%0 Journal Article %A Alberico, E. %A Baumann, W. %A de Vries, J. G. %A Drexler, H. J. %A Gladiali, S. %A Heller, D. %A Henderickx, H. J. %A Lefort, L. %D 2011 %T Unravelling the reaction path of rhodium-MonoPhos-catalysed olefin hydrogenation %J Chemistry %V 17 %N 45 %P 12683-95 %7 2011/10/01 %8 Nov 4 %! Unravelling the reaction path of rhodium-MonoPhos-catalysed olefin hydrogenation %@ 1521-3765 (Electronic) 0947-6539 (Linking) %R 10.1002/chem.201101793 %M 21956660 %K Alkenes/*chemistry Catalysis Hydrogenation Magnetic Resonance Spectroscopy Molecular Structure Organometallic Compounds/*chemistry Organophosphorus Compounds/*chemistry Rhodium/*chemistry Stereoisomerism %X The mechanism of the asymmetric hydrogenation of methyl (Z)-2-acetamidocinnamate (mac) catalysed by [Rh(MonoPhos)(2)(nbd)]SbF(6) (MonoPhos: 3,5-dioxa-4-phosphacyclohepta[2,1-a:3,4-a']dinaphthalen-4-yl)dimethylamine ) was elucidated by using (1)H, (31)P and (103)Rh NMR spectroscopy and ESI-MS. The use of nbd allows one to obtain in pure form the rhodium complex that contains two units of the ligand. In contrast to the analogous complexes that contain cis,cis-1,5-cyclooctadiene (cod), this complex shows well-resolved NMR spectroscopic signals. Hydrogenation of these catalyst precursors at 1 bar total pressure gave rise to the formation of a bimetallic complex of general formula [Rh(MonoPhos)(2)](2)(SbF(6))(2); no solvate complexes were detected. In the dimeric complex both rhodium atoms are ligated to two MonoPhos ligands but, in addition, each rhodium atom also binds to one of the binaphthyl rings of a ligand that is bound to the other rhodium metal. Upon addition of mac, a mixture of diastereomeric complexes [Rh(MonoPhos)(2)(mac)]SbF(6) is formed in which the substrate is bound in a chelate fashion to the metal. Upon hydrogenation, these adducts are converted into a new complex [Rh(MonoPhos)(2){mac(H)(2)}]SbF(6) in which the methyl phenylalaninate mac(H)(2) is bound through its aromatic ring to rhodium. Addition of mac to this complex leads to displacement of the product by the substrate. No hydride intermediates could be detected and no evidence was found for the involvement at any stage of the process of complexes with only one coordinated MonoPhos. The collected data suggest that the asymmetric hydrogenation follows a Halpern-like mechanism in which the less abundant substrate-catalyst adduct is preferentially hydrogenated to phenylalanine methyl ester. %Z Alberico, Elisabetta Baumann, Wolfgang de Vries, Johannes G Drexler, Hans-Joachim Gladiali, Serafino Heller, Detlef Henderickx, Huub J W Lefort, Laurent Research Support, Non-U.S. Gov't Germany Chemistry (Weinheim an der Bergstrasse, Germany) Chemistry. 2011 Nov 4;17(45):12683-95. doi: 10.1002/chem.201101793. Epub 2011 Sep 28. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21956660 %+ Istituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche, Sassari, Italy. Elisabetta.Alberico@cnr.it %G eng %0 Journal Article %A Ammerpohl, O. %A Haake, A. %A Pellissery, S. %A Giefing, M. %A Richter, J. %A Balint, B. %A Kulis, M. %A Le, J. %A Bibikova, M. %A Drexler, H. G. %A Seifert, M. %A Shaknovic, R. %A Korn, B. %A Kuppers, R. %A Martin-Subero, J. I. %A Siebert, R. %D 2012 %T Array-based DNA methylation analysis in classical Hodgkin lymphoma reveals new insights into the mechanisms underlying silencing of B cell-specific genes %J Leukemia %V 26 %N 1 %P 185-8 %7 2011/08/06 %8 Jan %! Array-based DNA methylation analysis in classical Hodgkin lymphoma reveals new insights into the mechanisms underlying silencing of B cell-specific genes %@ 1476-5551 (Electronic) 0887-6924 (Linking) %R leu2011194 [pii] 10.1038/leu.2011.194 %M 21818115 %Z Ammerpohl, O Haake, A Pellissery, S Giefing, M Richter, J Balint, B Kulis, M Le, J Bibikova, M Drexler, H G Seifert, M Shaknovic, R Korn, B Kuppers, R Martin-Subero, J I Siebert, R England Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K Leukemia. 2012 Jan;26(1):185-8. doi: 10.1038/leu.2011.194. Epub 2011 Aug 5. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21818115 %+ Institute of Human Genetics, Christian-Albrechts University Kiel & University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany. %G eng %0 Journal Article %A Arcangeli, M. L. %A Frontera, V. %A Bardin, F. %A Obrados, E. %A Adams, S. %A Chabannon, C. %A Schiff, C. %A Mancini, S. J. %A Adams, R. H. %A Aurrand-Lions, M. %D 2011 %T JAM-B regulates maintenance of hematopoietic stem cells in the bone marrow %J Blood %V 118 %N 17 %P 4609-19 %7 2011/08/27 %8 Oct 27 %! JAM-B regulates maintenance of hematopoietic stem cells in the bone marrow %@ 1528-0020 (Electronic) 0006-4971 (Linking) %R blood-2010-12-323972 [pii] 10.1182/blood-2010-12-323972 %M 21868569 %K Animals Bone Marrow/metabolism/physiology Bone Marrow Cells/cytology/metabolism/*physiology Cell Adhesion/genetics Cell Adhesion Molecules/genetics/metabolism/*physiology Cell Proliferation Hematopoiesis/genetics/physiology Hematopoietic Stem Cell Mobilization Hematopoietic Stem Cells/metabolism/*physiology Immunoglobulins/genetics/metabolism/*physiology Male Mesenchymal Stromal Cells/metabolism/physiology Mice Mice, Inbred C57BL Mice, Knockout %X In adult mammals, hematopoietic stem cells (HSCs) reside in the bone marrow (BM) and are maintained in a quiescent and undifferentiated state through adhesive interactions with specialized microenvironmental niches. Although junctional adhesion molecule-C (JAM-C) is expressed by HSCs, its function in adult hematopoiesis remains elusive. Here, we show that HSCs adhere to JAM-B expressed by BM stromal cells in a JAM-C dependent manner. The interaction regulates the interplay between HSCs and BM stromal cells as illustrated by the decreased pool of quiescent HSCs observed in jam-b deficient mice. We further show that this is probably because of alterations of BM stromal compartments and changes in SDF-1alpha BM content in jam-b(-/-) mice, suggesting that JAM-B is an active player in the maintenance of the BM stromal microenvironment. %Z Arcangeli, Marie-Laure Frontera, Vincent Bardin, Florence Obrados, Elodie Adams, Susanne Chabannon, Christian Schiff, Claudine Mancini, Stephane J C Adams, Ralf H Aurrand-Lions, Michel Research Support, Non-U.S. Gov't United States Blood Blood. 2011 Oct 27;118(17):4609-19. Epub 2011 Aug 25. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21868569 %+ Centre de Recherche en Cancerologie de Marseille, Unite Mixle de Recherche, Marseille, France. %G eng %0 Journal Article %A Baumeister, T. %A Uter, W. %A Weistenhofer, W. %A Drexler, H. %A Kutting, B. %D 2012 %T On the lookout for precursor lesions: where does dry skin end and slight hand eczema begin? %J Contact Dermatitis %V 66 %N 2 %P 63-71 %7 2011/09/29 %8 Feb %! On the lookout for precursor lesions: where does dry skin end and slight hand eczema begin? %@ 1600-0536 (Electronic) 0105-1873 (Linking) %R 10.1111/j.1600-0536.2011.01969.x %M 21943290 %X Background. The prognosis of occupational hand eczema is strongly associated with its duration, severity, and the onset of treatment. Objectives. The study was aimed at characterizing skin eruptions that might be potential precursors of occupational hand eczema, their pattern, and typical sites in a population at moderate risk of hand eczema. Patients/Materials/Methods. Eight hundred German male metal workers took part in a structured interview focused on their medical history combined with a dermatological examination of their hands, by use of the quantitative Hand Eczema Score for Occupational Screenings, with follow-up 1 year later. Results. The most frequent lesions were erythema (91.8%), lichenification (98.8%), crusting (70%), and scaling (35%); all other lesions were relatively rare (15%). The distribution of lesions remained stable between baseline and follow-up. The areas most affected were knuckles, palms, and finger shafts (excluding tips). Interdigital regions were uncommonly affected in this sample. Conclusions. Erythema, lichenification, and crusting, indicating constant skin 'strain', can be regarded as precursor lesions for slight hand eczema, and should be monitored quantitatively. As other occupations, for example hairdressing, have different predilection sites, it can be concluded that the pattern of occupational hand eczema is strongly influenced by the distinct strain profile of an occupation. %Z Baumeister, Thomas Uter, Wolfgang Weistenhofer, Wobbeke Drexler, Hans Kutting, Birgitta Denmark Contact dermatitis Contact Dermatitis. 2012 Feb;66(2):63-71. doi: 10.1111/j.1600-0536.2011.01969.x. Epub 2011 Sep 21. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21943290 %+ Institute and Outpatient Clinic of Occupational, Social and Environmental Medicine, University of Erlangen-Nuremberg, Schillerstr. 25 + 29, D-91054 Erlangen, Germany Department of Medical Informatics, Biometry and Epidemiology, University of Erlangen-Nuremberg, D-91054 Erlangen, Germany. %G eng %0 Journal Article %A Bernemann, C. %A Greber, B. %A Ko, K. %A Sterneckert, J. %A Han, D. W. %A Arauzo-Bravo, M. J. %A Scholer, H. R. %D 2011 %T Distinct Developmental Ground States of Epiblast Stem Cell Lines Determine Different Pluripotency Features %J Stem Cells %V 29 %N 10 %P 1496-1503 %8 Oct %! Distinct Developmental Ground States of Epiblast Stem Cell Lines Determine Different Pluripotency Features %Z Stem Cells %@ 1066-5099 %R Doi 10.1002/Stem.709 %M ISI:000295254600004 %K epiblast stem cells pluripotency developmental biology cell biology self-renewal mouse embryos embryogenesis gastrulation induction brachyury roles %X Epiblast stem cells (EpiSCs) are pluripotent stem cells derived from mouse postimplantation embryos at embryonic day (E) 5.5-E7.5 at the onset of gastrulation, which makes them a valuable tool for studying mammalian postimplantation development in vitro. EpiSCs can also be reprogrammed into a mouse embryonic stem cell (mESC)-like state. Some reports have shown that the reversion of EpiSCs requires transcription factor overexpression, whereas others have suggested that use of stringent mESC culture conditions alone is sufficient for the reversion of EpiSCs. To clarify these discrepancies, we systematically compared a panel of independent EpiSC lines. We found that-regardless of the embryonic day of derivation-the different EpiSC lines shared a number of defining characteristics such as the ability to form teratomas. However, despite use of standard EpiSC culture conditions, some lines exhibited elevated expression of genes associated with mesendodermal differentiation. Pluripotency (Oct4) and mesodermal (Brachyury) marker genes were coexpressed in this subset of lines. Interestingly, the expression of mesendodermal marker genes was negatively correlated with the cells' ability to efficiently undergo neural induction. Moreover, these mesodermal marker gene-expressing cell lines could not be efficiently reverted to an mESC-like state by using stringent mESC culture conditions. Conversely, Brachyury overexpression diminished the reversion efficiency in otherwise Brachyury-negative lines. Overall, our data suggest that different EpiSC lines may undergo self-renewal into distinct developmental states, a finding with important implications for functional readouts such as reversion of EpiSCs to an mESC-like state as well as directed differentiation. STEM CELLS 2011;29:1496-1503 %Z 825EU Times Cited:0 Cited References Count:27 %U ://000295254600004 %+ Max Planck Inst Mol Biomed, Dept Cell & Dev Biol, Rontgenstr 20, D-48149 Munster, Germany Max Planck Inst Mol Biomed, Dept Cell & Dev Biol, Rontgenstr 20, D-48149 Munster, Germany Max Planck Inst Mol Biomed, Dept Cell & Dev Biol, D-48149 Munster, Germany Konkuk Univ, Ctr Stem Cell Res, Inst Biomed Sci & Technol, Seoul, South Korea Konkuk Univ, Dept Neurosci, Sch Med, Seoul, South Korea Konkuk Univ, Dept Stem Cell Biol, SMART Inst Adv Biomed Sci, Seoul, South Korea Univ Munster, Fac Med, Munster, Germany %G English %0 Journal Article %A Bodor, C. %A O'Riain, C. %A Wrench, D. %A Matthews, J. %A Iyengar, S. %A Tayyib, H. %A Calaminici, M. %A Clear, A. %A Iqbal, S. %A Quentmeier, H. %A Drexler, H. G. %A Montoto, S. %A Lister, A. T. %A Gribben, J. G. %A Matolcsy, A. %A Fitzgibbon, J. %D 2011 %T EZH2 Y641 mutations in follicular lymphoma %J Leukemia %V 25 %N 4 %P 726-9 %7 2011/01/15 %8 Apr %! EZH2 Y641 mutations in follicular lymphoma %@ 1476-5551 (Electronic) 0887-6924 (Linking) %R leu2010311 [pii] 10.1038/leu.2010.311 %M 21233829 %K Adult Aged Aged, 80 and over Blotting, Western Cohort Studies DNA Methylation DNA-Binding Proteins/*genetics Epigenesis, Genetic Female Histones Humans Immunoenzyme Techniques Lymphoma, Follicular/diagnosis/*genetics/metabolism Lysine Male Middle Aged Mutation/*genetics Neoplasm Recurrence, Local/diagnosis/*genetics/metabolism Prognosis RNA, Messenger/genetics Reverse Transcriptase Polymerase Chain Reaction Survival Rate Tissue Array Analysis Transcription Factors/*genetics Young Adult %Z Bodor, C O'Riain, C Wrench, D Matthews, J Iyengar, S Tayyib, H Calaminici, M Clear, A Iqbal, S Quentmeier, H Drexler, H G Montoto, S Lister, A T Gribben, J G Matolcsy, A Fitzgibbon, J C1574/A6806/Cancer Research UK/United Kingdom Letter Research Support, Non-U.S. Gov't England Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K Leukemia. 2011 Apr;25(4):726-9. Epub 2011 Jan 14. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21233829 %G eng %0 Journal Article %A Boulday, G. %A Rudini, N. %A Maddaluno, L. %A Blecon, A. %A Arnould, M. %A Gaudric, A. %A Chapon, F. %A Adams, R. H. %A Dejana, E. %A Tournier-Lasserve, E. %D 2011 %T Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice %J J Exp Med %V 208 %N 9 %P 1835-47 %7 2011/08/24 %8 Aug 29 %! Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice %@ 1540-9538 (Electronic) 0022-1007 (Linking) %R jem.20110571 [pii] 10.1084/jem.20110571 %2 3171098 %M 21859843 %K Animals Carrier Proteins/*genetics/metabolism Central Nervous System Vascular Malformations/genetics/*metabolism/pathology/physiopathology Cerebellum/blood supply/metabolism/pathology Cerebral Hemorrhage/genetics/*metabolism/pathology/physiopathology Disease Models, Animal Endothelium, Vascular/*metabolism/pathology Gene Deletion Humans Mice Mice, Transgenic Microfilament Proteins/*genetics/metabolism Retina/metabolism/pathology/physiopathology %X Cerebral cavernous malformations (CCM) are vascular malformations of the central nervous system (CNS) that lead to cerebral hemorrhages. Familial CCM occurs as an autosomal dominant condition caused by loss-of-function mutations in one of the three CCM genes. Constitutive or tissue-specific ablation of any of the Ccm genes in mice previously established the crucial role of Ccm gene expression in endothelial cells for proper angiogenesis. However, embryonic lethality precluded the development of relevant CCM mouse models. Here, we show that endothelial-specific Ccm2 deletion at postnatal day 1 (P1) in mice results in vascular lesions mimicking human CCM lesions. Consistent with CCM1/3 involvement in the same human disease, deletion of Ccm1/3 at P1 in mice results in similar CCM lesions. The lesions are located in the cerebellum and the retina, two organs undergoing intense postnatal angiogenesis. Despite a pan-endothelial Ccm2 deletion, CCM lesions are restricted to the venous bed. Notably, the consequences of Ccm2 loss depend on the developmental timing of Ccm2 ablation. This work provides a highly penetrant and relevant CCM mouse model. %Z Boulday, Gwenola Rudini, Noemi Maddaluno, Luigi Blecon, Anne Arnould, Minh Gaudric, Alain Chapon, Francoise Adams, Ralf H Dejana, Elisabetta Tournier-Lasserve, Elisabeth Research Support, Non-U.S. Gov't United States The Journal of experimental medicine J Exp Med. 2011 Aug 29;208(9):1835-47. Epub 2011 Aug 22. %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21859843 %+ Institut National de la Sante et de la Recherche Medicale, UMR-S 740, 75010 Paris, France. %G eng %0 Journal Article %A Brachmann, J. %A Bohm, M. %A Rybak, K. %A Klein, G. %A Butter, C. %A Klemm, H. %A Schomburg, R. %A Siebermair, J. %A Israel, C. %A Sinha, A. M. %A Drexler, H. %D 2011 %T Fluid status monitoring with a wireless network to reduce cardiovascular-related hospitalizations and mortality in heart failure: rationale and design of the OptiLink HF Study (Optimization of Heart Failure Management using OptiVol Fluid Status Monitoring and CareLink) %J Eur J Heart Fail %V 13 %N 7 %P 796-804 %7 2011/05/11 %8 Jul %! Fluid status monitoring with a wireless network to reduce cardiovascular-related hospitalizations and mortality in heart failure: rationale and design of the OptiLink HF Study (Optimization of Heart Failure Management using OptiVol Fluid Status Monitoring and CareLink) %@ 1879-0844 (Electronic) 1388-9842 (Linking) %R hfr045 [pii] 10.1093/eurjhf/hfr045 %2 3125124 %M 21555324 %K Algorithms Cardiography, Impedance/*instrumentation Disease Management *Health Status Heart Failure/*mortality/pathology Humans Prospective Studies Quality of Life Questionnaires *Research Design *Telemetry Water-Electrolyte Balance/*physiology Wireless Technology/*instrumentation %X AIMS: The Optimization of Heart Failure Management using OptiVol Fluid Status Monitoring and CareLink (OptiLink HF) study is designed to investigate whether OptiVol fluid status monitoring with an automatically generated wireless CareAlert notification via the CareLink Network can reduce all-cause death and cardiovascular hospitalizations in an HF population, compared with standard clinical assessment. Methods Patients with newly implanted or replacement cardioverter-defibrillator devices with or without cardiac resynchronization therapy, who have chronic HF in New York Heart Association class II or III and a left ventricular ejection fraction