FISIOPATOLOGIA DE LA DISPLASIA BRONCOPULMONAR PDF

Parte 1: Epidemiología, fisiopatología y clínica. Seguimiento neumológico de los niños con displasia broncopulmonar al alta de la Unidad de Cuidados. Epidemia de displasia broncopulmonar: incidencia y factores asociados en una cohorte de niños prematuros en Bogotá, Colombia. Juan G. Ruiz-Peláez1,2,3. Displasia Broncopulmonar. ES. eliana silva. Updated 6 September Transcript. Displasia Broncopulmonar Diagnostico general. Nesecidad de mantener.

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Se fisplasia los factores maternos, presencia de anemia cercana al nacimiento y antecedentes de gestorragias de la segunda mitad. The “classic” CLD group received oxygen and presented longer survival Tissue microarrays were collected from lung samples from all the cases and analyzed immunohistochemically four samples for each case with 3 mm diameter eachsince this is the most suitable technique to analyze protein expression in this type of material 17 There were no statistically significant differences in PTEN tissue hroncopulmonar between the “classic” CLD group and the group “without” CLD, compatible with data in literature indicating that “classic” CLD is more associated with inflammatory response than with the fisiopatloogia processe This is an Open Access article distributed under the terms of the Creative Commons Displasix License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

We analyzed 32 infants autopsies at gestational age of less than 34 weeks exposed to oxygen therapy. These findings may be associated with the ability of a pulmonary cell to proliferate in response to mechanical strain 3334knowing that the “classic” form was submitted to mechanical ventilation for more days than the group “without” CLD.

The pathological bronxopulmonar of the “classic” form showed an obliterative bronchiolitis, an interstitial fibrosis that is compatible with proliferative activity.

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How to cite this article. TRADD was not submitted to morphometric analysis because most cases were negative for this protein.

Subsequent activation of the effector caspases through mitochondria dependent or independent pathways results in activation of Caspase 3, the key effector caspase.

Morphometric analysis The formalin-fixed paraffin-embedded lung tissue samples were reexamined and classified into one of the three groups according to the histopathological and morphometric changes without considering the clinical data: Studies in animal models and cell cultures show that apoptosis increases in the lungs of premature infants exposed to oxygen and mechanical ventilation 11 – The total score for each case were added to ve the total sum scores for the four samples.

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El universo de estudio estuvo constituido por 25 neonatos. Decreased alveolarization in baboon survivors with bronchopulmonary dysplasia.

Mechanical strain-induced proliferation and signaling in pulmonary epithelial H cells.

Pathogenesis and pathology of COPD. Peng H, Tong XM. However the postnatal infection bronchopneumonia, necrotizing enterocolitis and sepsis was greater in the “classic” CLD group, showing that infection could increase the risk of developing CLD, or because these neonates might be more exposed to oxygen and mechanical ventilation.

It is important to bear in mind that we use only pathological criteria to define these three groups, without considering the clinical data. Regarding the exposure to oxygen, some studies with cell cultures showed that hyperoxia inhibits cell proliferation 1314while another study say the opposite Proliferating cell nuclear antigen PCNA: Services on Demand Journal. The presence of maternal pathology such as hypertensive disorders of pregnancy and gestational diabetes did not influence the incidence of CLD.

From the pathological point of view, a injury and repair process, with early alveolar and interstitial inflammation and fibrosis, characterizes “classic” CLD.

Displasia broncopulmonar fisiopatologia — Поиск по картинкам — [RED]

B cell lymphoma 2; Fas: Moller N, Weber T. Bienvenido a siicsalud Contacto Inquietudes. For PTEN and Bcl-2, a score was assigned according to fisiopatooogia degree of positive staining as well broncouplmonar a pattern of staining. Immunohistochemical analysis of apoptosis and cell proliferation in lungs of premature infants with chronic lung disease bronchopulmonary dysplasia.

A study by Hargitai inalso found a high apoptotic index in alveolar and bronchial cells in lungs with BPD.

Bronchopulmonary dysplasia an update. Increased apoptosis “new” form and cell proliferation in lungs with CLD were observed in this study. J Bras Patol Med Lab. Inflammation and bronchopulmonary dysplasia. In the literature, the function of Caspase 3 is not clear, Caspase 3 could be involved in the pathophisiology of oxygen and ventilation inducing apoptosis The aim of this study is to investigate the expression of the proteins involved in the cell-cycle [proliferating cell nuclear antigen PCNAphosphatase and tensin homolog PTENB cell lymphoma 2 Bcl-2death receptor FasFas-associated protein with death domain FADDtumor necrosis factor receptor type 1-associated death domain protein TRADDcysteine-aspartic acid protease 3 Caspase 3 and cysteineaspartic acid protease 8 Caspase 8 ] in lung autopsy samples from premature infants that required assisted ventilation, with pathological evidence of “classic” or “new” CLD, and compare them to the expression of the same proteins in newborns without pathological evidence of CLD.

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It is known that apoptosis and cell proliferation are implicated in this process and that pulmonary exposure to oxygen and cyclic stretching in mechanical ventilation can trigger changes in the cell-cycle, particularly changes in apoptosis For each case, an average percentage of positive area was determined in 12 HPF images.

Anemia muy precoz del prematuro con peso ≤ 1 g:: prevalencia y factores asociados

Aberrant signaling pathways of the lung mesenchyme and their contributions to the pathogenesis of bronchopulmonary dysplasia. Statistically significant differences were found when expression of the proteins was analyzed. However, the most important risk factor is the exposure to oxygen and mechanical ventilation 5.

Camila M, Chaparro P.

Loss of this equilibrium may result in chronic lung pathologies in newborns as a result of impaired vascular and alveolar growth. Measurement of gene expression in archival paraffin-embedded tissues: The data were analyzed using SPSS Prediction of transfusions in extremely low-birthweight infants in the erythropoietin era.

Early versus delayed umbilical cord clamping in preterm infants. Active Caspase 8 initiates the subsequent cascade of caspases mediating apoptosis, and then FADD binding to Fas receptor is degraded.

The greater the number of cells expressing this protein in a particular tissue, the more likely the tissue would have a higher apoptotic index PTEN is a lipoprotein phosphatase that plays an important role in cell proliferation and apoptosis by negatively regulating the cell-cycle and suppressing growth

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