177 results on '"Parving, H. H."'
Search Results
2. Higher plasma high-mobility group box 1 levels are associated with incident cardiovascular disease and all-cause mortality in type 1 diabetes: a 12 year follow-up study
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Nin, J. W. M., primary, Ferreira, I., additional, Schalkwijk, C. G., additional, Jorsal, A., additional, Prins, M. H., additional, Parving, H.-H., additional, Tarnow, L., additional, Rossing, P., additional, and Stehouwer, C. D. A., additional
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- 2012
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3. Erratum to: Increased serum potassium affects renal outcomes: a post hoc analysis of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial
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Miao, Y., primary, Dobre, D., additional, Lambers Heerspink, H. J., additional, Brenner, B. M., additional, Cooper, M. E., additional, Parving, H.-H., additional, Shahinfar, S., additional, Grobbee, D., additional, and de Zeeuw, D., additional
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- 2011
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4. Increased serum potassium affects renal outcomes: a post hoc analysis of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial
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Miao, Y., primary, Dobre, D., additional, Lambers Heerspink, H. J., additional, Brenner, B. M., additional, Cooper, M. E., additional, Parving, H-H., additional, Shahinfar, S., additional, Grobbee, D., additional, and de Zeeuw, D., additional
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- 2010
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5. A polymorphism in the gene encoding carnosinase (CNDP1) as a predictor of mortality and progression from nephropathy to end-stage renal disease in type 1 diabetes mellitus
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Alkhalaf, A., primary, Bakker, S. J. L., additional, Bilo, H. J. G., additional, Gans, R. O. B., additional, Navis, G. J., additional, Postmus, D., additional, Forsblom, C., additional, Groop, P. H., additional, Vionnet, N., additional, Hadjadj, S., additional, Marre, M., additional, Parving, H. H., additional, Rossing, P., additional, and Tarnow, L., additional
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- 2010
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6. Multifactorial treatment increases endothelial progenitor cells in patients with type 2 diabetes
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Reinhard, H., primary, Jacobsen, P. Karl, additional, Lajer, M., additional, Pedersen, N., additional, Billestrup, N., additional, Mandrup-Poulsen, T., additional, Parving, H.-H., additional, and Rossing, P., additional
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- 2010
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7. Optimal antiproteinuric dose of aliskiren in type 2 diabetes mellitus: a randomised crossover trial
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Persson, F., primary, Rossing, P., additional, Reinhard, H., additional, Juhl, T., additional, Stehouwer, C. D. A., additional, Schalkwijk, C., additional, Danser, A. H. J., additional, Boomsma, F., additional, Frandsen, E., additional, and Parving, H.-H., additional
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- 2010
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8. Telomere length predicts all-cause mortality in patients with type 1 diabetes
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Astrup, A. S., primary, Tarnow, L., additional, Jorsal, A., additional, Lajer, M., additional, Nzietchueng, R., additional, Benetos, A., additional, Rossing, P., additional, and Parving, H.-H., additional
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- 2009
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9. Optimal dose of lisinopril for renoprotection in type 1 diabetic patients with diabetic nephropathy: a randomised crossover trial
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Schjoedt, K. J., primary, Astrup, A. S., additional, Persson, F., additional, Frandsen, E., additional, Boomsma, F., additional, Rossing, K., additional, Tarnow, L., additional, Rossing, P., additional, and Parving, H.-H., additional
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- 2008
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10. Plasma osteoprotegerin levels predict cardiovascular and all-cause mortality and deterioration of kidney function in type 1 diabetic patients with nephropathy
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Jorsal, A., primary, Tarnow, L., additional, Flyvbjerg, A., additional, Parving, H.-H., additional, Rossing, P., additional, and Rasmussen, L. M., additional
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- 2008
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11. Long-term prevention of diabetic nephropathy: an audit
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Schjoedt, K. J., primary, Hansen, H. P., additional, Tarnow, L., additional, Rossing, P., additional, and Parving, H.-H., additional
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- 2008
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12. Increased renal gene transcription of protein kinase C-β in human diabetic nephropathy: relationship to long-term glycaemic control
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Langham, R. G., primary, Kelly, D. J., additional, Gow, R. M., additional, Zhang, Y., additional, Cox, A. J., additional, Qi, W., additional, Thai, K., additional, Pollock, C. A., additional, Christensen, P. K., additional, Parving, H.-H., additional, and Gilbert, R. E., additional
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- 2008
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13. Plasma N-terminal pro-B-type natriuretic peptide and mortality in type 2 diabetes
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Tarnow, L., primary, Gall, M.-A., additional, Hansen, B. V., additional, Hovind, P., additional, and Parving, H.-H., additional
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- 2006
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14. Anaemia in diabetes: is there a rationale to TREAT?
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Thomas, M. C., primary, Cooper, M. E., additional, Rossing, K., additional, and Parving, H. H., additional
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- 2006
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15. Remission of nephrotic-range albuminuria reduces risk of end-stage renal disease and improves survival in type 2 diabetic patients
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Rossing, K., primary, Christensen, P. K., additional, Hovind, P., additional, and Parving, H.-H., additional
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- 2005
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16. Increased serum adiponectin levels in type 1 diabetic patients with microvascular complications
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Frystyk, J., primary, Tarnow, L., additional, Krarup Hansen, T., additional, Parving, H.-H., additional, and Flyvbjerg, A., additional
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- 2005
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17. The prevalence of coeliac disease in adult Danish patients with type 1 diabetes with and without nephropathy
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Skovbjerg, H., primary, Tarnow, L., additional, Locht, H., additional, and Parving, H.-H., additional
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- 2005
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18. Plasma N-terminal pro-brain natriuretic peptide as a major risk marker for cardiovascular disease in patients with type 2 diabetes and microalbuminuria
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G�de, P., primary, Hildebrandt, P., additional, Hess, G., additional, Parving, H.-H., additional, and Pedersen, O., additional
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- 2004
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19. Plasma N-terminal pro-brain natriuretic peptide as an independent predictor of mortality in diabetic nephropathy
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Tarnow, L., primary, Hildebrandt, P., additional, Hansen, B. V., additional, Borch-Johnsen, K., additional, and Parving, H.-H., additional
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- 2004
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20. Aldosterone escape during blockade of the renin?angiotensin?aldosterone system in diabetic nephropathy is associated with enhanced decline in glomerular filtration rate
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Schjoedt, K. J., primary, Andersen, S., additional, Rossing, P., additional, Tarnow, L., additional, and Parving, H.-H., additional
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- 2004
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21. Total plasma homocysteine is associated with hypertension in Type I diabetic patients
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Neugebauer, S., primary, Tarnow, L., additional, Stehouwer, C., additional, Teerlink, T., additional, Baba, T., additional, Watanabe, T., additional, and Parving, H.-H., additional
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- 2002
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22. Pregnancy and progression of diabetic nephropathy
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Rossing, K., primary, Jacobsen, P., additional, Hommel, E., additional, Mathiesen, E., additional, Svenningsen, A., additional, Rossing, P., additional, and Parving, H.-H., additional
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- 2002
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23. Lack of synergism between long-term poor glycaemic control and three gene polymorphisms of the renin angiotensin system on risk of developing diabetic nephropathy in Type I diabetic patients
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Tarnow, L., primary, Kjeld, T., additional, Knudsen, E., additional, Major-Pedersen, A., additional, and Parving, H. -H., additional
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- 2000
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24. Prevalence of left ventricular hypertrophy in Type I diabetic patients with diabetic nephropathy
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Sato, A., primary, Tarnow, L., additional, and Parving, H.-H., additional
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- 1999
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25. Renoprotection in diabetes: genetic and non-genetic risk factors and treatment
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Parving, H.-H., primary
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- 1998
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26. Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy
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Parving, H.-H., primary, Nielsen, F. S., additional, Bang, L. E., additional, Smidt, U. M., additional, Svendsen, T. L., additional, Chen, J.-W., additional, Gall, M.-A., additional, and Rossing, P., additional
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- 1996
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27. Glomerular hyperfiltration in microalbuminuric NIDDM patients
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Vedel, P., primary, Obel, J., additional, Nielsen, F. S., additional, Bang, L. E., additional, Svendsen, T. L., additional, Pedersen, O. B., additional, and Parving, H.-H., additional
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- 1996
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28. Cholesterol-lowering therapy may retard the progression of diabetic nephropathy
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Parving, H. -H., primary and Lam, K. S. L., additional
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- 1996
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29. 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., primary, Cambien, F., additional, Rossing, P., additional, Nielsen, F. S., additional, Hansen, B. V., additional, Lecerf, L., additional, Poirier, O., additional, Danilov, S., additional, Boelskifte, S., additional, Borch-Johnsen, K., additional, and Parving, H. -H., additional
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- 1995
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30. Long-term comparison of human insulin analogue B10Asp and soluble human insulin in IDDM patients on a basal/bolus insulin regimen
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Nielsen, F. S., primary, J�rgensen, L. N., additional, Ipsen, M., additional, Voldsgaard, A. I., additional, and Parving, H. -H., additional
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- 1995
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31. Monitoring kidney function in diabetic nephropathy
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Rossing, P., primary, Astrup, A.-S., additional, Smidt, U. M., additional, and Parving, H.-H., additional
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- 1994
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32. Reduction in albuminuria predicts a beneficial effect on diminishing the progression of human diabetic nephropathy during antihypertensive treatment
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Rossing, P., primary, Hommel, E., additional, Smidt, U. M., additional, and Parving, H. -H., additional
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- 1994
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33. Glomerular size-and charge selectivity in Type 2 (non-insulin-dependent) diabetic patients with diabetic nephropathy
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Gall, M. -A., primary, Rossing, P., additional, Kofoed-Enevoldsen, A., additional, Nielsen, F. S., additional, and Parving, H. -H., additional
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- 1994
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34. Glomerular structure and function in proteinuric Type 2 (non-insulin-dependent) diabetic patients
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Østerby, R., primary, Gall, M. -A., additional, Schmitz, A., additional, Nielsen, F. S., additional, Nyberg, G., additional, and Parving, H. -H., additional
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- 1993
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35. The course of kidney function in Type 2 (non-insulin-dependent) diabetic patients with diabetic nephropathy
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Gall, M. -A., primary, Nielsen, F. S., additional, Smidt, U. M., additional, and Parving, H. -H., additional
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- 1993
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36. Apolipoprotein(a) and cardiovascular disease in Type 2 (non-insulin-dependent) diabetic patients with and without diabetic nephropathy
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Nielsen, F. S., primary, Voldsgaard, A. I., additional, Gall, M. -A., additional, Rossing, P., additional, Hommel, E., additional, Andersen, P., additional, Dyerberg, J., additional, and Parving, H. -H., additional
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- 1993
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37. Plasma lipoproteins and renal function during simvastatin treatment in diabetic nephropathy
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Hommel, E., primary, Andersen, P., additional, Gall, M. -A., additional, Nielsen, F., additional, Jensen, B., additional, Rossing, P., additional, Dyerberg, J., additional, and Parving, H. -H., additional
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- 1992
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38. SNP in the genome-wide association study hotspot on chromosome 9p21 confers susceptibility to diabetic nephropathy in type 1 diabetes.
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Fagerholm, E., Ahlqvist, E., Forsblom, C., Sandholm, N., Syreeni, A., Parkkonen, M., McKnight, A., Tarnow, L., Maxwell, A., Parving, H.-H., Groop, L., and Groop, P.-H.
- Abstract
Aims/hypothesis: Parental type 2 diabetes mellitus increases the risk of diabetic nephropathy in offspring with type 1 diabetes mellitus. Several single nucleotide polymorphisms (SNPs) that predispose to type 2 diabetes mellitus have recently been identified. It is, however, not known whether such SNPs also confer susceptibility to diabetic nephropathy in patients with type 1 diabetes mellitus. Methods: We genotyped nine SNPs associated with type 2 diabetes mellitus in genome-wide association studies in the Finnish population, and tested for their association with diabetic nephropathy as well as with severe retinopathy and cardiovascular disease in 2,963 patients with type 1 diabetes mellitus. Replication of significant SNPs was sought in 2,980 patients from three other cohorts. Results: In the discovery cohort, rs10811661 near gene CDKN2A/B was associated with diabetic nephropathy. The association remained after robust Bonferroni correction for the total number of tests performed in this study (OR 1.33 [95% CI 1.14, 1.56], p = 0.00045, p = 0.016). In the meta-analysis, the combined result for diabetic nephropathy was significant, with a fixed effects p value of 0.011 (OR 1.15 [95% CI 1.02, 1.29]). The association was particularly strong when patients with end-stage renal disease were compared with controls (OR 1.35 [95% CI 1.13, 1.60], p = 0.00038). The same SNP was also associated with severe retinopathy (OR 1.37 [95% CI 1.10, 1.69] p = 0.0040), but the association did not remain after Bonferroni correction ( p = 0.14). None of the other selected SNPs was associated with nephropathy, severe retinopathy or cardiovascular disease. Conclusions/interpretation: A SNP predisposing to type 2 diabetes mellitus, rs10811661 near CDKN2A/B, is associated with diabetic nephropathy in patients with type 1 diabetes mellitus. [ABSTRACT FROM AUTHOR]
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- 2012
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39. Exposure to candesartan during the first trimester of pregnancy in type 1 diabetes: experience from the placebo-controlled diabetic retinopathy candesartan trials.
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Porta, M., Hainer, J., Jansson, S.-O., Malm, A., Bilous, R., Chaturvedi, N., Fuller, J., Klein, R., Orchard, T., Parving, H.-H., and Sjølie, A.-K.
- Abstract
ims/hypothesis: The teratogenic consequences of angiotensin-converting enzyme inhibitors angiotensin receptor blockers (ARBs) during the second and third trimesters of pregnancy are well described. However, the consequences of exposure during the first trimester are unclear, especially in diabetes. We report the experience from DIRECT (DIabetic REtinopathy and Candesartan Trials), three placebo-controlled studies designed to examine the effects of an ARB, candesartan, on diabetic retinopathy. Methods: Over 4 years or longer, 178 normotensive women with type 1 diabetes (86 randomised to candesartan, 32 mg once daily, and 92 assigned to placebo) became pregnant (total of 208 pregnancies). Results: More than half of patients were exposed to candesartan or placebo prior to or in early pregnancy, but all discontinued it at an estimated 8 weeks from the last menstrual period. Full-term pregnancies (51 vs 50), premature deliveries (21 vs 27), spontaneous miscarriages (12 vs 15), elective terminations (15 vs 14) and other outcomes (1 vs 2) were similar in the candesartan and placebo groups. There were two stillbirths and two 'sick babies' in the candesartan group, and one stillbirth, eight 'sick babies' and one cardiac malformation in the placebo group. Conclusions/interpretation: The risk for fetal consequences of ARBs in type 1 diabetes may not be high if exposure is clearly limited to the first trimester. Long-term studies in fertile women can be conducted with ARBs during pregnancy, provided investigators diligently stop their administration upon planning or detection of pregnancy. Trial registration: ClinicalTrials.gov DIRECT-Prevent 1 NCT00252733; DIRECT-Protect 1 NCT00252720; DIRECT-Protect 2 NCT00252694. Funding: The study was funded jointly by AstraZeneca and Takeda. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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40. Increased serum potassium affects renal outcomes: a post hoc analysis of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial.
- Author
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Miao, Y., Dobre, D., Lambers Heerspink, H., Brenner, B., Cooper, M., Parving, H-H., Shahinfar, S., Grobbee, D., and Zeeuw, D.
- Abstract
ims/hypothesis: To assess the effect of an angiotensin receptor blocker (ARB) on serum potassium and the effect of a serum potassium change on renal outcomes in patients with type 2 diabetes and nephropathy. Methods: We performed a post hoc analysis in patients with type 2 diabetes participating in the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) study. Renal outcomes were defined as a composite of doubling of serum creatinine or end-stage renal disease. Results: At month 6, 259 (38.4%) and 73 (10.8%) patients in the losartan group and 151 (22.8%) and 34 (5.1%) patients in the placebo group had serum potassium ≥5.0 mmol/l and ≥5.5 mmol/l, ( p < 0.001), respectively. Losartan was an independent predictor for serum potassium ≥5.0 mmol/l at month 6 (OR 2.8; 95% CI 2.0-3.9). Serum potassium at month 6 ≥ 5.0 mmol/l was in turn associated with increased risk for renal events (HR 1.22; 95% CI 1.00-1.50), independent of other risk factors. Adjustment of the overall treatment effects for serum potassium augmented losartan's renoprotective effect from 21% (6-34%) to 35% (20-48%), suggesting that the renoprotective effects of losartan are offset by its effect on serum potassium. Conclusions/interpretation: In this study, we found that treatment with the ARB losartan is associated with a high risk of increased serum potassium levels, which is in turn associated with an increased risk of renal outcomes in patients with diabetes and nephropathy. Whether additional management of high serum potassium would further increase the renal protective properties of losartan is an important clinical question. [ABSTRACT FROM AUTHOR]
- Published
- 2011
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41. Telomere length predicts all-cause mortality in patients with type 1 diabetes.
- Author
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Astrup, A., Tarnow, L., Jorsal, A., Lajer, M., Nzietchueng, R., Benetos, A., Rossing, P., and Parving, H.-H.
- Abstract
Type 1 diabetic patients with diabetic nephropathy have increased mortality and morbidity compared with normoalbuminuric patients. Telomere length in proliferative cells is inversely related to the total number of cell divisions, and therefore to biological age. We aimed to evaluate differences in telomere length in patients with type 1 diabetes with or without diabetic nephropathy; we also evaluated the prognostic value of telomere length. In a prospective follow-up study, 157 type 1 diabetic patients with diabetic nephropathy and a control group of 116 patients with type 1 diabetes and normoalbuminuria were followed for 11.1 years (range 0.2–12.9). Telomere length was measured from DNA samples extracted from white blood cells at baseline. The mean telomere length did not differ between patients with or without diabetic nephropathy, and was similar in men and women, but was inversely correlated with age and systolic blood pressure, p < 0.05. When dividing patients into tertiles after telomere length, 36 (37%) patients died in the tertile with the shortest telomere length, 24 (28%) died in the middle tertile, and 15 (17%) of patients in the tertile with the longest telomere length died, log rank test p = 0.017. After adjustment for traditional risk factors, telomere length was still predictive of all-cause mortality. In patients with type 1 diabetes we found no differences in telomere length between patients with or without diabetic nephropathy. We also found that telomere length was associated with all-cause mortality; however, confirmative studies are needed to verify our findings. [ABSTRACT FROM AUTHOR]
- Published
- 2010
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42. Prevalence of micro- and macroalbuminuria, arterial hypertension, retinopathy and large vessel disease in European Type 2 (non-insulin-dependent) diabetic patients
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Gall, M. -A., primary, Rossing, P., additional, Sk�tt, P., additional, Damsbo, P., additional, Vaag, A., additional, Bech, K., additional, Dejgaard, A., additional, Lauritzen, M., additional, Lauritzen, E., additional, Hougaard, P., additional, Beck-Nielsen, H., additional, and Parving, H. H., additional
- Published
- 1991
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43. Lack of familial predisposition to cardiovascular disease in Type 1 (insulin-dependent) diabetic patients with nephropathy
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N�rgaard, K., primary, Mathiesen, E. R., additional, Hommel, E., additional, Jensen, J. S., additional, and Parving, H. -H., additional
- Published
- 1991
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44. Optimal dose of lisinopril for renoprotection in type 1 diabetic patients with diabetic nephropathy: a randomised crossover trial.
- Author
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Schjoedt, K., Astrup, A., Persson, F., Frandsen, E., Boomsma, F., Rossing, K., Tarnow, L., Rossing, P., and Parving, H.-H.
- Abstract
The purpose of this study was to evaluate the optimal renoprotective effect of ultrahigh doses of lisinopril, as reflected by short-term changes in urinary albumin excretion rate (UAER), in type 1 diabetic patients with diabetic nephropathy. At the Steno Diabetes Center, 49 type 1 diabetic patients with diabetic nephropathy completed this double-masked randomised crossover trial consisting of an initial washout period followed by three treatment periods each lasting 2 months, where all patients received lisinopril 20, 40 and 60 mg once daily in randomised order in addition to slow-release furosemide. Allocation was concealed by sequentially numbered opaque sealed envelopes. UAER, 24 h ambulatory blood pressure (ABP) and estimated GFR were determined at baseline and after each treatment period. All 49 patients completed all three treatment periods. Baseline values were: UAER (geometric mean [95% CI]) 362 (240–545) mg/24 h, 24 h ABP (mean [SD]) 142 (14)/74 (8) mmHg and estimated GFR 75 (29) ml min
−1 1.73 m−2 . Reductions in UAER from baseline were 63%, 71% and 70%, respectively, with the increasing doses of lisinopril ( p < 0.001). Compared with lisinopril 20 mg there was a further reduction in UAER of 23% with lisinopril 40 mg and 19% with 60 mg, p < 0.05. ABP was reduced from baseline by 10/5, 13/7 and 12/7 mmHg ( p < 0.001 vs baseline, p < 0.05 for diastolic ABP 20 vs 40 mg, otherwise NS between doses). The difference in UAER between 20 and 40 mg lisinopril was significant after adjustment for changes in ABP ( p < 0.01). Two patients were excluded from the study because of an increase in plasma creatinine and one because of high BP; otherwise the study medication was well tolerated with few, mild, dose-independent adverse effects. Lisinopril 40 mg once daily is generally safe and offers additional reductions in BP and UAER in comparison with the currently recommended dose of 20 mg. Lisinopril 60 mg offers no further beneficial effect. Trial registration: ClinicalTrials.gov NCT00118976 Funding: This study was financed out of local funds and was not supported by the medical industry. [ABSTRACT FROM AUTHOR]- Published
- 2009
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45. Increased blood pressure and erythrocyte sodium/lithium countertransport activity are not inherited in diabetic nephropathy
- Author
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Jensen, J. S., primary, Mathiesen, E. R., additional, N�rgaard, K., additional, Hommel, E., additional, Borch-Johnsen, K., additional, Funder, J., additional, Brahm, J., additional, Parving, H. -H., additional, and Deckert, T., additional
- Published
- 1990
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46. Adverse effects of left ventricular hypertrophy in the reduction of endpoints in NIDDM with the angiotensin II antagonist losartan (RENAAL) study.
- Author
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Boner, G., Cooper, M. E., McCarroll, K., Brenner, B. M., de Zeeuw, D., Kowey, P. P., Shahinfar, S., Dickson, T., Crow, R. S., and Parving, H.-H.
- Subjects
ANGIOTENSIN-receptor blockers ,HYPERTROPHY ,LEFT heart ventricle ,HEART diseases ,ENDOCRINE diseases ,DIABETES ,PHARMACEUTICAL research ,MEDICAL research - Abstract
Aims/hypothesis: We explored the impact of baseline left ventricular hypertrophy (LVH) and losartan treatment on renal and cardiovascular (CV) events in 1,513 patients from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial, which studied the effects of losartan on the progression of renal disease and/or death in patients with type 2 diabetes and nephropathy. Materials and methods: LVH was assessed using ECG criteria (Cornell product and/or Sokolow—Lyon voltage). The risk of renal or CV events was determined by a proportional hazards model fit with treatment allocation and presence of LVH. Covariates at baseline included age, sex, systolic BP, mean arterial pressure, pulse, proteinuria, serum creatinine, albumin and haemoglobin. Results: A total of 187 subjects (12%) had LVH at baseline. Treatment with losartan resulted in a significant decrease in the Cornell product (-6.2%) and Sokolow-Lyon voltage (-6.3%). LVH was shown to be significantly associated with the primary endpoint, which was a composite of doubling of serum creatinine (DSCR), endstage renal disease (ESRD) or death (hazard ratio [HR]= 1.44, p=0.011), as well as with the composite renal endpoint of DSCR/ESRD (HR=1.42, p=0.031) and CV events (HR=1.68, p=0.001). Losartan treatment of patients with LVH decreased the CV as well as renal risk to a level similar to that of patients without LVH. Conclusions/ interpretation: In patients with type 2 diabetes and nephropathy, LVH is associated with significantly increased risk of CV events and the progression of kidney disease. Importantly, in patients with LVH, losartan reduced the CV as well as the renal risk to a level similar to that seen in subjects without LVH. [ABSTRACT FROM AUTHOR]
- Published
- 2005
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47. Aldosterone escape during blockade of the renin-angiotensin-aldosterone system in diabetic nephropathy is associated with enhanced decline in glomerular filtration rate.
- Author
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Schjoedt, K.J., Andersen, S., Rossing, P., Tarnow, L., and Parving, H.-H.
- Subjects
DIABETES complications ,ALDOSTERONE ,RENIN-angiotensin system ,GLOMERULAR filtration rate ,DIABETIC nephropathies ,KIDNEY diseases - Abstract
Aims/hypothesis. It has been suggested that aldosterone plays a role in the initiation and progression of renal disease independently of arterial blood pressure and plasma angiotensin II levels. We evaluated the influence of plasma aldosterone levels on progression of diabetic nephropathy during long-term blockade of the renin-angiotensin-aldosterone system. Methods. A total of 63 hypertensive patients with type 1 diabetes and diabetic nephropathy were treated with losartan, 100 mg once daily, for a mean folIow-up period of 35 months. Plasma aldosterone, GFR, albuminuria and 24-h blood pressure were determined at baseline and at regular intervals during the study. Results. Patients were divided according to their increasing or decreasing levels of plasma aldosterone during long-term losartan treatment in an escape group (n=26) and a non-escape group (n=37). In the escape group, aldosterone levels increased from (geometric mean [95% CI]) 57 pg/mI (43-76 pg/mI) at 2 months, to 102 pg/mI (78-134 pg/mI) at the end of the study (p<0.01). The corresponding levels in the non-escape group were 83 pg/mI (69-102 pg/mI) and 49 pg/mI (40-60 pg/mI; p<0.01). The median rate of decline in GFR was 5.0 ml·min
-1 ·year-1 (range 04-15.9 ml·min-1 ·year-1 ) in the escape group, compared with 2.4 ml·min-1 ·year-1 (-1.6 to 11.0 ml·min-1 ·year-1 ) in the non-escape group (p<0.005). The increase in plasma aldosterone correlated with the rate of decline in GFR (r²=0.19, p<0.00I), corresponding to a decline in GFR of 1.5 ml·min-1 ·year-1 for every two-foId increase in plasma aldosterone. Pre-treatment and treatment values of plasma aldosterone were not related to albuminuria or to changes in albuminuria during the study. Conclusions/interpretation. Our data suggest that aldosterone escape during long-term blockade of the renin-angiotensin-aldosterone system is associated with an enhanced decline in GFR in patients with type I diabetes and diabetic nephropathy. [ABSTRACT FROM AUTHOR]- Published
- 2004
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48. Effect of insulin on renal sodium handling in hyperinsulinaemic Type 2 (non-insulin-dependent) diabetic patients with peripheral insulin resistance.
- Author
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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/m) and eight age-matched control subjects (mean age 57 (43-68) years, mean body mass index 23.4 (20.8-26.6) kg/m). The renal clearances of Tc-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·m. 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·m, 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·1.73 m, p< 0.01) and in control subjects (1.7±0.3 vs 0.8±0.3 ml · min · 1.73 m, 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, 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. [ABSTRACT FROM AUTHOR]
- Published
- 1991
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49. 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. 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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.
- Published
- 1999
- Full Text
- View/download PDF
50. Eighth annual meeting of the European Association for the Study of Diabetes
- Author
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Alberti, K. G. M. M., Darley, J., Emerson, Pauline M., Hockaday, T. D. R., Amherdt, M., Like, A. A., Blondel, B., Marliss, B., Wollheim, C., Orci, L., Andersen, O. Ortved, Andersson, Arne, Antonini, F. M., Fumagalli, C., Petruzzi, E., Bertini, G., Mori, S., Tinti, P., Ashcroft, S. J. H., Weerasinghe, L. C. C., Randle, P. J., Assan, R., Slusher, N., Guy-Grand, B., Girard, F., Soufflet, E., Attali, J. R., Ballerio, G., Boillot, J., Atkins, T., Matty, A. J., Bailey, C. J., Aynsley-Green, A., Bloom, S. R., Bacchus, R. A., Meade, L. G., London, D. R., Balant, L., Zahnd, G., Petitpierre, B., Fabre, J., Balasse, E. O., Neef, M. A., Barta, L., Brooser, G., Molnar, Maria, Bataille, D. P., Freychet, P., Kitabgi, P., Rosselin, G. E., Berne, Christian, Beyer, J., Cordes, U., Sell, G., Rosak, C., Schöffling, K., Birkner, B., Henner, J., Wagner, P., Erhardt, F., Dieterle, P., Bloom, S. R., Vaughan, N. J. A., Edwards, A. V., Boquist, L., Brand, I., Söling, H. D., Brandenburg, D., Gliemann, J., Ooms, H. A., Puls, W., Wollmer, A., Camerini-Davalos, R. A., Bloodworth, J. M. B., Limburg, B., Oppermann, W., Campbell, A. K., Siddle, K., Cañadell, J. M., Barraquer, J., Muiños, A., Heredia, C. D., Castillo-Olivares, J., Guijo, J., Pallardo, L. F., Cerasi, E., Efendić, S., Luft, R., Cerasi, E., Wahren, J., Luft, R., Felig, P., Christensen, Niels Juel, Christiansen, A. H., Vølund, A., Connon, J. J., Trimble, E., Copinschi, G., Leclercq, R., Bruno, O. D., Cordes, U., Sell, G., Beyer, J., Haupt, E., Schöffling, K., Creutzfeldt, C., Track, N. S., Cuendet, G. S., Wollheim, C. B., Cameron, D. P., Balant, L., Stauffacher, W., Marliss, E. B., Czyzyk, A., Lao, B., Bartosiewicz, W., Szczepanik, Z., De Nobel, E., Laar, A. Van't, Koene, R. A. P., Benraad, Th. J., Dietze, G., Hepp, K. D., Wickmayr, M., Mehnert, H., Dixon, K., Exon, P. D., Hughes, H. R., Jones, D. W., Elkeles, R. S., Exon, P. D., Dixon, K., FitzGerald, M. G., Malins, J. M., Falorni, A., Massi-Benedetti, F., Gallo, G., Maffei, S., Fedele, D., Tiengo, A., Muggeo, M., Fabris, P., Crepaldi, G., Federlin, K., Helmke, K., Slijepčević, M., Pfeiffer, E. F., Felber, J. P., Oulès, J., Schindler, Ch., Chabot, V., Fernandez-Cruz, A., Catalán, E., Otero, M. Luque, Hermida, O. Garcia, Otero, M. Luque, Catalán, E., Flatt, J. P., Blackburn, G., Randers, G., Förster, H., Hoos, I, Lerche, D., Förster, H., Hoos, I., Matthäus, M., Franckson, J. R. M., Ooms, H. A., Frerichs, H., Daweke, H., Gries, F., Grüneklee, D., Hessing, J., Jahnke, K., Keup, U., Miss, H., Otto, H., Puls, W., Schmidt, D., Zumfelde, C., Funcke, H. v., Löffler, G., Wieland, O., Galton, D. J., Guttman, R., Gazzola, G. C., Franchi, R., Ronchi, P., Saibene, V., Guidotti, G. G., Gligore, V., Hîncu, N., Tecuceanu, Rodica, Goberna, R., Garcia-Albertos, F., Tamarit-Rodriguez, J., del Rio, E., Roca, R., Gomez-Acebo, José, Creco, A. V., Fedeli, G., Ghirlanda, G., Fenici, R., Lucente, M., Gutman, A., Agam, G., Nahas, N., Cazalis, P., Gylfe, E., Hellman, B., Hadden, D. R., Connolly, J. H., Montgomery, D. A. D., Weaver, J. A., Hellerström, Claes, Howell, Simon, Andersson, Arne, Edwards, John, Sehlin, J., Täljedal, I. -B., Heptner, W., Neubauer, H. B., Herchuelz, A., Pipeleers, D. G., Malaisse, W. J., Herrera, E., Montoya, Eladio, Hommel, H., Fischer, IT., Schmid, B., Fiedler, H., Bibergeil, H., Iversen, J., Iynedjian, P. B., Peters, G., Jacquemin, C., Lambert, B., Sutter, B. Ch. J., Jakob, A., Zapf, J., Froesch, E. R., Jansen, F. K., Freytag, G., Herberg, L., Jarrett, R. J., Baker, I. A., Jarrousse, C., Rancon, F., Rosselin, G. E., Job, D., Tchobroutsky, G., Eschwege, E., Guyot-Argenton, C., Aubry, J. P., Déret, M., Karman, H., Mialhe, P., Kissebah, A., Tulloch, B., Fraser, Russell, Kissebah, A., Tulloch, B., Vydelingum, N., Fraser, Russell, Kissing, J., Raptis, S., Dollinger, H., Faulhaber, J., Rothenbuchner, G., Pfeiffer, E. F., Kleineke, J., Sauer, H., Söling, H. D., Kloeze, J., Kohner, Eva M., Sutcliffe, Barbara A., Tudball, M., Dollery, C. T., Korp, W., Neubert, J., Bruneder, H., Lenhardt, A., Levett, R. E., Koschinsky, T., Gries, F. A., Landgraf-Leurs, M. M. C., Landgraf, R., Hörl, R., Langslow, D. R., Laube, H., Fussgänger, R., Mayer, R., Pfeiffer, E. F., Laube, H., Fussgänger, R., Klör, H., Pfeiffer, E. F., Lázaro, E., Leclercq-Meyer, V., Marchand, J. J., Malaisse, W., Ledet, Thomas, Lefébvre, P. J., Luyckx, A. S., Le Marchand, Y., Assimacopoulos, F., Singh, A., Amherdt, M., Rouiller, Ch., Jeanrenaud, B., Lenti, G., Frezzotti, R., Angotzi, G., Bardelli, A. M., Pagano, G., Basetti-Sani, A., Galli, M., Lernmark, Å., Fex, G., Lindsay, D. G., Loge, O., Lopez-Quijada, C., Chiva, L., Rodriguez-Lopez, M., Loten, E. G., Loubatières, A. L., Loubatières-Mariani, M. M., Ribes, G., Chapal, J., Lubetzki, J., Duprey, J., Sambourg, Cl., Lefebvre, P. J., Maier, V., Hinz, M., Schatz, H., Nierle, C., Pfeiffer, E. F., Malaisse, W. J., Pipeleers, D. G., Malaisse-Lagae, F., Orci, L., Malaisse-Lagae, F., Amherdt, M., Ravazzola, M., Stauffacher, W., Orci, L., Renold, A. E., Manzano, P., Rojas-Hidalgo, E., Marco, J., Diaz-Fierros, D., Calle, C., Roman, D., Villanueva, M. L., Valverde, I., Marliss, E. B., Wollheim, C. B., Blondel, B., Orci, L., Like, A., Amherdt, M., Stauffacher, W., Massi-Benedetti, F., Luycks, A. L., Fracassini, F., Lefebvre, P. J., Falorni, A., Menzel, R., Michaelis, D., Neumann, I., Bibergeil, H., Schulz, B., Wilke, W., Wulfert, P., Krämer, K., Menzinger, G., Fallucca, F., Tamburrano, F., Carratu', R., Andreani, D., Metzger, P., Franken, P., Balasse, E. O., Michael, R., Hildmann, W., Jutzi, E., Michl, J., Fankhauser, S., Schlichtkrull, J., Mirouze, J., Orsetti, A., Vierne, Y., Arnoux, N., Mølsted-Pederson, L., Tygstrup, Inge, Villumsen, Åge L., Pedersen, Jørgen, Montague, W., Howell, S. L., Moody, A. J., Agerbak, G. S., Sundby, F., Muggeo, M., Crepaldi, G., Fedele, D., Baritussio, A., Naeser, Peter, Navalesi, R., Pilo, A., Lenzi, S., Cecchetti, P., Corsini, G., Donato, L., Nerup, J., Andersen, O. Ortved, Bendixen, G., Egeberg, J., Poulsen, J. E., Nielsen, J. Høiriis, Hansen, F. Mølgaard, Gliemann, J., Niki, A., Niki, H., Koide, T., Lin, B. J., Nikkels, R. E., Terpstra, J., Gay, A., Oakman, R. H., Lazarus, Norman R., Orci, L., Amherdt, M., Stauffacher, W., Like, A. A., Rouiller, C., Renold, A. E., Malaisse-Lagae, F., Ravazzola, M., Ostman, J., Backman, L., Cerasi, E., Luft, R., Hallberg, D., Ostrowski, K., Panten, U., Christians, J., Parving, H. -H., Rasmussen, S. Munkgaard, Marichal, M., Platilovà, H., Dufek, M., Konopàsek, E., Pozuelo, V., Tamarit, J., Suner, A., Castell, C., Pruett, E. D. R., Maehlum, S., Raptis, S., Grebe, B., Chrissiku, M., Rothenbuchner, G., Müller, R., Hinze, H. J., Pfeiffer, E. F., Reinauer, H., Müller-Ruchholtz, E. R., Rietzler, X., Passa, P., Canivet, J., Schatz, H., Otto, J., Hinz, M., Maier, V., Nierle, C., Behrens, G., Bücher, T., Pfeiffer, E. F., Schlumpf, U., Morell, B., Zingg, A., Schönborn, J., Westphal, P., Panten, U., Bloom, G. D., Idahl, L. -A., Lernmark, A., Söderberg, M., Rios, M. Serrano, Hawkins, F. G., Escobar, F., Mato, J. M., Larrodera, L., de Oya, M., Rodriguez-Miñon, J. L., Shafrir, E., Gutman, A., Sitbon, G., Mialhe, P., Skrabalo, Z., Panajatović, N., Papić, Z., Posinovec, J., Stavljenić, A., Lipovac, V., Aganović, I., Soler, N. G., Bennett, M. A., Söling, H. D., Peters, H., Janson, G., Sönksen, P. H., Srivastava, M. C., Tompkins, C. V., Nabarro, J. D. N., Sørensen, N. Schwartz, Ladefoged, K., Wildenhoff, K. E., Sorge, F., Diehl, H. -J., Hoffmann, H., Schwartzkopff, W., Standl, E., Kolb, H., Standl, A., Mehnert, H., Sutherland, H. W., Stowers, J. M., Whetham, J. C. G., Sutter, B. C. J., Billaudel, B., Sutter, B. Ch. J., Sutter-Dub, M. T., Leclercq, R., Jacquot, R., Täljedal, I. B., Tamarit, J., Tamarit-Rodriguez, J., Goberna, R., Gobema, R., Tamás, Gy., Baranyi, Éva, Baranyi, A., Radvanyi, A., Tatoń, J., Hinek, A., Wiśniewska, A., Tattersall, R. B., Pyke, D. A., Terpstra, J., Slot, J. Bruins, Sande, P. L. M. v. d., Radder, J. K., Waldeok, K. J. J., Muijden, R. C. P. A. v., Tiengo, A., Assan, R., Frerichs, H., Creutzfeldt, W., Turner, D. S., Baker, R. W., Gent, W. G. L., Shabaan, A., Marks, V., Young, D. A. B., Vague, Ph., Heim, H., Laval, C. Martin, Vegezzi, M., Campo, C.Di, Rahamandridona, G., Garron, D., Heyraud, B., Vague, J., Valverde, I., Villanueva, M. L., Lozano, I., Diaz-Fierros, M., Marco, J., Van Assche, F. A., Gepts, W., Van Obberghen, E., Somers, G., Devis, G., Vaughan, G. D., Malaisse-Lagae, F., Orci, L., Malaisse, W. J., Veleminsky, J., Spirova, E., Waldhäusl, W., Frisch, H., Haydl, H., Weiss, L., Löffler, G., Wieland, O., Willms, B., Deuticke, U., Wollheim, C. B., Marliss, E. B., Blondel, B., Orci, L., Like, A., Renold, A. E., Zrůstová, M., and Roštlapil, J.
- Published
- 1973
- Full Text
- View/download PDF
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