., Christensen, H., Wu, X., Zhou, J., Yu, X., Tamakoshi, A., Pan, W., Chen, L., Shan, G., Sritara, P., Gu, D., Duan, X., Jackson, R., Li, Y., Jiang, C., Kiyohara, Y., Arima, H., Iida, M., Ho, S., Hong, Z., Huang, M., Zhou, B., Fuh, J., Kita, Y., Choudhury, S., Suh, I., Kim, I., Hashimoto, T., Sakata, K., Dobson, A., Imai, Y., Hozawa, A., the late, K., Hobbs, M., Broadhurst, R., Nakachi, K., Li, S., Yang, Q., Chen, Z., Tanaka, H., Nozaki, A., Horibe, H., Matsutani, Y., Kagaya, M., Hughes, K., Lee, J., Heng, D., Chew, S., Zhang, H., Shimamoto, K., Saitoh, S., Li, Z., Norman, P., Jamrozik, K., and He, Y.

Abstract

Background: Most of what is known regarding the epidemiology of mortality from heart failure (HF) comes from studies within Western populations with few data available from the Asia-Pacific region where the burden of heart failure is increasing.Methods: Individual level data from 543694 (85% Asian; 36% female) participants from 32 cohorts in the Asia Pacific Cohort Studies Collaboration were included in the analysis. Adjusted hazard ratios (HR) and 95% confidence intervals (CI) for mortality from HF were estimated separately for Asians and non-Asians for a quintet of cardiovascular risk factors: systolic blood pressure, diabetes, body mass index, cigarette smoking and total cholesterol. All analyses were stratified by sex and study.Results: During 3,793,229 person years of follow-up there were 614 HF deaths (80% Asian). The positive associations between elevated blood pressure, obesity, and cigarette smoking were consistent for Asians and non-Asians. There was evidence to indicate that diabetes was a weaker risk factor for death from HF for Asians compared with non-Asians: HR 1.26 (95% CI: 0.74-2.13) versus 3.04 (95% CI 1.76-5.25) respectively; p for interaction = 0.022. Additional adjustment for covariates did not materially change the overall associations. There was no good evidence to indicate that total cholesterol was a risk factor for HF mortality in either population.Conclusions: Most traditional cardiovascular risk factors including elevated blood pressure, obesity and cigarette smoking appear to operate similarly to increase the risk of death from HF in Asians and non-Asians populations alike. © 2014 Huxley et al.; licensee BioMed Central Ltd.

Published
2014

24. Adult height and the risks of cardiovascular disease and major causes of death in the Asia-Pacific region: 21 000 deaths in 510 000 men and women

Author

Lee, Crystal, Barzi, F., Woodward, M., Batty, G., Giles, G., Wong, J., Jamrozik, K., Lam, T., Ueshima, H., Kim, H., Gu, D., Schooling, M., Huxley, Rachel, Maegawa, H., Okayama, A., Nakamura, M., Aoki, N., Wu, Z., Yao, C., Luszcz, M., Welborn, T., Tang, Z., Liu, L., Xie, J., Norton, R., Ameratunga, S., MacMahon, S., Whitlock, G., Knuiman, M., Christensen, H., Wu, X., Zhou, J., Yu, X., Tamakoshi, A., Pan, W., Chen, L., Shan, G., Sritara, P., Duan, X., Jackson, R., Li, Y., Jiang, C., Kiyohara, Y., Arima, H., Iida, M., Woo, J., Ho, S., Hong, Z., Huang, M., Zhou, B., Fuh, J., Kita, Y., Choudhury, S., Suh, I., Jee, S., Kim, I., Hashimoto, T., Sakata, K., Dobson, A., Imai, Y., Ohkubo, T., Hozawa, A., Hobbs, M., Broadhurst, R., Nakachi, K., Fang, X., Li, S., Yang, Q., Chen, Z., Tanaka, H., Nozaki, A., Matsutani, Y., Horibe, H., Kagaya, M., Hughes, K., Lee, J., Heng, D., Chew, S., Zhang, H., Shimamoto, K., Saitoh, S., Li, Z., Norman, P., Lee, Crystal, Barzi, F., Woodward, M., Batty, G., Giles, G., Wong, J., Jamrozik, K., Lam, T., Ueshima, H., Kim, H., Gu, D., Schooling, M., Huxley, Rachel, Maegawa, H., Okayama, A., Nakamura, M., Aoki, N., Wu, Z., Yao, C., Luszcz, M., Welborn, T., Tang, Z., Liu, L., Xie, J., Norton, R., Ameratunga, S., MacMahon, S., Whitlock, G., Knuiman, M., Christensen, H., Wu, X., Zhou, J., Yu, X., Tamakoshi, A., Pan, W., Chen, L., Shan, G., Sritara, P., Duan, X., Jackson, R., Li, Y., Jiang, C., Kiyohara, Y., Arima, H., Iida, M., Woo, J., Ho, S., Hong, Z., Huang, M., Zhou, B., Fuh, J., Kita, Y., Choudhury, S., Suh, I., Jee, S., Kim, I., Hashimoto, T., Sakata, K., Dobson, A., Imai, Y., Ohkubo, T., Hozawa, A., Hobbs, M., Broadhurst, R., Nakachi, K., Fang, X., Li, S., Yang, Q., Chen, Z., Tanaka, H., Nozaki, A., Matsutani, Y., Horibe, H., Kagaya, M., Hughes, K., Lee, J., Heng, D., Chew, S., Zhang, H., Shimamoto, K., Saitoh, S., Li, Z., and Norman, P.

Abstract

Background: In Caucasian populations, adult height is inversely associated with cardiovascular disease (CVD) risk and positively related to some cancers. However, there are few data from Asian populations and from women. We sought to determine the sex- and region-specific associations between height and cardiovascular outcomes, and deaths due to cancer, respiratory and injury in populations from the Asia-Pacific region. Methods: Thirty-nine studies from the Asia Pacific Cohort Studies Collaboration database were included. We used Cox proportional hazard regression models to estimate the associations between height and pre-specified outcomes. Results: A total of 510 800 participants with 21 623 deaths were included. Amongst men, inverse linear associations were observed between height and coronary heart disease (CHD), stroke, CVD, injury and total mortality. The hazard ratios [95% confidence intervals, (CI)] for a 1-SD (= 6 cm) increment in height ranged from 0.85 (0.80-0.91) for injury to 0.97 (0.95-0.98) for total mortality. Similar trends were found between height and CHD, haemorrhagic stroke and CVD in women. A positive linear association was observed between height and cancer mortality. For each standard deviation greater height, the risk of cancer was increased by 5% (2-8%) and 9% (5-14%) in men and women, respectively. No regional difference was observed between Asian and Australasian cohorts. Adjusting for markers of education did not alter the results. Conclusions: The opposing relationships of height with CVD and cancer suggest that care is required in setting national policies on childhood nutrition lest they have unintended consequences on the incidence of major non-communicable diseases. Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2009; all rights reserved.

Published
2009

31. Transcatheter Arterial Infusion Chemotherapy with a Fine-powder Formulation of Cisplatin for Advanced Hepatocellular Carcinoma Refractory to Transcatheter Arterial Chemoembolization

Author

Iwasa, S., primary, Ikeda, M., additional, Okusaka, T., additional, Ueno, H., additional, Morizane, C., additional, Nakachi, K., additional, Mitsunaga, S., additional, Kondo, S., additional, Hagihara, A., additional, Shimizu, S., additional, Satake, M., additional, and Arai, Y., additional

Published
2011
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39. Gemcitabine alone or in combination with cisplatin in patients with biliary tract cancer: a comparative multicentre study in Japan

Author

Okusaka, T, primary, Nakachi, K, additional, Fukutomi, A, additional, Mizuno, N, additional, Ohkawa, S, additional, Funakoshi, A, additional, Nagino, M, additional, Kondo, S, additional, Nagaoka, S, additional, Funai, J, additional, Koshiji, M, additional, Nambu, Y, additional, Furuse, J, additional, Miyazaki, M, additional, and Nimura, Y, additional

Published
2010
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46. Changes of ROS during a Two-day Ultra-marathon Race

Author

Hattori, N., primary, Hayashi, T., additional, Nakachi, K., additional, Ichikawa, H., additional, Goto, C., additional, Tokudome, Y., additional, Kuriki, K., additional, Hoshino, H., additional, Shibata, K., additional, Yamada, N., additional, Tokudome, M., additional, Suzuki, S., additional, Nagaya, T., additional, Kobayashi, M., additional, and Tokudome, S., additional

Published
2009
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