Lung growth and development

Joshi, Suchita; Kotecha, Sailesh

doi:10.1016/j.earlhumdev.2007.09.007

Cited by 204 publications

(142 citation statements)

References 26 publications

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“…Infants born at 32 wk gestational age or less have underdeveloped lungs with impaired gas exchange (2). Most of these premature infants are at high risk of respiratory failure (3) and their primary care involves the promotion of respiratory function.…”

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confidence: 99%

Effect of time and body position on ventilation in premature infants

2016

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confidence: 99%

Effect of time and body position on ventilation in premature infants

2016

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“…Any condition that produces oligo-hydramnios (e.g., fetal renal insufficiency or prolonged premature rupture of membranes) may also lead to diminished lung growth. In these conditions, airway and arterial branching are inhibited, thereby limiting the capacity for capillary and gas exchange surface area 1,8,10 Development of the bronchial tree takes place at about 26th to 31st day of intrauterine life. Monaldi divided the mal-development of lung in four groups.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Hypoplasia with Pulmonary Tuberculosis in Healthy Infant A Case Report:-

Mushtaq¹,

Bhat²,

Wani³

et al. 2017

IOSR JDMS

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“…Previous studies in our laboratory have found these high levels of CSE to be cytotoxic. Fetal growth and development is influenced by intrauterine environment and governed by physical, environmental and hormonal factors [27]. This environment is carefully regulated and consists of various hormones including vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) [27].…”

Section: Discussionmentioning

confidence: 99%

“…Fetal growth and development is influenced by intrauterine environment and governed by physical, environmental and hormonal factors [27]. This environment is carefully regulated and consists of various hormones including vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) [27]. Both of these hormones contribute to type II alveolar cell differentiation as well as production and secretion of surfactant phospholipids and proteins [27].…”

Section: Discussionmentioning

confidence: 99%

“…This environment is carefully regulated and consists of various hormones including vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) [27]. Both of these hormones contribute to type II alveolar cell differentiation as well as production and secretion of surfactant phospholipids and proteins [27]. Moreover, alterations in the intra-uterine environment due to exposure to cigarette smoke may affect lung function [28].…”

Section: Discussionmentioning

confidence: 99%

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Cigarette Smoke Induces Apoptosis by Activation of Caspase-3 in Isolated Fetal Rat Lung Type II Alveolar Ep-ithelial Cells <i>in Vitro</i>

Ahmed¹,

Thliveris²,

Shaw³

et al. 2013

OJRD

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Smoking during pregnancy is a major source of fetal exposure to numerous harmful agents present in tobacco smoke. Lung development involves complex biochemical processes resulting in dramatic changes which continue even after birth. In addition to type I cells which form the blood-air barrier, type II alveolar epithelial (AE) cells have important and diverse functions related to immunological protection and stabilization of the alveolus through synthesis and secretion of the pulmonary surfactant. Apoptosis or programmed cells death is an important physiological process during lung embryogenesis and for the proper maintenance of homeostasis. Caspases are proteases that play important roles in regulating apoptosis. Caspase-3 is the key executioner caspase in the cascade of events leading to cell death by apoptosis. We explored the hypothesis that cigarette smoke extract (CSE) induces apoptosis in fetal rat lung type II AE cells by activation of caspase-3. To analyze these factors, isolated fetal rat lung type II AE cells were used. The cells were exposed to different concentrations of CSE (5%, 10% or 15%) (v/v) for 60 min. The results of the present study showed that CSE induced apoptosis in fetal rat lung type II AE cells with a significant increase (p < 0.05) in caspase-3 activity and decrease in cell proliferation at CSE concentrations of 10% and 15% (v/v). These observations indicate that cigarette smoke extract induces apoptosis by activation of caspase-3 in fetal rat lung type II AE cells in a dose-dependent manner and may potentially alter the regulated development of the lung and the appearance of the surfactant-producing type II alveolar cells which are critical for the establishment of adequate gas exchange at birth.

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Lung growth and development

Cited by 204 publications

References 26 publications

Effect of time and body position on ventilation in premature infants

Effect of time and body position on ventilation in premature infants

Pulmonary Hypoplasia with Pulmonary Tuberculosis in Healthy Infant A Case Report:-

Cigarette Smoke Induces Apoptosis by Activation of Caspase-3 in Isolated Fetal Rat Lung Type II Alveolar Ep-ithelial Cells <i>in Vitro</i>

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Lung growth and development

Cited by 204 publications

References 26 publications

Effect of time and body position on ventilation in premature infants

Effect of time and body position on ventilation in premature infants

Pulmonary Hypoplasia with Pulmonary Tuberculosis in Healthy Infant A Case Report:-

Cigarette Smoke Induces Apoptosis by Activation of Caspase-3 in Isolated Fetal Rat Lung Type II Alveolar Ep-ithelial Cells &lt;i&gt;in Vitro&lt;/i&gt;

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Cigarette Smoke Induces Apoptosis by Activation of Caspase-3 in Isolated Fetal Rat Lung Type II Alveolar Ep-ithelial Cells <i>in Vitro</i>