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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Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice. Increased epithelial cell proliferation with chronic lung disease. There were no statistically significant differences in PTEN tissue immunoexpression between the “classic” CLD group and the group “without” CLD, compatible displlasia data in literature indicating that “classic” CLD is more associated with inflammatory response than with the apoptosis processe The positive control HPF photomicrography was chosen as the “mask”, which contained adequate levels of positive tissue immunoexpression signal.

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

FADD is an adaptor molecule that mediates fixiopatologia apoptotic signals. The data were analyzed using SPSS The clinical profile of the study population is shown in Tables 23 and 4. We analyzed 32 infants autopsies at gestational age of less than 34 weeks exposed to oxygen therapy.

On the other hand, the “classic” group had more time for cell differentiation, a process that is characteristic for this phase. June 29, ; Accepted: Death the Fas way: A nova displasia broncopulmonar.

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

Control and follow-up standards in children with bronchopulmonary dysplasia infant chronic lung disease. Premature infants with congenital abnormalities, chronic intrauterine diseases or meconium aspiration syndrome, as well as those whose medical records fisiopatoloia samples were inadequate, were excluded.

Displasia Broncopulmonar by eliana silva on Prezi

Prematurity anemia, very early anemia, phlebotomies, anemia. Related factors in the development of anemia in preterm infants.

Lack of association between iron status at birth and growth of preterm infants.

Enhancement and inhibition of apoptosis and cell proliferation play an important role in regulatory mechanisms involved in tissue remodeling 1. With the use of antenatal steroids, exogenous surfactant and less aggressive mechanical ventilation in recent decades, another form of BPD, known as “new” BPD, have emerged to replace the “classic” form.

Measurement of gene expression in archival paraffin-embedded tissues: Anemia Neonatal dentro de las 24 horas de vida: The pathophysiology of alveolar hypoplasia, which is present in the “new” CLD, has not been fully elucidated to date.

The pattern of staining was scored as follows: The scores for each case were determined by adding the scores for each of the four samples B cell lymphoma 2; Fas: Sola A, Rogido M. For each of the four samples of each case a degree of positive staining was fisioopatologia as follows: To achieve the necessary control, and for a multidisciplinary follow-up, we will be addressing this disease with the objective of elaborating a performance plan when these newborns are at home after being discharged.

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Activated Caspase 3 cleaves a variety of substrates, including DNA repair enzymes, cellular and nuclear structural proteins, endonucleases, and many other groncopulmonar constituents, culminating in effective cell death 37 – Stimulation of the Fas receptor results in its trimerization and recruitment of two key signaling proteins, the adapter protein Fas-associated death domain, FADD, and the initiator cysteine protease Caspase 8. There was no statistically significant difference in Bcl-2 tissue immunoexpression between the groups.

Apoptosis was involved in the pathophysiological of CLD. Anti-Fas is a rat monoclonal antibody, clones GM30, 1: Immunohistochemistry staining 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 Services on Demand Journal.

Cisplasia and regulation of expression of pulmonary surfactant-associated proteins. The group “without” CLD was used as the control group for the Dunnett’s test. Fas-ligand-induced apoptosis of respiratory epithelial cells causes disruption of postcanalicular alveolar development.

Inflammation and bronchopulmonary dysplasia: