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1.
Hernia ; 15(2): 229-31, 2011 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-20155292

RESUMEN

Hernias are often associated with congenital defects or incisional breakdown. Even though most of the linea arcuata hernias are asymptomatic, we present a rare case of a symptomatic linea arcuata hernia with associated internal herniation of the colon sigmoideum in a woman without previous abdominal surgery.


Asunto(s)
Hernia Abdominal/diagnóstico , Hernia Abdominal/cirugía , Femenino , Humanos , Laparoscopía , Persona de Mediana Edad
2.
Acta Chir Belg ; 108(4): 447-50, 2008.
Artículo en Inglés | MEDLINE | ID: mdl-18807600

RESUMEN

Goblet cell carcinoids are uncommon tumours with histological features of both adenocarcinoma and carcinoid tumour. They occur predominantly in the appendix and although the malignant potential remains unclear, adenocarcinoids appear to be more aggressive than conventional carcinoids. In this case report, we present a goblet cell carcinoid with laparoscopic operative treatment in two stages. A 43-year-old female patient with constant dullness in the right lower quadrant was diagnosed with acute appendicitis and underwent laparoscopic appendectomy. Macroscopically, a diffusely inflamed appendix was found with no sign of perforation. Histopathological examination revealed a goblet cell carcinoid with characteristics of aggressive behaviour, indicating the need for laparoscopic right hemicolectomy in which, however, neither residual tumour nor metastatic lymph nodes could be found. The postoperative course was uneventful. As they may present the same clinical presentation, pathological diagnosis is required to distinguish goblet cell carcinoid from acute appendicitis. Two-stage surgery for goblet cell carcinoid is advocated in the literature, but the debate still continues as to whether the goblet cell carcinoid should be treated by appendectomy alone, as for most carcinoids, or by right hemicolectomy, as for the appendiceal adenocarcinoma.


Asunto(s)
Apendicectomía/métodos , Neoplasias del Apéndice/cirugía , Tumor Carcinoide/cirugía , Colectomía/métodos , Laparoscopía/métodos , Adulto , Neoplasias del Apéndice/patología , Tumor Carcinoide/patología , Diagnóstico Diferencial , Femenino , Estudios de Seguimiento , Humanos
3.
Mol Cell Endocrinol ; 165(1-2): 85-95, 2000 Jul 25.
Artículo en Inglés | MEDLINE | ID: mdl-10940487

RESUMEN

The authors previously reported that one of the cAMP-response elements (CREs) of the human beta3-AR gene, beta3CRE2, interacts with a nuclear factor which is distinct from CREB/ATF family. We named this factor WATSF-1 (white adipose tissue specific factor-1) since it is preferentially expressed in WAT. In this work, we have shown the absence of DNA binding or transcriptional activity of this factor in several non-adipose cells tested. By computer analysis, beta3CRE2 was found to constitute an octameric element that is highly homologous to the binding site for some members of the nuclear hormone receptor superfamily. Using the response elements of other adipocyte-specific nuclear receptors as competitors, a 'cross-talk' between WATSF-1 and these response elements has been demonstrated. However, the affinity of WATSF-1 for these response elements differs from that for beta3CRE2 (self), implying that WATSF-1 is distinct from these adipocyte-specific nuclear receptors. Furthermore the DNA-binding activity of WATSF-1 was shown to be enhanced by phosphatase treatment, suggesting that phosphorylation may play an important role in the functional modulation of this factor. In an effort to prove that it is indeed an adipocyte-specific factor, we used 3T3-L1 cells, a cellular model of WAT, that can undergo differentiation into adipocytes. The DNA binding and transcriptional activity of this factor appeared during differentiation of the cells. Taken together, these results demonstrate that WATSF-1 is a putative white adipocyte-specific nuclear orphan receptor induced during adipogenesis and is a transcriptional activator through one of the CREs of the human beta3-AR gene. Targeting this factor may be a novel therapeutic approach to stimulation of the beta3-AR signal transduction pathway in adipose tissues.


Asunto(s)
Tejido Adiposo/metabolismo , Receptores Adrenérgicos beta 3/genética , Receptores Citoplasmáticos y Nucleares/metabolismo , Células 3T3 , Adipocitos/citología , Adipocitos/metabolismo , Animales , Secuencia de Bases , Sitios de Unión/genética , Diferenciación Celular , AMP Cíclico/farmacología , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/genética , ADN/genética , ADN/metabolismo , Cartilla de ADN/genética , Humanos , Técnicas In Vitro , Ratones , Obesidad/terapia , Fosforilación , Receptor Cross-Talk , Receptores Citoplasmáticos y Nucleares/genética , Transcripción Genética
4.
Br J Cancer ; 82(6): 1123-30, 2000 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-10735494

RESUMEN

We have cloned a human Hevin cDNA from omental adipose tissue of different patients by reverse transcription polymerase chain reaction and shown a sequence variation due to a possible polymorphism at amino acid position 161 (E/G). Hevin protein expressed in vitro showed molecular weights of approximately 75 kDa and 150 kDa, suggesting that Hevin may form a homodimer in vitro. Using Northern blots and a human expressed sequence tAg database analysis, Hevin was shown to be widely expressed in human normal or non-neoplastic diseased tissues with various levels. In contrast to this, its expression was strongly down-regulated in most neoplastic cells or tissues tested. However, neither the mechanism nor the physiological meaning of this down-regulation is known. As an initial step towards investigating the functional role of Hevin in cell growth and differentiation, we transiently or stably expressed this gene in cancer cells (HeLa 3S) that are devoid of endogenous Hevin and measured DNA synthesis (cell proliferation) by 5-bromo-2'-deoxyuridine incorporation. Hevin was shown to be a negative regulator of cell proliferation. Furthermore, we have shown that Hevin can inhibit progression of cells from G1 to S phase or prolong G1 phase. This is the first report which describes the function of Hevin in cell growth and proliferation. Through database analysis, Hevin was found to be located on chromosome 4 which contains loss of heterozygosity of many tumour suppressor genes. Taken together, these results suggest that Hevin may be a candidate for a tumour suppressor gene and a potential target for cancer diagnosis/therapy.


Asunto(s)
Proteínas de Unión al Calcio/biosíntesis , Regulación hacia Abajo , Genes Supresores de Tumor/fisiología , Glicoproteínas/biosíntesis , Neoplasias/patología , Northern Blotting , Proteínas de Unión al Calcio/farmacología , Ciclo Celular/fisiología , División Celular/fisiología , Transformación Celular Neoplásica , ADN de Neoplasias/genética , Proteínas de la Matriz Extracelular , Glicoproteínas/farmacología , Humanos , Neoplasias/genética , Neoplasias/fisiopatología , Células Tumorales Cultivadas
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