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At least 487 records · Page 27Linked to original sources
PubMed1977

Influence of the central nervous system on fetal lung development. Experimental study.

Upper cervical cord injury was produced in fetal rabbits at 22-26 days' gestation. In 11 setuses with severe cord injury delivered at 28-29 days' gestation there was a median reduction in lung weight (expressed as a proportion of body weight) of 43% and a median reduction in estimated total lung DNA of 16% in comparison with paired operated littermates with intact cords. The hypoplastic lungs showed collapse on histology; if cord damage had been inflicted before 24 days' gestation there was retarded maturation. We conclude that the central nervous system plays a vital role in fetal lung growth and maturation, probably by maintenance of fetal respiratory movements.

Animals↗
PubMed1983

Fetal lung development in streptozotocin-induced experimental diabetes: cytidylyl transferase activity, disaturated phosphatidyl choline and glycogen levels.

The influence of streptozotocin-induced maternal diabetes on choline phosphate cytidylyltransferase activity (EC.2.7.7.15) glycogen content and disaturated phosphatidyl choline in fetal lung was studied between 19 and 21 days of gestation. In this experimental model, induction of maternal diabetes two days after mating, resulted in fetal hyperglycemia and hyperinsulinemia; the fetuses were neither macrosomic nor showed any evidence of fetal growth retardation. The glycogen content of lungs on days 19 and 20, but not on day 21 of gestation was significantly higher in fetuses of diabetic rats than in controls. The pulmonary cytosol cytidylyltransferase activity was similar in the two groups of fetuses on days 19 and 20. On day 21 of gestation the enzyme activity was significantly lower in fetuses of diabetic rats than in those of controls. On day 21 of gestation and in newborns of diabetic mothers, although there was no difference in the total pulmonary phospholipids, the levels of disaturated phosphatidyl cholines were significantly lower than in controls.

Animals↗
PubMed2004

Epithelial cell distribution and abundance in rhesus monkey airways during postnatal lung growth and development.

Lung development is both a pre- and postnatal process. Although many lung diseases have their origins in early childhood, few quantitative data are available on the normal growth and differentiation of both the conducting airways and the airway epithelium during the postnatal period. We examined rhesus monkey lungs from five postnatal ages: 4-6 days and 1, 2, 3, and 6 mo. Airways increase significantly in both length and circumference as monkeys increase significantly in body weight from 5 days to 6 mo. In this study we asked: as basement membrane surface area increases, does the epithelial cell organization change? To answer this question, we quantified total epithelial cell mass using high-resolution light micrographs and morphometric techniques on sections from defined airway regions: trachea, proximal intrapulmonary bronchus (generations 1 or 2), and distal intrapulmonary bronchus (generations 6-8). Epithelial thickness decreased in the smaller, more distal, airways compared with trachea but did not change with age in the trachea and proximal bronchus. The volume fraction of all cell types measured did not change significantly. Ciliated cells in the distal bronchus and goblet cells in the trachea both decreased in abundance with increasing age. Overall, the epithelial cell populations changed little in terms of mass or relative abundance to each other during this period of active postnatal lung growth. Regarding the proximal conducting airway epithelium, we conclude that 1) the steady-state abundance is tightly regulated to keep the proportion of cell types constant, and 2) establishment of these cell types occurs before 4-6 days postnatal age. We conclude that growth of the proximal airways occurs primarily in length and lags behind that of the lung parenchyma.

Animals↗
PubMed1975

Growth and development of the fetal Rhesus monkey. VI. Morphometric analysis of the developing lung.

Groups of fetal monkeys were studied at 50, 75, 100, 125 and 150 days gestational age, and postnatal monkeys were studied at 175 days gestational age and in adult life (full term gestation is 168 plus or minus 4 days). The ratios between the various tissues of which lung is composed were determined by light and electronmicroscopy. Characteristic changes in ratios were noted at each developmental age. Primitive bronchioles increased from 50 to 75 days, decreased as permanent bronchioles, alveolar ducts and alveoli developed, and were absent after 150 days. Mesenchymal tissue decreased progressively from 50 to 150 days. Alveoli were present at 100 days gestational age; alveolar lumens accounted for approximately 1/2 the volume of peripheral lung by 150 days, and 2/3 the volume of lung in adult animals. By 150 days alveolar epithelial cells could be identified as Type I (membranous) or Type II (granular) on the basis of the characteristic cytoplasmic lamellar inclusion bodies of the latter. The ratios of the Type II/Type I cells were .21-.23 at 150 and 175 days, and fell to approximately half that value in adult lungs.

Animals↗
PubMed1981

Fetal lung development in surgically induced prolonged gestation.

In our previous study we prolonged gestation in rats with daily subcutaneous injections of progesterone starting on gestation day 20 (P20). To determine whether exogenous progesterone affects the growth of post-term fetal lungs, we utilized surgical techniques to prolong gestation by retaining 4 living fetuses 1, 2, or 3 days beyond the date of spontaneous delivery of the rest of the litter. The retained fetuses were harvested by caesarean section on gestation days 21 through 25. In spite of an improved general appearance in the retained fetuses, there were many similarities between the retained and the post-term P20 fetuses such as: increase in fetal body, kidney and spleen weights; reduction in lung and liver weights; progressive lung atelectasis; loss of lung and liver glycogen; hypoglycemia; and reduction in placenta DNA content. The significant differences between the two were in the amount of lung disaturated phosphatidyl choline (DSPC) and lung DNA (cell number), expressed per lung or per body weight. In contrast to the P20 post-term fetuses, which exhibited a biphasic phenomenon in DSPC and DNA contents, the retained fetuses showed no change in lung DSPC and DNA contents after term. The P20 fetuses had larger adrenals, which increased with prolongation of gestation. The results suggest that exogenous progesterone does not affect the fetal lung growth post-term. It is speculated that the cellularity and the DSPC content of the post-term fetal lung is adversely affected by the degree of fetal distress.

Animals↗
PubMed2006

Lung development and susceptibility to chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease with emphysema has been considered to be an accelerated involutional disease of aging smokers. However, because only a proportion ( approximately 15%) of smokers develop chronic obstructive pulmonary disease with emphysema, clearly genetic susceptibility must play a significant part in determining both the age of onset and the rapidity of decline in lung function. In mice, interference with key genes, either by null mutation, hypomorphism, or gain or loss of function, results in phenotypes comprising either neonatal lethal respiratory distress if the structural effect is severe, or reduced alveolarization and/or early-onset emphysema if the effect is milder. Likewise, null mutants that interfere with matrix assembly and/or integrity, such as elastin, lysyl oxidase, or fibrillin, also result in alveolar dysplasia. Importantly, null mutation of Smad3, which encodes a receptor-activated Smad in the transforming growth factor-beta signaling pathway, results in a more subtle failure to correctly organize the alveolar matrix, which is in turn antecedent to early-onset emphysema mediated by matrix metalloproteinase-9. Furthermore, exposure to side-stream smoke profoundly exacerbates and accelerates alveolar destruction, leading to more severe early-onset emphysema in young Smad3-null mice (unpublished data). Interestingly, polymorphisms in the fibrillin, transforming growth factor-beta type II receptor, and matrix metalloproteinase-9 genes have been described in humans with emphysema. Thus, dysplastic or degraded matrix cannot provide the structural niche for alveolar stem/progenitor cells to assume the correct phenotype and/or repair the alveolar cell lineage niche. The hope is that providing the correct exogenous signals can coax them into doing so.

Age Factors↗
PubMed2002

A T2517C polymorphism in the GSTM4 gene is associated with risk of developing lung cancer.

The human Mu class Glutathione S-Transferases is a family of genes encoding phase II detoxifying enzymes thus playing a significant role in the detoxification of potential carcinogens. While there are many contradicting reports on the association of GSTM1 polymorphisms and cancer development, no studies exist to date describing polymorphisms in GSTM4. We have identified a new C-T polymorphism in intron 6 of the GSTM4 gene (T2517C, Genebank sequence accession number X68677) and termed the allele carrying T at this position allele *A and the allele carrying C, allele *B. Screening a population sample in Merseyside, England, revealed 23 carriers of the *B allele out of 156 healthy control individuals but only 12 carriers of the *B allele out of 163 individuals with lung cancer (O.R.=2.23, Fisher's test P=0.026). The polymorphism did not demonstrate any associations with tumour type, gender, and age at presentation. This is the first report on the implication of a polymorphism in the GSTM4 gene in lung cancer risk. Further studies are required to investigate the relation of this polymorphism to cancer risk to substantiate these findings.

Adult↗
PubMed1999

Genetic alterations in bronchial lavage as a potential marker for individuals with a high risk of developing lung cancer.

Using 12 microsatellite markers, we have studied DNAs from the bronchial lavage of 90 individuals who were referred to an early-lung-cancer clinic in the Northwest of England with suspected lung cancer. Genetic alterations were detected in 15 (35%) of 43 patients with lung cancer but also in 11 (23%) of 47 patients with no cytological or radiological evidence of bronchial neoplasia. No significant differences were found between the referring symptoms in any of the second group of individuals with and without genetic alterations. No correlation was found between smoking exposure and loss of heterozygosity (LOH)/microsatellite alterations (MAs) in the microsatellite markers. On comparing LOH with MAs based on cytology review, we found that the prevalent type of alteration in specimens with cytological evidence of malignancy was LOH; in contrast, the individuals with no cytological evidence of malignancy showed a preponderance of MAs (P = 0.01). Our results indicate that a substantial proportion of cells in the bronchial lavage from suspected lung cancer patients carry identifiable genetic alterations. However, the presence of genetic alterations in the bronchial lavage of individuals with no clinical evidence of lung cancer raises the question whether instability is a phenomenon solely associated with cancer or represents a feature of nonneoplastic diseases. Our results suggest that microsatellite PCR-based assays can be developed as tools for the earlier identification of genetic changes in cells exfoliating in the bronchus.

Adenocarcinoma↗