Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
1.
Int J Immunopathol Pharmacol ; 22(4): 1027-34, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-20074466

RESUMEN

Hodgkin's disease (HD) is a malignant lymphoma with frequent mediastinal involvement, characterized by a significant inflammatory infiltration. Exhaled nitric oxide (FENO), is present in healthy humans, and has been proven to be increased in eosinophilic diseases such as allergic asthma. We investigated whether FENO is increased in mediastinal HD and whether NO is produced by lymphoma tissue. To this aim FENO was measured in 56 HD patients, 17 with and 39 without bulky mediastinal involvement, in the period from January 2007 to December 2008. Thirty-seven patients were reassessed after remission. Lymph node biopsies of 10 patients were evaluated for inducible (iNOS) and constitutive (eNOS) nitric oxide synthase expression by immunohistochemistry. FENO resulted significantly related to the mediastinal mass maximum diameter (p=0.009) and was significantly higher in patients with as compared to those without bulky mediastinal disease (38.7 ppb, CI 95% 19.3-58.0, versus 20.7 ppb, CI 95% 16.6-24.7; p=0.009). iNOS and eNOS immunoreactivity was observed in tumour and inflammatory cells (eosinophils and histiocytes). Only in patients with bulky mediastinal HD there was a significant decrease in FENO (from 50.4 ppb CI 95% 18.0-82.8 to 11.1 ppb CI 95% 4.4-17.8, p=0.011). In conclusion, high FENO and NOS expression in lymph-nodes indicate that NO is a component of the inflammatory network of HD. FENO may be proposed for the assessment and follow up of bulky mediastinal HD patients.


Asunto(s)
Pruebas Respiratorias , Espiración , Enfermedad de Hodgkin/enzimología , Ganglios Linfáticos/enzimología , Neoplasias del Mediastino/enzimología , Óxido Nítrico Sintasa de Tipo III/metabolismo , Óxido Nítrico Sintasa de Tipo II/metabolismo , Óxido Nítrico/metabolismo , Adolescente , Adulto , Anciano , Antineoplásicos/uso terapéutico , Biopsia , Femenino , Enfermedad de Hodgkin/patología , Enfermedad de Hodgkin/fisiopatología , Enfermedad de Hodgkin/terapia , Humanos , Inmunohistoquímica , Ganglios Linfáticos/patología , Masculino , Neoplasias del Mediastino/patología , Neoplasias del Mediastino/fisiopatología , Neoplasias del Mediastino/terapia , Persona de Mediana Edad , Estadificación de Neoplasias , Radioterapia Adyuvante , Espirometría , Resultado del Tratamiento , Regulación hacia Arriba , Adulto Joven
2.
Minerva Stomatol ; 57(4): 189-98, 2008 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-18427363

RESUMEN

AIM: There is an increasing need for an appropriate and readily-available material to reconstruct large bone defects, one of the most significant problems in the dental and maxillo-facial fields. The in vitro study examines the effects of OSTEOPLANT ANGIOSTAD, a product developed to increase osteoinductivity. METHODS: The product's biological properties were assessed by examining: the viability of cultured bone-marrow mesenchymal stem cells (MSC) through the methylthiazol tetrazolium assay; transforming growth factor (TGF)-b release by these cells through the enzyme-linked immunosorbent assay (ELISA) and the migration capacity of MSC and endothelial cells, by the in vitro wound closure test and transwell-migration assay, respectively. RESULTS: OSTEOPLANT ANGIOSTAD preserved MSC's viability and improved their capacity to release TGF-b1. It also increased in vitro wound healing by MSC and migration of endothelial cells. CONCLUSION: The results show that, since it increases the production by MSC of proangiogenic factors such as TGF-beta and promotes endothelial cell migration, OSTEOPLANT ANGIOSTAD may be an appropriate adjunct to accelerate the osteointegration of bone substitutes.


Asunto(s)
Colágeno Tipo I/farmacología , Osteogénesis/efectos de los fármacos , Células Cultivadas , Células Endoteliales/efectos de los fármacos , Humanos , Células Madre Mesenquimatosas/efectos de los fármacos
3.
Minerva Med ; 96(2): 87-94, 2005 Apr.
Artículo en Italiano | MEDLINE | ID: mdl-16172578

RESUMEN

Pancreatic ductal carcinoma still is an aggressive disease with a fatal prognosis due to late diagnosis and resistance to pharmacological and surgical treatments. Molecular investigations of pancreatic cancer are complicated by the restricted accessibility of the organ for biopsies. However, recent studies have indicated that pancreatic cancer is a multi-stage process resulting from the accumulation of genetic changes in the somatic DNA of normal cells. These molecular alterations, including overexpression of receptor-ligand systems, oncogene activation and loss of tumour suppressor genes, leads to a profound disturbance in cell cycle regulation and continuous growth. The molecular findings are now integrated in a pancreatic tumour progression model, with genetically and morphological defined precursor lesions. However, it remains unclear whether the initial target cells of this cancer develop from ductal or acinar cells. This review will present recent emerging questions on the biology of pancreatic cancer with particular emphasis on the cell origin and tumour microenvironment.


Asunto(s)
Carcinoma Ductal Pancreático/genética , Neoplasias Pancreáticas/genética , Carcinoma Ductal Pancreático/patología , Citocinas/fisiología , Genes Supresores de Tumor/fisiología , Humanos , Neoplasias Pancreáticas/patología
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA