Search Results - (Author, Cooperation:M. Detmar)
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1Ma, Q., Dieterich, L. C., Ikenberg, K., Bachmann, S. B., Mangana, J., Proulx, S. T., Amann, V. C., Levesque, M. P., Dummer, R., Baluk, P., McDonald, D. M., Detmar, M.
American Association for the Advancement of Science (AAAS)
Published 2018Staff ViewPublication Date: 2018-08-09Publisher: American Association for the Advancement of Science (AAAS)Electronic ISSN: 2375-2548Topics: Natural Sciences in GeneralPublished by: -
2A. R. Forrest ; H. Kawaji ; M. Rehli ; J. K. Baillie ; M. J. de Hoon ; V. Haberle ; T. Lassmann ; I. V. Kulakovskiy ; M. Lizio ; M. Itoh ; R. Andersson ; C. J. Mungall ; T. F. Meehan ; S. Schmeier ; N. Bertin ; M. Jorgensen ; E. Dimont ; E. Arner ; C. Schmidl ; U. Schaefer ; Y. A. Medvedeva ; C. Plessy ; M. Vitezic ; J. Severin ; C. Semple ; Y. Ishizu ; R. S. Young ; M. Francescatto ; I. Alam ; D. Albanese ; G. M. Altschuler ; T. Arakawa ; J. A. Archer ; P. Arner ; M. Babina ; S. Rennie ; P. J. Balwierz ; A. G. Beckhouse ; S. Pradhan-Bhatt ; J. A. Blake ; A. Blumenthal ; B. Bodega ; A. Bonetti ; J. Briggs ; F. Brombacher ; A. M. Burroughs ; A. Califano ; C. V. Cannistraci ; D. Carbajo ; Y. Chen ; M. Chierici ; Y. Ciani ; H. C. Clevers ; E. Dalla ; C. A. Davis ; M. Detmar ; A. D. Diehl ; T. Dohi ; F. Drablos ; A. S. Edge ; M. Edinger ; K. Ekwall ; M. Endoh ; H. Enomoto ; M. Fagiolini ; L. Fairbairn ; H. Fang ; M. C. Farach-Carson ; G. J. Faulkner ; A. V. Favorov ; M. E. Fisher ; M. C. Frith ; R. Fujita ; S. Fukuda ; C. Furlanello ; M. Furino ; J. Furusawa ; T. B. Geijtenbeek ; A. P. Gibson ; T. Gingeras ; D. Goldowitz ; J. Gough ; S. Guhl ; R. Guler ; S. Gustincich ; T. J. Ha ; M. Hamaguchi ; M. Hara ; M. Harbers ; J. Harshbarger ; A. Hasegawa ; Y. Hasegawa ; T. Hashimoto ; M. Herlyn ; K. J. Hitchens ; S. J. Ho Sui ; O. M. Hofmann ; I. Hoof ; F. Hori ; L. Huminiecki ; K. Iida ; T. Ikawa ; B. R. Jankovic ; H. Jia ; A. Joshi ; G. Jurman ; B. Kaczkowski ; C. Kai ; K. Kaida ; A. Kaiho ; K. Kajiyama ; M. Kanamori-Katayama ; A. S. Kasianov ; T. Kasukawa ; S. Katayama ; S. Kato ; S. Kawaguchi ; H. Kawamoto ; Y. I. Kawamura ; T. Kawashima ; J. S. Kempfle ; T. J. Kenna ; J. Kere ; L. M. Khachigian ; T. Kitamura ; S. P. Klinken ; A. J. Knox ; M. Kojima ; S. Kojima ; N. Kondo ; H. Koseki ; S. Koyasu ; S. Krampitz ; A. Kubosaki ; A. T. Kwon ; J. F. Laros ; W. Lee ; A. Lennartsson ; K. Li ; B. Lilje ; L. Lipovich ; A. Mackay-Sim ; R. Manabe ; J. C. Mar ; B. Marchand ; A. Mathelier ; N. Mejhert ; A. Meynert ; Y. Mizuno ; D. A. de Lima Morais ; H. Morikawa ; M. Morimoto ; K. Moro ; E. Motakis ; H. Motohashi ; C. L. Mummery ; M. Murata ; S. Nagao-Sato ; Y. Nakachi ; F. Nakahara ; T. Nakamura ; Y. Nakamura ; K. Nakazato ; E. van Nimwegen ; N. Ninomiya ; H. Nishiyori ; S. Noma ; T. Noazaki ; S. Ogishima ; N. Ohkura ; H. Ohimiya ; H. Ohno ; M. Ohshima ; M. Okada-Hatakeyama ; Y. Okazaki ; V. Orlando ; D. A. Ovchinnikov ; A. Pain ; R. Passier ; M. Patrikakis ; H. Persson ; S. Piazza ; J. G. Prendergast ; O. J. Rackham ; J. A. Ramilowski ; M. Rashid ; T. Ravasi ; P. Rizzu ; M. Roncador ; S. Roy ; M. B. Rye ; E. Saijyo ; A. Sajantila ; A. Saka ; S. Sakaguchi ; M. Sakai ; H. Sato ; S. Savvi ; A. Saxena ; C. Schneider ; E. A. Schultes ; G. G. Schulze-Tanzil ; A. Schwegmann ; T. Sengstag ; G. Sheng ; H. Shimoji ; Y. Shimoni ; J. W. Shin ; C. Simon ; D. Sugiyama ; T. Sugiyama ; M. Suzuki ; N. Suzuki ; R. K. Swoboda ; P. A. t Hoen ; M. Tagami ; N. Takahashi ; J. Takai ; H. Tanaka ; H. Tatsukawa ; Z. Tatum ; M. Thompson ; H. Toyodo ; T. Toyoda ; E. Valen ; M. van de Wetering ; L. M. van den Berg ; R. Verado ; D. Vijayan ; I. E. Vorontsov ; W. W. Wasserman ; S. Watanabe ; C. A. Wells ; L. N. Winteringham ; E. Wolvetang ; E. J. Wood ; Y. Yamaguchi ; M. Yamamoto ; M. Yoneda ; Y. Yonekura ; S. Yoshida ; S. E. Zabierowski ; P. G. Zhang ; X. Zhao ; S. Zucchelli ; K. M. Summers ; H. Suzuki ; C. O. Daub ; J. Kawai ; P. Heutink ; W. Hide ; T. C. Freeman ; B. Lenhard ; V. B. Bajic ; M. S. Taylor ; V. J. Makeev ; A. Sandelin ; D. A. Hume ; P. Carninci ; Y. Hayashizaki
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-03-29Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*geneticsPublished by: -
3E. Arner ; C. O. Daub ; K. Vitting-Seerup ; R. Andersson ; B. Lilje ; F. Drablos ; A. Lennartsson ; M. Ronnerblad ; O. Hrydziuszko ; M. Vitezic ; T. C. Freeman ; A. M. Alhendi ; P. Arner ; R. Axton ; J. K. Baillie ; A. Beckhouse ; B. Bodega ; J. Briggs ; F. Brombacher ; M. Davis ; M. Detmar ; A. Ehrlund ; M. Endoh ; A. Eslami ; M. Fagiolini ; L. Fairbairn ; G. J. Faulkner ; C. Ferrai ; M. E. Fisher ; L. Forrester ; D. Goldowitz ; R. Guler ; T. Ha ; M. Hara ; M. Herlyn ; T. Ikawa ; C. Kai ; H. Kawamoto ; L. M. Khachigian ; S. P. Klinken ; S. Kojima ; H. Koseki ; S. Klein ; N. Mejhert ; K. Miyaguchi ; Y. Mizuno ; M. Morimoto ; K. J. Morris ; C. Mummery ; Y. Nakachi ; S. Ogishima ; M. Okada-Hatakeyama ; Y. Okazaki ; V. Orlando ; D. Ovchinnikov ; R. Passier ; M. Patrikakis ; A. Pombo ; X. Y. Qin ; S. Roy ; H. Sato ; S. Savvi ; A. Saxena ; A. Schwegmann ; D. Sugiyama ; R. Swoboda ; H. Tanaka ; A. Tomoiu ; L. N. Winteringham ; E. Wolvetang ; C. Yanagi-Mizuochi ; M. Yoneda ; S. Zabierowski ; P. Zhang ; I. Abugessaisa ; N. Bertin ; A. D. Diehl ; S. Fukuda ; M. Furuno ; J. Harshbarger ; A. Hasegawa ; F. Hori ; S. Ishikawa-Kato ; Y. Ishizu ; M. Itoh ; T. Kawashima ; M. Kojima ; N. Kondo ; M. Lizio ; T. F. Meehan ; C. J. Mungall ; M. Murata ; H. Nishiyori-Sueki ; S. Sahin ; S. Nagao-Sato ; J. Severin ; M. J. de Hoon ; J. Kawai ; T. Kasukawa ; T. Lassmann ; H. Suzuki ; H. Kawaji ; K. M. Summers ; C. Wells ; D. A. Hume ; A. R. Forrest ; A. Sandelin ; P. Carninci ; Y. Hayashizaki
American Association for the Advancement of Science (AAAS)
Published 2015Staff ViewPublication Date: 2015-02-14Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Binding Sites ; Cattle ; Cell Differentiation/*genetics ; Dogs ; *Enhancer Elements, Genetic ; *Gene Expression Regulation, Developmental ; Mice ; RNA, Messenger/genetics/metabolism ; Rats ; Stem Cells/*cytology/metabolism ; Transcription Factors/*metabolism ; *Transcription, GeneticPublished by: -
4DETMAR, M. ; PAULI, G. ; ANAGNOSTOPOULOS, I. ; WUNDERLICH, U. ; HERBST, H. ; GARBE, C. ; STEIN, H. ; ORFANOS, C. E.
Oxford, UK : Blackwell Publishing Ltd
Published 1991Staff ViewISSN: 1365-2133Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: A 72-year-old male patient from north-eastern Iran developed the typical clinical and histopathological features of mycosis fungoides with lymphadenopathy, but without any other systemic involvement. Human T-cell lymphotropic virus (HTLV-I) antibodies were detected in the patient's serum by two different ELISAs and by Western blot using purified viral particles from MT-2 culture supernatants. Cultured peripheral blood lymphocytes were positive for labelling with anti-HTLV-I serum. Southern blot hybridization of DNA extracted from a skin tumour and from an involved lymph node revealed integrated proviral DNA with identical restriction patterns. This case supports a relationship between mycosis fungoides and HTLV-I and may indicate a new region of endemic HTLV-I infection.Type of Medium: Electronic ResourceURL: -
5Yano, K. ; Kadoya, K. ; Kajiya, K. ; Hong, Y-K. ; Detmar, M.
Oxford, UK : Blackwell Science Ltd
Published 2005Staff ViewISSN: 1365-2133Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background We have previously demonstrated that skin-specific overexpression of the endogenous angiogenesis inhibitor thrombospondin (TSP)-1 prevented chronic ultraviolet (UV) B-induced angiogenesis, inflammatory cell infiltration and cutaneous photodamage in mice.Objectives To elucidate the mechanisms by which acute UVB-induced angiogenesis induces dermal damage, and to study the molecular regulation of acute UVB-induced angiogenesis in human skin.Methods We subjected five healthy volunteers to acute UVB irradiation (2 minimal erythema doses) and performed histological analysis at 48 h after UVB irradiation.Results Histology revealed epidermal hyperplasia, infiltration of elastase-producing neutrophils and elastin fibre damage. Immunohistochemistry for CD31 demonstrated pronounced angiogenesis with a significant increase in both vascular density and vessel size, associated with increased endothelial cell proliferation. Whereas constitutive expression of TSP-1 but only weak expression of vascular endothelial growth factor (VEGF) were detected in normal human epidermis, pronounced downregulation of TSP-1 and upregulation of VEGF were observed in epidermal keratinocytes after acute UVB irradiation. These findings were confirmed by quantitative reverse transcription–polymerase chain reaction analysis after UVB irradiation of cultured HaCaT keratinocytes in vitro.Conclusions Together, these data indicate that a disruption of the balance between VEGF and TSP-1 expression leads to a UVB-induced angiogenic switch, facilitating the infiltration of elastase-producing leucocytes and cutaneous photodamage.Type of Medium: Electronic ResourceURL: -
6Staff View
ISSN: 1432-069XKeywords: Tumor necrosis factor-alpha ; Keratinocyte cultures ; Class II antigens ; Cell Adhesion molecules ; Immunoelectron microscopySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary The effects of recombinant human tumor necrosis factor-alpha (TNF) on cell proliferation, cell morphology, and on the expression of class II alloantigens and intercellular adhesion molecule-1 (ICAM-1) were assessed in human keratinocytes cultured in serum-free medium. TNF inhibited cell proliferation in a time- and dose-dependent manner with a minimum effective dose of 10 U/ml and a 50% inhibitory dose of 100 U/ml. However, TNF did not induce cell death, and the growth inhibition induced by TNF was completely reversible after its withdrawal. In vitro combination of TNF with interferon-alpha (IFN-alpha) and IFN-beta resulted in additive growth inhibitory effects, while IFN-gamma enhanced the TNF mediated growth inhibition in a synergistic way. Furthermore, TNF altered the morphology of the growing keratinocytes inducing the appearance of a fusiform, fibroblast-like population. Also, treatment with TNF over 6 days markedly induced the expression of ICAM-1 on the cultured keratinocytes with a minimal effective dose of 10 U/ml, while HLA-DR was only moderately expressed after 1,000 U/ml. TNF did not induce HLA-DQ, but reduced the IFN-gamma induced expression of HLA-DR and HLA-DQ. By immunoelectron microscopy, an intense membrane-bound labeling for ICAM-1 was found after treatment with TNF, clearly pronounced in areas of microvillous membrane protrusions. These results indicate that epidermal keratinocytes are a major target for various biological effects of TNF. We also found that TNF differentially modulates IFN-gamma-induced effects, thus suggesting its potential role in the regulation of inflammatory skin disorders.Type of Medium: Electronic ResourceURL: -
7Imcke, E. ; Ruszczak, Zb. ; Mayer-da Silva, A. ; Detmar, M. ; Orfanos, C. E.
Springer
Published 1991Staff ViewISSN: 1432-069XKeywords: Endothelial cells ; Cell culture ; Retinoids ; Monoclonal antibodies ; LectinsSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary A new reliable and reproducible technique to culture endothelial cells from the small vessels and capillaries of human skin is introduced, and proliferation and differentiation of the growing cells are characterized. The endothelial origin of the culture cells was confirmed by light- and electron microscopy and by labelling with Ulex europaeus Agglutinin I and an antibody against Factor VIII-related antigen. Further immunocytochemical characterization showed that 92–100% of the cells were positive for Β 2-microglobulin and the entire cell population expressed vimentin, whereas cytokeratins, desmin, HLA-DR antigen, Leu 6 and S 100 protein, could not be detected. As vascular endothelium is a common site of inflammation and retinoids have been shown to be of good clinical efficacy in some chronic inflammatory skin diseases, we investigated the influence of etretinate, etretin and isotretinoin on proliferation and antigen expression of our culture cells. All retinoids applied inhibited proliferation of endothelial cells in a dose- and time-dependent manner whereas they induced neither HLA-DR nor intercellular adhesion molecule-1 (ICAM-1). Furthermore, none of the retinoids applied influenced the γ-interferon-induced expression of these surface antigens on endothelial cells. Our results suggest that the action of retinoids in skin inflammation is not mediated by modulation of HLA-DR or ICAM-1. The cell culture technique described here is an interesting and reliable model for studying the influence of drugs on endothelial cell growth and differentiation in vitro.Type of Medium: Electronic ResourceURL: -
8Kiessling, M. ; Mies, G. ; Paschen, W. ; Thilmann, R. ; Detmar, M. ; Hossmann, K. -A.
Springer
Published 1988Staff ViewISSN: 1432-0533Keywords: Hypoglycemia ; Selective vulnerability ; Neural grafts ; Cerebral blood flow ; Brain metabolismSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Hypoglycemia-induced disturbances of brain metabolism and neuronal injury exhibit a distinct predilection for forebrain structures, in particular the caudate-putamen, hippocampus and cerebral cortex, whereas the cerebellum is remarkably resistant. In an attempt to assess the biological basis of this differential regional vulnerability, we have used a neural transplantation technique to compare hemodynamic and metabolic changes in cerebellum during servere hypoglycemia with those in heterotopic cerebellar grafts. To this end, the cerebellar anlage of fetal rat brain (day 15 of gestation) was stereotactically transplanted into the vulnerable caudate-putamen. Following a differentiation period of 8 weeks the grafts had developed into an organotypic population of mature cells with laminar histoarchitecture. Host animals were then subjected to insulin-induced hypoglycemia. After 15 min of isoelectric EEG, blood flow was increased throughout the brain but residual glucose consumption was significantly higher in cerebellum (0.29 μmol/g per min) and cerebellar grafts (0.22 μmol/g per min) as a result of increased glucose extraction. Hypoglycemia caused a depletion of ATP in all brain structures except cerebellum where normal levels were maintained. Correlation of local ATP content and glucose utilization revealed a threshold-like decline of ATP at a glucose utilization rate of 0.27 μmol/g per min. ATP, in consequence, was normal in cerebellum but partially depleted in cerebellar grafts. It is concluded that the resistance of cerebellum to hypoglycemia is due to its capacity for higher glucose extraction at low blood glucose levels, and that this unique intrinsic property is preserved after heterotopic transplantation.Type of Medium: Electronic ResourceURL: -
9Staff View
ISSN: 1432-069XKeywords: Corticosteroids ; TNF ; IL-1Β ; ICAM-1 ; Human dermal microvascular endothelial cellsSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract The effects of hydrocortisone, dexamethasone, betamethasone 17-valerate and clobetasol propionate at concentrations of 10−5–10−12 M on the proliferation of human dermal microvascular endothelial cells (HDMEC) were studied in vitro. In addition, confluent HDMEC were treated with TNF (1000 U/ml) or IL-1Β (1000 U/ml) alone or in combination with the corticosteroids (10−5 M, 10−6 M) for 24 h, and cytokine-induced expression of intercellular adhesion molecule-1 (ICAM-1) was assessed by immunocytochemistry. Controls were treated either with growth medium or with the corticosteroids alone. All tested corticosteroids stimulated HDMEC growth after 4 and 6 days of treatment in a dose-dependent manner, as assessed by 3H-thymidine incorporation and the 4-methyl-umbelliferyl heptanoate (MUH) assay. The minimal effective concentration was 10−9 M for hydrocortisone, 10−10 M for dexamethasone and betamethasone, and 10−12 M for clobetasol. In untreated and in corticosteroid-treated cultures, less than 5% of the cells expressed ICAM-1. TNF and IL-1Β were strong inducers of ICAM-1 expression on 74% and 82% of the cells, respectively. None of the tested corticosteroids significantly influenced cytokine-induced ICAM-1 expression, suggesting that the anti-inflammatory effects of corticosteroids are not related to ICAM-1 modulation on HDMEC.Type of Medium: Electronic ResourceURL: -
10Staff View
ISSN: 1432-1920Keywords: Chymopapain ; Nucleolysis ; Diskography ; Animal experimental investigation ; Interaction contrast medium/chymopapainSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary A test was carried out on 11 young, full sized mongrels to determine whether there is an interaction between chymopapain and the contrast agents iotrolan and iopamidol. A total of 75 intervertebral disks were punctured: nucleolysis alone was performed on 20, diskography with iotrolan and subsequent nucleolysis on 20, and diskography with iopamidol and subsequent nucleolysis on 10. Diskography alone was performed 10 times with iotrolan and 5 times with iopamidol. Aqua dest. was given intradiskally 5 times, and puncture was carried out 5 times without the administration of any substance. Following puncture, x-rays of the lumbar vertebral column were taken laterally: daily for the first 10 days, then weekly. Disk space narrowing typical of nucleolysis with chymopapain was found among the disks that were nucleolyzed only to the same extent as among those that had undergone diskography previously. There was no evidence of narrowing of the other disk spaces which had been punctured but not treated with chymopapain. On some of the dogs, CT and MRI examinations were carried out. The CTs showed a homogenous hypodensity in all of the disks, in which chymopapain had been injected. The MRI revealed a signal loss in all ot the nucleolyzed disks. The results of short and long term follow up demonstrate that inhibition of chymopapain by iotrolan or iopamidol is not to be expected and therefore diskography prior to chemonucleolysis can be performed without danger of enzyme inactivation.Type of Medium: Electronic ResourceURL: