• Journal of Life Science
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• v.22 no.10
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• pp.1352-1358
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• 2012

In acute lung injury (ALI) by lipopolysaccharide (LPS), the underlying cause of infiltration and migration of neutrophils into the alveoli is considered to be from increased production of platelet-activating factor (PAF) in the pulmonary surfactant lining the alveolar lumen. In this study I partially confirmed this concept. LPS increased lung leak and the infiltration of neutrophils in the lung of rats given LPS intratracheally. The migration of neutrophils into the lung, which had caused oxidative stress, was also morphologically identified. I verified that the metabolism of the pulmonary surfactant was affected and that there was increased production of PAF in the pulmonary surfactant, both of which are considered to contribute to ALI by LPS in rats.

• Tuberculosis and Respiratory Diseases
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• v.40 no.2
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• pp.91-97
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• 1993

Pulmonary surfactant is a lipoprotein complex composed primarily of phospholipid and lung specific apoproteins that reduces surface tension in the alveolus and maintains alveolar stability at low lung volume. Adult respiratory distress syndrome still carries a very high morbidity and mortality. The surfactant system is vital to the maintenance of proper lung function, any type of surfactant deficiency, whether primary or secondary, will contribute significantly to the development of pulmonary pathophysiology. Various mechanisms in adult respiratory distress syndrome may be responsible for such alterations in the surfactant system. Surfactant replacement is now an established treatment for neonatal respiratory distress syndrome, reducing both incidence of complications and mortality. With the current knowledge of surfactant physiology and the pathophysiology of the adult respiratory distress syndrome exogenous surfactant treatment or stimulation of endogenous surfactant synthesis and secretion will prove to be beneficial in preventing and treating the adult respiratory distress syndrome. The study of clinical surfactant therapy for adult respiratory distress syndrome is just beginnig and this can be viewed as an area with exciting potential. As soon as surfactant preparations become more widely available trials should begin to define the role of surfactant treatment in the adult respiratory distress syndrome as an adjunct to available treatment techniques.

• Clinical and Experimental Pediatrics
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• v.57 no.4
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• pp.157-163
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• 2014

Respiratory distress syndrome (RDS) among preterm infants is typically due to a quantitative deficiency of pulmonary surfactant. Aside from the degree of prematurity, diverse environmental and genetic factors can affect the development of RDS. The variance of the risk of RDS in various races/ethnicities or monozygotic/dizygotic twins has suggested genetic influences on this disorder. So far, several specific mutations in genes encoding surfactant-associated molecules have confirmed this. Specific genetic variants contributing to the regulation of pulmonary development, its structure and function, or the inflammatory response could be candidate risk factors for the development of RDS. This review summarizes the background that suggests the genetic predisposition of RDS, the identified mutations, and candidate genetic polymorphisms of pulmonary surfactant proteins associated with RDS.

• The Korean Journal of Physiology
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• v.28 no.1
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• pp.71-77
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• 1994

In the animal model of acute respiratory distress syndrome (ARDS) induced by N-nitroso-N-methylurethane (NNNMU) the secretory activity of alveolar type H cells during acute alveolar injury was investigated by determining phospholipid and pulmonary surfactant associated proteins in crude surfactant. The mechanism of the secretory change was studied by determination of DNA and RNA levels in the lung tissue. After induction of acute alveolar injury with NNNMU, pulmonary hemorrhage, atelectasis and gross hypertrophy were observed. Seven days after NNNMU treatment the level of total DNA in lung homogenate was increased markedly indicating that a hypertrophy was induced by cellular proliferation. Although the total DNA level increased, the RNA/DNA ratio was gradually decreased after NNNMU treatment. Seven days after NNNMU treatment the RNA/DNA ratio returned to the normal control level. During the acute alveolar injury, phospholipid and surfactant associated proteins were reduced significantly as compared with the control, implying that the secretory activity of alveolar type II cells was altered during acute alveolar injury induced by NNNMU. The protein content in crude surfactant during peak injury(7 days after NNNMU) was decreased significantly but phospholipid/protein ratios were identical in both control and NNNMU treatment groups. SDS-PAGE of proteins in crude pulmonary surfactant showed a decrease in major surfactant associated protein(M.W. 38,000) during acute alveolar injury. The present study may suggest that while alveolar type H cells proliferate markedly, transcription of alveolar type ll cell gene was inhibited by an unknown mechanism such as DNA methylation induced by NNNMU. Such an inhibition of transcriptional activity is thought to be associated with the decreased secretory activity of alveolar type ll cells, which may lead to pulmonary atelectasis and edema during the acute alveolar injury.

• Tuberculosis and Respiratory Diseases
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• v.38 no.3
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• pp.228-235
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• 1991

Pulmonary surfactant is a lipoprotein complex composed primarily of phospholipid and lungspecific apoproteins that reduces surface tension in the alveolus and maintains alveolar stability at low lung volume. Three families of lung-specific apoproteins have been described: SP-A, a glycoprotein with a reduced molecular weight of 28~36 KDa. SP-B a hydrophobic protein with a nonreduced molecular weight of 18 KDa, and SP-C a hydrophobic protein with a non-reduced molecular weight of 5~8 KDa. Surfactant proteins have important roles in regulating surfactant metabolism as well as in determining its physical properties. The synthesis of the active surfactant peptides appears to be modulated by system with considerable complexity, including numerous levels of regulation such as cell-specific, hormonal and developmental controls. Endotoxin appears to alter surfactant protein mRNAs differentially. It is hoped that the elucidation of the factors controlling the synthesis and metabolism of the surfactant proteins will aid in understanding the pathogenesis of hyaline membrane disease and offer new avenues for the therapy and diagnosis of ther pulmonary disorders as well.

• Biomedical Science Letters
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• v.2 no.2
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• pp.159-166
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• 1996

In order to investigate the recycling of the pulmonary surfactant in association with morphological changes in macrophage after interleukin-1 $\alpha$ (IL-1) induced lung injury, an acute lung injury was induced by instillation of IL-1 into the trachea. Numbers of neutrophils and phospholipid content were increased significantly(P<0.01) in IL-1 treated BAL(brochoalveolar lavage) compared to control rat. By increased phagocytosis, the lamellar structures in the macrophges of IL-1 treated rats' BAL were increased and the compositions of the cellular organelles were changed in comparison to control rat. This difference in compositions of cellular organelles denotes difference of functions in macrophages between control and IL-1 treated rats. As macrophages have been said to implicate (in the difference in the recycling of pulmonary surfactant, it is highly probable that the difference in compositions of cellular organelles is closely related to the recycling of pulmonary surfactant. In the present study circular structures were synthesized in the cytoplasm of the macrophages in BAL of normal rats. Based on these experimental results, it is suggested that macrohages might synthesize during recycling of surfacuant in the lung.

• Journal of Yeungnam Medical Science
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• v.1 no.1
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• pp.59-66
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• 1984

Although it is well established that steroid is effective for treatment of neonatal respiratory distress syndrome (NRDS), the action mechanism of steroid on NRDS is not well known. Several authors have insisted that steroid increases secretion of pulmonary surfactant from type II pneumocyte, but others have insisted that steroid does not affect the secretory function of the type II pneumocyte. And some authors have suggested that steroid may ca use compositional change of pulmonary surfactant phospholipid. From these aspects, it is desirable to confirm the effect of steroid on (he secretory function of the type II pneumocyte. In order to know the effect of steroid on pulmonary surfactant activity, phospholipid phosphorus of lung lavage was measured and composition of pulmonary surfactant phospholipid of lung lavage was analyzed by thin layer chromatography (TLC) in control (C), pneumonectomized (PN), and pneumonectomized with betamethasone treated (PNS) rabbits. And lung weight and lung weight-body weight ratio were measured in each experimental group also. In PN group, right lung pneumonectomy was performed under general anesthesia with pentobarbital sodium (30mg/kg). On the fifth day after the surgery, the left lung was excised and measured above parameters. In PNS group, pneumonectomy was performed as PN group, and one day after the surgery, betamethasone was injected for four days intramusculary (4mg/day) and rabbits were sacrificed. The experiment yielded following results. PNS group's lung weight was significantly (p<0.01) heavier than C group's, but in comparison with PN group's it showed no significant change. PNS group's L/B ratio was significantly (p<0.05) higher than C group's, but compared with PN group's it showed no significant change. The value of phospholipid phosphorus content of PNS group was significantly (p<0.01) higher than that of C group. Even if the value of phospholipid phosphorus content in PNS group was not significantly higher than that of PN group, it showed increasing tendency compared with that of PN group. And in an analysis of the thin layer chromatogram, quantity (${\mu}mol/gm$ of wet weight lung) of phosphatidylcholine in PNS group decreased significantly (p<0.05) compared with C and PN group. From these results, it may be suggested that though steroid inhibits cellular hyperplasia in the compensatory growing lung, it auguments the secretory function of type II pneumocyte and causes compositional change of pulmonary surfactant phospholipid.

• Neonatal Medicine
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• v.16 no.2
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• pp.101-109
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• 2009

Pulmonary surfactant (PS) therapy in premature infants has a remarkable impact on improving survival and outcomes in neonatal respiratory distress syndrome (RDS). Early PS therapy involves instillation of PS upon delivery of very premature infants or if there is evidence of RDS, such as an increased requirement of oxygen 2 hours after birth, especially in infants <30 weeks gestation. Early PS treatment in very premature infants results in a significant reduction in the severity of RDS, mortality, and incidence of pneumothorax, pulmonary interstitial emphysema, and bronchopulmonary dysplasia in comparison with late PS treatment. According to European and American consensus guidelines on the management of neonatal RDS, early PS instillation should be considered for infants <30 weeks gestation, infants with a birth weight <1,250 g, or if the mother has not received antepartum corticosteroids. We suggest that the Korean health insurance policy on RDS be modified so that PS can be used for better clinical outcomes of very premature infants.

• Journal of Chest Surgery
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• v.24 no.8
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• pp.797-801
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• 1991

Reexpansion pulmonary edema following pneumothorax, atelectasis, massive pleural effusion are clinically uncommon, but sometimes life threatening progression. Reexpansion pulmonary edema is usually ipsilateral but rarely contralateral or both. Reexpansion pulmonary edema was occurred when chronically collapsed lung is rapidly reexpanded by evacuation of large amounts of air or fluid. The pathogenesis of the reexpansion pulmonary edema is unknown but is probably mutifactorial. The etiological factors of the reexpansion pulmonary edema are chronicity of the lung collapse, technique of the reexpansion, airway obstruction, loss of the surfactant, and pulmonary artery pressure changes. In the treatment of the chronically collapsed lung, physician must be remembered the possible events, and to prevent of the complication.

• Journal of Nutrition and Health
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• v.27 no.9
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• pp.940-948
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• 1994

The present study was designed to determine if prenatal and postnatal Se nutriture affects Se concentration, glutathione peroxidase(GSHPx) activity and phospholipid distribution of the neonatal rat lung. Female SD rats were bred and fed a semipurified Se-deficient(0.04ppm, Se-) or a Se-adequate(0.5ppm, Se+) diet through pregnancy and lactation. On d 2 of lactation, maternal dietary Se had no significant effect on pulmonary Se concentration of pups. On d 16 of lactation, mean milk Se concentration in Se- dams was significantly lower than that in Se+ dams. Milk Se concentration was reflected on lung Se concentration and GSHPx activity of d 16 pups, which were dramatically decreased in Se- pups. In addition, pulmonary disaturated phosphatidyl choline/total phosphatidyl choline ratio was also significantly decreased in Se- pups, implying impaired function of pulmonary surfactant. These data indicate that adequate Se nutrition is important in the maturation of neonatal rat lungs.