Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros

Banco de datos
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Rom J Morphol Embryol ; 51(4): 633-40, 2010.
Artículo en Inglés | MEDLINE | ID: mdl-21103619

RESUMEN

UNLABELLED: The systemic lupus erythematosus (SLE), a systemic autoimmune disorder with a multifactorial etiology, is characterized by the presence of autoantigens in some organs and tissues that induce the development of some antibodies with extended binding and with various specificities. The presence of antibodies is accompanied by disbalances in the immune cellular response, including alterations in the production of some cytokines. Cytokines, quite a heterogeneous group of protein molecules produced in small quantities by certain specifically stimulated cells, have the capacity to maintain the communication between different cell populations that participate in the immune response (messengers of the immune system), thus modeling a defense function. OBJECTIVES: The purpose of the study is to estimate the seric levels of some proinflammatory, anti-inflammatory and immunomodulating cytokines in patients diagnosed with SLE, as well as some correlations between the seric levels of these cytokines and the histopathological aspects. MATERIAL AND METHODS: There were included in the study 35 patients diagnosed with SLE (active÷remission stage of the disorder), in whom there were determined, before administering the treatment with the immunoenzymatic technique ELISA, the seric level of the following cytokines: interleukins (IL) IL-2, IL-6, IL-8, IL-10, and the tumor necrosis factor-alpha (TNF-alpha). The obtained results in the patients were compared to those observed in a control group, made up of 35 healthy subjects. RESULTS: The IL-2 production of T-lymphocytes was a deficient one (low seric levels in the majority of the patients), while cytokines IL-6, IL-8 and TNF-alpha showed high seric levels. IL-10 plays a very important role in the SLE pathogeny, through the high seric levels, and it may be involved, as a predictive biological marker, in the quantification of the activity degree of the disorder. CONCLUSIONS: SLE represents an autoimmune disorder, characterized, among others, by a disbalance in the cytokine network. Signaling and regulating abnormalities of B-lymphocytes by cytokines are responsible of the excessive production of antibodies. IL-6 and IL-10 were proved to be key factors in the intensification of the inflammation and regulation of B-lymphocytes activity, by their polyclonal activation. Alongside TNF-alpha, they play an important part in the development of severe dermo-epidermal alterations.


Asunto(s)
Citocinas/sangre , Lupus Eritematoso Sistémico/inmunología , Lupus Eritematoso Sistémico/patología , Adulto , Linfocitos B/inmunología , Estudios de Casos y Controles , Femenino , Humanos , Mediadores de Inflamación/sangre , Interleucinas/sangre , Masculino , Linfocitos T/inmunología , Factor de Necrosis Tumoral alfa/sangre
2.
Curr Health Sci J ; 40(2): 85-92, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25729587

RESUMEN

Pseudomonas aeruginosa genus bacteria are well known for their increased drug resistance (phenotypic ang genotypic resistance). The most important resistance mechanisms are: enzyme production, reduction of pore expression, reduction of the external membrane proteins expression, efflux systems, topoisomerase mutations. These mechanisms often accumulate and lead to multidrug ressitance strains emergence. The most frequent acquired resistance mechanisms are betalactamase-type enzyme production (ESBLs, AmpC, carbapenemases), which determine variable phenotypes of betalactamines resistance, phenotypes which are associated with aminoglycosides and quinolones resistance. The nonenzymatic drug resistance mechanisms are caused by efflux systems, pore reduction and penicillin-binding proteins (PBP) modification, which are often associated to other resistance mechanisms. Phenotypic methods used for testing these mechanisms are based on highlighting these phenotypes using Kirby Bauer antibiogram, clinical breakpoints, and "cut off" values recommended by EUCAST 2013 standard, version 3.1.

SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA