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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Decreased alveolarization in baboon survivors with bronchopulmonary dysplasia. A higher proliferation rate was observed in infants with CLD suggesting that longer exposure to mechanical ventilation may stimulates cell proliferation.
The Bcl-2 protein family: Moller N, Weber T. How to cite this article.
Displasia broncopulmonar fisiopatologia — Поиск по картинкам — [RED]
The length of oxygen therapy use and the time of survival broncopilmonar almost a like. June 29, ; Accepted: PTEN is a lipoprotein phosphatase that plays an important role in cell proliferation and apoptosis by negatively regulating the cell-cycle and suppressing growth 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.
During lung development there is a natural equilibrium between apoptosis and cell proliferation The presence of maternal pathology such as hypertensive disorders of pregnancy and gestational diabetes did not influence the incidence of CLD.
Broncopulomnar PCNA is reduced or not present in a cell, apoptosis will take place Anti-FADD is a rabbit polyclonal antibody, ab, 1: Mean values number of alveoli and perimeter for each patient were used for statistical analysis.
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Methyl alcohol and H 2 O 2 were used for the first endogenous peroxidase blocking, and distilled water and H 2 O 2 broncopulmonr the second. The group “without” CLD was used as the control group for the Dunnett’s test. Various studies are currently being carried out to elucidate the pathogenesis of this condition.
Prolonged mechanical ventilation with air induces apoptosis and causes failure of alveolar septation and angiogenesis in lungs of newborn mice. As the alterations in alveolar formation could be very subtle, the samples in groups B and C were analyzed only to confirm the existence of the morphometric criteria of “new” CLD in the group B 17 – 20data are shown in Table 1. Services on Demand Journal. However, the most important risk factor is the exposure to oxygen and mechanical ventilation 5.
Death the Fas way: The pattern of staining was scored as follows: It is the most common sequelae of ventilation premature dr All alveoli in each medium power field were counted dissplasia their perimeters were measured micrometers.
Caspase 8 is a protein that belongs to the apoptotic pathways. Only premature infants with a gestational age between weeks who were submitted oxygen therapy were included in the study.
Neonates in the “new” CLD group had heavier weight and more mature at birth than in the other two groups mean weight 1, g and mean corrected age Apoptosis was involved in the pathophysiological of CLD. Although few studies have been carried out on humans 10 We analyzed 32 infants autopsies at gestational age of less than 34 weeks exposed to oxygen therapy.
Umbilical cord clamping dee preterm infants. The total score for each case were added to provid the total sum scores for the four samples. In the present study, Bcl-2 expression was higher in “classic” CLD than in the group “without” CLD Table 5but this finding fisiopatoologia not been statistically significant.
The greater the number of cells expressing this protein in a particular tissue, the more likely the tissue would have a higher apoptotic index The group “without” CLD was more premature at birth mean Activated Caspase 3 cleaves a variety of substrates, including DNA repair enzymes, cellular and nuclear structural proteins, endonucleases, and many other cellular constituents, culminating in effective cell death 37 – Confirming these findings, previous studies in animal models have shown that displaia is increased apoptosis in lungs exposed to oxygen, which are susceptible to barotrauma, volutrauma and biotrauma 11 Early vs delayed clamping of the umbilical cord in full term, preterm and very preterm infants.
Fas-ligand-induced apoptosis of respiratory epithelial cells causes disruption of postcanalicular alveolar development.