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Your search keyword '"Kluin-Nelemans, H C"' showing total 7 results
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7 results on '"Kluin-Nelemans, H C"'

3. Mast cells as a unique hematopoietic lineage and cell system: From Paul Ehrlich's visions to precision medicine concepts

Author

Valent, P., Akin, C., Hartmann, K., Nilsson, G., Reiter, A., Hermine, O., Sotlar, K., Sperr, W. R., Escribano, L., George, T. I., Kluin-Nelemans, H. C., Ustun, C., Triggiani, M., Brockow, K., Gotlib, J., Orfao, A., Kovanen, P. T., Hadzijusufovic, E., Sadovnik, I., Horny, H. -P., Arock, M., Schwartz, L. B., Frank Austen, K., Metcalfe, D. D., Galli, S. J., Austrian Science Fund, National Institutes of Health (US), United States-Israel Binational Science Foundation, and Stanford University

Subjects
mastocytosis, tryptase, KIT, Cell Differentiation, History, 19th Century, Review, History, 20th Century, histamine, History, 21st Century, humanities, Immunity, Innate, Disease Models, Animal, Histamine, IgE receptor, Mast cell activation, Mastocytosis, Tryptase, Allergy and Immunology, mast cell activation, Hypersensitivity, Animals, Humans, Mast Cells, Molecular Targeted Therapy, Precision Medicine, Immunosuppressive Agents
Abstract

© The author(s)., The origin and functions of mast cells (MCs) have been debated since their description by Paul Ehrlich in 1879. MCs have long been considered 'reactive bystanders' and 'amplifiers' in inflammatory processes, allergic reactions, and host responses to infectious diseases. However, knowledge about the origin, phenotypes and functions of MCs has increased substantially over the past 50 years. MCs are now known to be derived from multipotent hematopoietic progenitors, which, through a process of differentiation and maturation, form a unique hematopoietic lineage residing in multiple organs. In particular, MCs are distinguishable from basophils and other hematopoietic cells by their unique phenotype, origin(s), and spectrum of functions, both in innate and adaptive immune responses and in other settings. The concept of a unique MC lineage is further supported by the development of a distinct group of neoplasms, collectively referred to as mastocytosis, in which MC precursors expand as clonal cells. The clinical consequences of the expansion and/or activation of MCs are best established in mastocytosis and in allergic inflammation. However, MCs have also been implicated as important participants in a number of additional pathologic conditions and physiological processes. In this article, we review concepts regarding MC development, factors controlling MC expansion and activation, and some of the fundamental roles MCs may play in both health and disease. We also discuss new concepts for suppressing MC expansion and/or activation using molecularly-targeted drugs., P.V. was supported by the Austrian Science Fund (FWF), grants F4701-B28, F4704-B28 and P32470-B. DDM is supported by the Division of Intramural Research, NIAID. SJG's research is supported by the NIH, USA, the US-Israel Binational Foundation, and the Department of Pathology and the Sean N. Parker Center for Allergy and Asthma Research at Stanford University, Stanford, CA.

Published
2020

5. POOLED SURVIVAL ANALYSIS OF MIDOSTAURIN CLINICAL STUDY DATA (D2201+A2213) IN PATIENTS WITH ADVANCED SYSTEMIC MASTOCYTOSIS COMPARED WITH HISTORICAL CONTROLS

Author

Reiter, A., Kluin-Nelemans, H. C., George, T., Akin, C., DeAngelo, D. J., Hermine, O., Awan, F., Hexner, E., Mauro, M., Schwaab, J., Jawhar, M., Sternberg, D., Berkowitz, N., Niolat, J., Labed, A. Huntsman, Hartmann, K., Horny, H-P., Valent, P., Gotlib, J., Reiter, A., Kluin-Nelemans, H. C., George, T., Akin, C., DeAngelo, D. J., Hermine, O., Awan, F., Hexner, E., Mauro, M., Schwaab, J., Jawhar, M., Sternberg, D., Berkowitz, N., Niolat, J., Labed, A. Huntsman, Hartmann, K., Horny, H-P., Valent, P., and Gotlib, J.

Published
2017

6. Advanced systemic mastocytosis: from molecular and genetic progress to clinical practice

Author

Ustun, C., primary, Arock, M., additional, Kluin-Nelemans, H. C., additional, Reiter, A., additional, Sperr, W. R., additional, George, T., additional, Horny, H.-P., additional, Hartmann, K., additional, Sotlar, K., additional, Damaj, G., additional, Hermine, O., additional, Verstovsek, S., additional, Metcalfe, D. D., additional, Gotlib, J., additional, Akin, C., additional, and Valent, P., additional

Published
2016
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7. The impact of a male or female thrombotic family history on contraceptive counseling: a cohort study.

Author

van Vlijmen EF, Veeger NJ, Middeldorp S, Hamulyák K, Prins MH, Kluin-Nelemans HC, and Meijer K

Subjects
Cohort Studies, Factor V genetics, Family Health, Female, Humans, Male, Mutation, Netherlands, Postpartum Period, Pregnancy, Proportional Hazards Models, Risk Assessment, Thrombophilia genetics, Venous Thromboembolism genetics, Venous Thrombosis genetics, Contraception methods, Contraceptive Agents therapeutic use, Contraceptives, Oral, Combined adverse effects, Thrombosis genetics
Abstract

Unlabelled: Essentials It is unknown if a male or female thrombotic family history influences risk in female relatives. We assessed thrombotic risk in female relatives of male and female patients with thrombosis. A hormonally related female thrombotic family history further increases risk in female relatives. This information could be important in counseling women on contraceptive options. Click to hear Prof. Rosendaal's perspective on venous thrombosis: etiology, pathogenesis, and prognosis, Summary: Background Women from thrombophilic families have increased risk of venous thromboembolism (VTE), which increases further during oral contraceptive (COC) use and pregnancy-postpartum. Whether this additional risk differs between relatives of male and female patients, or is different when that female patient had a hormonally related VTE (during COC use/pregnancy), is unknown. Methods One thousand five female relatives of consecutive patients with VTE from a family-based cohort were retrospectively followed for incident VTE from ages 15 to 50, first VTE, or study inclusion. Absolute and relative VTE risks adjusted for factors of patients (sex, age) and relatives (thrombophilia, COC use, pregnancy) were estimated in relatives of female and male patients and in relatives of female patients with and without hormonally related VTE. Results Absolute risk in relatives of female (0.32 [95% confidence interval [CI] 0.23-0.43]) vs. male patients (0.39 [95% CI 0.28-0.53]) was comparable. However, the heterogeneity analysis of risk estimates suggested that in relatives of female vs. male patients, the contribution of pregnancy-postpartum (hazard ratio [HR] 11.6 [95% CI 6.3-21.3] vs. HR6.6 [95% CI 2.8-15.2]) and, to a lesser extent, COC use (HR3.6 [95% CI 1.8-7.1] vs. HR2.7 [95% CI 1.5-5.0]) to the VTE risk differs. Absolute risk was significantly higher in relatives of female patients with hormonally related VTE (0.43 [95% CI 0.3-0.6]) vs. relatives of female patients without hormonally related VTE (0.13 [95% CI 0.05-0.27]), HR3.28 [95% CI 1.5-7.9]). The higher contribution of pregnancy-postpartum and COC use to the VTE risk was mainly observed in relatives of patients with hormonally related VTE. Conclusions These findings suggest that a family history from a female patient, especially when VTE was hormonally related, may further increase VTE risk in her female relatives. This information could be important in counseling women on contraceptive options., (© 2016 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals, Inc. on behalf of International Society on Thrombosis and Haemostasis.)

Published
2016
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