Normal Lung Structure and Pulmonary Function in a Twin with Agenesis of the Cloacal Membrane and Persistent Severe Oligohydramnios

1992 ◽  
Vol 1 (1) ◽  
pp. 24-28 ◽  
Author(s):  
David M. Sherer ◽  
David M. Sherer ◽  
Susan A. Smith ◽  
Carol L. Cusson ◽  
Leon A. Metlay ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Normal Lung ◽  
Cloacal Membrane ◽  
Lung Structure

scholarly journals Tenascin-C: Friend or Foe in Lung Aging?

2021 ◽  
Vol 12 ◽  
Author(s):  
Sandrine Gremlich ◽  
Tiziana P. Cremona ◽  
Eveline Yao ◽  
Farah Chabenet ◽  
Kleanthis Fytianos ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Smooth Muscle Actin ◽  
Lung Parenchyma ◽  
Normal Lung ◽  
Matricellular Protein ◽  
Ecm Remodeling ◽  
Tenascin C ◽  
Lung Structure ◽  
Regulatory Functions ◽  
Lung Aging

Lung aging is characterized by lung function impairment, ECM remodeling and airspace enlargement. Tenascin-C (TNC) is a large extracellular matrix (ECM) protein with paracrine and autocrine regulatory functions on cell migration, proliferation and differentiation. This matricellular protein is highly expressed during organogenesis and morphogenetic events like injury repair, inflammation or cancer. We previously showed that TNC deficiency affected lung development and pulmonary function, but little is known about its role during pulmonary aging. In order to answer this question, we characterized lung structure and physiology in 18 months old TNC-deficient and wild-type (WT) mice. Mice were mechanically ventilated with a basal and high tidal volume (HTV) ventilation protocol for functional analyses. Additional animals were used for histological, stereological and molecular biological analyses. We observed that old TNC-deficient mice exhibited larger lung volume, parenchymal volume, total airspace volume and septal surface area than WT, but similar mean linear intercept. This was accompanied by an increase in proliferation, but not apoptosis or autophagy markers expression throughout the lung parenchyma. Senescent cells were observed in epithelial cells of the conducting airways and in alveolar macrophages, but equally in both genotypes. Total collagen content was doubled in TNC KO lungs. However, basal and HTV ventilation revealed similar respiratory physiological parameters in both genotypes. Smooth muscle actin (α-SMA) analysis showed a faint increase in α-SMA positive cells in TNC-deficient lungs, but a marked increase in non-proliferative α-SMA + desmin + cells. Major TNC-related molecular pathways were not up- or down-regulated in TNC-deficient lungs as compared to WT; only minor changes in TLR4 and TGFβR3 mRNA expression were observed. In conclusion, TNC-deficient lungs at 18 months of age showed exaggerated features of the normal structural lung aging described to occur in mice between 12 and 18 months of age. Correlated to the increased pulmonary function parameters previously observed in young adult TNC-deficient lungs and described to occur in normal lung aging between 3 and 6 months of age, TNC might be an advantage in lung aging.

Il-17A contributes to maintenance of pulmonary homeostasis in a murine model of cigarette smoke-induced emphysema

2015 ◽  
Vol 309 (2) ◽  
pp. L188-L195 ◽  
Author(s):  
Meike Voss ◽  
Lisa Wolf ◽  
Andreas Kamyschnikow ◽  
Bodo Wonnenberg ◽  
Anja Honecker ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Cigarette Smoke ◽  
Murine Model ◽  
Lung Damage ◽  
Disease Assessment ◽  
Normal Lung ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Lung Structure ◽  
Induced Changes

Smoking is the main risk factor for the development of the chronic obstructive pulmonary disease (COPD) in Western countries. Recent studies suggest that IL-17A and Th17 cells play a role in the pathogenesis of COPD. We used a murine model of chronic cigarette smoke (CS) exposure to explore the contribution of IL-17A to CS-induced lung damage and loss of pulmonary function. Histology and morphometry showed that IL-17A deficiency spontaneously resulted in a loss of lung structure under basal conditions. Even though inflammatory markers [IL-1β and granulocyte colony-stimulating factor (G-CSF)] were decreased in IL-17A-deficient mice (IL-17A−/−) exposed to CS compared with wild-type (WT) mice, IL-17A−/− mice were per se not protected from CS-induced emphysematous disease. Assessment of pulmonary function showed that IL-17A−/− mice were partially protected from CS-induced changes in total lung capacity. However, the respiratory elastance decreased and respiratory compliance increased in IL-17A−/− mice after exposure to CS. Morphometry revealed destruction of lung tissue in CS-exposed IL-17A−/− mice similar to WT mice. The expression of elastin was decreased in air-exposed IL-17A−/− mice and in CS-exposed WT and IL-17A−/− mice. Thus, in the present model of sterile CS-exposure, IL-17A contributes to normal lung homeostasis and does not mediate CS-induced loss of lung structure and pulmonary function.

scholarly journals CT densitovolumetry in children with obliterative bronchiolitis: correlation with clinical scores and pulmonary function test results

2013 ◽  
Vol 39 (6) ◽  
pp. 701-710 ◽  
Author(s):  
Helena Mocelin ◽  
Gilberto Bueno ◽  
Klaus Irion ◽  
Edson Marchiori ◽  
Edgar Sarria ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Function Test ◽  
Clinical Score ◽  
Obliterative Bronchiolitis ◽  
Normal Lung ◽  
Test Results ◽  
Air Trapping ◽  
Clinical Scores ◽  
Function Test ◽  
Minute Walk

OBJECTIVE: To determine whether air trapping (expressed as the percentage of air trapping relative to total lung volume [AT%]) correlates with clinical and functional parameters in children with obliterative bronchiolitis (OB).METHODS: CT scans of 19 children with OB were post-processed for AT% quantification with the use of a fixed threshold of −950 HU (AT%950) and of thresholds selected with the aid of density masks (AT%DM). Patients were divided into three groups by AT% severity. We examined AT% correlations with oxygen saturation (SO2) at rest, six-minute walk distance (6MWD), minimum SO2 during the six-minute walk test (6MWT_SO2), FVC, FEV1, FEV1/FVC, and clinical parameters.RESULTS: The 6MWD was longer in the patients with larger normal lung volumes (r = 0.53). We found that AT%950 showed significant correlations (before and after the exclusion of outliers, respectively) with the clinical score (r = 0.72; 0.80), FVC (r = 0.24; 0.59), FEV1 (r = −0.58; −0.67), and FEV1/FVC (r = −0.53; r = −0.62), as did AT%DM with the clinical score (r = 0.58; r = 0.63), SO2 at rest (r = −0.40; r = −0.61), 6MWT_SO2 (r = −0.24; r = −0.55), FVC (r = −0.44; r = −0.80), FEV1 (r = −0.65; r = −0.71), and FEV1/FVC (r = −0.41; r = −0.52).CONCLUSIONS: Our results show that AT% correlates significantly with clinical scores and pulmonary function test results in children with OB.

Inhaled NO restores lung structure in eNOS-deficient mice recovering from neonatal hypoxia

2006 ◽  
Vol 291 (1) ◽  
pp. L119-L127 ◽  
Author(s):  
Vivek Balasubramaniam ◽  
Anne M. Maxey ◽  
Danielle B. Morgan ◽  
Neil E. Markham ◽  
Steven H. Abman
Keyword(s):  
Nitric Oxide ◽  
Nodal Point ◽  
Fold Increase ◽  
Normal Lung ◽  
Lung Growth ◽  
Vascular Growth ◽  
Neonatal Hypoxia ◽  
Compensatory Lung Growth ◽  
Lung Structure ◽  
Inhaled No

We have previously shown that neonatal mice deficient in endothelial nitric oxide synthase (eNOS−/−) are more susceptible to hypoxic inhibition of alveolar and vascular growth. Although eNOS is downregulated, the role of nitric oxide (NO) during recovery after neonatal lung injury is poorly understood. We hypothesized that lung vascular and alveolar growth would remain impaired in eNOS−/− mice during recovery in room air and that NO therapy would augment compensatory lung growth in the eNOS−/− mice during recovery. Mice (1 day old) from heterozygous (eNOS+/−) parents were placed in hypobaric hypoxia (FiO2= 0.16). After 10 days, pups were to recovered in room air (HR group) or inhaled NO (10 parts/million; HiNO group) until 3 wk of age, when lung tissue was collected. Morphometric analysis revealed that the eNOS−/− mice in the HR group had persistently abnormal lung structure compared with eNOS-sufficient (eNOS+/+) mice (increased mean linear intercept and reduced radial alveolar counts, nodal point density, and vessel density). Lung morphology of the eNOS+/− was not different from eNOS+/+. Inhaled NO after neonatal hypoxia stimulated compensatory lung growth in eNOS−/− mice that completely restored normal lung structure. eNOS+/− mice (HR group) had a 2.5-fold increase in lung vascular endothelial growth factor (VEGFR)-2 protein compared with eNOS+/+ ( P < 0.05). eNOS−/− mice (HiNO group) had a 66% increase in lung VEGFR-2 protein compared with eNOS−/− (HR group; P < 0.01). We conclude that deficiency of eNOS leads to a persistent failure of lung growth during recovery from neonatal hypoxia and that, after hypoxia, inhaled NO stimulates alveolar and vascular growth in eNOS−/− mice.

A human acinar structure for simulation of realistic alveolar plateau slopes

2000 ◽  
Vol 89 (5) ◽  
pp. 1859-1867 ◽  
Author(s):  
Brigitte Dutrieue ◽  
Frederique Vanholsbeeck ◽  
Sylvia Verbanck ◽  
Manuel Paiva
Keyword(s):  
Normal Subjects ◽  
Sensitivity Study ◽  
Phase Iii ◽  
Normal Lung ◽  
Acinar Structure ◽  
Lung Structure ◽  
Solving Equations ◽  
Different Depths ◽  
Lung Periphery ◽  
Successive Generations

We simulated the intra-acinar contribution to phase III slope ( S acin) for gases of differing diffusivities (He and SF6) by solving equations of diffusive and convective gas transport in multi-branch-point models (MBPM) of the human acinus. We first conducted a sensitivity study of S acin to asymmetry and its variability in successive generations. S acin increases were greatest when asymmetry and variability of asymmetry were increased at the level of the respiratory bronchioles (generations 17–18) for He and at the level of the alveolar ducts (generations 20–21) for SF6, corresponding to the location of their respective diffusion fronts. On the basis of this sensitivity study and in keeping with reported acinar morphometry, we built a MBPM that actually reproduced experimental S acin values obtained in normal subjects for He, N2, and SF6. Ten variants of such a MBPM were constructed to estimate intrinsic S acin variability owing to peripheral lung structure. The realistic simulation of S acin in the normal lung and the understanding of how asymmetry affects S acin for different diffusivity gases make S acin a powerful tool to detect structural alterations at different depths in the lung periphery.

scholarly journals Bone marrow-derived angiogenic cells restore lung alveolar and vascular structure after neonatal hyperoxia in infant mice

2010 ◽  
Vol 298 (3) ◽  
pp. L315-L323 ◽  
Author(s):  
Vivek Balasubramaniam ◽  
Sharon L. Ryan ◽  
Gregory J. Seedorf ◽  
Emily V. Roth ◽  
Thatcher R. Heumann ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fluorescent Protein ◽  
Normal Lung ◽  
Vascular Density ◽  
Alveolar Type ◽  
Endothelial Progenitor ◽  
Lung Structure ◽  
Neonatal Hyperoxia

Neonatal hyperoxia impairs vascular and alveolar growth in mice and decreases endothelial progenitor cells. To determine the role of bone marrow-derived cells in restoration of neonatal lung structure after injury, we studied a novel bone marrow myeloid progenitor cell population from Tie2-green fluorescent protein (GFP) transgenic mice (bone marrow-derived angiogenic cells; BMDAC). We hypothesized that treatment with BMDAC would restore normal lung structure in infant mice during recovery from neonatal hyperoxia. Neonatal mice (1-day-old) were exposed to 80% oxygen for 10 days. BMDACs (1 × 105), embryonic endothelial progenitor cells, mouse embryonic fibroblasts (control), or saline were then injected into the pulmonary circulation. At 21 days of age, saline-treated mice had enlarged alveoli, reduced septation, and a reduction in vascular density. In contrast, mice treated with BMDAC had complete restoration of lung structure that was indistinguishable from room air controls. BMDAC comprised 12% of distal lung cells localized to pulmonary vessels or alveolar type II (AT2) cells and persist (8.8%) for 8 wk postinjection. Coculture of AT2 cells or lung endothelial cells (luEC) with BMDAC augmented AT2 and luEC cell growth in vitro. We conclude that treatment with BMDAC after neonatal hyperoxia restores lung structure in this model of bronchopulmonary dysplasia.

Lung Structure Abnormalities, But Normal Lung Function in Pediatric Bronchiectasis

CHEST Journal ◽  
2006 ◽  
Vol 130 (2) ◽  
pp. 480-486 ◽  
Author(s):  
Francesca Santamaria ◽  
Silvia Montella ◽  
Luigi Camera ◽  
Cristiana Palumbo ◽  
Luigi Greco ◽  
...  
Keyword(s):  
Lung Function ◽  
Normal Lung ◽  
Normal Lung Function ◽  
Lung Structure

scholarly journals DETECTION OF PULMONARY FUNCTION ON ACTIVE SMOKERS WHOM REGULARY PLAY WIND INSTRUMENT “PUI-PUI”

2019 ◽  
Vol 14 (2) ◽  
pp. 104
Author(s):  
Sri Wahyuni ◽  
Framita Rahman
Keyword(s):  
Lung Function ◽  
Pulmonary Function ◽  
General Hospital ◽  
Sampling Technique ◽  
Smoking Habits ◽  
Normal Lung ◽  
Purposive Sampling ◽  
Lung Capacity ◽  
Wind Instrument ◽  
Mild Restriction

The method used to increase the lung capacity value is to practice using a wind instrument, one of which is the traditional Makassar wind instrument, the Pui-Pui. The purpose of this study was to look at the description of the lung capacity values of pui-pui wind instrument players in Makassar City. This research was conducted at the Pulmonary Polyclinic of Wahidin Sudirohusodo General Hospital with 27 smokers using a purposive sampling technique. Examination of lung capacity is carried out using a spirometry device by converting its value based on values based on Pneumobile Indonesia. The results of this study indicate that smokers who have been "Pui-Pui" blown music artists for more than 6 years have lung function: 24 people (89%) who have normal lung impression, 2 people (7.4%) mild obstruction, and 1 person (3.7) mild restriction. The conclusion is the occurrence of lung function disorders due to smoking is minimized by the habit of playing a wind instrument "Pui-Pui", so that this can be used as a medium of prevention or treatment to improve the lung function of those who have smoking habits.

scholarly journals Medium-Term Pulmonary Function Test After Thoracoscopic Lobectomy and Segmentectomy for Congenital Lung Malformation: A Comparative Study With Normal Control

2021 ◽  
Vol 9 ◽  
Author(s):  
Jin-Xi Huang ◽  
Song-Ming Hong ◽  
Jun-Jie Hong ◽  
Qiang Chen ◽  
Hua Cao
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Function Test ◽  
Small Airway ◽  
Normal Lung ◽  
Control Group ◽  
Medium Term ◽  
Thoracoscopic Lobectomy ◽  
Congenital Lung Malformation ◽  
Significant Difference ◽  
Function Test

Purpose: This study aimed to compare the outcomes and pulmonary function test (PFT) of thoracoscopic segmentectomy and lobectomy in infants with congenital lung malformation and study the result of PFT on a medium-term basis.Methods: The clinical data of 19 infants with congenital lung malformation who underwent thoracoscopic surgery in our hospital from January 2018 to March 2019 were retrospectively studied; these infants were paired with another 19 infants who underwent thoracoscopic lobectomy during the same period using propensity score matching. Age-matched healthy individuals with similar body sizes were recruited for PFT as the control group. Patient characteristics, postoperative PFT, and outcomes were extracted for statistical analysis.Results: The average length of hospital stay did not significantly differ between segmentectomy and lobectomy groups. The segmentectomy group had more chest tube drainage than the lobectomy group. PFT 1 month after the operation showed that the tidal volume of the lobectomy group was lower than that of the segmentectomy group. Time to peak expiratory flow/time of expiration and peak flow/terminal airway velocity (V25%) indicated small airway dysfunction in the lobectomy group, and no obvious abnormalities were found in “time of inspiratory/time of expiration” in either group. Reexamination of pulmonary function 2 years after the operation showed that the small airway function of the segmentectomy group returned to normal, and no significant difference in pulmonary function was noted among the three groups.Conclusion: The short-term pulmonary function recovery was better after segmentectomy than after lobectomy. Patients who underwent thoracoscopic lobectomy and segmentectomy have normal lung function 2 years after the operation.

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