75 results on '"Parving, H H"'
Search Results
2. Short stature and diabetic nephropathy
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Rossing, P., Tarnow, L., Nielsen, F.S., Boelskifte, S., Brenner, B.M., and Parving, H.-H.
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Stature, Short -- Health aspects -- Risk factors ,Diabetic nephropathies -- Risk factors -- Health aspects ,Health ,Risk factors ,Health aspects - Abstract
Recent studies have suggested that low birth weight is associated with a reduced number of nephrons and hypertension in later life,[1 2] both well known risk factors for renal disease. [...]
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- 1995
3. Pulse pressure is not an independent predictor of outcome in type 2 diabetes patients with chronic kidney disease and anemia—the Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT)
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Theilade, S, Claggett, B, Hansen, T W, Skali, H, Lewis, E F, Solomon, S D, Parving, H-H, Pfeffer, M, McMurray, J J, and Rossing, P
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Pulse pressure (PP) remains an elusive cardiovascular risk factor with inconsistent findings. We clarified the prognostic value in patients with type 2 diabetes, chronic kidney disease (CKD) and anemia in the Trial to Reduce cardiovascular Events with Aranesp (darbepoetin alfa) Therapy. In 4038 type 2 diabetes patients, darbepoetin alfa treatment did not affect the primary outcome. Risk related to PP at randomization was evaluated in a multivariable model including age, gender, kidney function, cardiovascular disease (CVD) and other conventional risk factors. End points were myocardial infarction (MI), stroke, end stage renal disease (ESRD) and the composite of cardiovascular death, MI or hospitalization for myocardial ischemia, heart failure or stroke (CVD composite). Median (interquartile range) age, gender, eGFR and PP was 68 (60–75) years, 57.3% women, 33 (27–42) ml min−1per 1.73 m2and 60 (50–74) mm Hg. During 29.1 months (median) follow-up, the number of events for composite CVD, MI, stroke and ESRD was 1010, 253, 154 and 668. In unadjusted analyses, higher quartiles of PP were associated with higher rates per 100 years of follow-up of all end points (P⩽0.04), except stroke (P=0.52). Adjusted hazard ratios (95% confidence interval) per one quartile increase in PP were 1.06 (0.99–1.26) for MI, 0.96 (0.83–1.11) for stroke, 1.01 (0.94–1.09) for ESRD and 1.01 (0.96–1.07) for CVD composite. Results were similar in continuous analyses of PP (per 10 mm Hg). In patients with type 2 diabetes, CKD and anemia, PP did not independently predict cardiovascular events or ESRD. This may reflect confounding by aggressive antihypertensive treatment, or PP may be too rough a risk marker in these high-risk patients.
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- 2016
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4. A prediction of the renal and cardiovascular efficacy of aliskiren in ALTITUDE using short-term changes in multiple risk markers
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Smink, PA, Hoekman, J, Grobbee, DE, Eijkemans, MJC, Parving, H-H, Persson, F, Ibsen, H, Lindholm, L, Wachtell, K, de Zeeuw, D, and Heerspink, HJ
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IntroductionWe recently developed and validated in existing trials a novel algorithm (PRE score) to predict long-term drug efficacy based on short-term (month-6) drug-induced changes in multiple risk markers. To show the value of the PRE score for ongoing and planned clinical trials, we here report the predicted long-term cardio-renal efficacy of aliskiren in type 2 diabetes, which was investigated in the ALTITUDE trial, but unknown at the time this study was conducted.MethodsWe established the relation between multiple risk markers and cardio-renal endpoints (as defined in ALTITUDE) using a background database from past clinical trials. The short-term effect of aliskiren on multiple risk markers was taken from the AVOID trial. A PRE score was developed by multivariate Cox analysis in the background population and was then applied to the baseline and month-6 measurements of the aliskiren treatment arm of the AVOID trial to predict cardio-renal risk. The net risk difference at these time-points, after correction for placebo effects, was taken to indicate the estimated long-term cardio-renal risk change.ResultsBased on the PRE score, we predicted that aliskiren treatment in ALTITUDE would confer a relative risk change of −7.9% (95% CI −2.5 to −13.4) for the cardio-renal endpoint, a risk change of −5.1% (−1.2 to −9.0) for the CV endpoint and a non-significant risk change of −19.9% (−42.1 to +2.1) for the renal endpoint.ConclusionsPRE score estimations suggested that aliskiren has only a marginal additive protective effect on cardio-renal endpoints. These predictions were validated by the results of the ALTITUDE trial, confirming the potential of the PRE score to prospectively predict drug efficacy on cardio-renal outcomes.
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- 2014
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5. Dual Blockade of the Renin-angiotensin-aldosterone System in Diabetic Nephropathy: The Role of Aldosterone
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Schjoedt, K. J., Jacobsen, P., Rossing, K., Boomsma, F., and Parving, H. H.
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- 2005
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6. Controlling hypertension in diabetes
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Parving, H. H.
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Abstract Patients with type 2 diabetes are especially vulnerable to both large and small vessel injury from elevated arterial blood pressure. The frequent combination of hypertension and diabetes is, therefore, associated with a high risk of cardiovascular events and end-stage renal disease. The beneficial therapeutic effects of angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers (CCBs), and other antihypertensive drugs in patients with type 2 diabetes have been well established in placebo-controlled trials, and there appears to be no evidence of differences between treatment regimens based on different drug classes. In addition, a number of major clinical trials have supported a policy of aggressive blood pressure lowering in patients with type 2 diabetes. In the UK Prospective Diabetes Study, for example, tight control of blood pressure was demonstrated to produce clinically important reductions in the risk of complications related to type 2 diabetes compared with less tight control. In most hypertensive patients, however, a reduction to a recommended levels <130/85 mm Hg is unlikely to be achieved by monotherapy. Consequently, the combination of ACE inhibitors with other first-line drugs, such as CCBs, diuretics and beta-blockers, is recommended for the therapeutic management of hypertensive diabetic patients.
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- 2002
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7. Cataract surgery on diabetic patients. A prospective evaluation of risk factors and complications
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Flesner, P., Sander, B., Henning, V., Parving, H-H., Cour, M.D. de la, and Lund-Andersen, H.
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.Purpose: This study presents an evaluation of cataract surgery on diabetic patients. One experienced surgeon carried out phaco emulsification on all subjects and the same surface-coated one-piece PMMA-lens-type was implanted. The lens fluorescence and the blood-aqueous barrier (BAB) were then evaluated as experimental preoperative risk indicators.Results: During follow-up, 10 out of 39 diabetic patients progressed unilaterally in diabetic retinopathy or developed macular oedema, a significant relative risk. Neither lens fluorescence, BAB, HbA1c, level of retinopathy, type/duration of diabetes, diabetes treatment or antihypertensive treatment differed significantly between the group of patients with postoperative progression of retinopathy/macular oedema and those without. Results indicated NIDDM (non-insulin-dependent diabetes mellitus/type 2 diabetes) patients might have increased risk of a postoperative macular oedema.Conclusion:When diabetic retinopathy (DR) is not in a proliferative phase it should not be regarded as a contraindication to modern cataract surgery. Neither lens fluorescence nor BAB is valuable as a risk indicator for postoperative progression of DR.
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- 2002
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8. Renal function and structure in albuminuric type 2 diabetic patients without retinopathy.
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Christensen, P K, Larsen, S, Horn, T, Olsen, S, and Parving, H H
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In type 2 diabetic patients without retinopathy the cause of albuminuria is heterogeneous and our knowledge of the relationship between kidney structure and function in these patients is limited. Therefore, a long-term study evaluating the structural-functional relationship in albuminuric type 2 diabetic patients without retinopathy was performed.
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- 2001
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9. Elevated levels of plasma von Willebrand factor and the risk of macro- and microvascular disease in type 2 diabetic patients with microalbuminuria.
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Gaede, P, Vedel, P, Parving, H H, and Pedersen, O
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The purpose of this study was to examine the concept suggesting that microalbuminuria in combination with high levels of plasma von Willebrand factor is a stronger predictor for cardiovascular disease and microvascular complications than microalbuminuria alone in type 2 diabetic patients.
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- 2001
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10. Diabetic microvascular complications are not associated with two polymorphisms in the GLUT-1 and PC-1 genes regulating glucose metabolism in Caucasian type 1 diabetic patients.
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Tarnow, L, Grarup, N, Hansen, T, Parving, H H, and Pedersen, O
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An XbaI polymorphism in the gene encoding the glucose transporter, GLUT-1, is associated with development of diabetic nephropathy in Chinese type 2 diabetic patients. In addition, an amino acid variant (K121Q) in the gene encoding the glycoprotein plasma cell differentiating antigen (PC-1), a specific inhibitor of insulin receptor signalling, has been reported to predict a faster progression of nephropathy in Italian and British type 1 diabetic patients.
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- 2001
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11. Plasminogen activator inhibitor-1 and apolipoprotein E gene polymorphisms and diabetic angiopathy.
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Tarnow, L, Stehouwer, C D, Emeis, J J, Poirier, O, Cambien, F, Hansen, B V, and Parving, H H
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A point mutation in the plasminogen activator inhibitor-1 (PAI-1) gene and a three-allelic variation in the apolipoprotein-E (ApoE) gene have been suggested as risk factors for the development of diabetic micro- and macrovascular complications.
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- 2000
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12. Prevalence of left ventricular hypertrophy in Type I diabetic patients with diabetic nephropathy
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Sato, A., Tarnow, L., and Parving, H.-H.
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The increased mortality of patients with diabetic nephropathy is mainly due to cardiovascular disease and end stage renal failure. Left ventricular hypertrophy is an independent risk factor for myocardial ischaemia and sudden death. The aim of our cross-sectional study was to evaluate left ventricular structure and function in Type I (insulin-dependent) diabetic patients with diabetic nephropathy. M-mode and Doppler echocardiography were done on 105 Type I diabetic patients with diabetic nephropathy [61 men, age (means ± SD) 44 ± 9 years, and albuminuria [median(range)] 567(10–8188) mg/24 h, serum creatinine 109 (53–558) μmol/l], and 140 Type I diabetic patients with persistent normoalbuminuria [79 men, 47 ± 10 years, urinary albumin excretion rate 8 (0–30) mg/24 h, and serum creatinine 81 (55–121) μmol/l]. Patients with and without nephropathy were comparable with respect to sex, body mass index, and duration of diabetes. Arterial blood pressure was slightly higher in patients with nephropathy: 140/79 ± 17/9 mm Hg vs 134/78 ± 15/8 mm Hg, p< 0.01, and the majority of proteinuric patients received antihypertensive drugs, 84 vs 17 %, respectively, p< 0.001. Left ventricular mass index was increased in the nephropathic group (means ± SD) 100.6 ± 23.9 g/m2compared with the normoalbuminuric group 91.4 ± 21.9 g/m2, p= 0.002. Left ventricular hypertrophy was found more often in patients with nephropathy 23 (14–31)% compared with patients with normoalbuminuria 9 (5–14)%, p< 0.005. Diastolic function, assessed by the ratio between the peak diastolic velocity and the peak atrial systolic velocity (E/A ratio) and isovolumic relaxation time, was reduced in patients with vs without nephropathy: 1.17 ± 0.29 vs 1.34 ± 0.32, and 81.7 ± 16.5 vs 74.6 ± 14.5, p< 0.001 and p= 0.002, respectively. Systolic function was about the same and normal in both groups. Our study suggests that an increase in left ventricular mass index and a decrease in diastolic function occurs early in the course of diabetic nephropathy. [Diabetologia (1999) 42: 76–80]The increased mortality of patients with diabetic nephropathy is mainly due to cardiovascular disease and end stage renal failure. Left ventricular hypertrophy is an independent risk factor for myocardial ischaemia and sudden death. The aim of our cross-sectional study was to evaluate left ventricular structure and function in Type I (insulin-dependent) diabetic patients with diabetic nephropathy. M-mode and Doppler echocardiography were done on 105 Type I diabetic patients with diabetic nephropathy [61 men, age (means ± SD) 44 ± 9 years, and albuminuria [median(range)] 567(10–8188) mg/24 h, serum creatinine 109 (53–558) μmol/l], and 140 Type I diabetic patients with persistent normoalbuminuria [79 men, 47 ± 10 years, urinary albumin excretion rate 8 (0–30) mg/24 h, and serum creatinine 81 (55–121) μmol/l]. Patients with and without nephropathy were comparable with respect to sex, body mass index, and duration of diabetes. Arterial blood pressure was slightly higher in patients with nephropathy: 140/79 ± 17/9 mm Hg vs 134/78 ± 15/8 mm Hg, p< 0.01, and the majority of proteinuric patients received antihypertensive drugs, 84 vs 17 %, respectively, p< 0.001. Left ventricular mass index was increased in the nephropathic group (means ± SD) 100.6 ± 23.9 g/m2compared with the normoalbuminuric group 91.4 ± 21.9 g/m2, p= 0.002. Left ventricular hypertrophy was found more often in patients with nephropathy 23 (14–31)% compared with patients with normoalbuminuria 9 (5–14)%, p< 0.005. Diastolic function, assessed by the ratio between the peak diastolic velocity and the peak atrial systolic velocity (E/A ratio) and isovolumic relaxation time, was reduced in patients with vs without nephropathy: 1.17 ± 0.29 vs 1.34 ± 0.32, and 81.7 ± 16.5 vs 74.6 ± 14.5, p< 0.001 and p= 0.002, respectively. Systolic function was about the same and normal in both groups. Our study suggests that an increase in left ventricular mass index and a decrease in diastolic function occurs early in the course of diabetic nephropathy. [Diabetologia (1999) 42: 76–80]
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- 1999
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13. 35th Annual Meeting of the European Association for the Study of Diabetes
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessières-Lacombe, S., Tauber, J.-P., Home, P. D., Lindholm, A., Riis, A., Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Steiner, G., Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Vergès, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph., Benko, B., Ljubić, S., Turk, Z., Granić, M., März, W., Wollschläger, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O’Rahilly, S., Hattersley, A. T., McCarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., de Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Van Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Simán, C., Wisse, Bert, Gittenberger-de Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ożegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rość, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Škrha, J., Kvasnička, J., Kalvodová, B., Hilgertová, J., Schatteman, K., Goossens, F., Scharpé, S., De Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th. D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Häring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., McKinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnæs, A. M., Andersen, N. Aa., Osterhoff, M., Möhlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Fürnsinn, C., Nowotny, P., Waldhäusl, W., Roden, M., Neeft, M., Meijer, A. J., Båvenholm, P., Pigon, J., Efendic, S., Kästenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Van Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovská, A., Kasalicky, P., Hosová, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefèbvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valéro, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., de Galan, B., Netea, M. G., Hancu, N., Smits, P., Van der Meer, J. W. M., Osterbye, T., Jørgensen, K. H., Tranum-Jensen, J., Fredman, P., Høy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patanè, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., de Vos, P., Visser, L., de Haan, B. J., Klok, P., van Schilfgaarde, R., Poppema, S., Juang, J.-H., Kuo, C.-H., Hsu, B. R.-S., Nacher, V., Pérez, M., Biarnés, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Büsing, M., Becker, T., Klempnauer, J., Hücking, K., Schmiegel, W. H., Nauck, M. A., Bouček, P., Saudek, F., Adamec, M., Kožitarová, R., Jedináková, T., Vlasáková, Z., Skibová, J., Bartoš, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J.-C., Gillespie, J. S., McMaster, D., Mercer, C., Trimble, E. R., Lecomte, M., Véricel, E., Paget, C., Ruggiero, D., Lagarde, M., Wiernsperger, N., Pricci, F., Leto, G., Amadio, L., Cordone, S., Iacobini, C., Catalano, S., Violi, F., Rotella, C. M., Pugliese, G., Zicari, A., Gradini, R., Sale, P., Pala, L., Cresci, B., Giannini, S., Manuelli, C., Dahlfors, G., Arnqvist, H. J., Gonelle-Gispert, C., Halnan, P. A., Sadoul, K., Wolter, S., Lang, J., Niwa, T., Yu, W., Hidaka, H., Senda, T., Niki, I., Fukasawa, T., Renstrom, E., Barg, S., Seward, E., Rorsman, P., Rutter, G. A., Molinete, M., Lilla, V., Ravazzola, M., Halban, P. A., Efanov, A. M., Bertorello, A. M., Zaitsev, S. V., Zwiller, J., Berggren, P.-O., MŞengül, A., Salman, F., Sargrn, M., Özer, E., Karşidaǧ, K., Salman, S., Gedik, S., Satman, İ., Dinççaǧ, N., Yılmaz, M. T., Lloyd, A., Hopkinson, P. K., Testa, M. A., Blonde, L., Turner, R. R., Hayes, J., Simonson, D. C., van der Ven, N. C. W., Lubach, C. H. C., Snoek, F. J., Mollema, E. D., van der Ploeg, H. M., Danne, T., Hoey, H., McGee, H., Fitzgerald, H., Lernmark, B., Thernlund, G., Fredin, K., Hägglöf, B., Lugari, R., Dell’Anna, C., Ugolotti, D., Dei Cas, A., Barilli, A. L., Sard, L., Marani, B., Iotti, M., Zandomeneghi, R., Gnudi, A., Kjems, L. L., Volund, Aa., Toft-Nielsen, M., Damholt, M. B., Hilsted, L., Hughes, T. E., Krarup, T., Holst, J. J., Young, A., Gottlieb, A., Fineman, M., Kolterman, O., Cancelas, J., García-Martínez, J. A., Villanueva-Peñacarrillo, M. L., Valverde, I., Malaisse, W. J., Filipsson, K., Ahrén, B., Balkan, B., Kwasnik, L., Battle, B., Li, X., Egan, J. M., Clocquet, A. R., Elahi, D., Petrella, E., Pricket, K., Petersen, K. F., Sullivan, J. T., Amatruda, J. M., Livingston, J. N., Shulman, G. I., Freyse, E.-J., Knospe, S., Glund, K., Demuth, H.-U., Walker, D., Malik, R. A., Reljanovic, M., Barada, A., Milicevic, Z., Tack, Cees J., Goldstein, David S., Van Huysen, C., Stevens, M. J., Cao, X., Sundkvist, G., Dahlin, L.-B., Eriksson, K.-F., Rosén, I., Lattimer, S. A., Sima, A. A. F., Sullivan, K., Shaw, J. E., de Courten, M. P., Zimmet, P. Z., Gourdy, P., Ruidavets, J. B., Arveiler, D., Amouyel, Ph., Bingham, A., Tauber, J. P., Lam, K. S. L., Wat, N. M. S., Lam, T. H., Janus, E. D., de Pablos, P., Rodriguez, F., Martínez, J., Sánchez, V., Santana, C., García, I., Macías, A., Levin, K., Hother-Nielsen, O., Henriksen, J. E., Beck-Nielsen, H., Brechtel, K., Machann, J., Koch, M., Nielsen, M., Löblein, K., Becker, R., Denignger, M., Renn, W., Machicao, F., Claussen, C. D., Schick, F., Diraison, F., Moulin, P., Beylot, M., Thams, P., Capito, K., Eliasson, Lena, Barg, Sebastian, Göpel, Sven, Kanno, Takahiro, Renström, Erik, Meda, P., Charollais, A., Gjnovci, A., Calabrese, A., Wonkam, A., Caton, D., Wisznievski, L., Serre, V., Cogne, F., Bauquis, J., Bosco, D., Huarte, J., Herrera, P., Gotfredsen, C. F., Vessby, B., Manuel y Keenoy, B., Engelen, W., Vertommen, J., Schrans, S., Louheranta, A., Lindström, J., Tuomilehto, J., Segal, K. R., Heymsfield, S., Hauptman, J., Boldrin, M., Lucas, C., Pandolfi, A., Cetrullo, D., Polishchuck, R., Alberta, M., Pellegrini, G., Calafiore, A., Vitacolonna, E., Capani, F., Consoli, A., Halleux, C. M., Gillot, E. F., Brichard, S. M., Van der Planken, M., Corthouts, B., Peiffer, F., Scholten, D., Walke, M., Assert, R., Pirags, V., Pedula, K. L., Hillier, T. A., Brown, J. B., Santini, S. A., Marra, G., Cotroneo, P., Manto, A., Di Leo, M. A. S., Di Gregorio, S., Tordi, A., Pitocco, D., Ruotolo, V., Ghirlanda, G., Temelkova-Kurktschiev, T., Schaper, F., Koehler, C., Henkel, E., Hanefeld, M., Mancini, L., Citterio, F., Cotroneo, A., Ceroone, S., Castagneto, M., Rajbhandari, S. M., Dent, M. T., Plater, M. E., Harris, N. D., Tesfaye, S., Ward, J. D., Dupuy, O., Mayaudon, H., Lecoules, S., Bauduceau, B., Palou, M., Farret, O., Molinié, C., Antonelli-Incalzi, R., Fuso, L., Giordano, A., Calcagni, M. L., Todaro, L., Basso, S., Tramaglino, L. M., Troncone, L., Pistelli, R., Guillot, R., Bringuier, A., Porokhov, B., Guillausseau, P. J., Feldmann, G., Zivanic, S., Cizmic, M., Dragojevic, R., Vanovic, M., Borghouts, L. B., van Kranenburg, G. P. J., Schaart, G., Keizer, H. A., Niess, A. M., Dickuth, H. H., Lutz, O., Barbe, P., Calazel-Fournier, C., Hernandez, G., Saint-Martin, F., Galitzky, J., Gonçalves, A. A., da Silva, E. C., Brito, I. J. L., da Silva, C. A., Lawrence, N. J., Kousta, E., Mulnier, H., Penny, A., Millauer, B., Johnston, D. G., Robinson, S., Perriello, G., Pimenta, W., Pampanelli, S., Lucidi, P., Lepore, M., Porcellati, F., Cordoni, M. C., De Feo, P., Bolli, G. B., Sjöstrand, M., Holmäng, A., Lönnroth, P., Hauer, B., Grauer, P., Artzner, S., Lang, R., Stumvoll, M., Monti, L. D., Piatti, P. M., Gemone, F., Valsecchi, G., Magni, M., Barbieri, E., Setola, E., Sandoli, E. P., Galli-Kienle, M., Pontiroli, A. E., Nichols, Gregory A., Brown, Jonathan B., Salzsieder, E., Boltz, H., Ramirez, J. C., Rutscher, A., Fischer, U., Koenig, Ch., Friske, M., Schramm, W., Landgraf, R., Bachmann, W., Bangemann, M., Groeneveld, G., Edvell, Anders, Lindström, Per, Tsiotra, P., Koukourava, A., Raptis, S. A., Tsigos, C., Boutou, E., Triandaffilopoulou, A., Egido, E. M., Rodríguez-Gallardo, J., Gutiérrez, E., García, P., Silvestre, R. A., Marco, J., Khan, Akhtar, Ling, Zong-Chao, Ahren, Bo, Efendic, Suad, Bünting, C., Du, X., Zhi Sui, G., Rösen, P., Koschinsky, T., Kearney, T. M., Sharp, P. S., Lapolla, A., Fedele, D., Martano, L., Garbeglio, M., Seraglia, R., Favretto, D., Traldi, P., Meerwaldt, R., Smit, A. J., Links, Th. P., v. Roon, A. M., Graaf, R., Gans, R. O. B., Deynelİ, O., Ersöz, H. Ö., Gogas, D., Fak, A. S., Akalin, S., Veglio, M., Sivieri, R., Chinaglia, A., Scaglione, L., Le, T., Wong, N., Detrano, R., Charles, M. A., Colhoun, H. M., Francis, D. P., Rubens, M., Underwood, S. R., Fuller, J. H., Knudsen, E., Sato, A., Nielsen, F. S., Bonora, E., Kiechl, S., Willeit, J., Oberhollenzer, F., Egger, G., Bonadonna, R., Muggeo, M., Festa, A., D’Agostino, R., Howard, G., Mykkänen, L., Tracy, R. P., Haffner, S. M., Poulsen, P., Vach, K., Ijzerman, R. G., Bakker, S. J. L., Truster, J., Crowther, N. J., Cameron, N., Gray, I. P., Chaillous, L., Carel, J. C., Thivolet, C., Boitard, C., Charbonnel, B., Saï, P., Decochez, K., Keymeulen, B., Somers, G., Dorchy, H., Rottiers, R., Winnock, F., ver Elst, K., Weets, I., Pipeleers, D., Gorus, F., Seebaum, S., Schumm-Draeger, P.-M., Petzoldt, R., Federlin, K., Bonnevie-Nielsen, V., Martensen, P. M., Justesen, J., Worsaa, A., Karlsson, Maria, Sederholm, Sofia, Ludvigsson, Johnny, Bélicar, P., Dale, C., Vague, Ph., Alessis, C., Lassmann-Vague, V., Bode, B. W., Gross, T. M., Ghegan, M., Steed, R. D., Davidson, P. C., Ordoñez, A., Rubio, J. L., Sulleiro, J. M., Buendía, J. P., Zamora, J., Castillo, M., Schaupp, L., Ellmerer, M., Brunner, G. A., Sendlhofer, G., Schlack, Ch., Skrabal, F., Wach, P., Pieber, T. R., Heinemann, L., Krämer, U., Klötzer, H. M., Hermann, M., Cosgrove, K. E., Chapman, J. C., Shepherd, R. M., McIntyre, S., Butler, P. C., Dunne, M. J., Brekardin, E., Dörschner, H., Schwanstecher, C., Schwanstecher, M., Uhde, I., Emmanouilidou, E., Teschemacher, A. G., Pouli, A. E., Gylfe, E., Tengholm, A., Hellman, B., Perfetti, R., Aggarwal, S., Müller, Günter, Welte, Stefan, Wied, Susanne, Valverde, A. M., Mur, C., Kahn, C. R., Benito, M., Rondinone, C. M., Peterson, T., Laviola, L., Belsanti, G., Logoluso, F., Napoli, R., Davalli, A. M., Weir, G. C., Giorgino, R., Giorgino, F., Flesch, S., Hompesch, B., Rave, K., Susanto, F., Kühn-Velten, W. N., Heise, T., Rendell, M., Dole, J., Esper, R. J., Stein, E., Lemme, L., Rubinstein, A., Maritz, F. J., Soule, S., Market, A., Chajek-Shaul, T., Maislos, M., Tal, S., Stolero, D., Josefsen, K., Beckmann, H., Petersen, C., Ekman, R., Efanova, I., Zaitsev, S., Berggren, P. O., Birkenbach, M., Holl, R. W., Rosenbauer, J., Grabert, M., Icks, A., Schwab, O., Reile, K., Janssen, M. M. J., de Jongh, R. T., Casteleijn, S., Masurel, N., Hoogma, R. P. L. M., Santeusanio, F., Brunetti, P., Fanelli, C. G., Laureti, S., Bartocci, L., Maran, A., Crepaldi, C., Trupiani, S., Macdonald, I. A., Avogaro, A., Bouman, S. D., Keitz, M., Bruggink, J. E., Scheurink, A. J. W., Strubbe, J. H., Steffens, A. B., Ferguson, S. C., McCrimmon, R. J., Perros, P., Best, J. J. K., Deary, I. J., Frier, B. M., Robinson, R. T. C. E., Ireland, N. H., Bedford, C., Fairclough, E., Hudson, S., Heller, S. R., Borch-Johnsen, K., Berger, M., Overmann, H., Bender, R., Blank, M., Sawicki, P., Jörgens, V., Mühlhauser, I., Nosadini, R., Sailer, A., Dalla Vestra, M., Brocco, E., Piarulli, F., Frigato, F., Sambataro, M., Velussi, M., Baggio, B., Fioretto, P., Jager, A., van Hinsbergh, V. W. M., Kostense, P. J., Nrjpels, G., Gæde, P., Pedersen, O., Andrysiak-Mamos, E., Majkowska, L., Krzyżanowska, B., Pilarska, K., Czekalski, S., Mazzon, C., Brocco, S., Field, L. L., Nejentsev, S., Gombos, Z., Veijola, R., Knip, M., Simell, O., Vaarala, O., Åkerblom, H. K., Ilonen, J., Krokowski, M., Bodalski, J., Andrzejewski, W., Ławnik, M., Teodorczyk, A., Heinrich, A., Caillat-Zucman, S., Buzzetti, R., Petrone, A., Mesturino, C., Giorgi, G., Fiori, R., Nisticò, L., Di Genova, G., Cascino, I., Klöting, I., Kovacs, P., McKinney, P. A., Okasha, M., Parslow, R. C., Law, G. R., Gurney, K. A., Williams, R., Bodansky, H. J., Herzig, P., Giani, G., Vervoort, G., Lutterman, J. A., Berden, J. H. M., Wetzels, J. F. M., Paniagua, O., Shaw, L., Austin, C., Heagerty, A. M., Seppälä-Lindroos, A., Vehkavaara, S., Yki-Järvinen, H., Caballero, A. E., Lim, S. C., LoGerfo, F. W., Horton, E. S., Zembowicz, A., Fragasso, G., Caumo, A., Phan, V. C., Costa, S., Conti, M., Chierchia, S. L., Vigili de Kreutzenberg, S., Marchetto, S., Calò, L., Wascher, T. C., Wölkart, G., Brunner, F., Tripathy, Devjit, Carlsson, Martin, Isomaa, Bo, Tuomi, Tiinamaija, Groop, Leif, Stoffers, D. A., Muller, D. C., Wideman, L., Chin, G. A., Clarke, W. L., Hanks, J. B., Habener, J. F., Guazzarotti, L., Toffolo, G., Clementi, L., Vespasiani, G., Cobelli, C., Clauin, S., Bellanné-Chantelot, C., Bartolotta, E., Gautier, J.-F., Wilson, C., Weyer, C., Mort, D., Knowler, W. C., Polonsky, K., Bogardus, C., Pratley, R. E., Porksen, N., Veldhuis, J. D., Polonsky, K. S., Byrne, M. M., Brandt, A., Arnold, R., Katschinski, M., Göke, B., Hardt, E., Fritsche, A., Stefan, N., Schützenauer, S., Lüddeke, H. J., Renner, R., Hepp, K. D., Shnawa, N., Krugluger, W., Hopmeier, P., Schernthaner, G., Kautzky-Willer, A., Prager, R., Fallucca, F., Sabbatini, A., Sciullo, E., Torresi, P., Mazziotti, F., Maroccia, E., Napoli, A., Buongiorno, A., Deberg, M., Dozio, N., Castiglioni, M. T., Sodoyez-Goffaux, F., Carvalheiro, M., Fagulha, I., Fagulha, A., Gomes, L., Paiva, S., Marta, E., Sobral, E., Leitão, F., Pinto, L., Ruas, M., Buchanan, T., Di Cianni, G., Volpe, L., Casadidio, I., Bottone, P., Teti, G., Boldrini, A., Benzi, L., Rasera, T., Becciu, V., Beretta, A., Almirante, G., Castiglioni, M., Kerényi, Zs., Stella, P., Nádasdi, Á., Baranyi, É., Csákány, M. Gy., Tamás, Gy., Mehta, Z. M., Manley, S., Zimmett, P., Bottazzo, G. F., Hoey, Hilary, Mollensen, Henrik, Hougaard, Philip, McGee, Hanna, Vidal, J., Fernández, M., Sesmilo, G., Casamitjana, R., Gomis, R., Conget, I., Rathmann, W., Curran, S., Mitchell, J., Hennings, S., Katsaros, T., Saflianis, I., Gigiakou, E., Kasi, E., Polychroniades, V., Dzien, A., Dzien-Bischinger, Ch., Hadjidakis, D., Apostolopoulou, N., Sfakianakis, M., Raptis, A. E., Ryysy, L., Häkkinen, A.-M., Goto, T., Westerbacka, J., Halavaara, J., Libman, I., Pietropaolo, M., LaPorte, R., Pietropaolo, S., Becker, D., Pirie, F. J., York, D. F., Motala, A. A., Omar, M. A. K., Tzaneva, V., Iotova, V., Jaeger, C., Hatziagelaki, E., Stroedter, A., Becker, F., Bretzel, R. G., Strebelow, M., Schlosser, M., Ziegler, B., Ziegler, M., Wassmuth, R., Ostrauskas, R., Žalinkevičius, R., Norkus, A., Jarosz-Chobot, P., Otto-Buczkowska, E., Koehler, B., Maklakiewicz, E., Green, A., Ionescu-Tirgoviste, C., Serban, V., Guja, C., Mota, M., Creteanu, G., Calin, A., Morosanu, M., Ferariu, I., Halmagy, I., Cristescu, I., Strugariu, M., Minescu, A., Barbul, R., Visalli, N., Sabastiani, L., Adorisio, E., Cassone Faldetta, M. R., Multari, G., Casu, A., Songini, M., Pozzilli, P., Muntoni, Sa., Wäänänen, S., Law, G., Muntoni, S., Shubnikov, E., Choubnikova, J., Mikulecký, M., Michalková, D., Hlava, P., Teuscher, A. U., Reinli, K., Teuscher, A., Zhao, H. X., Stenhouse, E., Moyeed, R., Demaine, A. G., Millward, B. A., Feltbower, R. G., Holland, P., Campbell, F., Fear, N. T., Wasmuth, H. E., Elliott, R. B., McLachlan, C., Erhardt, G., Kolb, H., Guaita, G., Pelligra, I., Motzo, C., Obinu, M., Cossu, E., Cirillo, R., Kinalski, M., Krętowski, A., Bingley, P., Kinalska, I., Douek, I. F., Bingley, P. J., Gale, E. A. M., Imagawa, A., Hanafusa, T., Miyagawa, J., Matsuzawa, Y., Todd, J. A., Welsh, K., Marshall, S., Nolsøe, R., Kristiansen, O. P., Larsen, Z., Johannesen, J., Jahromi, M. M., Larsen, Z. M., Kyvik, K. O., Jeanclos, E., Schork, N. J., Aviv, A., Sieradzki, J., Małecki, M. T., Klupa, T., Hanna, L., Sieradzka, J., Frey, J., Królewski, A. S., Calvo, B., Bilbao, J. R., Perez de Nanclares, G., Castaño, L., Santos, J. L., Pérez-Bravo, F., Piquer, S., Puig-Domingo, M., Carrasco, E., Calvillán, M., De Leiva, A., Albala, C., Cavallo, M. G., Manca Bitti, M. L., Suraci, C., Crinò, A., Giordano, C., Cervoni, M., Sbriglia, M. S., Bizzarri, C., Marietti, G., Füchtenbusch, M., Bonifacio, E., Kredel, K., Schnell, O., Ziegler, A. G., Assaad-Khalil, S. H., Michelsen, B. K., El-Azzouni, O., Abou-Seif, M., Kamel, F., Fouad, K., Abdel-Aty, T., El-Sheikh, S., Zamani, Mahdi, Pociot, Hemming, Nerup, Jorn, Cassiman, Jean-Jacques, Olivares, E., Ladrière, L., Laghmich, A., Sener, A., Scott, F. W., Ivanova, O., Poltorack, V., Gorbenko, N., Gladkich, A., Nikitchenko, I., Dunger, A., Augstein, P., Berg, S., Williams, A. J. K., Norcross, A. J., Gillmor, H. A., Lampasona, V., Bernasconi, L., Hermite, L., Martin-Moutot, N., Boucraut, J., Seagar, M., Couraud, F., Scirpoli, M., Maioli, M., Tonolo, G., Bekris, L., Schranz, D., Ciccarese, M., Lernmark, A., Lee, H. C., Nam, J. H., Ahn, C. W., Song, Y. D., Lim, S. K., Kim, K. R., Huh, K. B., Fajardo, C., Carmona, E., Sanchez-Cuenca, J. M., Campos, V., Carles, C., Brazales, A., Merino, F., Piñón, F., Mašek, Z., Perušičová, J., Bárová, H., Šterzl, I., Hejduková, H., Schneiderka, P., Hink, S., Muzyka, B., Streit, G., Kopp, H. P., Kroiss, A., Tankova, T., Dakovska, L., Kirilov, G., Koev, D., Abrams, P., De Block, C., Rooman, R., Du Caju, M., Eibl, N. L., Wolf, H., Eibl, M. M., Di Cesare, E., Previti, M., Lombardo, F., Di Benedetto, A., Romano, G., De Luca, F., Cucinotta, D., Brunelle, R. L., Huang, J., Fineberg, S. E., Anderson, J. H., List, C., Lamesch, P., Kohlhaw, K., Schwarz, C., Wenzke, M., Richter, O., Hauss, J., Zeng, S. F., Xu, X. S., Zheng, S. X., Shii, K., Baba, S., Bonfanti, R., Bazzigaluppi, E., Meschi, F., Bognetti, E., Bosi, E., Chiumello, G., Cinapri, V., Quilici, S., Forotti, G., Giampietro, O., Matteucci, E., Luppi, P., Zanone, M. M., Rudert, W., Haluszczak, C., Alexander, A., Bertera, S., Gottlieb, P., Trucco, M., Irnstetter, A., Jäger, G., Schenker, M., Ziegler, M. A. G., Myśliwiec, J., Szelachowska, M., Monetini, L., Valente, L., Coppolino, G., Stefanini, L., Corbi, S., Spera, S., Matteoli, M. C., Ferrazzoli, F., Cantagallo, A., De Mattia, G. C., Walker, B., Sonnet, E., Gibassier, J., Derrien, C., Massart, C., Allannic, H., Maugendre, D., Leech, N. J., Elsegood, K. A., Narendran, P., Hubbard, A., Dayan, C. M., Mianowska, B., Bodalska-Lipińska, J., Chrul, S., Wyka, K., Geissler, A., Schneider, M. L., Bochow, B., Koop, I., Zhang, T. M., Zhang, Y., Han, C. H., Jin, S. X., Dervogormiyacıyan, H., Araslı, M., Aydemir, D., Yıllar, G., Deniz, G., Gürol, A. O., Aktaş, E., Tütüncü, Y., Pertyñska, M. P., Banasik, M., Zeman, K., Cypryk, K., Wilczyñski, J., Tchórzewski, H., Müser, E. S., Baier, J. E., Bergbauer, M., Schmutz, G., Figge, A., Reiser, M., Schmiegel, W., Burkart, V., Kim, Y.-E., Kauer, M., Utsugi, T., Kanda, T., Kobayashi, I., Uchiyama, T., Ito, H., Ohyama, Y., Tomono, S., Kawazu, S., Nagai, R., Hehmke, B., Heinke, P., Kelemen, K., Wegmann, D., Hutton, J. C., Wachlin, G., Schröder, D., Schmidt, S., Schloot, N. C., Hanifi-Moghaddam, P., Goebel, C., Rothe, H., Hausmann, A., Laureys, J., Depovere, J., Waer, M., Karsten, V., Tritschler, S., Belcourt, A., Pinget, M., Kessler, L., Gregori, S., Sala, L., Smiroldo, S., Davalli, A., Adorini, L., Bo, S., Repetti, E., Gentile, L., Fornengo, P., Bruno, A., Ferrero, L., Kanoun, F., Harzallah, F., Ftouhi, B., Mekaouar, A., Bellaaj, R., Fekih, M., Mebazaa, A., Zouari, B., Ben Khalifa, F., Spijkerman, A. M. W., Ruige, J. B., Colagiuri, S., Colagiuri, R., Palu, T., Na’ati, E., Muimui-heata, S., Samiu, O., deBlieck, C., Ta’ai, A., Foliaki, S., Hussain, Z., McLennan, M., Hansen, C. N., Ibsen, H., Dogadin, S. A., Nozdratchev, K. G., Lidfeldt, J., Nerbrand, C., Lindholm, L. H., Samsioe, G., Scherstén, B., Agardh, C.-D., Wójcikowski, Cz., Grzeszczak, W., Łopatyński, J., Bandurska-Stankiewicz, E., Mardarowicz, G., Król, H., Matej, A., Czupryniak, L., Kropiwnicka, A., Drzewoski, J., Viljoen, E., Costa, A., Martinez, S., Carmona, F., Levy, I., Baruffaldi, L., Solerte, B., Mantovani, E., Boullu, S., Jeandidier, N., Legaludec, V., Costa, B., Franch, J., Martín, F., Morató, J., Donado, A., Basora, J., Daniel, J., Sayeed, M. A., Mahtab, H., Kibriya, M. G., Khanam, P. A., Azad Khan, A. K., de Courten, M., Chitson, P., Cox, H., King, R., Dachtler, J., Johnston, D., Ito, C., Kataoka, M., Lakhdar, A. A., Myers, M. A., Fuecker, K., Echwald, S. M., Hansen, T., Ekstrøm, C. T., Urhammer, S. A., Eiberg, H., Roberts, S., Barrow, B. A., Hainsworth, J., Schousboe, K., Henriksenog, J. E., Sørensen, T. I. A., Herlihy, O. M., Timmer, B., Grant, P. J., Bennett, S. M. A., Ghunaim, S. A., Stewart, M. W., Baroni, M. G., Sentinelli, F., Lovari, S., Vitali, M., Capici, F., Barbetti, F., Weng, J. P., Lehto, M., Li, H., Forsblom, C., Groop, L., Blanche, H., Morel, V., Hansen, L., Stanojevic, V., Petersen, H. V., Urioste, S., Stoffers, D., Møller, A. M., Serup, P., Ek, J., Durviaux, S., Clausen, J. O., Rousseau, G. G., Lemaigre, F. P., Bjørkhaug, L., Njølstad, P. R., Lindner, T., Cockburn, B. N., Molven, A., Søvik, O., Lindner, T. H., Horikawa, Y., Sovik, O., Frederiksen, S. K., Almind, K., Van Obberghen, E., Kovács, P., van den Brandt, J., Fenger, M., Vaag, A., Haist, K., Weisser, M., Rettig, A., Zhang, M., Chung, S. S. M., Pihlajamäki, J., Karjalainen, L., Karhapää, P., Vauhkonen, I., Cassell, P., Uwakwe, N., Kopelman, P., Ramachandran, A., Snehalatha, C., Rasmussen, S. K., Lautier, C., Grigorescu, F., Smith, R. J., Frayling, T., Turner, R., Hitman, G., Subba Rao, P., Bennett, A. J., Jones, E., Lathrop, G. M., Menzel, S., Wahid, F., Cooper, L., Scott, J., Aitman, T. J., Galli, J., Fakhrai-Rad, H., Kamel, A., Marcus, C., Norgren, S., Luthman, H., Wallis, R. H., Collins, S. C., Kaisaki, P. J., Ktorza, A., Lathrop, M., Gauguier, D., Huxtable, S., McCarthy, M., Shimomura, H., Hanabusa, T., Tsunoda, K., Lazdins, M., Dalgaard, L. T., Jensen, N. M., Jensen, J. N., Lynn, S., Turnbull, D. M., Pérez de Nanclares, G., Gaztambide, S., Vázquez, J. A., Groves, C. J., Izmajlowicz, M. L., Horton, V. A., Owen, R. J., Stratton, I. R., Green, F. R., Groves, C., Horton, V., Owen, R., Stratton, I., Clark, L. A., Voigt, A., Rochlitz, H., Rau, H., Braun, J., Schmidt, K., Plock, K., Donner, H., Schöneberger, A., Usadel, K. H., Badenhoop, K., Bendlová, B., Mazura, I., Včelák, J., Vondra, K., Palyzová, D., Svatoš, J., Mikšová, P., Russo, G., Couture, P., Wilson, P. W. F., Cupples, L. A., Otvos, J. D., Schaefer, E. J., Ordovas, J. M., Malecki, M. T., Ji, L., Curtis, S., Rich, S. S., Warram, J. H., Krolewski, A. S., Gudayol, M., Usac, E. F., van Essen, E. H. R., Roep, B. O., ’t Hart, L. M., Janssen, J. J., van den Ouweland, J. M. W., Lemkes, H. H. P. J., Maassen, A. J., Nakano, S., Fukuda, M., Maejima, K., Imaizumi, N., Kitazawa, M., Nishizawa, M., Kigoshi, T., Uchida, K., Le Gall, J. Y., David, V., Baltrusch, S., Richter, T., da Silva Xavier, G., Dickens, M., Belin, V. D., Green, I. C., Burns, C. J., Squires, P. E., Howell, S. L., Persaud, S. J., Ban, N., Yamada, Y., Someya, Y., Ihara, Y., Tsuda, K., Seino, Y., Alcazar, O., Tyrberg, B., Carlsson, C., Andersson, A., Mukai, E., Ishida, H., Fujimoto, S., Kajikawa, M., Fujita, J., Tsuura, Y., Malaisse-Lagae, F., Picton, S., Tamarit-Rodriguez, J., Mukala-Nsengu-Tshibangu, A., Fernández, S., Giné, E., Ortsäter, H., Liss, P., Åkerman, K. E. O., Bergsten, P., Hu, S., Wang, S., Roos, E. S., Gounarides, J. S., Shapiro, M. J., de Souza, C. J., Papas, K. K., Nishimura, M., Kadiata, M. M., Louchami, K., Jijakli, H., Rajan, A. S., Kuang, S., Iyer, D., Waddell, I. D., Holloway, B. R., Ishihara, H., Wang, H., Wollheim, C. B., Ayvaz, G., Mercan, D., Rasschaert, J., Giroix, M.-H., Scruel, O., Portha, B., Broca, C., Fernandez-Alvarez, J., Manteghetti, M., Gross, R., Sauvaire, Y., Petit, P., Ribes, G., McClenaghan, N. H., Ball, A. J., Flatt, P. R., Rustenbeck, I., Dickel, C., Winkler, M., Grimmsmann, T., Meyer, U., Gross, I., Barnes, P. D., O’Brien, R. E., Abdel-Wahab, Y. H. A., Hashmi, M. N., Giesberts, A. N., White, S. J., Cooper, E. J., Hudson, A. L., Eglen, R. M., Dillon, M. P., Chan, S. L. F., Morgan, N. G., Parini, A., Gotfredsen, C., Ullrich, S., Su, J., Rösier, M., Hescheler, J., Greger, R., Wardt, R., Arredouani, A., Gailly, P., Henquin, J. C., Gilon, P., Macfarlane, W. N., Docherty, K., Jonkers, F. C., Schöfl, C., Börger, J., von zur Mühlen, A., Brabant, G., Grapengiesser, E., Harris, T. E., Buchan, A. M. J., Jones, P. M., Jaikaran, E. T. A. S., Marcon, G., St George-Hyslop, P. H., Fraser, P. E., Clark, A., Lebrun, P., Antoine, M.-H., Nguyen, Q.-A., Rorsman, Patrik, Wasmeier, C., Antinozzi, P., Maechler, P., Schwartz, E., Wollheim, C., Roderigo, H. M., Matsumoto, K., Ebihara, K., Yamamoto, H., Tabuchi, H., Fukunaga, K., Yasunami, M., Ohkubo, H., Miyamoto, E., Horn, P. A., García-Barrado, M. J., Sancho, C., Martín, M., Moratinos, J., Westerlund, J., Lin, J. M., Brown, R., Björklund, A., Grill, V., Detimary, P., Guiot, Y., Rahier, J., Elmi, A., Sehlin, J., Hauge-Evans, A. C., Cybal, M., Druzyńska, J., Wierzchowska, J., Krippeit-Drews, P., Drews, G., Krämer, C., Jornot, L., Düfer, M., Nöda, M., Yamashita, S., Takahashi, N., Tsubamoto, Y., Kasai, H., Sharp, G. W. G., Lembert, N., Joos, H. C., Ammon, H. P. T., Wahl, M. A., Ainscow, E. K., Zhao, C., Fabregat, M. E., Fernández-Álvarez, J., Franco, C., Novelli, M., Fernàndez-Alvarez, J., Masiello, P., Lajoix, A., Beffy, P., Roux, S., Chardès, T., Roye, M., Lajoix, A. D., Reggio, H., Peraldi-Roux, S., Henningsson, R., Salehi, A., Lundquist, I., Stickings, P., Mistry, S., Ratcliff, H., Morris, S. M., Cunningham, J. M., Ekelund, M., Ermakova, N. V., Paulssen, R. H., Florholmen, J., Carmellini, M., Mosca, F., Patané, G., Longo, D., Squatrito, S., Clement, L., Magnan, C., Vincent, M., Penicaud, L., Assimacopoulos-Jeannet, F., Vigneri, R., Rolfsen, S. E. D., Gregersen, S., Hermansen, K., Blondeau, B., Rojas, I., Novials, A., Femández-Usac, E., Cristóbal, P., Higham, C. E., Lawrie, L., Sherman, K. I. J., Birch, N., Tito, P., Robinson, C. V., de Koning, E. J. P., Verbeek, J. S., Esapa, C., Laube, B., Powell, D. S., Maksoud, H., Chargé, S. B. P., Matthews, D. R., Stratton, I. M., Karlsson, S., Myrsén-Axcrona, U., Östlund, B., Sundler, F., Bertrand, G., Puech, R., Bockaert, J., Persson-Sjögren, S., Täljedal, I.-B., Mooney, M. H., O’Harte, F. P. M., Simonsson, E., Abdel-Halim, Samy M., Efendić, Suad, Ahrén, Bo, Yanagida, K., Arima, T., Yada, T., Egéa, J. C., Hirtz, C., Deville de Périère, D., Meoni, C., Falqui, L., Arcelloni, C., Paroni, R., Folli, F., Barry, R., Turner, N. C., Tadayyon, M., Arch, J. R., Sutti, F., Perego, L., Baglioni, S., Otte, A., Socci, C., Raffaele, H. S., Stumpf, E., Aalto, Y., Otonkoski, T., Knuutila, S., Andersson, L. C., Berra, C., Furlan, R., Coppelli, A., Tellini, C., Bordignon, C., Rouiller, D. G., Lister, C. A., Moore, G. B. T., Piercy, V., Newman, M., Chapman, H., Smith, S. A., Anastasi, E., Bulotta, A., Tiberti, C., Ponte, E., Liddi, R., Taruscio, D., Falchi, M., Annerén, C., Welsh, M., Bernard, C., Ilic, C., Guilbert, V., Palgi, J., Korbutt, G. S., Rayat, G. R., Rajotte, R. V., Kieffer, T. J., Karlsson, Ella, Sandler, Stellan, Boujendar, S., Huotari, M.-A., Miettinen, P. J., Keski-Oja, J., Breda, E., Pacini, G., Vilsbøll, T., Toft-Nielsen, M.-B., Dinesen, B., Corssmit, E. P. M., Qvigstad, E., Mostad, I. L., Bjerve, K., Ann, C. W., Kume, M., Hiramatsu, M., Taniguchi, J., Saito, Y., Kawasaki, Y., Kanazawa, M., Notoya, Y., Hayashi, T., Djemli, A., Gallice, P., Coste, T., Jannot, M. F., Dufayet, D., Raccah, D., Vague, P., Sattar, S., Basak, R. C., Hasan, Z., Ali, L., Nikulina, M. A., Karlsen, A. E., Hong, T. P., Andersen, N. A., Puren, A. J., Fantuzzi, G., Dinarello, C. A., Gysemans, C. A., Sparre, T., Fey, S., Larsen, P. M., Andersson, A. K., John, N. E., Fey, S. J., Mose Larsen, P., Frigerio, S., Ghayur, T., Holländer, G. A., Zumsteg, U., Pinach, S., Monge, L., Grassi, G., Pasquero, P., Ruiu, G., Dall’Omo, A., Carta, Q., Hadjivassiliou, V., Dunger, A. M., Green, M. H. L., Rasilainen, S., Roivainen, M., Ylipaasto, P., Bouwens, L., Hovi, T., Sekine, N., Takahashi, K., Ishikawa, T., Okazaki, T., Fujita, T., Elliott, J., Scarpello, J. H. B., Conroy, S., Byrne, P., Newsholme, P., Harrison, M., Greenl, I. C., Kaya, F., Süsleyici, B., Öztürk, M., Eisner, M., Guldbakke, B., Karpenko, N., Brizgalova, G., Alesina, M., Røder, M. E., Schwartz, R. S., Prigeon, R., Kahn, S. E., Kendereški, A., Micić, D., Šumarac, M., Macut, Dj., Zonć, S., Čolić, M., Cvijović, G., Gligorović, P., Courtney, C. H., Atkinson, A. B., Ennis, C., Sheridan, B., Bell, P. M., Jolly, M., Amin, R., Godsland, I., Horvoka, R., Anyaoku, V., Lawrence, N., Krasova, N., Sergienko, L., Mingrone, G., Plat, L., Balasse, E. O., Zykova, T., Jenssen, T., Strelkova, A., Zykova, S., Tipisova, E., Féry, F., Wijenaike, A. N., Watt, P. W., Jung, R. T., Bolton-Smith, C., Rennie, M. J., Ludvik, B., Aigmueller, Th., Waldhaeusl, W., Courtois, P., Bource, F., Guenat, E., Philippe, J., Jéquier, E., Tappy, L., Benny, Santosa, Grönemeyer, Dietrich, Aygen, Sitke, Scholz, Nicole, Busch, Martin, Tauveron, I., Rochon, C., Dejax, C., Benoit, P., Capitan, P., Bayle, G., Prugnaud, J., Fabricio, A., Champredon, C., Thieblot, P., Grizard, J., Nielsen, M. F., Nyholm, B., Chandramouli, V., Schumann, W. C., Landau, B. R., Rizza, R. A., Mitrakou, A., Meyer, C., Tolias, A., Platanisiotis, D., Vlachos, L., Gerich, J., Wajngot, A., Sprangers, F., Jellema, W. T., Lopuhaä, C. E., van Lieshout, J. J., van der Zee, J. S., Mithieux, G., Croset, M., Zitoun, C., Hurot, J. M., Rajas, F., Montano, S., Willem, R., Verbruggen, I., Grue-Sørensen, G., Björkling, F., Watson, N. D., Burns, S. P., Murphy, H. C., Iles, R. A., Cohen, R. D., Rooney, K., Swan, V., Phuyal, J., Millar, J., Bryson, J., Denyer, G., Caterson, I., Thompson, C., Gaster, M., Handberg, Aa., Schrøder, H. D., Alzaid, A., Sobki, S., Thye-Rønn, P., Alford, F., Christopher, M., Gras, F., Brunmair, B., Neschen, S., Py, G., Lambert, K., Raynaud, E., Mercier, J., Tsuchihashi, K., Sumida, Y., Fujimoto, H., Nakamura, M., Miyata, E., Furuta, M., Katsuki, A., Ito, K., Sasaki, R., Hori, Y., Yano, Y., Adachi, Y., Lauritz, J., Eriksson, J. W., Burén, J., Zhao, L. J., Li, Z.-C., Kullin, M., Karlsson, F. A., Redondo, A., Puente, J., Clemente, F., González, N., Moberg, E., Amer, P., Hagström-Toft, E., Bolinder, J., Björnholm, M., Krook, A., Galuska, D., Myers, M., Zierath, J. R., Wallberg-Henriksson, H., Niklasson, M., Strindberg, L., Sternberg, F., Hebeda, S., Kratzer, W., Salgado, M. I., Hoss, U., Kalatz, B., Lohmann, S., Fussgänger, R., Khomazjuk, A. I., Ncscheret, A. P., Gonchar, I. V., Quinones-Galvan, A., Sironi, A. M., Cominacini, L., Nagai, Y., Yamashita, H., Takamura, T., Kobayashi, K., Szanto, I., Peth, J. A., Kinnick, T. R., Youngblood, E. B., Tritschler, H. J., Henriksen, E. J., Gašperíková, D., Rufo, C., Teran-Garcia, M., Nakamura, M. T., Clarke, S. D., Pye, S., Zhang, Z., Radziuk, J., Guignot, L., Bell, K. S., Lim-Fraser, M., Cooney, G., Kraegen, E. W., Takayama, S., Legare, D. J., Macedo, M. P., Lautt, W. W., Bradley, B., Barron, P., Davies, J., Ader, M., Richey, J. M., Ait El Mkadem, S., Macari, F., Renard, E., Méchaly, I., Brun, J. F., Cros, G., Bringer, J., del Aguila, L. F., Krishnan, R. K., Farrell, P. A., Ulbrecht, J., Correll, P. H., Kirwan, J. P., Mei, J., Rahn-Landström, T., Brindley, D., Manganiello, V., Degerman, E., Ziv, E., Shafrir, E., Kaiman, R., Galer, S., Bar-On, H., Gerő, L., Földes, K., Janssen, J., Járay, J., Perner, F., Haap, M., Houdali, B., Schmit, M. B., Dietze, G. J., Perrini, S., Natalicchio, A., Montrone, C., de Robertis, O., De Pergola, G., Strack, V., Kellerer, M., Kausch, C., Condorelli, G., Beguinot, F., Häring, H.-U., Song, X. M., Chibalin, A. V., Ryder, J. W., Jiang, X. J., Alessi, D. R., Hennige, A. M., Metzinger, E., Seipke, G., Trüb, T., Hey, A., Sørensen, A. R., Schäffer, L., Drejer, K., Kurtzhals, P., Hansen, B. F., Matozaki, T., Noguchi, T., Yamao, T., Takada, T., Ochi, F., Takeda, H., Inagaki, K., Hosoka, T., Kasuga, M., Schürt, M., Meier, M., Drenckhan, M., Meyer, M., Aries, S. P., Klein, H. H., Telting, D., van der Zon, G. C. M., Dorrestijn, J., Maassen, J. A., Clapham, J. C., Holder, J. C., Tomlinson, K. M., Pickavance, L., Buckingham, R., Wilding, J., Jacinto, S. M., Harrold, J., Ljung, B., Kjellstedt, A., Thalén, P., Widdowson, P., Williams, G., Oakes, N., Aoki, K., Saito, T., Satoh, S., Mukasa, K., Kaneshiro, M., Kawasaki, S., Hoshino, K., Okamura, A., Sekihara, H., Smith, U., Johansson, A., Nilsson, E., Olausson, T., Nakazawa, T., Suzuki, M., Martinez, J., Murado, P., Azal, Ö., Yönem, A., Çakır, B., Polat, Z., Kutlu, M., Çorakçı, A., Bayraktar, M., Gürlek, A., Koray, Z., Damian, M. S., Linn, T., Laube, H., Arzner, S., Meißner, H.-P., Giunti, S., Comune, M., Cassader, M., Conte, M. R., Sacchi, C., Musso, G., Mecca, F., Depetris, N., Gambino, R., Perin, P. Cavallo, Kawakami, S., Sandqvist, M., Jansson, P.-A., Šindelka, G., Widimský, J., Haas, T., Prázný, M., Mari, A., Nolan, J. J., Uusitupa, M. I. J., Karşıdağ, K., Hacıhanefioğlu, B., Dinççağ, N., Drivsholm, T., Palacios, R. T., Vølund, A., Pedersen, Oluf B., Letiexhe, M. R., Scheen, A. J., Quiñones Galvan, A., Simeoni, M., Basu, A., Uosukainen, A., Mäkimattila, S., Schlenzka, A., Adler, A. I., Levy, J., Stevens, R., Matthews, D., Holman, R., Boland, B. J., Jeanjean, M., Hermans, M. P., Maudoigt, C., Tonglet, R., Robert, A., Quiñones-Galvan, A., Cini, G., Galetta, F., Sanna, G., Gernone, F., Janssen, M. J., Gonera, R. K., Wolffenbuttel, B. H. R., de Leeuw, P. W., Schaper, N. C., Molęda, P., Kuczerowski, R., Czech, A., Tatoń, J., Taddei, S., Patiag, D., Qu, X., Wilkes, M., Gray, S., Seale, J. P., Donnelly, R., Campión, J., Maestro, B., Dávila, N., Carranza, M. C., Calle, C., Hales, C. N., Fernández-Real, J. M., Grasa, M., Pugeat, M., Barret, C., Ricart, W., Lindmark, S., Olsson, T., Tufvesson, M., Loeblein, K., Mehnert, B., Haering, H. U., Rave, Klaus, Heise, Tim, Clauson, Per, Hirschberger, Sabine, Heinemann, Lutz, Claret, M., Nadal, B., Truc, A., Rossi, L., Hildebrand, P., Ketterer, S., Beglinger, C., Keller, U., Gyr, K., Parvin, S., Overkamp, D., Vayreda, M., González-Huix, F., G-Huix, F., Zavaroni, I., Gasparini, P., Massironi, P., Zuccarelli, A., Delsignore, R., Reaven, G. M., Sheu, W. H. H., Lee, W. J., Chen, Y.-T., Iraklianou, S., Tournis, S., Volonakis, I., Spylopoulou, M., Bilianou, E., Melidonis, A., Foussas, S., Güler, Serdar, çakir, Bekir, Demi̇rbaş, Berrin, Gürsoy, Gül, Serter, Rüştü, Aral, Yalçin, Morton, G., Lee, S., Fahey, R., de Silva, A., Cai, X. J., Buckingham, R. E., Arch, J. R. S., Wilson, S., Clausen, J. T., Kristensen, P., Nielsen, P. F., Wulff, B. S., Thim, L., Holness, M. J., Sugden, M. C., Fryer, L. G. D., Munns, M. J., Mannucci, E., Ognibene, A., Cremasco, F., Bardini, G., Mencucci, A., Ciani, S., Pierazzuoli, E., Tsuchihashil, K., Rigalleau, V., Delafaye, C., Baillet, L., Vergnot, V., Brunou, P., Gatta, B., Gin, H., Felber, J. P., Munger, R., Assimacopoulos, F., Bobbioni, E., Golay, A., Wilken, M., Larsen, F. S., Buckley, D., Molina, L. M., Marquez, L., Arbeo, A., Hernandez, C., Kofod, H., Damholt, A. B., Buchan, A., Márquez, L., Luque, M. A., Sarti, L., Sutton, P. J., Behle, K., Heimesaat, M. M., Hüfner, M., Gravholt, Claus Højbjerg, Mølier, Niels, Christiansen, Jens Sandahl, Schmitz, Ole, Deacon, C. F., Brock, B., Knudsen, L. B., Agersø, H., Huusfeldt, P. O., Kelly, C. M. N., Brunn, C., Schioos, J., Sewing, S., Lemansky, P., Wawro, S., Mest, H. J., Taguchi, T., Motoshima, H., Yoshizato, K., Guenifi, Amel, Henriksson, M., Johansson, J., Shafqat, J., Tally, M., Wahren, J., Jömvall, H., Ekberg, K., Rigler, R., Pramanik, A., Kratz, G., Johansson, B.-L., Uhlén, M., Jörnvall, H., Forst, T., Dufayet De La Tour, D., Kunt, T., Pfützner, A., Goitom, K., Pohlmann, T., Schneider, S., Johansson, B. L., Löbig, M., Engelbach, M., Beyer, J., Ekman, Bertil, Nyström, Fredrik, Arnqvist, Hans J., Halvatsiotis, P. G., Meek, S., Bigelow, M., Nair, K. S., Maghsoudi, S., Fisker, S., Vølund, A. A., Jörgensen, J. O. L., Christiansen, J. S., Hilsted, J., Mazerkina, N. A., Tiulpakov, A. N., Gorelyshev, S. K., Peterkova, V. A., Macut, D. J., Dieguez, C., Casanueva, F. F., Catalina, P. F., Mallo, F., Andrade, A., García-Mayor, R. V. G., Popova, V. V., ter Maaten, J. C., Popp-Snijders, C., Madsen, L., Ukropec, J., Bergene, E., Rnstan, A. C., Berge, R., Arner, P., Wahl, G., Häring, H., Bryson, J. M., Curtis, S. E., Caterson, I. D., Winzell, M. Sörhede, Svensson, H., Ahnén, B., Holm, C., Phillips, C., Madigan, C., Owens, D., Collins, P., Johnson, A., Tomkin, G. H., Cabezas, M. Castro, van Oostrom, A. J. H. H. M., Erkelens, D. W., Summers, L. K. M., Fielding, B. A., Ilic, V., Clark, M. L., Frayn, K. N., Pietzsch, J., Julius, U., Nitzsche, S., Fischer, S., Lindgren, C., Amrot-Fors, L., Hoffmann, M. M., Luft, D., Schmülling, R.-M., D’Adamo, M., Leonetti, F., Paoloni, A., Ribaudo, M. C., Basso, M. S., Elmore, U., Restuccia, A., Sbraccia, P., Emilsson, V., O’Dowd, J., Heyman, R., Cawthorne, M. A., Pelikánová, T., Kazdová, L., Žák, A., Chvojková, Š., Özer, E. M., Kadıoğlu, P., Korugan, Ü., Hatemi, H., Rivellese, A. A., Dullaart, R. P. F., Riemens, S. C., Sluiter, W. J., van Tol, A., Farnier, M., Megnien, S., Turpin, G., Stulp, B. K., Brambilla, P., Brunelli, A., Riva, M. C., Manzoni, P., de Poli, S., Riboni, S., Stolk, R. P., Meijer, R., Wink, O., Zelissen, P. M. J., van Gils, A. P. G., Grobbee, D. E., Vilarrasa, N., Gimenez, O., Lopez, L., Insa, R., Fdez Castañer, M., Cabrera-Rode, E., Perich, P., Diaz-Horta, O., Molina, G., Fernández Castañer, M., López, L., Jiménez, O., Boltaña, A., Ampudia-Blasco, F. J., Martínez, I., Civera, M., Ascaso, J. F., Carmena, R., Ahmed, K., Luzio, S., Furmaniak, V., Owens, D. R., Dionadji, Mbainguinam, Mbaissouroum, Mouanodji, Anderson, J., Garg, S., MacKenzie, T., Shephard, M., Peery, B., Chase, H., Holstein, A., Thießen, E., Kaufmann, N., Egberts, E.-H., Lutgers, H. L., Hullegie, L. M., Hoogenberg, K., Wientjes, K. J., Schoonen, A. J., Wientjes, K. J. C., Schoonen, A. J. M., Weitgasser, R., Gappmayer, B., Pichler, M., Sapin, R., Friess, P., Eskes, S. A., de Vries, J. H., Pouwer, F., van Ballegooie, E., Spijker, A. J., Jeng, L., Winsett, J., Tubiana-Rufi, N., Munz-Licha, G., Polak, M., Sheehan, J., Ulchaker, M., Toeller, M., Üstün, A., Yilmaz, M. T., Aparicio, M., Peyron, E., Rizkalla, S. W., Taverna, M., Guerre-Millo, M., Chevalier, A., Pacher, N., Slama, G., Gorshunska, M., Buyken, A. E., Heitkamp, G., Kabir, M., Oppert, J. M., Wursch, P., Bruzzo, F., Rahman, M. H., Fatima, K., Ahmed, S., Mondal, H. N., Yilmaz, M., Öztok, U., Karakoç, A., Çakır, N., Düzgün, E., Yetkin, İ., Arslan, M., Şardaş, S., Wilding, John, Géloën, A., Baret, G., Dalmaz, Y., Peyronnet, J., Clémenceau, B., Martignat, L., Lalain, S., Gouin, E., Kenda-Ropson, N., Miller, A. O. A., You, S., Aguilera, E., Recasens, M., Flores, L., Ricart, M. J., Fernández-Cruz, L., Esmatjes, E., Crenier, L., Noël, C., Le Moine, A., Mahy, M., Danguy, A., Kiss, R., Goldman, M., Bracci, C., De Haan, B., Nilsson, K., Deschamps, J. Y., Glagoličová, A., Smrčková, I., Dieterle, C., Illner, W. D., Land, W., Feldmeier, H., Scheuer, R., Lalli, C., Di Loreto, C., Ellringmann, U., Balks, H. J., v. zur Mühlen, A., Dengler, R., Weissenborn, K., Rasmussen, B. M., Ørskov, L., Watson, J., Owen, G., Barrett, G., Ingleby, J., Weiss, M., Deary, I., Cavan, D., Kerr, D., Bruneiii, A., Cuce’, A., Elsing, H. G., Kühne, D., Quinn, N. D., Warner, D. P., Buysschaert, M., Jamal, R., O’Brien, T., Latare, P., Mullen, J., Rein, A., Wargo, M., Parkes, J. L., Ginsberg, B., Sotiropoulos, A., Peppas, Th. A., Kotsini, V., Apostolou, O., Bousboulas, S., Michailidis, E., Sawala, M., Pappas, S., Nilsson, P. M., Nilsson, J. Å., Berglund, G., Molins, T., Esteban, J. I., Genescà, J., Paris, I., Haufroid, V., Selvais, Ph., Petit, J. M., Duong, M., Grappin, M., Guiguet, M., Rudoni, S., Portier, H., Brun, J. M., Bagg, W., Plank, L., Drury, P. L., Sharpe, N., Braatvedt, G. D., Carrascosa, J. M., Molero, J. C., Fermίn, Y., Andrés, A., Satrústegui, J., Rietzsch, H., Patzak, A., Schwanebeck, U., Simpson, H., Robertson-Mackay, F., Montegriffo, E., Fox, C., Chiasson, J.-L., Josse, R. G., Dorman, J. M., Gerstein, H. C., Lau, D., Leiter, L. A., Maheux, P., Meneilly, G. S., Murphy, L., Rodger, N. W., Ross, S. A., Ryan, E., Yale, J.-F., Wolever, T. M. S., Haller, T., Elias, I., Segal, P., Standi, E., Rybka, J., Sencer, E., Satman, I., Schlcnzka, A., Vakkilainen, J., Tsaglis, H., Ioannidis, I., Giakoumaki, A., Amantou, A., Komitopoulos, N., Georgiou, S., Varsamis, E., Katsilambros, N., El Gayar, M., Shereba, N., Botros, R., Fikry, R., Jackson, D., Balme, M., Silva-Nunes, J., Alves, J., Bogalho, P., Gardete-Correia, L., Nunes-Corrêa, J., Kot’átková, A., Němcová, D., Vrbíková, J., Zamrazil, V., Meyer, L., Delbachian, I., Lehert, P., Cugnardey, N., Drouin, P., Guerci, B., Wagner, O. F., Jones, N. P., Vallance, S. E., Thompson, K. A., Miller, A. K., Inglis, A. M. L., Patterson, S., Jorkasky, D., Freed, M. I., Mathisen, A. L., Schneider, R., Rubin, C., Houser, V., Beebe, K. L., Kortboyer, J. M., Eckland, D. J. A., Cranmer, H., Mori, Y., Kurokawa, N., Komiya, H., Horikoshi, H., Yokoyama, J., Tajima, N., Ikeda, Y., Bakst, A., Hemyari, P., Lönnqvist, F., Owen, S., Vikramadithyan, R. K., Chakrabarti, R., Misra, P., Prem Kumar, M., Sunil Kumar, K. B., Ghosh, A., Rajagopalan, R., Goldstein, B., Katoh, S., Tsuruoka, N., Hata, S., Matsushima, M., Ikemoto, S., Inoue, Y., Edwards, G., Fonseca, V., Biswas, N., Bakris, G., Viberti, G., Rebuck, A. S., Weill, S., Abel, M. G., Klappoth, W., Brodesser, A., Linkeschowa, R., Pushparaj, P., Tan, C. H., Tan, B. K. H., Bahner, A., Parker, J., Waite, G., Lipson, V., Nahar, N., Rokeya, B., Parveen, S., Nur-e-Alam, M., Mosihuzzaman, M., Hansen, A. Kornerup, Lepore°, M., Kurzhals, R., Pampanelli°, S., Fanelli°, C. G., Bolli°, G. B., Ratner, R. E., Hirsch, I. B., Mecca, T. E., Wilson, C. A., Mohideen, P., Mudaliar, S., Deutsch, R., Ciaraldi, T., Armstrong, D., Kim, B., Morrill, B., Sha, X., Henry, R., Meyer, B. H., Scholtz, H. E., van Niekerk, N., Rosenkranz, B., Schoenle, E., Witthaus, Elke, Bradley, Clare, Stewart, John, Barbeau, M., Myers, S., Flora, D., DiMarchi, R., Chance, R., Plum, A., Larsen, P. S., Larsen, U. D., Kristensen, J. B., Jansen, J. A., Olsen, B., Mortensen, H., Hylleberg, B., Jacobsen, L. V., Gall, M.-A., Søgaard, B., Ewing, F. M., Ireland, R. H., Hoogwerf, B., Raskin, P., Jovanovic, L., Leiter, L., Boss, A. H., Bott, U., Ebrahim, S., Hirschberger, S., Leukel, P., Sieber, H. J., McGill, J., Kilo, C., Kamp, N. M., Wutte, A., Le Thai, F., Balarac, N., Allicar, M. P., Cazeneuve, B., Augendre, B., Wise, S. D., Seah, E. S., Koivisto, V., Torlone, E., Del Sindaco, P., Ciofetta, M., Hedman, C., Orre Pettersson, A.-C., Lindström, T., Cernigoi, A. M., Kong, N., Kitchen, M. M., Ryder, R. E. J., Petkova, M., Angelova-Gateva, P., Malone, J., Arora, V., Bue-Valleskey, J., Pein, M., Diebler, F., Roach, P., Gudat, U., Dreyer, M., Hanusch, U., Ristic, S., McLeod, J., Hirschberg, Y., Garreffa, S., Keilson, L., Mather, S., Gagen, K., Chen, W., Dragonas, N., Chuang, L. M., Juang, J. H., Wu, H. P., Chiang, Y. D., Li, K. L., Jorgensen, L. N., Tai, T. Y., Cheatham, W. W., Kennedy, F., Woo, V., Jain, R., Boss, A., Moses, R., Clauson, P., Fischer, T., Björk, S., Østergaard, A., Langendorf, K. W., Hatorp, V., Hasslacher, C., Farrar, N. S., Chambers, N. J., Denyer, G. S., Johnston, G. A. R., Hashiguchi, S., Jönsson, A., Hallengren, B., Rydberg, T., Herbaut, C., Turc, A., Mourand, I., Chevassus, H., Molinier, N., Christensen, A.-B. L., Mathiesen, E. R., Stage, E., Damm, P., Boivin, S., Gross, P., Pennington, M., Harder, T., Kohlhoff, R., Dörner, G., Rohde, W., Plagemann, A., Ferdeghini, M., Murru, S., Maffei, M., Cecchetti, P., Dunne, F., Brydon, P., Smith, T., Proffitt, M., Holder, R., Gee, H., Goulis, D. G., Teoh, T. G., Asatiani, N., Elphick, A., Natsvlishvili, M., Chanturia, T., Shelestova, E., Ramazashvili, M., Hod, M., Cederberg, J., Casi, A. Leunda, Pampfer, S., De Hertogh, R., Hinck, L., Aly, S., Bertie, J., Botta, R. M., Imbergamo, M. P., Impiccichè, M. G., Todaro, B., Greco, D., Ekbom, P., Clausen, P., Feldt-Rasmussen, U., Feldt-Rasmussen, B., Mølsted Pedersen, L., Nørgaard, K., Svenningsen, A., Nielsen, L., Zmudzińska, M., Ziętek, I., Min, Y., Crawford, M. A., Bozzoni, F., Corubolo, C., Borrello, E., Di Biase, N., Spagnolo, S., Hawthorne, G., Sen, D., Bagust, A., Maier, W., Currie, C. J., Sailesh, S., Patel, V., Hayes, D., Cockrill, B., Gatling, W., Budd, S., Mullee, M. A., Savill, A. W., Smithers, M. G., Davies, R. R., Sandford, A., Stutz, L., Vadstrup, S., Simonsen, V., Musaeus, L., Molsing, B., Lyholm, B., Turner, B. C., Jenkins, E., Hejlesen, O. J., Andreassen, S., Hovorka, R., Cavan, D. A., Klinge, A., Strauss, K. W., Guthrie, R., Testa, M., Zimmerman, R., Sandberg, M., Steinfatt, H., Hardenberg, R., Gottsmann, M., König, A., Schmauß, S., Hierl, F. X., Renders, C. M., Valk, G. D., van Eijk, J. Th. M., van der Wal, G., Jermendy, G., Hídvégi, T., Müller, U. A., Junghänel, J., Köhler, S., Köhler, C., Schumann, M., Use, G., de Valk, H. W., Blankestijn, J. G., de Bruin, H. J., Bottomley, J., Gillam, S., Holmes, J., Murphy, M., Madani, S. F., Müller, R., Hunger Dathe, W., Grüßer, M., Roien, D., Hussain, M., Vibe-Petersen, J., Braun, A., Schiel, R., Höfer, A., Leppert, K., Trento, M., Passera, P., Tomalino, M., Bajardi, M., Vaccari, P., Pagnozzi, F., Pomero, F., Molinatti, G. M., Porta, M., Blaauwwiekel, E. E., Hania, M., Scholten-Jaegers, S. M. H. J., Links, T. P., Perciun, R., Dumitrescu, C., Skeie, S., Thue, G., Sandberg, S., Nordfeldt, S., Ludvigsson, J., García, Rosario, Suárez, Rolando, Henry, J. L., Kangas, M., Wilson, P. H., Pibernik, M., Szabo, S., Metelko, Ž., González-Clemente, J. M., Galdon, G., De Pedro, B., Fontanals, Ll., Miñarro, A., Topsever, P., Azık, A., Karşıdaǧ, K., Dündar, Y., Şengül, A., Vileikyte, L., Apostolou, T., Tomenson, B., Bundy, C. H., Gokal, R., Gormley, D. A., Baksi, A. K., Hrachovinová, T., Csémy, L., Bartášková, D., Krch, F. D., Gåfvels, M. C., Lithner, F., Branchtein, L., Matos, M. C. G., Gaio, D., Yamashita, T., Pousada, J. M. D. C., Duncan, B. B., Schmidt, M. I., Buchanan, T. A., Xiang, A. H., Tan, S., Peters, R. K., Trigo, E., Kjos, S. L., Lee, W. P., Azen, S., Ilic, S., Mezic, J., Pettitt, D. J., Bastyr, E. J., Camps, I., Salcedo, M. D., Rius, F., Rubio, M., Baptista, C., Martins, T., Ruas, M. M. A., Acosta, D., Cerrillos, L., Soto, A., Quijada, D., Morales, F., Silva, H., García-Hernandez, N., Villamil, F., Astorga, R., Selby, P. L., Jude, E. B., Biggs, A. M., Al-Sabbagh, S., Kumar, S., Rowbotham, J., McKenzie, W. E., Dodson, P. M., Barnett, A. H., Maresh, M., Alevizaki, M., Anastasiou, E., Grigorakis, S. I., Philippou, G., Michalopoulou, G., Souvatzoglou, A., Corcoy, R., Pau, E., Pascual, E., García-Patterson, A., Albareda, M. L., Ccrmeño, J., Altirriba, O., Adelantado, J. M., Ubeda, J., Endocrinologia, S., Reichelt, A. J., Nucci, L., Teixeira, M. M., Costa-e-Forti, A., Ciampalini, P., Giannone, G., Benedetti, S., Borrelli, P., Czerniawska, M., Manowska, B., Rami, B., Schober, E., Hueppe, A., Granditsch, G., Huber, W., Bittmann, B., Jaeger, A., Saukkonen, T., Väisänen, S., Savilahti, E., Šumník, Z., Kotalová, R., Loudová, M., Cinek, O., Šnajderová, M., Kolousková, S., Vavřinec, J., Barbato, M., Viola, T., Formisano, M., Hovind, P., Adler, I. A., Makita, Z., Takeuchi, M., Kamada, Y., Koike, T., Courrèges, J. P., Pradier, P., Bacha, J., Aboud, E., André, L., Lamarca, R., Janeczko-Sosnowska, E., Lewandowski, Z., Janeczko, D., Kopczyñski, J., Nakagami, T., Tomonaga, O., Babazono, T., Iwamoto, Y., Nakanishi, K., Higa, M., Kosugi, E., Elving, L. D., Szadkowska, A., Mirecka, M. W., Czerniawska, E., Weekers, L., Hadjadj, S., Belloum, R., Gallois, Y., Bouhanick, B., Marre, M., Saucha, W., Skwarna, B., Zychma, M., Żukowska-Szczechowska, E., Zychma, M. J., Zukowska-Szczechowska, E., Nazim, J., Dziatkowiak, H., Sanak, M., Cieślik, G., Nannipieri, M., Viberti, G. C., De Cosmo, S., Piras, G., Errannini, E., Uchigata, Y., Miura, J., Okada, T., Gong, J.-S., Zhang, J., Tanaka, M., Wamoto, Y., Zucaro, L., Bacci, S., Miscio, G., Thomas, M., Piras, G. P., Cavallo Perin, P., Mauer, M., Barzon, I., Bortoloso, E., Saller, A., Crepaldi, G., Latif, Z. A., Christensen, P. K., v. Larsen, S., Olsen, S., Bombonato, G., Sacerdoti, D., Chiesura-Corona, M., Marangon, A., Rudberg, S., Rasmussen, L., Bangstad, H.-J., Ösrterby, R., Sivous, G. I., Kasatkina, E. P., Demurov, L. M., Nosikov, V. V., Kotova, A. K., Kuraeva, T. L., Mishina, I. I., Gorashko, N. M., Nosicov, V. V., Petercova, V. A., Berrut, G., Alhenc-Gelas, F., Tsimaratos, M., Gerbi, A., Barone, R., Ollerton, R. L., Playle, R. A., Luzio, S. D., Evans, W. D., Burch, A., Siebenhofer, A., Meinitzer, A., Brandmaier, H., Brunner, G., Plank, J., West, P., Tindall, H., McKenna, K., Smith, D., Tormey, W., Kesson, C. M., Thompson, C. J., Penno, G., Anichini, R., Bandinelli, S., Boldrini, E., Giannarelli, R., Piazza, F., Pucci, L., Karunakaran, S., Morris, R. J., Nádas, J., Farkas, K., Daróczy, A., Péterfai, É., Svensson, M., Weigert, C., Facchin, S., Gambaro, G., Brodbeck, K., Schleicher, E., Tada, H., Nomura, K., Kuboki, K., Tsukamoto, M., Inokuchi, T., Menè, P., Pugliese, F., Iino, K., Yoshinari, M., Iwase, M., Asano, T., Sonoki, K., Wakisaka, M., Takata, Y., Ujishima, M., Del Prete, D., Anglani, F., Antonucci, F., Mauri, J. M., Vallés, M., Gutiérrez, C., Vendrell, J., Shinada, M., Akdeniz, A., Panagiotopoulos, P., Bach, L. A., Law, V. A., Lecomte, P. P., Yokota, C., Okuda, Y., Odawara, M., Yamashita, K., Yamada, N., Kawai, K., Açbay, Ö., Mazlum, A., Kural, E., Gündoğdu, S., Jensen, C., Körner, A., Eklöf, A.-Ch, Jaremko, G., Lal, M., DiBona, G., Aperia, A., Yavuz, D. G., Tuncer, M., Sargon, M., Küçükkaya, B., Ahıskalı, R., Akalın, Sema, Nohara, E., Oates, P. J., Ellery, C. A., Yonem, A., Azal, O., Cakýr, B., Erdogan, M. F., Corakcý, A., Ozdemir, I. C., Stevens, R. J., Yudkin, J. S., Webber, J., Wheeler, D. C., Taylor, K. G., Jones, S. L., Srivatsa, A., Anderson, S. G., Cruikshank, J. K., Florkowski, C. M., Scott, R. S., Graham, P. J., Moir, C. L., Flores, C., Ruggenenti, P., Dodesini, A. R., Vasile, B., Gaspari, F., Arnoldi, F., Ferrari, S., Ciocca, I., Spalluzzi, A., Remuzzi, G., Delvigne, C., Ballaux, D., Bosman, D. R., Winkler, A. S., Marsden, J., Watkins, P. J., Strutton, D., Erbey, J. R., Jacobsen, P., Rossing, K., Jensen, J. S., Mansfield, M. W., Kowalska, I., Telejko, B., Bachórzewska-Gajewska, A., Prokop, J., Kochman, W., Musiał, W., Naskręt, D., Oleksa, R., Zozulińska, D., Sowiński, J., Wierusz-Wysocka, B., Klamann, A., Jonas, M., Müller-Lung, U., Heuser, L., Launhardt, V., Valensi, P., Pariès, J., Torremocha, F., Brulport, V., Sachs, R. N., Vanzetto, G., Levy, M., Lormeau, B., Halimi, S., Perfornis, A., Boumal, D., Zimmermann, C., Bernard, Y., Sabbah, A., Meneveau, N., Gautier, S., Bassand, J. P., Anděl, M., Kraml, P., Potočková, J., Dvořáková, H., Trešlová, L., Nuttall, S. L., Martin, U., Kendall, M. J., Schiaffini, R., Pantaleo, A., Battocletti, T., Vaccari, V., Brufani, C., Martuscelli, E., Gargiulo, P., Nieszner, E., Posa, I., Kocsis, E., Préda, I., Pogatsa, G., Koltai, M. Z. S., Stefanidis, A., Manoussakis, S., Handanis, S., Zairis, M., Vitalis, D., Dadiotis, L., Fiorina, P., La Rocca, E., Astorri, E., Rossetti, C., Lucignani, G., Giudici, D., Castoldi, R., Mazarakis, N., Giagiakou, E., Karavidas, A., Agellou, A., Karamani, O., Matsakas, E., Caviezel, F., Morricone, L., Ranucci, M., Denti, S., Cazzaniga, A., Enrini, R., Isgrò, G., González de Molina, F. J., Sala, J., Masià, R., Marrugat, J., Kruszewski, P., Wolnik, B., Bieniaszewski, L., Świerblewska, E., Semetkowska-Jurkiewicz, E., Krupa-Wojciechowska, B., Vasilikos, P. G., Alaveras, A. E. G., Anastasopoulos, N. G., Chala, E., Sidira, M., Christakopoulos, P. D., Poulsen, P. L., Hansen, K. W., Ebbehøj, E., Knudsen, S. T., Mogensen, C. E., Ramu, Y., Vidyullatha, Y., Strojek, K., Gorska, J., Morawin, E., Ritz, E., Ciavarella, A., Malini, P. L., Strocchi, E., Fiumi, N., Ambrosioni, E., Idzior-Waluś, B., Stevens, L., McEneny, J., O’Kane, M. J., Moles, K. W., McMaster, C., Young, I. S., Leonhardt, W., Konstadelou, E., Gürlek, Alper, Soedamah-Muthu, S., Taskinen, M. R., Ehnholm, C., Wägner, A., Bayen, Laia, Rigla, M., Ortega, E., Caixàs, A., Mestrón, A., Ordóñez, J., Pérez, A., Sotiropoulou, G., Servais, P. L., Bertolotto, A., Pilo, M., Suchánková, G., Andratschke, S., Tschöp, M., Strasburger, C.-J., Rizzo, L., Aerts, P., Vinckx, M., Ansquer, J. C., Ryan, M., Buter, H., Navis, G. J., de Jong, P. E., de Zeeuw, D., Carreras, G., Giménez, G., Pou, J. M., Howorka, K., Gabriel, M., Pumprla, J., Köves, A., Bhowmik, N. B., Haque, A., Rahman, A., Paleari, F., Gamba, P., Mauri, G., Rovaris, G., Giannattasio, C., Piatti, M. L., Zincone, A., Cavaletti, G., Mancia, G., Lan, S., Arezzo, J., Gerber, R. A., Klioze, S. S., Saponara, C., Tartaglione, T., Cercone, S., Caputo, S., Meloni, T., Brunetti, D., Di Lazzaro, V., Xu, G., Jiang, H. Y., Shy, M. E., Sugimoto, K., Zhang, W.-X., Kuchmerovskaya, T., Donchenko, G., Shymansky, I., Kuchmerovsky, N., Pakyrbaeva, L., Cameron, N. E., Keegan, A., Cotter, M. A., Mirrlees, D., Smale, S. E., Biessels, G. J., Duis, S. E. J., Kamal, A., Gispen, W. H., Carrington, A., Carman, S., Smiarowski, H., Lavoie, D., Sawicki, D., Sabetta, A., Litchfield, J., Van Zandt, M., Sredy, J., Smirnova, V., Strokov, I., Ivanova, L., Ichunina, A., Nakamura, J., Nakayama, M., Hamada, Y., Chaya, S., Kato, K., Kasuya, Y., Mizubayashi, R., Miwa, K., Yasuda, Y., Kamiya, H., Hotta, N., Bíró, K., Kukorelli, T., Szilágyi, N., Kürthy, M., Komáromy, A., Mogyorosi, T., Nagy, K., Çakir, M., Baskal, N., Güllü, S., Elhan, A. H., Erdogan, G., Ziegler, D., Piolot, R., Neubauer, J., Senesi, B., Bonetti, R., Napolitano, A., Canepa, F., Ottonello, P., Schabmann, A., Giménez-Pérez, G., Arroyo, J. A., López, T., Ponz, E., Mauricio, D., Diem, P., Zanchin, L., Suter, S. L., Lefrandt, J. D., Smit, A., van Roon, A. M., Dullaart, R., Voita, D., Mackevics, V., Vitols, A., Lengyel, Cs., Farkas, Gy., Török, T., Légrády, P., Várkonyi, T. T., Kardos, A., Gingl, Z., Kempler, P., Rudas, L., Lonovics, J., Marchand, M., Stevens, L. K., Tarnás, Gy., Estrella, F., Christensen, N. J., Keresztes, K., Barna, I., Hermányi, Zs., Vargha, P., Bonnevie, L., Chanudet, X., Larroque, P., Tutuncu, N. Bascil, Deger, A., Batur, M. K., Yildirir, A., Onalan, O., Aksöyek, S., Kabakçι, G., Erbaş, T., Galicka-Latała, D., Surdacki, A., Gerritsen, J., TenVoorde, B. J., Heethaar, R. M., Tagawa, T. S., Kodama, M., Yoshioka, R., Yamasaki, Y., Didangelos, T., Athyros, V., Kontopoulos, A., Papageorgiou, A., Karamitsos, D., Lacigová, S., Rušavý, Z., Kárová, R., Perrild, H., Kay, L., Jørgensen, T., Bień, A. I., Witek, P., Geraldes, Elizabete, Rodrigues, D., Pereira, L., Doménech, A., Leitão, P., Anagnostopoulos, D., Foster, A. V. M., Nag, S., Barsoum, M., Lewis, G., Dunlop, N., Connolly, V., Bilous, R., Kelly, W., Chantelau, E., Gede, A., Sharman, D., O’Halloran, D., Best, C., Abbas, Z. G., Lutale, J., Gill, G. V., Jarvis, W. R., Archibald, L. K., Corcoran, S., Mansell, J., Pibworth, L., Terada, H., Shiba, T., Utugi, N., Utugi, T., Blum, M., Strobel, J., Höffken, K., Razvi, F. M., Kritzinger, E. E., Taylor, K., Jones, S., Illahi, W., Grüβer, M., Hartmann, P., Hoffstadt, K., van Leiden, H. A., Moll, A. C., Polak, B. C. P., Pietragalla, G. B., Maurino, M., Montanaro, M., Karadeniz, Ş., Tommasini, P., Quadrini, C., Demiraj, V., Rispoli, E., Ota, A., Takama, H., Saito, N., Hemández, C., Lepore, D., Antico, L., Giardina, B., Franconi, F., Michoud, E., Chamot, S., Riva, Ch., Hammes, H.-P., Renner, O., Breier, G., Lin, J., Alt, A., Betzholtz, C., Bretzel, R. G., Manti, R., Gallo, M., Molinar Hin, A., Brignardello, E., Boccuzzi, G., Li, Shanfang, Xiang, Kunsan, Zhang, Rugeng, Shangguan, Xinhong, Wu, Jianrong, Donnan, P. T., Broomhall, J., Hunter, K., Morris, A. D., Ioannidis, G., Peppa, M., Rontogianni, E., Kallifronas, M., Lekatsas, I., Chrysanthopoulou, G., Anthopoulos, L., Kesse, M., Thalassinos, N., Neves, C., Medina, J. L., Lopes, F., Yılmaz, M., Güvener, N., Güvener, M., Kocagöz, T., Böke, E., Paşaoglu, I., Bascil Tutuncu, N., Oto, A., Karvonen, M. K., Koulu, M., Pesonen, U., Mercuri, M., Rauramaa, R., Rutter, M. K., Kestevan, P., McComb, J. M., Marshall, S. M., Sobieska, M., Wiktorowicz, K., Kanters, S. D. J. M., Banga, J. D., Algra, A., Frijns, C. J. M., Beutler, J. J., Fijnheer, R., Nicoloff, G., Baydanoff, S., Stanimirova, N., Petrova, Ch., Lario, S., Campistol, J. M., Cases, A., Clària, J., Iñigo, P., Esmatjcs, E., Sármán, B., Tóth, M., Kocsis, I., Somogyi, A., Bumbure, A., Jachimowicz, K., Samson, J., Tomasiak, M., Sobol, A., Stańczyk, L., Watala, C., Stradina, P., Wiśniewska-Jarosińska, M., Marciniak, D., Więcławska, B., Watała, C., Golański, J., Zinnat, R., Mahmud, I., Büyükasik, Yahya, Demiroğlu, H., Szczepanik, A., Skowroński, M., Murawska, A., Meeking, D. R., Allard, S., Munday, J., Chowienczyk, P., Shaw, K. M., Cummings, M. H., Šimková, R., Jirsa, M., Hadoke, P. W. F., McIntyre, C. A., Jones, G. C., Williams, B. C., Elliott, A. I., McKnight, J. A., Pernow, J., Bombonato, G. C., Finucci, G. F., Zotta, L., Senses, V., Ozyazgan, S., Ince, E., Tunçdemir, M., Oztürk, M., Sultuybek, G., Akkan, A. G., Özyazgan, S., Unlücerci, Y., Bekpınar, S., Meyer, M. F., Lee, B. C., Shore, A. C., Humphreys, J. M., Tooke, J. E., Dell’Omo, G., Giovannitti, G., Caricato, F., Mariani, M., Pedrinelli, R., Kiviet-Boehm, C., Schwelling, V., Matthäei, S., Pfohl, M., McInerney, D., Itoh, H., Ohno, T., Katoh, N., Baumgartner-Parzer, S., Artwohl, M., Graier, W., Ludwig, C., Tachi, Y., Bannai, C., Shinohara, M., Shimpuku, H., Ohura, K., Bertacca, A., Sasvári, M., Szaleczki, E., Pusztai, P., Boes, U., Klaus, E., Dittrich, P., Wagner, Z., Wittmann, I., Pótó, L., Wagner, L., Mazák, I., Nagy, J., Feletto, F., Taboga, C., Tonutti, L., Lizzio, S., Russo, A., Selmo, V., Ceriello, A., Lekakis, J., Papamichael, C. M., Stamatelopoulos, K., Stamatelopoulos, S., Yillar, D. O., Gay, M., Lillaz, E., Passaro, A., Vanini, A., Calzoni, F., D’Elia, K., Carantoni, M., Zuliani, G., Fellin, R., Solini, A., Chwatko, G., Bald, E., Dramais, A.-S., Wallemacq, P. E., Vandeleene, B., Ciaria, M. V., Ariano, M., Strom, R., Gibney, J., Weiss, U., Turner, B., O’Gorman, P., Watts, G., Powrie, J., Crook, M., Shaw, K., and Cummings, M.
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- 1999
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14. Plasma renin and prorenin and renin gene variation in patients with insulin-dependent diabetes mellitus and nephropathy.
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Deinum, J, Tarnow, L, van Gool, J M, de Bruin, R A, Derkx, F H, Schalekamp, M A, and Parving, H H
- Abstract
The most striking abnormality in the renin angiotensin system in diabetic nephropathy (DN) is increased plasma prorenin. Renin is thought to be low or normal in DN. In spite of altered (pro)renin regulation the renin gene has not been studied for contribution to the development of DN.
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- 1999
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15. Effects of hyperglycaemia on kidney function, atrial natriuretic factor and plasma renin in patients with insulin-dependent diabetes mellitus
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Skøtt, P., Vaag, A., Hother-Nielsen, O., Andersen, P., Bruun, N. E., Giese, J., Beck-Nielsen, H., and Parving, H. -H.
- Abstract
In normoalbuminuric patients with insulin-dependent diabetes mellitus, plasma atrial natriuretic factor (ANF), cyclic GMP and active renin and the renal clearances of [99Tcm] diethylenetriaminepentaacetic acid (DTPA) lithium and sodium were studied on a hyperglycaemia day and a euglycaemia day. Baseline euglycaemia was achieved by an overnight variable insulin infusion, which during study days was fixed at the rate necessary to maintain euglycaemia in the morning. After a baseline euglycaemic clearance period of 90 min, measurements were repeated in a new 90-min period beginning 150 min later. On the hyperglycaemia day i.v. infusion of 20% glucose was started at the end of the euglycaemic baseline period, increasing blood glucose (5.3±1.3 vs 12.1±1.2 mmol l-1, p<0.01). On the euglycaemia day blood glucose declined (5.1±1.0 vs 4.2±1.0 mmol 1-1, p<0.02). Glomerular filtration rate (GFR) was unchanged by acute hyperglycaemia (127+16 vs 129±24 ml min-1, NS), but nearly normalized during maintained euglycaemia on the euglycaemia day (124±17 vs 105+16 ml min-1, p<0.01). When comparing the hyperglycaemic study period with the similarly timed period on the euglycaemia day, GFR was elevated by hyperglycaemia (129±24 vs 105±16 ml min -1, p<0.01), while the renal clearances of lithium and sodium were similar. Consequently, the calculated absolute proximal reabsorption rate of sodium and water was elevated during hyperglycaemia. Hyperglycaemia reduced the slight decline in plasma concentrations of ANF and cyclic GMP observed on the euglycaemia day. Active renin, glucagon and plasma osmolality were unchanged. In conclusion, marked changes in glomerular filtration rate are induced by changes in blood glucose concentration, but the effect is delayed and thus not directly related to renal tubular transport of glucose. Hyperglycaemia does not affect renal clearances of lithium and sodium, while proximal tubular reabsorption is markedly stimulated. These changes are not related to changes in ANF, renin, glucagon or plasma osmolality.
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- 1991
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16. Hearing Sensitivity in Patients with Myxoedema Before and After Treatment with L-Thyroxine
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Parving, A., Parving, H. H., and Lyngsøe, J.
- Abstract
Fifteen patients with confirmed myxoedema, median age 76 years, were consecutively referred for audiological evaluation. The diagnosis of myxoedema was based on the symptomatology, typical clinical appearance, increased TSH level and decreased T4. The audio-logical evaluation included routine ENT-examination, pure-tone octave audiometry, determination of speech reception threshold and discrimination score. The function of the middle ear was evaluated by impedance audiometry, indicating both middle ear pressure and stapedial reflex thresholds elicited by contralateral stimulation. All patients were evaluated in the myxoedematous state before treatment with 1-thyroxine and reevaluated when treated and found euthyroid, both by the clinical investigation and as judged by chemical thyroid parameters. Bilateral symmetrical or nearly symmetrical sensorineural hearing loss was demonstrated in all patients before treatment. The results indicate that in elderly patients with myxoedema no improvement in hearing sensitivity can be demonstrated upon 1-thyroxine medication. Patients with myxoedema at this age demonstrate neither more nor less degree of hearing loss when related to an age-matched group of hearing impaired patients. In patients with myxoedema the hearing impairment is found to be equal to that of an age and sex matched control group exhibiting true age-related hearing loss.
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- 1983
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17. Renoprotection in diabetes: genetic and non-genetic risk factors and treatment
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Parving, H.-H.
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- 1998
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18. Metabolism and Transcapillary Escape Rate of Albumin in Acromegaly
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Rossing, N., Parving, H. H., and Korsgaard, O.
- Abstract
Albumin metabolism was studied with 131 I-labeled albumin in 6 patients with acromegaly and raised plasma levels of growth hormone. The objective was to see whether the rate of albumin synthesis was increased, as animal experiments may suggest. The fractional catabolic rate of albumin (i.e. fraction of intravascular albumin mass catabolized per unit time) was increased by 64 % (form 8.5 to 13.8 % per 24 h), and the rate of synthesis must have been increased to the same extent, since the intravascular albumin mass was quite normal. Plasma albumin concentration and the intravascular and total masses were normal. The transcapillary escape rate, i.e. the fraction of the intravascular mass passing extravascularly per unit time, was increased on an average 40% above normal levels. It is concluded that growth hormone acts primarily by increasing albumin production.
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- 1974
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19. The acute effect of smoking on systemic haemodynamics, kidney and endothelial functions in insulin-dependent diabetic patients with microalbuminuria
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Hansen, H. P., Rossing, K., Jacobsen, P., Jensen, B. R., and Parving, H. -H.
- Abstract
The acute effect of smoking upon arterial blood pressure, urinary albumin excretion rate, glomerular filtration rate and transcapillary escape rate of albumin were investigated in nine normotensive insulin-dependent diabetic patients with microalbuminuria, who had been smoking for 19 (range 4-30) years. In a prospective, open randomized cross-over design, patients were investigated with and without smoking three cigarettes per hour during a 5.5-h period. A rise in systolic blood pressure and heart rate (Takeda TM2420, median (range)) was observed during the smoking day (10 ( - 11 to 14) mmHg and 8 ( - 1 to 19) beats min-1), compared to the non-smoking day (1 mmHg ( - 7 to 13) (p=0.05) and 0 beats min-1 ( - 2 to 4) (p<0.01)). Urinary albumin excretion rate (ELISA), glomerular filtration rate (plasma clearance of 51Cr-EDTA) and transcapillary escape rate of albumin (125I-albumin) remained the same with or without smoking. Our study suggests that heavy smoking induces an abrupt rise in systolic blood pressure and heart rate, while vascular leakage of albumin and glomerular filtration rate remain unaltered in normotensive insulin-dependent diabetic patients with microalbuminuria who had been smoking for several years.
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- 1996
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20. Changes in plasma volume, in transcapillary escape rate of albumin and in subcutaneous blood flow during hypoglycaemia in man
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Hilsted, J., Bonde-Petersen, F., Madsbad, S., Parving, H.-H., Christensen, N. J., Adelhøj, B., Bigler, D., and Sjøntoft, E.
- Abstract
1. Hypoglycaemia was induced by insulin injected intravenously (0.15 i.u./kg body weight) in seven healthy young males. 2. Plasma volume was measured before and during hypoglycaemia by intravenous injection of 125I before hypoglycaemia and of 131I during hypoglycaemia. Plasma volume decreased and transcapillary escape rate increased significantly during hypoglycaemia. 3. Skin temperature and local subcutaneous adipose tissue blood flow were measured in four different regions. Both tended to decrease during hypoglycaemia and decreased significantly 2 h after hypoglycaemia. There was no correlation between changes in the two measurements, suggesting that there is no simple relationship between subcutaneous blood flow and skin temperature during hypoglycaemia.
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- 1985
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21. Meta analysis. Diabetic nephropathy and the insertion/deletion polymorphism of the angiotensin-converting enzyme gene
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Tarnow, L., Gluud, C., and Parving, H-H.
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- 1998
22. Audiological and Temporal Bone Findings in Myxedema
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Parving, A., Ostri, B., Hansen, J., Bretlau, P., and Parving, H.-H.
- Abstract
Fifteen patients with confirmed myxedema at a median age of 48 years (range 32 to 60 years) were referred for audiological evaluation before and after treatment with levothyroxine. The median interval between the pretreatment and posttreatment investigations was 18 months (range 9 to 27 months). In addition, 13 patients at a median age of 78 years (range 64 to 95 years) were audiologically reexamined after long-standing levothyroxine treatment. The observation period upon treatment with levothyroxine was 40 months (range 32 to 46 months). No improvement in hearing sensitivity could be demonstrated either in the younger patients or in the elderly. When compared to an age- and sex-matched unscreened population, the myxedematous patients did not demonstrate any different degree of hearing loss. Histological investigation of the temporal bones from an 83-year-old woman with myxedema, however, showed no morphological changes or deposition of glycosaminoglycans, changes which are compatible with true age-related hearing loss. It is concluded that no association exists between myxedema and hearing impairment and that no morphological or structural changes due to myxedema can be demonstrated in the temporal bones.
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- 1986
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23. Microalbuminuria as an early indicator of osteopenia in male insulin‐dependent diabetic patients
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Clausen, P., Feldt‐Rasmussen, B., Jacobsen, P., Rossing, K., Parving, H‐H., Nielsen, P.K., Feldt‐Rasmussen, U., and Olgaard, K.
- Abstract
Reduced bone mineral density (BMD), termed diabetic osteopenia, has been reported in patients with insulin‐dependent (Type 1) diabetes mellitus (IDDM). To examine BMD in long‐term IDDM patients with normal kidney function, but with different degrees of urinary albumin excretion rate (UAER), compared to that of patients with elevated plasma creatinine, 36 IDDM male patients (mean duration 27 years) were subdivided according to UAER (<30, 30–300, >300, >300 mg 24 h−1and plasma creatinine 0.120–0.350 mmol l−1) and 15 controls were recruited. BMD was measured by dual energy X‐ray absorptiometry and UAER by enzyme linked immunosorbent assay. BMD was normal in IDDM patients with normal UAER and reduced in the femoral neck, the trochanter major, and the Wards triangle in patients with increased UAER (p< 0.01, p< 0.05, p< 0.02). BMD correlated to creatinine clearance in both cortical and cancellous bone sites (p< 0.001, p< 0.0001), and inversely to the levels of plasma PTH (p< 0.0005). We conclude that BMD is normal in long‐term IDDM male patients with normal kidney function and normal UAER and reduced in patients with increased UAER. Diabetic osteopenia seems to be a progressive phenomenon related to diabetic nephropathy and associated with the decrease in creatinine clearance and with the resulting rise in plasma PTH. © 1997 John Wiley & Sons, Ltd.
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- 1997
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24. Left Ventricular Hypertrophy in Non‐insulin‐dependent Diabetic Patients With and Without Diabetic Nephropathy
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Nielsen, F.S, Ali, S., Rossing, P., Bang, L.E., Svendsen, T.L., Gall, M.‐A., Smidt, U.M., Kastrup, J., and Parving, H.‐H.
- Abstract
The aim of our cross‐sectional case–control study was to evaluate putative mechanisms of the increased cardiac morbidity and mortality in NIDDM patients with or without diabetic nephropathy. Fifty‐one NIDDM patients with diabetic nephropathy (38 males, age 61 ± 8 years, group 1), 53 NIDDM patients with normoalbuminuria (42 males, 61 ± 7 years, group 2), and 22 non‐diabetic control subjects (15 males, 58 ± 8 years, group 3) were investigated. Previous antihypertensive treatment was withdrawn 2 weeks before the study. Left ventricular mass index (LVMI) and systolic function were determined by echocardiography. LVMI was elevated, mean ± SE, in group 1: 157 ± 6 g m−2, and in group 2: 139 ± 7 g m−2, as compared with group 3: 95 ± 5 g m−2(p< 0.001, for both), and in group 1 as compared with group 2 (p= 0.05). The prevalence of left ventricular hypertrophy (LVH) (LVMI > 131 g m−2in men and > 100 g m−2in women) was much higher in group 1: 75 % (95 % CI, 60–86), and group 2: 51 % (95 % CI, 37–65), as compared with group 3: 9 % (95 % CI, 1–29) (p< 0.001, for both), and in group 1 as compared with group 2 (p< 0.01). Shortening fraction of the left ventricle, % ± SE, was relatively reduced in group 1: 32.5 ± 1.1 %, and group 2: 33.4 ± 1.1 %, as compared with group 3: 41.2 ± 1.2 % (p< 0.01, for both). In a subgroup of 26 normoalbuminuric normotensive NIDDM patients, LVMI was higher than in 14 normotensive non‐diabetic control subjects: 137 ± 10 g m−2vs 96 ± 7 g m−2, respectively (p< 0.005). The prevalence of LVH was 42 % (95 % CI, 23–63) and 14 % (95 % CI, 2–43) (p= 0.07) in these two groups, respectively. In conclusion, normotensive and hypertensive NIDDM patients with and without diabetic nephropathy frequently suffer from LVH and relatively reduced systolic function which may constitute independent risk factors for fatal and non‐fatal cardiac events. © 1997 John Wiley & Sons, Ltd.
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- 1997
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25. Improved visual function in IDDM patients with unchanged cumulative incidence of sight-threatening diabetic retinopathy.
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Rossing, K, Jacobsen, P, Rossing, P, Lauritzen, E, Lund-Andersen, H, and Parving, H H
- Abstract
OBJECTIVE: To evaluate trends in visual acuity and the cumulative incidence of diabetic retinopathy in a clinic-based observational follow-up study. RESEARCH DESIGN AND METHODS: All patients visiting Hvidore Hospital in 1984 whose diagnosis of IDDM had been made before 41 years of age and between 1965 and 1979 (n = 356) were followed until 1994 or until their deaths. All patients were Caucasians and resided in Copenhagen. Patients were divided into three prevalence cohorts based on time of diabetes onset: group A, 1965-1969 (n = 113); group B, 1970-1974 (n = 130); and group C, 1975-1979 (n = 113). RESULTS: Fifteen years after diabetes onset, the visual acuity was significantly improved in patients with increasing calendar year of the disease onset. The median (interquartile range) visual acuity was 1.0 (0.8-1.0), 1.0(0.9-1.0), and 1.0 (1.0-1.0) in groups A, B, and C, respectively (P < 0.01 overall; P = 0.28 for group A vs. group B; and P < 0.01 for group A vs. group C) with 60, 66, and 93 having a visual acuity of 1.0 in groups A, B, and C, respectively. The cumulative incidence (+/-SEM), expressed as a percentage and calculated according to the life-table method, of proliferative retinopathy, maculopathy, and laser-treated retinopathy 15 years after onset of diabetes were, respectively, 13+/-3, 11+/-3, and 12+/-3 in group A; 16+/-3, 12+/-3, and 21+/-4 in group B; 11+/-3, 5+/-2, and 12+/-3 in group C, respectively (NS). The development of proliferative retinopathy was associated with the degree of retinopathy and albuminuria at baseline and the mean HbA1c during follow-up. CONCLUSIONS: The study revealed an improvement in visual acuity with increasing calendar year of diabetes onset but an unchanged cumulative incidence of diabetic retinopathy.
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- 1998
26. Increased left ventricular mass in normotensive type 1 diabetic patients with diabetic nephropathy.
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Sato, A, Tarnow, L, and Parving, H H
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OBJECTIVE: Diabetic nephropathy increases the risk of premature cardiovascular disease and sudden death, particularly in type 1 diabetic patients. One possible mechanism for this risk may be left ventricular hypertrophy. In our study, we aimed to evaluate left ventricular structure and function in normotensive type 1 diabetic patients with and without nephropathy. RESEARCH DESIGN AND METHODS: M-mode and Doppler echocardiography was performed in 17 type 1 diabetic patients with nephropathy (albuminuria [median (range)], 345 (135-2,846) mg/24 h) and compared with 34 normotensive, normoalbuminuric (10 [3-30] mg/24 h) type 1 diabetic patients matched for arterial blood pressure (mean +/- SD) ([134/77] +/- [13/7] vs. [129/78] +/- [12/7] mmHg), age (40 +/- 11 vs. 42 +/- 10 years), duration of diabetes (28 +/- 7 vs. 28 +/- 6 years), and BMI (24.2 +/- 4.2 vs. 24.6 +/- 2.4 kg/m2). RESULTS: Left ventricular mass (LVM) index was significantly higher in patients with nephropathy compared with patients with normoalbuminuria (100.8 +/- 10.3 vs. 88.2 +/- 21.0 g/m2, respectively; P = 0.02). Greater ventricular septum width was demonstrated in the nephropathic group compared with the control group (9.4 +/- 1.0 vs. 8.2 +/- 1.3 mm, respectively; P = 0.002). No significant difference in posterior wall thickness was apparent. The nephropathic group tended to have reduced diastolic function (E/A ratio, 1.2 +/- 0.3 vs. 1.4 +/- 0.4; P = 0.09). Fractional shortening was normal and about the same in the two groups. The groups did not differ with respect to serum creatinine or hemoglobin, while metabolic control (assessed by HbA1c) and plasma renin and prorenin levels were elevated in the nephropathic group compared with the normoalbuminuric group. CONCLUSIONS: A blood pressure-independent increase in LVM may contribute to the increased cardiac morbidity and mortality in normotensive type 1 diabetic patients with diabetic nephropathy. Glycemic abnormalities and activation of the renin-angiotensin system may lead to the ventricular enlargement.
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- 1998
27. Beneficial impact of ramipril on left ventricular hypertrophy in normotensive nonalbuminuric NIDDM patients.
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Nielsen, F S, Sato, A, Ali, S, Tarnow, L, Smidt, U M, Kastrup, J, and Parving, H H
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OBJECTIVE: To evaluate the effect of the ACE inhibitor ramipril as compared with placebo on left ventricular mass index (LVMI) in normotensive, nonalbuminuric NIDDM patients with left ventricular hypertrophy (LVH). Patients with NIDDM are characterized by excessive cardiovascular morbidity and mortality, and LVH, an independent risk factor for cardiac events, is often present in NIDDM patients. RESEARCH DESIGN AND METHODS: A total of 38 normotensive, nonalbuminuric (albuminuria < 100 mg/24 h) NIDDM patients with LVH (LVMI > 131 g/m2 in men and > 100 g/m2 in women) were enrolled in a 6-month randomized, double-blind parallel group study to compare the effects of ramipril (5 mg/day) with placebo on LVMI (echocardiography, Vingmed CFM725, Diasonics Sonotron), QTc dispersion determined as the interlead variation in QTc interval on standard electrocardiogram (ECG), and 24-h ambulatory blood pressure (A&D TM2420, Tokyo, Japan). A total of 16 ramipril (10 men, 60 +/- 9 years [mean +/- SD]) and 15 placebo-treated (8 men, 55 +/- 10 years) patients completed the study, and their data are presented. RESULTS: Ambulatory blood pressure was almost identical at baseline (132/76 +/- 3/1 vs. 133/74 +/- 5/2 mmHg [mean +/- SEM]) and remained stable during follow-up (134/76 +/- 3/1 vs. 136/74 +/- 6/2 mmHg) in the ramipril and placebo group, respectively. LVMI was comparable at baseline (137.1 +/- 7.0 vs. 129.6 +/- 3.7 g/m2) in the ramipril and placebo group, respectively, and decreased significantly more in the ramipril group as compared with the placebo group (17.6 +/- 3.0 vs. 5.7 +/- 4.6 g/m2, respectively, 11.9 [0.7-23.1] g/m2, mean difference [95% CI]; P = 0.037). QTc dispersion was comparable at baseline (60.2 [5.5] vs. 64.1 [6.5] ms) and did not change significantly during follow-up: -2.5 [7.0] vs. -12.2 [9.5] ms; mean difference 9.8 (-14.2 to 33.8 ms) in the ramipril and placebo group, respectively. CONCLUSIONS: Ramipril induces regression of LVH in normotensive, nonalbuminuric NIDDM patients, independent of reduction in systemic blood pressure.
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- 1998
28. Diabetic nephropathy and the insertion/deletion polymorphism of the angiotensin-converting enzyme gene.
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Tarnow, L, Gluud, C, and Parving, H H
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- 1998
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29. KIDNEY FUNCTION IN NORMAL MAN DURING SHORT-TERM GROWTH HORMONE INFUSION
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Parving, H.-H., Noer, I., Mogensen, C. E., and Svendsen, P. Aa.
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Kidney function was studied in 9 normal males before and during a 2 h growth hormone (GH) infusion of 50 ng/kg/min. The following variables were measured during each 20 min clearance period: glomerular filtration rate, GFR, effective renal plasma flow, RPF (steady state infusion technique with urinary collections using [125I]iothalamate and [131I]iodohippurate), and urinary albumin and β2-microglobulin excretion rates (radioimmunoassays).The GH infusion resulted in a 10-fold increase in plasma GH concentration.All the above mentioned variables remained practically unchanged during the infusion except for a small (−5%) but significant decrease in renal plasma flow (P< 0.01). Our negative results contrast to the findings of increased GFR and RPF during prolonged GH administration and suggest that GH requires several hours or days for its renal effects to become manifest.
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- 1978
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30. Early detection of patients at risk of developing diabetic nephropathy. A longitudinal study of urinary albumin excretion
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Parving, H.-H., Oxenbøll, B., Svendsen, P. Aa., Christiansen, J. Sandahl, and Andersen, A. R.
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In an attempt to detect patients at high risk of developing diabetic nephropathy, a longitudinal study of urinary albumin excretion rate (radial immunodiffusion) was carried out in 15 female and 8 male long-term insulin-dependent diabetics without proteinuria (negative Albustix test).Five females and 3 males had an elevated urinary albumin excretion at the time of screening, mean 115 ± 26 (sd) mg/24 h. Our upper normal range for urinary albumin excretion is ≤ 40 mg/24 h. The 5 patients with the highest albumin excretion subsequently developed persistent albuminuria, 132 → 1007 mg/24 h, P< 0.05, elevated serum creatinine, 83 → 128 μmol/l, P< 0.05, and raised blood pressure, 135/86 → 163/112 mmHg, P< 0.05. One patient developed intermittent albuminuria (positive Albustix test), while the variables in the remaining 2 patients were about the same during the 6 years observation period. Fifteen patients had a normal urinary albumin excretion, mean 17 ± 9 (sd) mg/24 h, at the time of the screening. Intermittent and persistent albuminuria developed in 2 patients, while albumin excretion, serum creatinine, and blood pressure were nearly unchanged in the remaining 13 patients after 6 years.Our longitudinal study indicates that early detection of patients at high and low risk of developing persistent proteinuria i.e. diabetic nephropathy, is possible by using a sensitive method for measuring urinary albumin excretion.
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- 1982
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31. Glomerular hyperfiltration in microalbuminuric NIDDM patients
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Vedel, P., Obel, J., Nielsen, F. S., Bang, L. E., Svendsen, T. L., Pedersen, O. B., and Parving, H.-H.
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Glomerular hyperfiltration and microalbuminuria are both regarded as risk factors for the development of diabetic nephropathy in insulin-dependent diabetic patients. Information on glomerular hyperfiltration is scarse in microalbuminuric non-insulin-dependent diabetic (NIDDM) patients. Therefore, we performed a cross-sectional study of glomerular filtration rate (single i. v. bolus injection of 51Cr-EDTA, plasma clearance for 4 h) in 158 microalbuminuric NIDDM patients compared to 39 normoalbuminuric NIDDM patients and 20 non-diabetic control subjects. The groups were well-matched with regard to sex, age and body mass index. The uncorrected (ml/min) and the adjusted (ml · min–1· 1.73 m–2) glomerular filtration rate were both clearly elevated in the microalbuminuric patients: 139 ± 29 and 117 ± 24 as compared to 115 ± 19 and 99 ± 15; 111 ± 23 and 98 ± 21 in normoalbuminuric NIDDM patients and control subjects, respectively (p< 0.001). The glomerular filtration rate (ml · min–1· 1.73 m–2) in NIDDM patients who had never received antihypertensive treatment was also clearly elevated in the microalbuminuric patients (n= 96): 119 ± 22 as compared to 100 ± 14 and 98 ± 21 in normoalbuminuric NIDDM patients (n= 27) and control subjects (n= 20), respectively (p< 0.001). Glomerular hyperfiltration (elevation above mean glomerular filtration rate plus 2 SD in normoalbuminuric NIDDM patients) was demonstrated in 37 (95 % confidence interval 30–45)% of the microalbuminuric patients. Multiple regression analysis revealed that HbA1 c, 24-h urinary sodium excretion, age and known duration of diabetes were correlated with glomerular filtration rate in microalbuminuric NIDDM patients (r2= 0.21, p< 0.01). Our cross-sectional study indicates that NIDDM patients at high risk of developing diabetic nephropathy are also characterized by an additional putative risk factor for progression, glomerular hyperfiltration. [Diabetologia (1996) 39: 1584–1589]
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- 1996
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32. Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy
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Parving, H.-H., Nielsen, F. S., Bang, L. E., Smidt, U. M., Svendsen, T. L., Chen, J.-W., Gall, M.-A., and Rossing, P.
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The Steno hypothesis suggests that albuminuria reflects widespread vascular damage (proliferative retinopathy and severe macroangiopathy) due to a generalized vascular (endothelial) dysfunction. We assessed this concept in NIDDM (non-insulin-dependent diabetic) patients with (13 female/39 male, age 60 ± 7 years, group 1) and without (12 female/41 male, age 61 ± 7 years, group 2) diabetic nephropathy compared to matched non-diabetic subjects (7 female/15 male, age 58 ± 8 years, group 3). A 12-lead ECG was recorded and coded blindly using the Minnesota Rating Scale; the World Health Organization cardiovascular questionnaire was used to assess past and present evidence of myocardial infarction, angina pectoris, stroke, and peripheral vascular disease (digital systolic blood pressure determination). The degree of diabetic retinopathy was scored from fundus photography. The following variables were measured: transcapillary escape rate of albumin (initial disappearance of intravenously injected 125I-labelled human serum albumin), plasma concentrations of prorenin (radioimmunoassay) and serum concentrations of von Willebrand factor (enzyme-linked immunoadsorbent assay). Prevalence of ischaemic heart disease (ECG reading) (49/20/5)% and peripheral vascular disease as indicated by reduced systolic blood pressure on big toe (69/30/14)% was significantly higher in group 1 vs group 2 (p< 0.01) and in group 2 vs group 3 (p< 0.01), respectively. The prevalence and severity of retinopathy was higher in group 1 vs 2 (p< 0.01). Transcapillary escape rate of albumin (%/h) was elevated in group 1 and 2 as compared to control subjects: 7.9 (4.3–13.7); 7.4 (3.7–16.4) vs 6.0 (3.4–8.7), (p< 0.005), respectively. Plasma prorenin activity (IU/ml) was raised in group 1 and group 2 as compared to group 3: 272 (59–2405); 192 (18–813), and 85 (28–246), p< 0.001, respectively. Serum von Willebrand factor (IU/ml)was elevated in group 1 as compared to group 2 and 3: 2.07 (0.83–4.34); 1.60 (0.30–2.99) and 1.50 (1.00–2.38), p< 0.001, respectively. Our study demonstrated that NIDDM patients with and without albuminuria had increased transcapillary escape of albumin and raised prorenin activity, whereas only those with albuminuria had increased von Willebrand factor. Patients with NIDDM may have abnormal endothelial function in the absence of albuminuria. [Diabetologia (1996) 39: 1590–1597]
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- 1996
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33. Prevention of diabetic renal disease with special reference to microalbuminuria
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Mogensen, C.E., Keane, W.F., Bennett, P.H., Striker, G.E., Jerums, G., Parving, H-H., Passa, P., Steffes, M.W., and Viberti, G.C.
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- 1995
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34. Increased minimal vascular resistance and arteriolar hyalinosis in skin on the leg in insulin-dependent diabetic patients
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Kastrup, J., Nørgaard, T., Parving, H.-H., and Lassen, N. A.
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Minimal vascular resistance (MVR) was determined in a paralysed cutaneous vascular bed at the dorsum of the foot in diabetic patients. Twelve long-term insulin-dependent diabetic (IDDM) patients with and nine short-term IDDM patients without nephropathy and retinopathy and eight control subjects were investigated. The vascular bed was paralysed by local injection of histamine. Skin perfusion pressure was varied by applying graded external counter pressure over the investigated area. Skin blood flow was measured by the local 99mTc wash-out technique before, during and after three to five step-wise increases of external counter pressure. The MVR was calculated from the reciprocal of the slope of the relationship between blood flow and applied pressure. The MVR was significantly increased in diabetic patients with (mean: 9.3 mmHg ml-1·100 g·min) and without nephropathy and retinopathy (8.5 mmHg ml-1·100 g·min) compared with non-diabetic subjects (5.2 mmHg ml-1·100 g·min) (p<0.001 and p<0.005, respectively). Diabetic microangiopathy (increased hyalinusis of the basement membranes in the terminal arterioles) was found in skin biopsies in nine of the 12 long-term IDDM patients and in four of the nine short-term IDDM patients, but not in the control subjects. Multiple regression analysis demonstrated a highly significant direct association between MVR and degree of diabetic microangiopathy in the same skin area (p<0.0002). A less significant direct association between MVR and arm diastolic blood pressure (p<0.05) and blood glucose concentration (p<0.05) was also found. Our results indicate, that terminal arteriolar hyalinosis is the main determinant of the increased minimal vascular resistance in skin in short- and long-term IDDM patients.
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- 1987
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35. Arteriolar hyalinosis does not interfere with the local veno-arteriolar reflex regulation of subcutaneous blood flow in insulin-dependent diabetic patients
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Kastrup, J., Nørgaard, T., Parving, H.-H., and Lassen, N. A.
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The function of the local nervous veno-arteriolar reflex regulation of blood flow in subcutaneous tissue of the lower leg was studied in diabetic patients. The material comprised 11 long-term insulin-dependent diabetic (IDDM) patients with retinopathy and nephropathy and eight short-term IDDM patients without retinopathy or nephropathy and 11 non-diabetic subjects. The diabetic patients had no or a slight to moderate degree of peripheral autonomic and sensoric neuropathy. Blood flow was measured by the local 133Xe wash-out technique. Blood flow was determined before, during and after an approximately 40 mmHg increase in venous transmural pressure, induced by lowering the lower leg 50 cm below heart level. During lowering of the leg, the subcutaneous blood flow decreased to the same level in long-term IDDM patients (mean: 46), short-term IDDM patients (53) and control subjects (53). There was no association between the relative local blood flow during lowering and the degree of terminal arteriolar hyalinosis studied in skin biopsies from the same tissue area. Our results suggest that terminal arteriolar hyalinosis does not interfere with the local sympathetic-mediated veno-arteriolar reflex regulation of blood flow. Moreover, the vasoconstriction mediated by the veno-arteriolar reflex probably occurs in the larger arterioles (>50–100 μm) or small arteries.
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- 1987
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36. Lisinopril improves endothelial dysfunction in hypertensive NIDDM subjects with diabetic nephropathy
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Nielsen, F. S., Rossing, P., Gall, M. A., Smidt, U. M., Chen, J. W., Sato, A., and Parving, H. H.
- Abstract
Endothelial dysfunction is a prevalent phenomenon in non-insulin dependent diabetic (NIDDM) patients with hypertension and albuminuria, and may contribute to the development and progression of cardiovascular disease, which is the main cause of the high morbidity and mortality observed in these patients. Therefore the aim of our study was to evaluate whether inhibition of angiotensin-converting enzyme (with lisinopril 10-20 mg day-1) could ameliorate endothelial dysfunction more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg day-1), usually in combination with a diuretic. We performed a 12-month prospective, randomized, double-blind, parallel study in 43 hypertensive NIDDM patients with diabetic nephropathy (21 treated with lisinopril and 22 with atenolol). The following variables were measured: 24-h ambulatory blood pressure (ABP); transcapillary escape rate of albumin (TERalb; i.e. initial disappearance of intravenously injected 125I-labelled human serum albumin); serum concentrations of von Willebrand factor (vWF), using ELISA, and urinary albumin excretion rate (UAE). Data are presented for 32 patients (16 lisinopril and 16 atenolol; age 60 years, SD 8; 25 males) out of 35 who completed the study and had valid measurements of TERalb. At baseline the two groups were comparable: TERalb (8.5 (SEM 0.6) vs. 7.2 (0.4) %); vWF (2.09 (range 0.82-4.34) vs. 1.97 (0.95-3.86) IU ml-1; UAE 916 (x/÷ antilog SEM 1.3) vs. 1444 (1.2), and mean ABP 110 (SEM 3) vs. 113 (2) mmHg, in the lisinopril and atenolol group, respectively. During follow up, the mean ABP was equally reduced in the lisinopril and atenolol group, by 12 (SEM 2) vs. 10 (2) mmHg, respectively. TERalb decreased in the lisinopril group by 0.6 (SEM 0.7) %, whereas it increased in the atenolol group 1.5 (0.5) %; the mean difference was 2.2% (95% CI, 0.5 to 3.9; p=0.015). UAE was reduced by 45% (95% CI, 25 to 60) in the lisinopril group vs. 10% (-15 to 30) in the atenolol group (p=0.014). Serum vWF was not changed during follow up in either group. Our study suggests that lisinopril has both reno- and vasculo-protective properties in hypertensive NIDDM patients with diabetic nephropathy.
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- 1997
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37. Extracellular fluid volume determined by a single injection of inulin in men with untreated essential hypertension
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Poulsen, H. Løønsmann, Jensen, H. ÆÆ., and Parving, H.-H.
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The extracellular volume (ECV) and plasma volume (PV) were determined simultaneously in nine men with untreated essential hypertension and in nine healthy matched control subjects, using a single injection of inulin and of 131I-labelled human serum albumin, respectively. The average mean arterial blood pressure in the hypertensive group was 178/118 mmHg. ECV was nearly the same in the two groups, viz. 151 ml/kg body weight (SD 17) in the hypertensive group compared to 147 ml/kg (SD 16) in the control group. The corresponding figures for PV were 38.2 ml/kg body weight (SD 4.7) and 43.7 ml/kg (SD 7.9) respectively (P<0.1). The calculated interstitial fluid volume (IV) was 113 ml/kg (SD 16) and 103 ml/kg (SD 10) (P<0.2). The PV/IV ratio was significantly lower (P<0.02) in the hypertensive group (0.34, SD 0.06) than in the normal group (0.42, SD 0.06). The difference might suggest increased transcapillary water filtration in hypertension.
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- 1977
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38. Increased transcapillary escape rate of albumin in patients with cirrhosis of the liver
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Parving, H. -H., Ranek, L., and Lassen, N. A.
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The transcapillary escape rate of albumin (TERalb), i.e. the fraction of intravascular mass of albumin that passes to the extravascular space per unit time, was determined from the disappearance of intravenously injected 125I-labelled human serum albumin during the first 60 min after injection in nine patients with cirrhosis of the liver. Six of the patients had ascites. The wedged hepatic venous pressure or splenic pulp pressure ranged from 20 to 30 mmHg, mean 26 mmHg. Plasma albumin concentration was low, but plasma volume was slightly enlarged, and thus the intravascular mass of albumin was only moderately reduced. The transcapillary escape rate of albumin was significantly elevated in all the cirrhotics, mean 10.2%/h, range 8.8 to 12.3%/h, in comparison to values for twenty-eight normal subjects 5.4%/h, range 3.5-7.2%/h. Our results can best be explained by increased filtration out of the vessels in the portal system, due to the increased portal venous pressure. The increased TERalb probably contributes to the formation of oedema and ascitic fluid.
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- 1977
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39. Insertion/deletion polymorphism in the angiotensin-l-converting enzyme gene is associated with coronary heart disease in IDDM patients with diabetic nephropathy
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Tarnow, L., Cambien, F., Rossing, P., Nielsen, F. S., Hansen, B. V., Lecerf, L., Poirier, O., Danilov, S., Boelskifte, S., Borch-Johnsen, K., and Parving, H. -H.
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Insulin-dependent diabetic (IDDM) patients with diabetic nephropathy have a highly increased morbidity and mortality from coronary heart disease. An insertion (I) /deletion (D) polymorphism in the angiotensin-I-converting enzyme (ACE) gene has been shown to be associated with coronary heart disease. Therefore, we have investigated the role of this ACE/ID polymorphism in 198 IDDM patients with diabetic nephropathy and 190 normoalbuminuric IDDM patients. The prevalence of myocardial infarction and other coronary heart disease was significantly elevated in patients with nephropathy, 19% (38/198) vs 8% (15/190), p< 0.001. In the nephropathic group 12 of 63 (19%), 23 of 95 (24%), and 3 of 40 (7.5 %) patients with the DD, ID and II genotypes, respectively had a history of coronary heart disease, II vs DD and ID, p< 0.05 when compared to nephropathic patients without coronary heart disease. Multiple logistic regression analysis of the risk factors associated with coronary heart disease in univariate analysis revealed that the II genotype acts as an independent protective factor against coronary heart disease, odds ratio II/DD + ID 0.27 (95 % confidence interval 0.07–0.97, p< 0.05). There was no difference in genotype or allele frequency (D/I) between patients with and without nephropathy, 0.56/0.44 in both groups, but plasma ACE concentration was elevated in patients with nephropathy 609 (151–1504) ng/ml as compared to patients with normoalbuminuria, 428 (55–1630) ng/ml, p< 0.001. We suggest that ACE/ID polymorphism may influence the frequency of life-threatening cardiac complications in IDDM patients suffering from diabetic nephropathy, a condition characterized by increased plasma ACE concentration.
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- 1995
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40. Reduction in albuminuria predicts a beneficial effect on diminishing the progression of human diabetic nephropathy during antihypertensive treatment
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Rossing, P., Hommel, E., Smidt, U. M., and Parving, H. -H.
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Diabetic nephropathy is the main cause of increased mortality and morbidity in IDDM patients. The effect of antihypertensive treatment on the progression of the nephropathy is highly variable. The aim of this study was to evaluate putative predictors of the progression in diabetic nephropathy during long-term antihypertensive treatment. Eighteen hypertensive IDDM patients with diabetic nephropathy, who had not been treated previously, were followed during 3 years of treatment with captopril and frusemide or bendrofluazide. Glomerular filtration rate, arterial blood pressure, albuminuria and adjusted albuminuria were used as putative predictors of rate of decline in glomerular filtration. Fall rate in glomerular filtration rate was 4.6 (4.0) mlmhr-1year-1(mean (SD)) during treatment. Relative change in albuminuria (ratio of first year of treatment/baseline) and albuminuria during first year of treatment were significantly correlated to fall rate in glomerular filtration rate during 3 years of treatment (r =0.73, p> 0.001) and (r =0.60, p >0.01), respectively. Arterial blood pressure and glomerular filtration rate measured at baseline, during first year of treatment or relative changes in these variables did not correlate with fall rate in glomerular filtration rate during 3 years of treatment. Haemoglobin Alc, serum-cholesterol, protein intake and sodium excretion remained unchanged during treatment, and were not correlated with loss of kidney function. Reduction in albuminuria during captopril treatment predicts an attenuated rate of decline in glomerular filtration rate in early diabetic nephropathy (glomerular filtration rate <70 ml· mirr-1· 1.73 nr-2). The finding suggests a clinical application in monitoring the efficacy of antihypertensive treatment in early diabetic nephropathy.
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- 1994
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41. Glomerular size-and charge selectivity in Type 2 (non-insulin-dependent) diabetic patients with diabetic nephropathy
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Gall, M. -A., Rossing, P., Kofoed-Enevoldsen, A., Nielsen, F. S., and Parving, H. -H.
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In an attempt to evaluate the mechanisms of proteinuria in diabetic kidney disease, we measured the renal clearances of albumin, total IgG, and IgG4 in 20 male Type 2 (non-insulin-dependent) diabetic patients with diabetic glomerulosclerosis (biopsy proven), in 10 male Type 2 diabetic patients without nephropathy (urinary albumin excretion rate < 30 mg/24 h), and in 10 healthy male subjects. The fractional clearance of albumin was increased in patients with nephropathy: 659 (42–4355) · 10−6(median (range)), compared to 2.6 (0.2–14.2) · 10−6in patients without nephropathy, and 2.3 (0.4–4.2) · 10−6in healthy subjects. The fractional clearance of total IgG (neutral) and of IgG4 (anionic) was 40–50 times higher in patients with nephropathy compared to the two other groups. The IgG/IgG4 selectivity index was not significantly different in the three groups, being: 1.12 (0.06–5.65), 1.16 (0.45–3.72) and 1.35 (0.65–3.34) in patients with nephropathy, patients without nephropathy, and healthy subjects, respectively. The IgG/albumin selectivity index was decreased in patients with nephropathy: 0.27 (0.01–1.26) compared to 1.29 (0.07–2.67) (p< 0.05) and 1.23 (0.76–7.84) (p< 0.001) in patients without nephropathy and healthy subjects, respectively. No significant change in IgG/albumin selectivity index was observed between patients without nephropathy and healthy subjects. The systolic blood pressure was elevated in the patients with nephropathy: 164 ± 21 mm Hg (mean ± SD) compared to patients without nephropathy: 145 ± 20 mm Hg (p< 0.05) and to healthy subjects: 133 ± 19 mm Hg (p< 0.005). The diastolic blood pressure was higher in patients with and without nephropathy: 92 ± 7 vs 90 ± 10 mm Hg compared to 79 ± 8 mm Hg (p< 0.005) in healthy subjects. Our cross-sectional study suggests that impaired barrier size selectivity, probably due to an increase in large pore area (“shunt pathway”) in the glomerular capillary wall and systemic hypertension are the major pathogenic mechanisms of proteinuria in Type 2 diabetic patients with diabetic nephropathy.
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- 1994
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42. Effect of insulin on renal sodium handling in hyperinsulinaemic Type 2 (non-insulin-dependent) diabetic patients with peripheral insulin resistance
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Skøtt, P., Vaag, A., Bruun, N., Hother-Nielsen, O., Gall, M.-A., Beck-Nielsen, H., and Parving, H.-H.
- Abstract
The sodium retaining effect of insulin was studied in ten Type 2 (non-insulin-dependent) diabetic patients (mean age 56 (43–73) years, mean body mass index 29.5 (24.2–33.7) kg/m2) and eight age-matched control subjects (mean age 57 (43–68) years, mean body mass index 23.4 (20.8–26.6) kg/m2). The renal clearances of 99mTc-DTPA, lithium, sodium and potassium were measured over a basal period of 90 min. Then insulin was infused at a rate of 40 mU·mirr−1·m−2. After an equilibration period of 90 min, the clearance measurements were repeated during a new 90 min period. Blood glucose was clamped at the basal level (diabetic patients: 9.9±3.5, control subjects: 5.3±0.5 mmol/l) by a variable glucose infusion. Basal plasma insulin concentration was elevated in the diabetic patients (0.12±0.05 vs 0.05±0.02 pmol/ml, p<0.01). Insulin infusion resulted in comparable absolute increments in plasma insulin concentrations in the diabetic group and in the control group (0.44±0.13 vs 0.36±0.07 pmol/ml, NS). The metabolic clearance rate of glucose during the last 30 min of insulin infusion was lower in the diabetic patients (155±62 vs 320±69 ml·min−1·m2, p<0.01), reflecting peripheral insulin resistance. The decline in sodium clearance during insulin infusion was similar in diabetic subjects (1.8±1.1 vs 0.7±0.4 ml·min−1·1.73 m−2, p< 0.01) and in control subjects (1.7±0.3 vs 0.8±0.3 ml · min−1· 1.73 m−2, p<0.01). The glomerular filtration rate and lithium clearance was unchanged, consequently calculated distal tubular fractional sodium reabsorption increased (diabetic patients: 92.9±4.1 vs 97.1±1.5, p<0.01, control subjects: 93.1±1.1 vs 96.5±0.6%, p< 0.01). Estimated extracellular fluid volume was 10% higher in the diabetic subjects (16.3±2.1 vs 14.8±2.01·1.73 m−2, NS). In conclusion, the sodium retaining effect of insulin is preserved in Type 2 diabetic patients with peripheral insulin resistance. Insulin may contribute to sodium and fluid retention and thus to the increased frequency of hypertension in hyperinsulinaemic Type 2 diabetic patients.
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- 1991
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43. Effects of nisoldipine and lisinopril on microvascular dysfunction in hypertensive Type I diabetes patients with nephropathy
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SØRENSEN, V. B., ROSSING, P., TARNOW, L., PARVING, H.-H., NØRGAARD, T., and KASTRUP, J.
- Abstract
1. Our objective was to compare the effect of a long-acting calcium antagonist (nisoldipine) compared with an angiotensin-converting enzyme inhibitor (lisinopril) on the non-neurogenic regulation of the microvascular blood flow in hypertensive Type I diabetes patients with diabetic nephropathy. 2. We performed a 1-year double-blind, double-dummy randomized controlled study comparing nisoldipine (20–40 mg once daily) with lisinopril (10–20 mg once daily) in 48 hypertensive Type I diabetes patients with diabetic nephropathy. For comparison, 22 age-matched normotensive healthy control subjects were included. Measurements were performed at baseline and after 1 year of antihypertensive treatment. The minimal vascular resistance and distensibility (stiffness) of resistance vessels in skin and skeletal muscle were measured using the local isotope washout method. 3. Mean arterial pressure was reduced to the same extent in both groups: nisoldipine, 113±2.1 to 105±1.6 mmHg (P< 0.001); lisinopril, 110±2.7 to 101±2.1 mmHg (P< 0.002) (controls, 88±2.2 mmHg; P< 0.0001 compared with diabetic patients). Nisoldipine improved the skin vascular distensibility from 28±3.3 to 43±3.8% (P< 0.005) and decreased skin minimal vascular resistance from 16.9±1.0 to 13.6±0.8 mmHg·ml-1·min·100 g (P< 0.02). Lisinopril had no significant effect on skin vascular distensibility (40±4.0% and 41±4.4%), but minimal vascular resistance tended to diminish (18.1±0.9 to 15.8±1.3 mmHg·ml-1·min·100 g (P =0.09). Nisoldipine significantly increased the skin distensibility (P = 0.05) after 1 year of antihypertensive treatment compared with lisinopril. 4. The control group had a skin vascular distensibility of 54±3.2% and a minimal vascular resistance of 10.8±0.7 mmHg·ml-1·min·100 g, both significantly different from the values in the diabetic groups (P< 0.0001 for all). Skeletal muscle vascular distensibility was unaltered after 1 year of treatment with both nisoldipine (22±3.3% and 19±2.7%) and lisinopril (19±2.1% and 24±2.5%), but was reduced compared with a control value of 43±3.7% (P< 0.0001 for diabetes patients versus controls). However, neither nisoldipine nor lisinopril had any effect on the increased minimal vascular resistance or the reduced skeletal muscle distensibility. 5. Enhanced thickening of the basement membranes of the terminal arteriolar wall was found in skin biopsy specimens in 91% of diabetic patients and 38% only in control subjects (P< 0.000001 both before and after treatment for diabetic patients versus controls). There was no significant effect of antihypertensive treatment on arteriolar hyalinosis. 6. The reduction in systemic blood pressure was identical during 1 year of treatment with nisoldipine or lisinopril. The abnormal arteriolar stiffness was more pronounced in the group treated with nisoldipine than with lisinopril and only nisoldipine compared with lisinopril improved the abnormal arteriolar stiffness and minimal vascular resistance in the skin. This suggests that nisoldipine can reverse the peripheral skin perfusion and thereby improve the local protection against development of ischaemic skin lesions in Type I diabetes patients with clinical diabetic nephropathy.
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- 1998
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44. Decreased distensibility of resistance vessels of the skin in type 1 (insulin-dependent) diabetic patients with microangiopathy
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Kastrup, J., Nørgaard, T., Parving, H.-H., and Lassen, N. A.
- Abstract
1. The distensibility of the resistance vessels of the skin at the dorsum of the foot was determined in 11 long-term type 1 (insulin-dependent) diabetic patients with nephropathy and retinopathy, nine short-term type 1 diabetic patients without clinical microangiopathy and in nine healthy non-diabetic subjects. 2. Blood flow was measured by the local 133Xexenon washout technique in a vascular bed locally paralysed by the injection of histamine. Blood flow was measured before, during and after a 40 mmHg increase of the vascular transmural pressure, induced by head-up tilt. 3. The mean increase in blood flow during headup tilt was only 24% in diabetic subjects with and 48% in diabetic patients without clinical microangiopathy, compared with 79% in normal non-diabetic subjects (P < 0.0005 and P < 0.05, respectively). 4. An inverse correlation between microvascular distensibility and degree of hyalinosis of the terminal arterioles in biopsies from the skin was demonstrated (r = − 0.57, P < 0.001). 5. Our results suggest that terminal arteriolar hyalinosis reduces the microvascular distensibility and probably increases the minimal vascular resistance, thereby impeding hyperaemic responses.
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- 1987
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45. Apolipoprotein(a) in insulin-dependent diabetic patients with and without diabetic nephropathy
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Gall, M-A., Rossing, P., Hommel, E., Voldsgaard, A. I., Andersen, P., Nielsen, F. S., Dyerberg, J., and Parving, H-H.
- Abstract
Insulin-dependent diabetic patients with diabetic nephropathy have a highly increased morbidity and mortality from cardiovascular diseases. To determine whether altered levels of apolipoprotein(a) (apo(a)), the glycoprotein of the potentially atherogenic lipoprotein(a) (Lp(a)), contribute to the increased risk of ischaemic heart disease, apo(a) was determined in 50 insulin-dependent diabetic patients with diabetic nephropathy (group 1), in 50 insulin-dependent diabetic patients with microalbuminuria (group 2), in 50 insulin-dependent diabetic patients with normoalbuminuria (group 3), and in 50 healthy subjects (group 4). The groups were matched with regard to sex, age and body mass index. The diabetic groups were also matched with regard to diabetes duration. The level of apo(a) was approximately the same in the four groups, being: 122 (×//4.2) U 1-1, 63 (×//.4) U 1-l, 128 (×//3.5) U 1-1 and 126 (×//3.7) U 1-1 (geometric mean (×//antilog SD)) in group 1, 2, 3 and 4, respectively. 1 U 1-1 apo(a) approximates 0.7 mg 1-1 Lp(a). The serum concentration of the following apolipoproteins and lipids was higher in patients with nephropathy as compared to the three other groups (group 1 vs group 3): apolipoprotein B 1.36 ± 0.38 vs 1.11 ± 0.30 g 1-1 (mean ± SD) (p < 0.01), total-cholesterol 6.0 ± 1.6 vs 5.3 ± 1.1 mmol 1-1 (p < 0.05), low-density lipoprotein (LDL)-cholesterol 3.85 ± 1.35 vs 3.22 ± 1.09 mmol 1-1 (p < 0.01) and triglyceride 1.28 (×//1.7) vs 0.85 (×//1.6 mmol 1-1 (p < 0.01). High-density lipoprotein (HDL)-cholesterol was lower in patients with nephropathy as compared to patients with micro-and normoalbuminuria (group 1 vs group 3): 1.42 ± 0.42 vs 1.61 ± 0.41 mmol 1-1 (p < 0.05). Our case-control study has revealed that insulin-dependent diabetic patients with diabetic nephropathy have hyperlipidaemia but a serum concentration of apo(a) comparable to healthy subjects.
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- 1992
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46. On the pathogenesis of arterial blood pressure elevation early in the course of diabetic nephropathy
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Hommel, E., Mathiesen, E. R., Giese, J., Nielsen, M. D., Schütten, H. J., and Parving, H-H.
- Abstract
We measured plasma- and extracellular fluid volume (125I-albumin, 51Cr-EDTA), plasma concentrations of renin, angiotensin I and II, aldosterone and atrial natriuretic peptide by radio-immunoassays in insulin-dependent diabetic (IDDM) patients with (n=28) and without (n=ll) nephropathy and in 14 normal control subjects matched for sex and age. Glomerular filtration rate (GFR) (ml/min/1.73 m2, single intravenous bolus 51Cr-EDTA technique) was within normal range in all nephropathy patients; 107 (range 78-134). Mean arterial blood pressure (mmHg) was elevated 102±13 (±S.D.) compared to the diabetic and normal control group, 92±8 and 87±5, respectively (p<0.01). Plasma volume was identical in all three groups while extracellular volume (1/1.73 m2) was expanded in nephropathic patients, 14.5±1.5 vs 13.1±0.9 and 12.4± 1.3 in the diabetic and non-diabetic control groups, respectively (p<0.05). A significant correlation between extracellular fluid volume and mean arterial blood pressure was found (n=53, r=0.49, p<0.001). Active renin was signficantly increased in patients with diabetic nephropathy compared with the normal control subjects, while all the remaining hormones were about the same in the three groups. Our study suggests that fluid retention plays a dominant role in the initiation and maintenance of arterial blood pressure elevation early in the course of diabetic nephropathy.
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- 1989
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47. The acute effect of acetazolamide on glomerular filtration rate and proximal tubular reabsorption of sodium and water in normal man
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Skøtt, P., Hommel, E., Bruun, N. E., Arnold-Larsen, S., and Parving, H-H.
- Abstract
The acute effects on kidney function of acetazolamide (250 mg) given intravenously were evaluated in seven healthy subjects. Glomerular filtration rate was measured as the renal clearance of 5lCr-EDTA, and fluid flow rate out of the proximal tubules was assessed by measurement of the renal lithium clearance. An 18% decline in glomerular filtration rate (ml/min) was observed after acetazolamide administration (109±16 vs 89±14, p<0.02), while lithium clearance (ml/min) increased by 35% (30±5 vs 38±8, p<0.02). Absolute proximal tubular reabsorption of water (ml/min) was reduced by about one third (79±12 vs 51±9, p<0.02), and fractional proximal reabsorption of water and sodium (%) declined (73±2 vs 58±6, p<0.02). Renal sodium clearance and absolute distal reabsorption of sodium increased, while fractional distal reabsorption of sodium declined.Acetazolamide reduces absolute and fractional proximal tubular reabsorption of sodium and water, and glomerular filtration rate. Primarily, this induces an increase in the output of fluid from the proximal tubules accounting for the diuretic effect of the drug. The acute fall in glomerular filtration rate is probably mediated by a temporary increase in proximal intratubular pressure and activation of the tubuloglomerular feedback mechanism.
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- 1989
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48. The increased proximal tubular reabsorption of sodium and water is maintained in long-term insulin-dependent diabetics with early nephropathy
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Skøøtt, P., Mathiesen, E. R., Hommel, E., Gall, M-A., Bruun, N. E., and Parving, H-H.
- Abstract
Proximal tubular reabsorption of sodium and water was investigated in long-term insulin-dependent diabetic patients with normoalbuminuria (group I, n=19), microalbuminuria (group II, n=39), diabetic nephropathy (group III, n=12) and in 13 healthy age-matched subjects. Glomerular filtration rate was measured with the single injection 51Cr-EDTA technique. The fluid flow rate out of the proximal tubules was assessed by the renal lithium clearance. Although glomerular filtration rate was significantly elevated in the diabetic patients (Group I: 122±±16, Group II: 121 ±±18, Group III: 110117, Controls: 105 + 13 ml/minxl.73 m2), lithium clearance was similar in the four groups (Group I: 19+6, Group II: 22±±7, Group III: 19±±5, Controls: 23±±4 ml/ minx 1.73 m2). Both absolute and fractional proximal reabsorption of sodium and water was enhanced in diabetes. Indices of distal tubular function did not differ between controls and patients with insulin-dependent diabetes. Sodium clearance was about the same in the four groups. Our study suggests that the enhanced proximal reabsorption of sodium and water in insulin-dependent diabetic patients is still observed despite the presence of incipient or overt diabetic nephropathy.
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- 1989
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49. Increased transcapillary escape rate of albumin and IgG in essential hypertension
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Parving, H. H., Jensen, H. Æ., and Westrup, M.
- Abstract
Transcapillary escape rates of albumin and IgG (fractions of intravascular mass of albumin and IgG that pass to the extravascular space per unit time) were determined simultaneously from the initial disappearance of intravenously injected 131I human albumin and 125I human IgG in seven untreated subjects suffering from essential hypertension. The average mean arterial blood pressure of these subjects was 193/119 mmHg; four subjects had grade I-III funduscopic changes. Transcapillary escape rates of albumin (TERalb) and IgG (TERIgG) were found significantly increased in the hypertensive subjects, average 7.8±0.9 (SD) and 4.7±1.0 (SD) %/h, respectively, compared with normal values of mean 5.2±1.0 (SD) and 3.0±0.7 (SD) %/h, respectively (P<0.01). There was a statistically significant positive correlation between the mean arterial blood pressure and TER of albumin and of IgG (P<0.001). The TER1gG/TERalb ratio was about the same in the hypertensives and the normals. Confirming a previous observation, we found an increase in the daily urinary albumin excretion rate from a normal average of 9.1 (range, 2.4-20.4)mg/24 h to 96 (range, 5.6-565) mg/24 h, P<005. The present findings can best be explained by increased filtration through normal pores between the endothelial cells in the microvascula-ture, due to the high arterial blood pressure.
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- 1977
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50. Clinical Physiology: Increased Metabolic Turnover Rate and Transcapillary Escape Rate of Albumin in Long-Term Juvenile Diabetics
- Author
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Parving, H. -H., Rossing, N., and Sander, E.
- Abstract
Parving, H.-H., Rossing, N. & Sander, E. Increased Metabolic Turnover Rate and Transcapillary Escape Rate of Albumin in Long-Term Juvenile Diabetics. Scand. J. din. Lab. Invest. 35, 59-66, 1975.The metabolic turnover rate and transcapillary escape rate of albumin were studied with 131I-labelled human albumin in nine patients with long-term diabetes mellitus. Retinopathy was present in all patients and nephropathy in four. Plasma albumin concentration and plasma volume were reduced (P < 0.05). The previously reported decrease in the intravascular albumin mass in long-term diabetics was thus confirmed by an average of 59.0 g/m2 surface area, compared with a normal value of 71.7 g/m2 (-18yo) (P < 0.005). The albumin metabolic rate was increased, the fractional disappearance rate being an average 13.2yo of the intravascular albumin mass per 24 hr, compared with a normal value of 8.4% (+ 57%) (P < 0.001). The rate of synthesis was 7.7 g. 24 h-1. m-2 in contrast to a normal rate of 6.2 g. 24 h-1. m-2 (+24%) (P < 0.001). Total body albumin mass was decreased proportionally to the intravascular mass. Confirming previous observations, we found an increase in the transcapillary escape rate of albumin (fraction of intravascular albumin mass passing to the extravascular space per unit time) from a normal average of 5.6% hr-1 to 7.4y0. hr-1 (+ 32%) (P < 0.001). This finding can best be explained by an increased microvascular permeability to plasma proteins. A positive correlation between the transcapillary escape rate and fractional disappearance rate of albumin was demonstrated (r = 0.74; P < 0.01). This supports the concept that albumin is catabolized in connection with its permeation through the microvascular endothelium.
- Published
- 1975
- Full Text
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