Examinando por Autor "Gonzalez, Carlos M."

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    Oral masses in African pygmy hedgehogs
    (SAGE Publications Inc., 2019-11) Del Aguila, Gabriela; Torres, Cristian G.; Carvallo, Francisco R.; Gonzalez, Carlos M.; Cifuentes, Federico F.
    African pygmy hedgehogs (Atelerix albiventris) frequently develop oral neoplasms, and most of these neoplasms are malignant. We characterized oral masses detected in hedgehogs at clinical examination. During a 1-y period, we diagnosed oral cavity masses in 27 privately owned hedgehogs; 16 were female and 11 were male, with ages of 2–7y (mean: 4.3 y). Eight masses were non-neoplastic and were diagnosed as gingival hyperplasia (GH). Nineteen masses were neoplastic, of which 17 were squamous cell carcinomas (SCCs) and 2 were mesenchymal tumors (1 spindle cell tumor of probable neural origin, and 1 hemangiosarcoma). The GHs were noninvasive, exophytic, and did not recur after surgical excision. The SCCs were highly invasive tumors that induced facial deformation and were located in the caudal portion of the oral cavity, with 12 of them arising from the right-caudal maxilla. Thus, clinical signs, growth pattern, and anatomic location can be used to suspect a diagnosis of SCC among the other possible diagnoses, such as GH, in this location. However, histopathology is necessary for confirmation. Also, hemangiosarcoma should be considered among the differential diagnoses.
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    Regulation of the Intestinal Extra-Adrenal Steroidogenic Pathway Component LRH-1 by Glucocorticoids in Ulcerative Colitis
    (MDPI, 2022-06-02) Landskron, Glauben; Dubois-Camacho, Karen; Orellana-Serradell, Octavio; De la Fuente, Marjorie; Parada-Venegas, Daniela; Bitrán, Mirit; Diaz-Jimenez, David; Tang, Shuang; Cidlowski, John A.; Li, Xiaoling; Molina, Hector; Gonzalez, Carlos M.; Simian, Daniela; Lubascher, Jaime; Pola, Victor; Montecino, Martín; Blokzijl, Tjasso; Faber, Klaas Nico; González, María-Julieta; Quera, Rodrigo; Hermoso, Marcela A.
    Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) and can be treated with glucocorticoids (GC), although some patients are unresponsive to this therapy. The transcription factor LRH-1/NR5A2 is critical to intestinal cortisol production (intestinal steroidogenesis), being reduced in UC patients. However, the relationship between LRH-1 expression and distribution with altered corticosteroid responses is unknown. To address this, we categorized UC patients by their steroid response. Here, we found that steroid-dependent and refractory patients presented reduced glucocorticoid receptor (GR)-mediated intestinal steroidogenesis compared to healthy individuals and responder patients, possibly related to increased colonic mucosa GR isoform beta (GRβ) content and cytoplasmic LRH-1 levels in epithelial and lamina propria cells. Interestingly, an intestinal epithelium-specific GR-induced knockout (GRiKO) dextran sodium sulfate (DSS)-colitis mice model presented decreased epithelial LRH-1 expression, whilst it increased in the lamina propria compared to DSS-treated control mice. Mechanistically, GR directly induced NR5A2 gene expression in CCD841CoN cells and human colonic organoids. Furthermore, GR bound to two glucocorticoid-response elements within the NR5A2 promoter in dexamethasone-stimulated CCD841CoN cells. We conclude that GR contributes to intestinal steroidogenesis by inducing LRH-1 in epithelial cells, suggesting LRH-1 as a potential marker for glucocorticoid-impaired response in UC. However, further studies with a larger patient cohort will be necessary to confirm role of LRH-1 as a therapeutic biomarker. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.