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3. Mitochondrial diseases in Hong Kong: prevalence, clinical characteristics and genetic landscape

Author

Wong, T.Y., Belaramani, Kiran M., Chan, C.-k., Chan, W.K., Chan, W.L., Chang, Shek-kwan, Rodenburg, R.J.T., Smeitink, J., Yün, Chi-lap, Fung, Cheuk-Wing, Wong, T.Y., Belaramani, Kiran M., Chan, C.-k., Chan, W.K., Chan, W.L., Chang, Shek-kwan, Rodenburg, R.J.T., Smeitink, J., Yün, Chi-lap, and Fung, Cheuk-Wing

Abstract

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Published
2023

5. Mitochondriopathien

Author

Smeitink, J., Wendel, U., Lentze, Michael J., editor, Schulte, Franz J., editor, Schaub, Jürgen, editor, and Spranger, Jürgen, editor

Published
2007
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6. Mitochondriopathien

Author

Smeitink, J., Wendel, U., Lentze, Michael J., editor, Schulte, Franz J., editor, Schaub, Jürgen, editor, and Spranger, Jürgen, editor

Published
2003
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7. Stoffwechselkrankheiten

Author

Ullrich, K., Schaub, J., Spranger, J., Kohlschütter, A., Bachmann, C., Harms, E., Wendel, U, Baerlocher, K., Böhles, H., Smeitink, J., Gärtner, J., Roscher, A., Widhalm, K., van Gennip, A. H., Lentze, Michael J., editor, Schaub, Jürgen, editor, Schulte, Franz J., editor, and Spranger, Jürgen, editor

Published
2001
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10. CONGENITAL MUSCULAR DYSTROPHIES

Author

Bouman, K., primary, Groothuis, J., additional, Doorduin, J., additional, van Alfen, N., additional, ten Cate, F. Udink, additional, van den Heuvel, F., additional, Nijveldt, R., additional, van Tilburg, W., additional, Buckens, S., additional, Dittrich, A., additional, Draaisma, J., additional, Janssen, M., additional, Kamsteeg, E., additional, van Kleef, E., additional, Smeitink, J., additional, van Tienen, F., additional, Smeets, H., additional, van Engelen, B., additional, Erasmus, C., additional, and Voermans, N., additional

Published
2021
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12. High FGF-21 level in a cohort of 22 patients with Dravet Syndrome-Possible relationship with the disease outcomes

Author

Kwong, A.K., Wong, V.C., Wong, S.S., Chu, V.L., Koene, S., Smeitink, J., Fung, C.W., Kwong, A.K., Wong, V.C., Wong, S.S., Chu, V.L., Koene, S., Smeitink, J., and Fung, C.W.

Abstract

Contains fulltext : 241407.pdf (Publisher’s version ) (Open Access), OBJECTIVE: Dravet syndrome (DS) is a severe and intractable form of epilepsy with prolonged seizures which may evolve to other seizure types and associated with mild-to-severe intellectual disabilities. Fibroblast growth factor 21 (FGF-21) is a stress hormone mediating metabolic and oxidative stress and circulating level of FGF-21 had been shown to increase in some patients with impairment of oxidative phosphorylation in muscles. In DS, FGF-21 is of interest for further study as mitochondrial oxidative stress was identified previously in patients. METHODS: Plasma FGF-21 levels were compared between 22 DS patients and 22 normal controls, and their clinical characteristics of DS patients at the time of plasma sampling were studied retrospectively. Besides, the relationships of FGF-21 level with intellectual development, seizure frequency, valproate treatment, and types of SCN1A mutations were analyzed. Logarithmic transformation of FGF-21 levels was performed before comparison and statistical analysis. RESULTS: Mean of log(10) FGF-21 level was significantly higher in DS patients when comparing with normal controls (P = .0042). Mean of log(10) FGF-21 level was significantly higher in DS patients with normal-to-mild ID versus mild-to-severe ID (P = .0193) and with valproate treatment versus without valproate treatment (P = .015). No significant difference was shown in FGF-21 level in DS patients with missense versus truncating SCN1A variants, and no correlation could be demonstrated between seizure frequency and FGF-21 level. SIGNIFICANCE: Significantly higher level of plasma FGF-21 was identified in DS patients. The high FGF-21 levels were shown to be associated with developmental outcome and valproate treatment. These results support further investigation on the relationship of FGF-21 with the clinical outcomes of DS and other related mechanism which is important for possible therapeutic development for this epileptic encephalopathy.

Published
2021

13. Cognitive functioning and mental health in mitochondrial disease: A systematic scoping review

Author

Klein, I.L., Loo, K.F.E. van de, Smeitink, J., Janssen, M.C., Kessels, R.P.C., Karnebeek, C.D. van, Veer, E. van der, Custers, J.A.E., Verhaak, C.M., Klein, I.L., Loo, K.F.E. van de, Smeitink, J., Janssen, M.C., Kessels, R.P.C., Karnebeek, C.D. van, Veer, E. van der, Custers, J.A.E., and Verhaak, C.M.

Abstract

Contains fulltext : 230490.pdf (publisher's version ) (Open Access), Mitochondrial diseases (MDs) are rare, heterogeneous, hereditary and progressive in nature. In addition to the serious somatic symptoms, patients with MD also experience problems regarding their cognitive functioning and mental health. We provide an overview of all published studies reporting on any aspect of cognitive functioning and/or mental health in patients with MD and their relatives. A total of 58 research articles and 45 case studies were included and critically reviewed. Cognitive impairments in multiple domains were reported. Mental disorders were frequently reported, especially depression and anxiety. Furthermore, most studies showed impairments in self-reported psychological functioning and high prevalence of mental health problems in (matrilineal) relatives. The included studies showed heterogeneity regarding patient samples, measurement instruments and reference groups, making comparisons cautious. Results highlight a high prevalence of cognitive impairments and mental disorders in patients with MD. Recommendations for further research as well as tailored patientcare with standardized follow-up are provided. Key gaps in the literature are identified, of which studies on natural history are of highest importance.

Published
2021

14. Human d-lactate dehydrogenase deficiency by LDHD mutation in a patient with neurological manifestations and mitochondrial complex IV deficiency

Author

Kwong, A.K., Wong, S.S., Rodenburg, R.J.T., Smeitink, J., Chan, G.C.F., Fung, C.W., Kwong, A.K., Wong, S.S., Rodenburg, R.J.T., Smeitink, J., Chan, G.C.F., and Fung, C.W.

Abstract

Contains fulltext : 237483.pdf (Publisher’s version ) (Open Access), BACKGROUND: d-lactate, one of the isomers of lactate, exists in a low concentration in healthy individuals and it can be oxidized to pyruvate catalyzed by d-lactate dehydrogenase. Excessive amount of d-lactate causes d-lactate acidosis associated with neurological manifestations. METHODS AND RESULTS: We report here a patient with developmental delay, cerebellar ataxia, and transient hepatomegaly. Enzyme analysis in the patient's skin fibroblast showed decreased mitochondrial complex IV activity. Using whole exome sequencing, we identified compound heterozygous variants in the LDHD gene, which encodes the d-lactate dehydrogenase, consisting of a splice site variant c.469+1dupG and a missense variant c.752C>T, p.(Thr251Met) which are pathogenic and likely pathogenic respectively according to the American College of Medical Genetics and Genomics (ACMG) classification. The serum d-lactate level was subsequently detected to be elevated (0.61 mmol/L, reference value: 0-0.25 mmol/L). CONCLUSION: This is the third report on LDHD mutations associated with d-lactate elevation and was first reported to have decreased mitochondrial complex IV activity. The study provides more information on this rare metabolic condition but the association of LDHD deficiency with the clinical presentations requires further investigations.

Published
2021

15. Exome sequencing in paediatric patients with movement disorders

Author

Kwong, A.K., Tsang, Mandy Ho-Yin, Fung, J.L.F., Mak, C.C., Chan, K.L.S., Rodenburg, R.J.T., Smeitink, J., Chung, Brian Hon-Yin, Fung, Cheuk-Wing, Kwong, A.K., Tsang, Mandy Ho-Yin, Fung, J.L.F., Mak, C.C., Chan, K.L.S., Rodenburg, R.J.T., Smeitink, J., Chung, Brian Hon-Yin, and Fung, Cheuk-Wing

Abstract

Contains fulltext : 230163.pdf (publisher's version ) (Open Access)

Published
2021

16. Sonlicromanol improves neuronal network dysfunction and transcriptome changes linked to m.3243A>G heteroplasmy in iPSC-derived neurons

Author

Klein Gunnewiek, T.M., Verboven, A.H.A., Pelgrim, I.M., Hogeweg, M., Schoenmaker, C., Renkema, H., Beyrath, J.D., Smeitink, J., Vries, B.B.A. de, Hoen, P.A.C. 't, Kozicz, T., Nadif Kasri, N., Klein Gunnewiek, T.M., Verboven, A.H.A., Pelgrim, I.M., Hogeweg, M., Schoenmaker, C., Renkema, H., Beyrath, J.D., Smeitink, J., Vries, B.B.A. de, Hoen, P.A.C. 't, Kozicz, T., and Nadif Kasri, N.

Abstract

Contains fulltext : 237505.pdf (Publisher’s version ) (Open Access), Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is often caused by an adenine to guanine variant at m.3243 (m.3243A>G) of the MT-TL1 gene. To understand how this pathogenic variant affects the nervous system, we differentiated human induced pluripotent stem cells (iPSCs) into excitatory neurons with normal (low heteroplasmy) and impaired (high heteroplasmy) mitochondrial function from MELAS patients with the m.3243A>G pathogenic variant. We combined micro-electrode array (MEA) measurements with RNA sequencing (MEA-seq) and found reduced expression of genes involved in mitochondrial respiration and presynaptic function, as well as non-cell autonomous processes in co-cultured astrocytes. Finally, we show that the clinical phase II drug sonlicromanol can improve neuronal network activity when treatment is initiated early in development. This was intricately linked with changes in the neuronal transcriptome. Overall, we provide insight in transcriptomic changes in iPSC-derived neurons with high m.3243A>G heteroplasmy, and show the pathology is partially reversible by sonlicromanol.

Published
2021

24. Oxidative switch drives mitophagy defects in dopaminergic parkin mutant patient neurons

Author

Schwartzentruber, A., Boschian, C., Lopes, F.M., Myszczynska, M.A., New, E.J., Beyrath, J.D., Smeitink, J., Ferraiuolo, L., Mortiboys, H., Schwartzentruber, A., Boschian, C., Lopes, F.M., Myszczynska, M.A., New, E.J., Beyrath, J.D., Smeitink, J., Ferraiuolo, L., and Mortiboys, H.

Abstract

Contains fulltext : 229911.pdf (publisher's version ) (Open Access), Mutations in PRKN are the most common cause of early onset Parkinson's disease. Parkin is an E3 ubiquitin ligase, functioning in mitophagy. Mitochondrial abnormalities are present in PRKN mutant models. Patient derived neurons are a promising model in which to study pathogenic mechanisms and therapeutic targets. Here we generate induced neuronal progenitor cells from PRKN mutant patient fibroblasts with a high dopaminergic neuron yield. We reveal changing mitochondrial phenotypes as neurons undergo a metabolic switch during differentiation. Fibroblasts from 4 controls and 4 PRKN mutant patients were transformed into induced neuronal progenitor cells and subsequently differentiated into dopaminergic neurons. Mitochondrial morphology, function and mitophagy were evaluated using live cell fluorescent imaging, cellular ATP and reactive oxygen species production quantification. Direct conversion of control and PRKN mutant patient fibroblasts results in induced neuronal progenitor and their differentiation yields high percentage of dopaminergic neurons. We were able to observe changing mitochondrial phenotypes as neurons undergo a metabolic switch during differentiation. Our results show that when pre-neurons are glycolytic early in differentiation mitophagy is unimpaired by PRKN deficiency. However as neurons become oxidative phosphorylation dependent, mitophagy is severely impaired in the PRKN mutant patient neurons. These changes correlate with changes in mitochondrial function and morphology; resulting in lower neuron yield and altered neuronal morphology. Induced neuronal progenitor cell conversion can produce a high yield of dopaminergic neurons. The mitochondrial phenotype, including mitophagy status, is highly dependent on the metabolic status of the cell. Only when neurons are oxidative phosphorylation reliant the extent of mitochondrial abnormalities are identified. These data provide insight into cell specific effects of PRKN mutations, in particular in relatio

Published
2020

25. Psychological functioning in children suspected for mitochondrial disease: the need for care.

Author

Loo, K.F.E. van de, Custers, J.A.E., Koene, S., Klein, I.L., Janssen, M.C.H., Smeitink, J., Verhaak, C.M., Loo, K.F.E. van de, Custers, J.A.E., Koene, S., Klein, I.L., Janssen, M.C.H., Smeitink, J., and Verhaak, C.M.

Abstract

Contains fulltext : 218702.pdf (publisher's version ) (Open Access), BACKGROUND: Mitochondrial diseases (MD) are generally serious and progressive, inherited metabolic diseases. There is a high comorbidity of anxiety and depression and limitations in daily functioning. The complexity and duration of the diagnostic process and lack of knowledge about prognosis leads to uncertainty. In this study, we investigated the psychological well-being of children who are suspected for MD and their parents. METHODS: In total 122 children suspected for MD and their parents, received questionnaires as part of standard clinical investigation. RESULTS: Parent proxy report revealed a lower quality of life (QoL) compared to norms and even more physical problems compared to chronically ill patients. They also reported more behavioral problems in general and more internalizing problems compared to the norms. Most frequent reported somatic complaints were tiredness and pain. Parents did not report enhanced levels of stress regarding parenting and experienced sufficient social support. At the end of the diagnostic process, 5.7% of the children received the genetically confirmed diagnosis of MD, 26% showed non-conclusive abnormalities in the muscle biopsy, 54% did not receive any diagnosis, and the remaining received other diagnoses. Strikingly, children without a diagnosis showed equally QoL and behavioral problems as children with a diagnosis, and even more internalizing problems. CONCLUSIONS: This study highlights the psychological concerns of children with a suspicion of MD. It is important to realize that as well as children with a confirmed diagnosis, children without a diagnosis are vulnerable since explanation for their complaints is still lacking.

Published
2020

26. The genotypic and phenotypic spectrum of MTO1 deficiency

Author

O'Byrne, J.J., Tarailo-Graovac, M., Ghani, Aisha, Champion, M.P., Deshpande, Charu, Dursun, Ali, Kluijtmans, L.A.J., Smeitink, J., Wevers, R.A., Engelke, U.F.H., Rodenburg, R.J.T., Salvarinova, R., and Karnebeek, C.D. van

Subjects
All institutes and research themes of the Radboud University Medical Center, Other Research Radboud Institute for Molecular Life Sciences [Radboudumc 0], Metabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6], Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]
Abstract

Contains fulltext : 184066.pdf (Publisher’s version ) (Open Access)

Published
2018

36. Genotype and phenotype in patients with dihydropyrimidine dehydrogenase deficiency

Author

Van Kuilenburg, A. B. P., Vreken, P., Abeling, N. G. G. M., Bakker, H. D., Meinsma, R., Van Lenthe, H., De Abreu, R. A., Smeitink, J. A. M., Kayserili, H., Apak, M. Y., Christensen, E., Holopainen, I., Pulkki, K., Riva, D., Botteon, G., Holme, E., Tulinius, M., Kleijer, W. J., Beemer, F. A., Duran, M., Niezen-Koning, K. E., Smit, G. P. A., Jakobs, C., Smit, L. M. E., Moog, U., Spaapen, L. J. M., and Van Gennip, A. H.

Published
1999
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38. Sonlicromanol improves neuronal network dysfunction and transcriptome changes linked to m.3243A>G heteroplasmy in iPSC-derived neurons

Author

Gunnewiek, T.M. Klein, primary, Verboven, A. H. A., additional, Hogeweg, M., additional, Schoenmaker, C., additional, Renkema, H., additional, Beyrath, J., additional, Smeitink, J., additional, de Vries, B. B. A., additional, ’t Hoen, P.A.C., additional, Kozicz, T., additional, and Kasri, N. Nadif, additional

Published
2020
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47. De Slappe Baby

Author

Schrander-Stumpel, C. T. R. M., primary, Brouwer, O. F., additional, Smeitink, J. A. M., additional, and De Nijs Bik, H., additional

Published
2003
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50. Royal academy of medicine in Ireland international conference on homocysteine metabolism from basic science to clinical medicine: Proceedings of meeting held at Dromoland Castle, Co. Clare on July 2nd–6th, 1995

Author

Björkegren, K., Bergmark, C., de Faire, U., Mansoor, M. Azam, Svardal, A., Bostom, A. G., Roubenoff, R., Dellaripa, P., Nadeau, M. R., Sutherland, P., Wilson, P. W. F., Jacques, P. F., Selhub, J., Rosenberg, I. H., Bostom, A. G., Brosnan, J. T., Hall, B., Nadeau, M. R., Selhub, J., Bostom, A. G., Shemin, D., Lapane, K. L., Sutherland, P., Nadeau, M. R., Wilson, P. W. F., Selhub, J., Bostom, A. G., Shemin, D., Nadeau, M. R., Selhub, J., Bostom, A. G., Selhub, J., Jacques, P. F., Nadeau, M. R., Williams, R. R., Ellison, R. C., Cuskelly, G. J., McNulty, H., Strain, J. J., McPartlin, J. M., Scott, J. M., Chadefaux-Vekemans, B., Coudé, M., Aupetit, J., Kamoun, P., Coudé, M., Aral, B., Zabot, M. T., Aupetit, J., Kamoun, P., Chadefaux-Vekemans, B., Calaf, R., Ghiringelli, O., Barlatier, A., Charpiot, P., Rolland, P. H., Garçon, D., Charpiot, P., Augier, T., Chareyre, C., Rolland, P. H., Garçon, D., Chango, A., Hodez, F., Tronel, H., Nuel, G., Michel, F., Frémont, S., Méjean, L., Nicolas, J. P., Candito, M., Chambon, P., Gibelin, P., Amsellem, J., Baudouy, M., Morand, P., Candito, M., Chambon, P., Pringuey, D., Aubin-Brunet, V., Beaulieu, F., Darcourt, G., Bedoucha, P., Alchaar, H., Chatel, M., Candito, M., de Valk, H. W., van der Griend, R., Eeden, M. K. G. van, de Groot, E., Duran, M., Smeitink, J. A. M., de Klerk, J. B. C., Wittebol-Post, D., Rolland, M. -O., Haas, F. J. L. M., Meuwissen, O. J. A. Th., Banga, J. D., Poll-The, B. T., de Vries, J. I. P., Dekker, G. A., van Geijn, H. P., Huigens, P. C., Jakobs, C., von Blomberg, B. M. E., Deulofeu, R., Giralt, M., Aibar, C., Bauchet, C., Ballesta, A. M., Varela, G., Vila, N., Chamorro, A., Casals, F. J., Cremades, J. Diaz, Daly, L., Meleady, R., Graham, I., den Heijer, M., Brouwer, I. A., Gerrits, W. B. J., Bos, G. M. J., Blom, H. J., den Heijer, M., Bos, G. M. J., Koster, T., Vandenbroucke, J. P., Blom, H. J., Briët, E., Rosendaal, F. R., Fischer, G., Behrend, C., Bartholmes, P., Fermo, I., Paroni, R., Vigano, S., D’Angelo, A., Fermo, I., Paroni, R., Vigano, S., D’Angelo, A., Franken, D. G., Boers, G. H. J., Blom, H. J., Hamel, B. C. J., Franken, D. G., Boers, G. H. J., Blom, H. J., Ruijs, J. H. J., Franken, D. G., Blom, H. J., Boers, G. H. J., Tangerman, A., Guttormsen, A. B., Ueland, P. M., Refsum, H., Svarstad, E., Gao, W., Goldman, E., Jakubowski, H., Sebastio, G., Sperandeo, M. P., de Franchis, R., Andria, G., Garrow, T. A., Hladovec, J., Sommerova, Z., Písariková, A., Halsted, C. H., Villanueva, J., Chandler, C. J., Stabler, S. P., Allen, R. H., Muskhelishvili, L., James, S. J., Poirer, L., Jacobsen, D. W., Savon, S. R., DiCorleto, P. E., Jourdheuil-Rahmani, D., Rolland, P. H., Garçon, D., Joosten, E., Riezler, R., Allen, R., Joosten, E., Riezler, R., Allen, R., Marquardt, T., Ullrich, K., Harms, E., Koch, H. G., Koch, H. G., Evers, S., Grotemeyer, K. H., Vogelpohl, L., von Eckardstein, A., Ullrich, K., Deufel, T., Kraus, J., Harms, E., Kozich, V., Janosik, M., Sokolová, J., Bukovská, G., Kraus, J. P., Kluitmans, L. A. J., van den Heuvel, L. P., Stevens, E., Trubels, J. M. F., Blom, H. J., Boers, G. H. J., van Oost, B. A., Kraus, J. P., Kittner, S., Macko, R., Hebel, J. R., Rohr, J., Malinow, M. R., Upson, B., Buchholz, D., Earley, C., Johnson, C., Price, T. R., Rosario, J., Sloan, M., Stern, B., Wityk, R., Wozniak, M., Sherwin, R., Stolley, P., Kluijtmans, L., Heuvel, L. van den, Stevens, E., Trijbels, F., Blom, H., Boers, G., van Oost, B., den Heijer, M., Rozen, R., Löhrer, F., Angst, C., Fowler, B., Zaugg, M., Brunner, F., Haefeli, W. E., Nedrebø, B., Ericsson, U. -B., Ueland, P. M., Refsum, H., Lien, E. A., London, J., Paly, E., Paul, V., Paris, D., Kamoun, P., Chassé, J. F., Møller, J., Rasmussen, K., Meleady, R., Graham, I., Daly, L., Verhoef, P., Meleady, R., Graham, I., Daly, L., McMartin, K. E., Phifer, T. J., Alexander, J. S., Middlebrooks, M., Childress, L. E., Nicolas, J. P., Tronel, H., Chango, A., Fremont, S., Felden, F., Guerci, B., Creton, C., Drouin, P., Oakley, G. P., Elias, P. R. P., Hann, A. C., Curtis, C. G., Rose, F. A., Tudball, N., Parrot-Roulaud, F., Cochet, C., Catargi, B., Leprat, F., Latapie, J. -L., Perna, A. F., De Santo, N. G., Ingrosso, D., Galletti, P., Zappia, V., Parrot-Roulaud, F., Sassoust, G., Boissieras, P., Blom, H. J., Majors, A. K., Ehrhart, L. A., Pezacka, E. H., Perry, I. J., Morris, R. W., Ebrahim, S. B., Shaper, A. G., Refsum, H., Ueland, P. M., Pietrzik, K., Dierkes, J., Kroesen, M., Bung, P., Rasmussen, K., Moller, J., Rasmussen, K., Remacha, A., Garcia-Die, F., Cadafalch, J., Barceló, H. J., Parellada, H., Regland, B., Gottfries, C. -G., Andersson, M., Bagby, J., Dyrehag, L. -E., Abrahamsson, L., Ronge, E., Kjellman, B., Frosst, P., Christensen, B., Goyette, P., Rosenblatt, D. S., Genest, J., Rozen, R., Riedel, B., Ueland, P. M., Svardal, A. M., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X. W., Xie, L., Dudman, N., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X. W., Xie, L., Dudman, N., Silberberg, J., Crooks, R., Fryer, J., Ray, C., Guo, X., Xie, L., Dudman, N., Smith, B., Kohlman-Trigoboff, D., Simsir, S., Stabler, S. P., Allen, R. H., Strydom, A. J. C., Schlüssel, E., Preibisch, G., Elstner, E. F. E., Pütter, S., Spuijbroek, M. D. E. H., Goddijn-Wessel, T. A. W., Wouters, M. G. A. J., Molen, E. F. v. d., Blom, H. J., Boers, G. H. J., Steegers-Theunissen, R. P. M., Trijbels, J. M. F., Thomas, C. M. G., Eskes, T. K. A. B., Tsai, M. Y., Hanson, N., Key, N., Schwichtenberg, K., Garg, U., Todesco, L., Fowler, B., Pollaert, N., Haefeli, W. E., Thorand, B., Hages, M., Pietrzik, K., Bung, P., Holzgreve, W., Vila, N., Chamorro, A., Deulofeu, R., Aibar, C., Giralt, M., Ballesta, A. M., van der Mooren, M. J., Wouters, M. G. A. J., Schellekens, L. A., Eskes, T. K. A. B., Rolland, R., Blom, H. J., Put, N. v. d., Trijbels, F., Heuvel, L. v. d., Blom, H., Eskes, T., Steegers-Theunissen, R., Mariman, E., Heyer, M. d., Rozen, R., Daher, R., Van Lente, F., Vilkovsky, A. B., Maev, I. V., Richter, E. L., Kirnus, M. D., Varela-Moreiras, G., Alonso-Aperte, E., Rubio, M., Gassó, M., Deulofeu, R., Alvarez, L., Caballeria, J., Rodés, J., Mato, J. M., van Aerts, L. A. G. J. M., Peereboom-Stegeman, J. H. J. Copius, Noordhoek, J., Eskes, T. K. A. B., Molen, E. F. v. d., Spuijbroek, M. D. E. H., Eskes, T. K. A. B., Heuvel, L. P. v. d., Monnens, L. A. H., Blom, H. J., van Guidener, C., Janssen, M. J. F. M., Surachno, J., Stehouwer, C. D. A., van den Berg, M., Bierdrager, E., Rauwerda, J. A., Wilcken, B., Hammond, J., Wouters, M. G. A. J., Hamilton, C. J. C. M., Blom, H. J., Boers, G. H. J., Thomas, C. M. G., Borm, G. F., Eskes, T. K. A. B., Wang, H., Tsai, J. -C., Perrella, M. A., Yoshizumi, M., Sibinga, N. E. S., Haber, E., Chang, T. H. -T., Schlegel, R., Lee, M. -E., Woodside, J., McMaster, D., Yarnell, J., Young, I., Mercer, C., Byrne, K., Evans, A., Gey, F., Gao, X. M., Dougan, G., Wordsworth, P., McMichael, A., Young, P. B., Kennedy, D. G., Molloy, A. M., Scott, J. M., Ward, P., Naughten, E., Cahalane, S., Murphy, D., Mayne, P., Chauveau, P., Chadefaux-Vekemans, B., Coudé, M., Aupetit, J., Kamoun, P., Jungers, P., van Asselt, D. Z. B., Blom, H. J., de Wild, G. M., van Staveren, W. A., Hoefnagels, W. H. L., Naruszewicz, M., Staniewicz, A., Dziewanowski, K., Evrovski, J., Cole, D. E. C., Callaghan, Michael, Lindgren, A., Brattström, L., Hultberg, B., Verhoef, P., Hennekens, C. H., Allen, R. H., Stabler, S. P., Willett, W. C., Stampfer, M. J., Frantzen, F., Sundrehagen, E., Verhoef, P., Kok, F. J., Stampfer, M. J., Willett, W. C., Gaziano, J. M., Hennekens, C. H., Allen, R. H., Stabler, S. P., Reynolds, R. 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1995
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