ABSTRACT
Paciente de género femenino de 51 años que en una revisión de rutina se observó lesión sospechosa de mama derecha, BIRADS IVa. Patología reportó cáncer ductal infiltrante moderadamente diferenciado con dos focos de carcinoma invasor separados de 2 y 1 mm, receptores de estrógeno y progesterona positivos. El cáncer de mama familiar abarca entre el 5 por ciento al 10 por ciento de cáncer de mama de la población en general. Los genes involucrados en este padecimiento son: BRCA1 en 20 por ciento, BRCA 2 en 20 por ciento, CHEK2 en 5 por ciento, TP 53 en 1 por ciento, sin embargo, en más del 50 por ciento de los casos se desconoce en gen asociado. El BRCA1 es un gen localizado en el cromosoma 17q21, supresor de tumor, involucrado en la regulación del ciclo celular, reparación del ADN dañado, mantenimiento de la estabilidad genómica y regulación de la transcripción. Existen indicaciones precisas para la búsqueda intencionada del gen BRCA en pacientes con historia familiar o personal de cßncer de mama y ovario.
51 year old female found on check up a suspicious lesion in right breast, BIRADS IVa. Pathology reported a ductal infiltrative moderately differentiated cancer with two separate carcinomas of 2 and 1 mm each, progesterone and estrogen receptors. Familiar breast cancer is calculated to be about 5-10 percent of all breast cancers. The genes involved are: BCRA1 in 20 percent, BRCA2 in 20 percent, CHEK2 in 5 percent, TP 53 in 1 percent, although more than 50 percent of cases are not associated with a gen. BRCA1 is a gene in chromosome 17q21, tumor suppressor, involved in the regulation of the cellular cycle, repair of damaged DNA, maintenance of genomic stability and regulation of transcription. Specific indications are in use for BCRA gene scouting in women with family or personal history of breast or ovary cancer.
Subject(s)
Humans , Female , Middle Aged , Carcinoma, Ductal, Breast/genetics , Genes, BRCA1 , Genetic Predisposition to Disease , Breast Neoplasms/genetics , MutationABSTRACT
BACKGROUND: This study evaluates whether bosentan (endothelin [ET] receptor antagonist) or preconditioning (mechanism that inhibits the postischemic ET release) could reduce the microvascular disorders and the injurious effects of tumor necrosis factor (TNF) associated with hepatic ischemia-reperfusion (I/R). METHODS: Hepatic I/R was induced in rats and the effects of bosentan or preconditioning on the deleterious effects of ET in hepatic I/R were evaluated. Transaminase and TNF levels in plasma; edema, vascular permeability, lactate, ET, and TNF levels in liver; and edema and myeloperoxidase activity levels in lung were measured after hepatic reperfusion. RESULTS: The administration of bosentan or the induction of preconditioning previous to I/R attenuated the increase in vascular permeability, edema and lactate levels observed in liver after I/R. However, the addition of ET before preconditioning abolished its benefits. Preconditioning prevented both the increase in hepatic TNF and its release from the liver into the systemic circulation. This resulted in an attenuation of liver and lung damage. Addition of ET or TNF to the preconditioned group abolished the benefits of preconditioning, whereas the previous inhibition of TNF release with GdCl3 in the preconditioned group pretreated with ET did not modify the effects of preconditioning. The inhibition of ET with bosentan prevented the increase of both hepatic and plasma TNF, thus attenuating the liver and lung injury, whereas TNF addition abolished the benefits of bosentan. CONCLUSIONS: These findings suggest that both bosentan and preconditioning, by inhibition of ET could attenuate the microvascular disorders and the deleterious effect of TNF on the liver and lung elicited by hepatic I/R.
Subject(s)
Endothelin-1/physiology , Liver Transplantation/adverse effects , Liver/blood supply , Liver/injuries , Reperfusion Injury/prevention & control , Animals , Bosentan , Endothelin-1/antagonists & inhibitors , Liver/physiopathology , Liver Transplantation/physiology , Lung Injury , Male , Microscopy, Electron , Rats , Rats, Wistar , Reperfusion Injury/etiology , Reperfusion Injury/physiopathology , Sulfonamides/pharmacology , Transplantation Conditioning , Tumor Necrosis Factor-alpha/physiologyABSTRACT
Long mitochondria containing paracrystalline inclusions have been detected in the epithelial cells of the basal layer of the rat ureter close to the bladder (Barastegui and Ruano-Gil, 1978). In the first part of this investigation the origin of these inclusions from alterations of the cristae has been suggested. The current report deals with an analysis by microdensitometry, optical diffraction and goniometry of the inclusions as well as with their possible architecture. A tridimensional model of the paracrystalline inclusions is proposed.
