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- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ classification A1.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ date "2023".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ language "eng".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ type journalArticle.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ hasPart 01HAC9ABRYN7TZF461MW815Z4M.pdf.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ subject "Medicine and Health Sciences".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ doi "10.1371/journal.pone.0288347".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ issn "1932-6203".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ issue "7".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ volume "18".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ abstract "This study is the first to investigate the transcriptomic changes occurring in severe udder cleft dermatitis lesions (UCD) in Holstein-Friesian cows. An examination of the gene expression levels in natural UCD lesions and healthy udder skin through RNA Seq-Technology provided a deeper insight into the inflammatory pathways associated with this disease. A clear distinction between the gene expression patterns of UCD lesions and healthy skin was shown in the principal component analysis. Genes coding for inflammatory molecules were upregulated such as the chemokines C-X-C motif ligand 2 (CXCL2), 5 (CXCL5) and 8 (CXCL8), and C-C motif ligand 11 (CCL11). Moreover, the genes coding for the multifunctional molecules ADAM12 and SLPI were amongst the highest upregulated ones, whereas the most downregulated genes included the ones coding for keratins and keratin-associated molecules. Predominantly inflammatory pathways such as the chemokine signaling, cytokine receptor interaction and IL-17 signaling pathway were significantly upregulated in the pathway analysis. These results point towards a fulminant, dysregulated inflammatory response concomitant with a disruption of the skin barrier integrity and a hampered wound repair mechanism in severe UCD lesions.".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author 1f957e26-9c0f-11ec-976e-bb5548f6f8d1.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author 2C1D9392-1352-11E3-B75B-E7B310BDE39D.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author 374B2838-F0EE-11E1-A9DE-61C894A0A6B4.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author F3ECBCBE-F0ED-11E1-A9DE-61C894A0A6B4.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author F49F793A-F0ED-11E1-A9DE-61C894A0A6B4.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author F4D02620-F0ED-11E1-A9DE-61C894A0A6B4.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author F57157B6-F0ED-11E1-A9DE-61C894A0A6B4.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author F5BC58D8-F0ED-11E1-A9DE-61C894A0A6B4.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ author urn:uuid:879d43fb-5693-4db1-9316-d432dcec32e2.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ dateCreated "2023-08-16T15:13:43Z".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ dateModified "2025-02-03T11:15:42Z".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ editor urn:uuid:e5c2de8c-6280-4808-9300-78f1c5f85687.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ name "Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis".
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ pagination urn:uuid:4d540415-d999-4066-9650-6a6f718b40fa.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ publisher urn:uuid:c027e241-cac6-4c27-9da6-07c37365bbbc.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ sameAs LU-01H7ZEHSAHSJJT9Z6T2GMR1MDJ.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ sourceOrganization urn:uuid:03c0c021-0f16-41e9-88c9-b81d50d65eb3.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ sourceOrganization urn:uuid:6848758e-7600-40a9-9892-09b516515178.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ sourceOrganization urn:uuid:bd6f0851-36bc-451e-80b2-24de5479878c.
- 01H7ZEHSAHSJJT9Z6T2GMR1MDJ type A1.