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350 results on '"Enjolras O"'

35. Blue Rubber Bleb Nevus (BRBN) Syndrome Is Caused by Somatic TEK (TIE2) Mutations.

Author

Soblet, J., Kangas, J., Nätynki, M., Mendola, A., Helaers, R., Uebelhoer, M., Kaakinen, M., Cordisco, M., Dompmartin, A., Enjolras, O., Holden, S., Irvine, A.D., Kangesu, L., Léauté-Labrèze, C., Lanoel, L., Lokmic, Z., Maas, S., McAleer, M.A., Penington, A., Rieu, P.N.M.A., Syed, S., Vleuten, C.J.M. van der, Watson, R., Fishman, S.J., Mulliken, J.B., Eklund, L., Limaye, N., Boon, L.M., Vikkula, M., Soblet, J., Kangas, J., Nätynki, M., Mendola, A., Helaers, R., Uebelhoer, M., Kaakinen, M., Cordisco, M., Dompmartin, A., Enjolras, O., Holden, S., Irvine, A.D., Kangesu, L., Léauté-Labrèze, C., Lanoel, L., Lokmic, Z., Maas, S., McAleer, M.A., Penington, A., Rieu, P.N.M.A., Syed, S., Vleuten, C.J.M. van der, Watson, R., Fishman, S.J., Mulliken, J.B., Eklund, L., Limaye, N., Boon, L.M., and Vikkula, M.

Abstract

Item does not contain fulltext

Published
2016

36. Angiome plan épaissi de la face : réponse à la sclérothérapie au polidocanol 2 % combinée à la rapamycine orale

Author

Salhi, A., primary, Belateche, K., additional, Allem, L., additional, Aitbelkacem, F., additional, Djéridane, A., additional, Benkaidali, I., additional, Belkaid, Z., additional, Ammarkhodja, A., additional, Saadi, A., additional, Lounis, Y., additional, Toukkal, F., additional, Bouadjar, B., additional, Aitbenamar, A., additional, and Enjolras, O., additional

Published
2015
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37. Phénomène de Kasabach-Merritt réfractaire traité par sirolimus : réponse inconstante (3 cas)

Author

Salhi, A., primary, Slaouti, M., additional, Laadjal, M., additional, Hasnaoui, A., additional, Aitbelkacem, F., additional, Djéridane, A., additional, Lebane, J., additional, Benkaidali, I., additional, Mani, S., additional, Ammarkhodja, A., additional, Bouadjar, B., additional, Boukari, R., additional, Belkaid, Z., additional, Aitbenamar, A., additional, Syed, S., additional, and Enjolras, O., additional

Published
2015
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38. Hémangiome infantile hépatique géant avec hypothyroïdie de consommation chez un nourrisson de 3 mois : sauvetage par le propranolol

Author

Salhi, A., primary, Gacem, O., additional, Salah, L., additional, Tounsi, T., additional, Laadjouze, A., additional, Mekki, A., additional, Aitbelkacem, F., additional, Benkaidali, I., additional, Bouadjar, B., additional, Laraba, A., additional, Ammarkhodja, A., additional, Djéridane, A., additional, Belkaid, A., additional, Aitbenamar, A., additional, and Enjolras, O., additional

Published
2015
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41. Le syndrome de Kasabach-Merritt versus le pseudo syndrome de Kasabach-Merritt : comment traiter ?

Author

Salhi, A., primary, Enjolras, O., additional, Wassef, M., additional, Khalef, K., additional, Drouet, L., additional, Labreze, C., additional, Taieb, A., additional, Maiche, L., additional, Tablit, I., additional, Syed, S., additional, Ait Belkacem, F., additional, Himeur, Z., additional, Boudghen, O., additional, Benhafsa, L., additional, Ammarkhodja, A., additional, Bouadjar, B., additional, Kedji, L., additional, Mertani, M., additional, Laraba, A., additional, Labyad, M., additional, Boukari, M., additional, Jamil, L., additional, Arfi, H., additional, Khiati, A., additional, Bensenouci, M., additional, Benkaidali, I., additional, Bouharati, F., additional, Otsman, F., additional, and Ait Benamar, A., additional

Published
2014
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42. A cAMP binding abnormality in psoriasis

Author

Raynaud, F., Enjolras, O., Donnadieu, M., Gerbaud, P., Gorin, I., Anderson, W.B., and Evain-Brion, D.

Subjects
Protein kinases -- Analysis, Retinoids -- Health aspects, Cyclic adenylic acid -- Physiological aspects, Erythrocyte disorders -- Analysis, Psoriasis -- Causes of
Published
1989

43. Syndrome pelvis/sacral associé à des brides amniotiques des jambes

Author

Salhi, A., primary, Enjolras, O., additional, Wassef, M., additional, Bisdorff, A., additional, Bouadjar, B., additional, Bouharati, D., additional, Aitbelkacem, F., additional, Ammarkhodja, A., additional, Benjkaidali, I., additional, Lebyed, M., additional, Laraba, A., additional, Boukari, M., additional, and Ait Benamar, A., additional

Published
2013
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44. Four common glomulin mutations cause two thirds of glomuvenous malformations ('familial glomangiomas'): evidence for a founder effect.

Author

UCL - MD/BICL - Département de biochimie et de biologie cellulaire, UCL - MD/CHIR - Département de chirurgie, Brouillard, Pascal, Ghassibé, Michella, Penington, A, Boon, Laurence M., Dompmartin, Anne, Temple, I K, Cordisco, M, Adams, D., Piette, F, Harper, J I, Syed, S, Boralevi, F, Taïeb, A, Danda, S, Baselga, E, Enjolras, O, Mulliken, J B, Vikkula, Miikka, UCL - MD/BICL - Département de biochimie et de biologie cellulaire, UCL - MD/CHIR - Département de chirurgie, Brouillard, Pascal, Ghassibé, Michella, Penington, A, Boon, Laurence M., Dompmartin, Anne, Temple, I K, Cordisco, M, Adams, D., Piette, F, Harper, J I, Syed, S, Boralevi, F, Taïeb, A, Danda, S, Baselga, E, Enjolras, O, Mulliken, J B, and Vikkula, Miikka

Abstract

BACKGROUND: Glomuvenous malformation (GVM) ("familial glomangioma") is a localised cutaneous vascular lesion histologically characterised by abnormal smooth muscle-like "glomus cells" in the walls of distended endothelium lined channels. Inheritable GVM has been linked to chromosome 1p21-22 and is caused by truncating mutations in glomulin. A double hit mutation was identified in one lesion. This finding suggests that GVM results from complete localised loss of function and explains the paradominant mode of inheritance. OBJECTIVE: To report on the identification of a mutation in glomulin in 23 additional families with GVM. RESULTS: Three mutations are new; the others have been described previously. Among the 17 different inherited mutations in glomulin known up to now in 43 families, the 157delAAGAA mutation is the most common and was present in 21 families (48.8%). Mutation 108C-->A was found in five families (11.8%), and the mutations 554delA+556delCCT and 1179delCAA were present together in two families (4.7% each). Polymorphic markers suggested a founder effect for all four mutations. CONCLUSIONS: Screening for these mutations should lead to a genetic diagnosis in about 70% of patients with inherited GVM. So far, a mutation in glomulin has been found in all GVM families tested, thus demonstrating locus homogeneity.

Published
2005

50. Rapidly involuting congenital hemangioma: Clinical and histopathologic features

Author

UCL - MD/CHIR - Département de chirurgie, UCL - (SLuc) Service de chirurgie plastique, UCL - (SLuc) Centre de malformations vasculaires congénitales, Berenguer, B, Mulliken, JB, Enjolras, O, Boon, Laurence M., Wassef, M, Josset, P, Burrows, PE, Perez-Atayde, AR, Kozakewich, HPW, Symposium on Vascular Anomalies, UCL - MD/CHIR - Département de chirurgie, UCL - (SLuc) Service de chirurgie plastique, UCL - (SLuc) Centre de malformations vasculaires congénitales, Berenguer, B, Mulliken, JB, Enjolras, O, Boon, Laurence M., Wassef, M, Josset, P, Burrows, PE, Perez-Atayde, AR, Kozakewich, HPW, and Symposium on Vascular Anomalies

Abstract

We define the histopathologic findings and review the clinical and radiologic characteristics of rapidly involuting congenital hemangioma (RICH). The features of RICH are compared to the equally uncommon noninvoluting congenital hemangioma (NICH) and common infantile hemangioma. RICH and NICH had many similarities, such as appearance, location, size, and sex distribution. The obvious differences in behavior served to differentiate RICH, NICH, and common infantile hemangioma. Magnetic resonance imaging (MRI) of the three tumors is quite similar, but some RICH also had areas of inhomogeneity and larger flow voids on MRI and arterial aneurysms on angiography. The histologic appearance of RICH differed from NICH and common infantile hemangioma, but some overlap was noted among the three lesions. RICH was composed of small-to-large lobules of capillaries with moderately plump endothelial cells and pericytes; the lobules were surrounded by abundant fibrous tissue. One-half of the specimens had a central involuting zone(s) characterized by lobular loss, fibrous tissue, and draining channels that were often large and abnormal. Ancillary features commonly found were hemosiderin, thrombosis, cyst formation, focal calcification, and extramedullary hematopoiesis. With one exception, endothelial cells in RICH (as in NICH) did not express glucose transporter-1 protein, as does common infantile hemangioma. One RICH exhibited 50% postnatal involution during the 1st year, stopped regressing, was resected at 18 months, and was histologically indistinguishable from NICH. In addition, several RICH, resected in early infancy, also had some histologic features suggestive of NICH. Furthermore, NICH removed early (2-4 years), showed some histologic findings of RICH or were indistinguishable from RICH. We conclude that RICH, NICH, and common infantile hemangioma have overlapping clinical and pathologic features. These observations support the hypothesis that these vascular tumors may be var

Published
2003

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