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1
Harding, R., and S. B. Hooper. "Regulation of lung expansion and lung growth before birth." Journal of Applied Physiology 81, no. 1 (July 1, 1996): 209–24. http://dx.doi.org/10.1152/jappl.1996.81.1.209.
Abstract:
Fetal lung growth depends on the degree to which lungs are distended with luminal liquid. Fetal lungs are highly distended such that mean luminal volume exceeds the static relaxation volume. This high level of expansion is maintained by fetal breathing movements and by resistive effects of the upper airway during apnea; both factors oppose lung recoil. Mechanical stress in lung and other tissues stimulates cell division and tissue remodeling. Potential transduction mechanisms involve direct effects of cellular tension and mediation of locally released mitogenic factors. Further studies are required to further define links between lung tissue stress, increased growth, structural remodeling, and the endocrine environment. A common cause of fetal lung hypoplasia is a sustained reduction in mean lung expansion. Studies of mechanisms controlling fetal lung expansion have led to insights into the etiology of fetal lung hypoplasia and how it may be remedied in utero. Fetal lung hypoplasia can have long-lasting effects on postnatal lung function, as airway and alveolar formation may be compromised. Preterm birth may also result in incomplete structural development of the lungs as it shortens the period of increased intrauterine lung expansion.
2
Kirillova, E., N. Shamsutdinova, and G. Nurullina. "THU0534 LUNG ULTRASOUND IN PATIENTS WITH SECONDARY INTERSTITIAL LUNG DISEASES." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 506.2–507. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5168.
Abstract:
Background:Currently, lung ultrasound (LUS) is increasingly used in rheumatology.Objectives:To evaluate the relationship between lung ultrasound and pulmonary function and disease activity in patients with rheumatic diseases with secondary lung involvement.Methods:Thirty patients with rheumatic diseases were included in the study, who, according to the data of the high-resolution RCT of lungs (64-slice CT system Philips Diamond Select Brilliance), showed interstitial lung involvement as a type of nonspecific interstitial pneumonia. In 4 patients, mixed connective tissue disease (MCTD) was diagnosed, 20 had systemic vasculitis (SV), and 6 had rheumatoid arthritis (RA). The mean age of the patients was 56,55 ± 10,59, the duration of the disease was 2,3 ± 1,2 years. All patients underwent a standard clinical examination, the following indices and scales were used to assess the activity of the underlying disease: VDI damage index, Bermingham systemic vasculitis activity scale (BVAS), RA activity scale (DAS 28-CRP). The functional state of the lungs was assessed using spirometry, bodipletismography, gas diffusion “single breath”. LUS was carried out for the evaluation of the location and number of B-lines on both right and left hemithoraces using commercially available echographic equipment with a 5-12 MHz linear transducer (Accuvix A30, Samsung Medison).Results:Most patients had an average number of B-lines 24,5[11,5;34,0]. Тhere were no significant differences in the number of В-lines between groups of patients of different nosologies. The total number of В-lines correlated with the index of activity of systemic vasculitis BVAS (р<0,05; r=0,83). There were no statistically significant correlations with clinical manifestations of pulmonary involvement.Conclusion:Lung ultrasound may be useful in screening secondary lung involvement in patients with rheumatic diseases with high activity.References:[1]Dietrich CF, Mathis G, Blaivas M, Volpicelli G, Seibel A, Wastl D, Atkinson NS, Cui XW, FanM, Yi D. Lung B-line artefacts and their use. J Thorac Dis 2016;8(6):1356-1365. doi: 10.21037/jtd.2016.04.55[2]Tatiana Barskova, Luna Gargani, Serena Guiducci, et al. Lung ultrasound for the screening of interstitial lung disease in very early systemic sclerosis Ann Rheum Dis 2013 72: 390-395 originally published online May 15 2012 doi: 10.1136/annrheumdis-2011-201072Disclosure of Interests:None declared
3
Chen, Jiawen, Ting Li, Chun Ye, Jiasheng Zhong, Jian-Dong Huang, Yiquan Ke, and Haitao Sun. "The Lung Microbiome: A New Frontier for Lung and Brain Disease." International Journal of Molecular Sciences 24, no. 3 (January 21, 2023): 2170. http://dx.doi.org/10.3390/ijms24032170.
Abstract:
Due to the limitations of culture techniques, the lung in a healthy state is traditionally considered to be a sterile organ. With the development of non-culture-dependent techniques, the presence of low-biomass microbiomes in the lungs has been identified. The species of the lung microbiome are similar to those of the oral microbiome, suggesting that the microbiome is derived passively within the lungs from the oral cavity via micro-aspiration. Elimination, immigration, and relative growth within its communities all contribute to the composition of the lung microbiome. The lung microbiome is reportedly altered in many lung diseases that have not traditionally been considered infectious or microbial, and potential pathways of microbe–host crosstalk are emerging. Recent studies have shown that the lung microbiome also plays an important role in brain autoimmunity. There is a close relationship between the lungs and the brain, which can be called the lung–brain axis. However, the problem now is that it is not well understood how the lung microbiota plays a role in the disease—specifically, whether there is a causal connection between disease and the lung microbiome. The lung microbiome includes bacteria, archaea, fungi, protozoa, and viruses. However, fungi and viruses have not been fully studied compared to bacteria in the lungs. In this review, we mainly discuss the role of the lung microbiome in chronic lung diseases and, in particular, we summarize the recent progress of the lung microbiome in multiple sclerosis, as well as the lung–brain axis.
4
Margulies, S. S., R. W. Schriner, M. A. Schroeder, and R. D. Hubmayr. "Static lung-lung interactions in unilateral emphysema." Journal of Applied Physiology 73, no. 2 (August 1, 1992): 545–51. http://dx.doi.org/10.1152/jappl.1992.73.2.545.
Abstract:
Motivated by the introduction of single-lung transplantation into clinical practice, we compared the static mechanical properties of the respiratory system in six supine dogs before (at baseline) with those after the induction of unilateral emphysema. Relaxation volume (Vrel), total lung capacity (TLC), and static compliance of the emphysematous lung increased to 214 +/- 68, 186 +/- 39, and 253 +/- 95% (SD) of baseline, respectively. Vrel of the nonemphysematous lung fell to 81 +/- 28% of baseline, with no significant change in TLC of the nonemphysematous lung or its pressure-volume relationship, indicating that unilateral hyperinflation does not cause dropout of contralateral lung units. After unilateral emphysema, the chest wall shifted to a higher unstressed or neutral volume (when pleural pressure equals atmospheric pressure) in three of six animals, minimizing the anticipated decrease in lung recoil pressure at the higher respiratory system Vrel. The pattern of relative lung emptying in the intact dog and in the excised lungs was similar during stepwise deflations from TLC, suggesting that mean pleural pressure of the hemithoraces is equal. We conclude that in the dog the static volume distribution between emphysematous and nonemphysematous lungs is determined only by differences in lung recoil and compliance.
5
Chen, Fengshi, Toru Bando, Tatsuo Fukuse, Mitsugu Omasa, Toshihiro Okamoto, Naoki Satoda, Akihiro Aoyama, et al. "LTC-2 Recurrent Lymphangioleiomyomatosis after Lung Transplantation(Lung Transplant Conference)." Journal of the Japanese Association for Chest Surgery 20, no. 3 (2006): 981. http://dx.doi.org/10.2995/jacsurg.20.981_2.
6
Syed, Ahad, Sarah Kerdi, and Adnan Qamar. "Bioengineering Progress in Lung Assist Devices." Bioengineering 8, no. 7 (June 28, 2021): 89. http://dx.doi.org/10.3390/bioengineering8070089.
Abstract:
Artificial lung technology is advancing at a startling rate raising hopes that it would better serve the needs of those requiring respiratory support. Whether to assist the healing of an injured lung, support patients to lung transplantation, or to entirely replace native lung function, safe and effective artificial lungs are sought. After 200 years of bioengineering progress, artificial lungs are closer than ever before to meet this demand which has risen exponentially due to the COVID-19 crisis. In this review, the critical advances in the historical development of artificial lungs are detailed. The current state of affairs regarding extracorporeal membrane oxygenation, intravascular lung assists, pump-less extracorporeal lung assists, total artificial lungs, and microfluidic oxygenators are outlined.
7
Horalskyi, L., N. Hlukhova, and I. Sokulskyi. "Morphological traits of rabbit lung." Scientific Horizons 93, no. 8 (2020): 180–88. http://dx.doi.org/10.33249/2663-2144-2020-93-8-180-188.
Abstract:
In the article, following the results of complex methods (anatomic, histologic, organometric, histometric and statistical) researches are shown the features of morphological structure and morphometric parameters of the lungs of mature rabbits. It was found out, that macro- and microscopic architecture of rabbit lungs has similar histoarchitectonics, inherent in other species of farm animals of the class "mammals" and the characteristic features of morphological structures. Lungs in clinically healthy rabbits structurally reflect the shape of thoracic cavity and gradually expand ventrally. Subsequent to the results of performed organometry, the absolute lung mass of mature rabbits is 18,05±1,32 g, relative 0,624±0,013 %. The Right and left rabbit lungs are surrounded by pleural sacs (right and left): in rabbits pleural spaces of the right and left lungs are not connected. According to morphological and organometric investigations the rabbit lungs are relating to VIII type – the reduction of the superior lobe of left lung is observed, consequently right lung is more developed than left ( the length of right lung is 6,40±0,45 mm, the width – 3,54±0,30 mm, the thickness – 3,28±0,30 mm; the length of left lung is 6,84±0,40 mm; 4,18±0,30 mm and 1,52±0,30 mm relatively) and the coefficient of lung asymmetry (right to left) according to their absolute mass is 1.16. Although, rabbit lungs have dilatated base and superior. Right lung divides into four lobes – cranial (the superior), cardio, diaphragmatic and ancilla, left one divides into three lobes – the reduced superior, cardio and diaphragmatic. Histoarchitecture of lungs is formed by lobes of the lungs, that are separated by connective tissue, which contains blood and lymphatic vessels. Lung parenchyma is created by airways and respiratory divisions that blood vessels accompany to. Respiratory lung parenchyma is formed by respiratory bronchioles, alveolar ducts and alveolar saccules, in which walls the alveolus are located and shape the alveolar tree. According to the analysis of histometry results, respiratory (breathing) lobe of lungs of experimental rabbits is 52,3± 0,62 %, connective tissue base – 69,6±1,27 %, and the average volume of alveolus (small, middle and big) is equal to 42,3±4,35 thousand mkm3.
8
Srinivasan, Hari B., Stephen M. Vogel, Dharmapuri Vidyasagar, and Asrar B. Malik. "Protective effect of lung inflation in reperfusion-induced lung microvascular injury." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 3 (March 1, 2000): H951—H957. http://dx.doi.org/10.1152/ajpheart.2000.278.3.h951.
Abstract:
We used the isolated-perfused rat lung model to study the influence of pulmonary ventilation and surfactant instillation on the development of postreperfusion lung microvascular injury. We hypothesized that the state of lung inflation during ischemia contributes to the development of the injury during reperfusion. Pulmonary microvascular injury was assessed by continuously monitoring the wet lung weight and measuring the vessel wall125I-labeled albumin (125I-albumin) permeability-surface area product ( PS). Sprague-Dawley rats ( n = 24) were divided into one control group and five experimental groups ( n = 4 rats per group). Control lungs were continuously ventilated with 20% O2and perfused for 120 min. All lung preparations were ventilated with 20% O2before the ischemia period and during the reperfusion period. The various groups differed only in the ventilatory gas mixtures used during the flow cessation: group I, ventilated with 20% O2; group II, ventilated with 100% N2; group III, lungs remained collapsed and unventilated; group IV, same as group IIIbut pretreated with surfactant (4 ml/kg) instilled into the airway; and group V, same as group III but saline (4 ml/kg) was instilled into the airway. Control lungs remained isogravimetric with baseline125I-albumin PS value of 4.9 ± 0.3 × 10−3ml ⋅ min−1⋅ g wet lung wt−1. Lung wet weight in group III increased by 1.45 ± 0.35 g and albumin PSincreased to 17.7 ± 2.3 × 10−3, indicating development of vascular injury during the reperfusion period. Lung wet weight and albumin PS did not increase in groups I and II, indicating that ventilation by either 20% O2or 100% N2prevented vascular injury. Pretreatment of collapsed lungs with surfactant before cessation of flow also prevented the vascular injury, whereas pretreatment with saline vehicle had no effect. These results indicate that the state of lung inflation during ischemia (irrespective of gas mixture used) and supplementation of surfactant prevent reperfusion-induced lung microvascular injury.
9
Koch, Achim, Nikolaus Pizanis, Carolin Olbertz, Omar Abou-Issa, Christian Taube, Alexis Slama, Clemens Aigner, Heinz G. Jakob, and Markus Kamler. "One-year experience with ex vivo lung perfusion: Preliminary results from a single center." International Journal of Artificial Organs 41, no. 8 (July 5, 2018): 460–66. http://dx.doi.org/10.1177/0391398818783391.
Abstract:
Objective: To enlarge the donor pool for lung transplantation, an increasing number of extended criteria donor lungs are used. However, in more than 50% of multi-organ donors the lungs are not used. Ex vivo lung perfusion offers a unique possibility to evaluate and eventually recondition the injured donor lungs. The aim of our study was to assess the enlargement of the donor pool and the outcome with extended criteria donor lungs after ex vivo lung perfusion. Patients and Methods: Data were prospectively collected in our lung transplant database. We compared the results of lung transplants after ex vivo lung perfusion with those after conventional cold static preservation. In total, 11 extended criteria donor lungs processed with ex vivo lung perfusion and 41 cold static preservation lungs transplanted consecutively between May 2016 and May 2017 were evaluated. Normothermic ex vivo lung perfusion was performed according to the Toronto protocol for 4 h. Cold static preservation lungs were stored in low-potassium dextran solution. Results: Ex vivo lung perfusion lungs before procurement had significantly lower PaO2/FiO2 (P/F) ratios and more X-ray abnormalities. There were no statistically significant differences for pre-donation ventilation time, smoking history, or sex. After reconditioning with ex vivo lung perfusion, 9 out of 11 processed lungs were considered suitable and successfully transplanted. The mean postoperative ventilation time and in-hospital stay were not significantly different in ex vivo lung perfusion and cold static preservation recipients. Conclusion: Ex vivo lung perfusion can safely be used in the evaluation of lungs initially considered not suitable for transplantation. The primary outcome was not negatively affected and normothermic ex vivo lung perfusion is a useful tool to increase the usage of potentially transplantable lungs.
10
Neumann, Peter, Jan Erik Berglund, Enrique Fernández Mondéjar, Anders Magnusson, and Göran Hedenstierna. "Dynamics of lung collapse and recruitment during prolonged breathing in porcine lung injury." Journal of Applied Physiology 85, no. 4 (October 1, 1998): 1533–43. http://dx.doi.org/10.1152/jappl.1998.85.4.1533.
Abstract:
Oleic acid (OA) injection, lung lavage, and endotoxin infusion are three commonly used methods to induce experimental lung injury. The dynamics of lung collapse and recruitment in these models have not been studied, although knowledge of this is desirable to establish ventilatory techniques that keep the lungs open. We measured lung density by computed tomography during breath-holding procedures. Lung injury was induced with OA, lung lavage, or endotoxin in groups of six mechanically ventilated pigs. After a stabilization period, repetitive computed tomography scans of the same slice were obtained during prolonged expirations with and without positive end-expiratory pressure and during prolonged inspirations after 5 and 30 s of expiration. Lung collapse and recruitment occurred mainly within the first 4 s of breath-holding procedures in all three lung injury models, and some collapse and recruitment occurred even within 0.6 s. OA-injured lungs were significantly more unstable than lungs injured by bronchoalveolar lavage or endotoxin infusion. In this experimental setting, expiration times <0.6 s are required to avoid cyclic alveolar collapse during mechanical ventilation without extrinsic positive end-expiratory pressure.
11
Stella, Giulia M., Stefan Kolling, Silvia Benvenuti, and Chandra Bortolotto. "Lung-Seeking Metastases." Cancers 11, no. 7 (July 19, 2019): 1010. http://dx.doi.org/10.3390/cancers11071010.
Abstract:
Metastases from different cancer types most often affect the lung parenchyma. Moreover, the lungs are among the most frequent sites of growth of metastatic masses of uncertain/unknown lineage of origin. Thus, with regards to pulmonary neoplastic parenchymal nodules, the critical issue is to determine if they are IN the lung or OF the lung. In this review, we highlight the clinical, instrumental and molecular features which characterize lung metastases, mainly focusing on recently advancing and emerging concepts regarding the metastatic niche, inflammation, angiogenesis, immune modulation and gene expression. A novel issue is related to the analysis of biomechanical forces which cooperate in the expansion of tumor masses in the lungs. We here aim to analyze the biological, genetic and pathological features of metastatic lesions to the lungs, here referred to as site of metastatic growth. This point should be a crucial part of the algorithm for a proper diagnostic and therapeutic approach in the era of personalized medicine.
12
Lawrence, E. Clinton. "Lung transplantation for COPD: one lung, two lungs, or none?" Lancet 371, no. 9614 (March 2008): 702–3. http://dx.doi.org/10.1016/s0140-6736(08)60319-0.
13
Bilali, Aishan, Shunichi Kurata, Satoshi Ikeda, Gabriela S. Georgieva, Chenting Zhu, Makoto Tomita, Iyoko Katoh, Chieko Mitaka, Yoshinobu Eishi, and Takasuke Imai. "Lung–lung interaction in isolated perfused unilateral hyperventilated rat lungs." Translational Research 155, no. 5 (May 2010): 228–37. http://dx.doi.org/10.1016/j.trsl.2010.01.001.
14
Wright, Casey M., Rayleen V. Bowman, Maxine E. Tan, Maria U. Martins, Rebecca E. McLachlan, Linda H. Passmore, Morgan N. Windsor, et al. "Lung Asbestos Content in Lungs Resected for Primary Lung Cancer." Journal of Thoracic Oncology 3, no. 6 (June 2008): 569–76. http://dx.doi.org/10.1097/jto.0b013e318174e046.
15
Milross, Luke, Chelsea Griffiths, and Andrew J. Fisher. "Ex Vivo Lung Perfusion: A Platform for Donor Lung Assessment, Treatment and Recovery." Transplantology 2, no. 4 (September 27, 2021): 387–95. http://dx.doi.org/10.3390/transplantology2040037.
Abstract:
Lung transplantation offers a lifesaving therapy for patients with end-stage lung disease but its availability is presently limited by low organ utilization rates with donor lungs frequently excluded due to unsuitability at assessment. When transplantation does occur, recipients are then vulnerable to primary graft dysfunction (PGD), multitudinous short-term complications, and chronic lung allograft dysfunction. The decision whether to use donor lungs is made rapidly and subjectively with limited information and means many lungs that might have been suitable are lost to the transplant pathway. Compared to static cold storage (SCS), ex vivo lung perfusion (EVLP) offers clinicians unrivalled opportunity for rigorous objective assessment of donor lungs in conditions replicating normal physiology, thus allowing for better informed decision-making in suitability assessments. EVLP additionally offers a platform for the delivery of intravascular or intrabronchial therapies to metabolically active tissue aiming to treat existing lung injuries. In the future, EVLP may be employed to provide a pre-transplant environment optimized to prevent negative outcomes such as primary graft dysfunction (PGD) or rejection post-transplant.
16
Gilpin, Sarah E., and Darcy E. Wagner. "Acellular human lung scaffolds to model lung disease and tissue regeneration." European Respiratory Review 27, no. 148 (June 6, 2018): 180021. http://dx.doi.org/10.1183/16000617.0021-2018.
Abstract:
Recent advances in whole lung bioengineering have opened new doors for studying lung repair and regeneration ex vivo using acellular human derived lung tissue scaffolds. Methods to decellularise whole human lungs, lobes or resected segments from normal and diseased human lungs have been developed using both perfusion and immersion based techniques. Immersion based techniques allow laboratories without access to intact lobes the ability to generate acellular human lung scaffolds. Acellular human lung scaffolds can be further processed into small segments, thin slices or extracellular matrix extracts, to study cell behaviour such as viability, proliferation, migration and differentiation. Recent studies have offered important proof of concept of generating sufficient primary endothelial and lung epithelial cells to recellularise whole lobes that can be maintained for several days ex vivo in a bioreactor to study regeneration. In parallel, acellular human lung scaffolds have been increasingly used for studying cell–extracellular environment interactions. These studies have helped provide new insights into the role of the matrix and the extracellular environment in chronic human lung diseases such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. Acellular human lung scaffolds are a versatile new tool for studying human lung repair and regeneration ex vivo.
17
Shibuya, Soichi, Jessica Allen-Hyttinen, Paolo De Coppi, and Federica Michielin. "In vitro models of fetal lung development to enhance research into congenital lung diseases." Pediatric Surgery International 37, no. 5 (March 31, 2021): 561–68. http://dx.doi.org/10.1007/s00383-021-04864-8.
Abstract:
AbstractPurposeThis paper aims to build upon previous work to definitively establish in vitro models of murine pseudoglandular stage lung development. These can be easily translated to human fetal lung samples to allow the investigation of lung development in physiologic and pathologic conditions.MethodsLungs were harvested from mouse embryos at E12.5 and cultured in three different settings, i.e., whole lung culture, mesenchyme-free epithelium culture, and organoid culture. For the whole lung culture, extracted lungs were embedded in Matrigel and incubated on permeable filters. Separately, distal epithelial tips were isolated by firstly removing mesothelial and mesenchymal cells, and then severing the tips from the airway tubes. These were then cultured either in branch-promoting or self-renewing conditions.ResultsCultured whole lungs underwent branching morphogenesis similarly to native lungs. Real-time qPCR analysis demonstrated expression of key genes essential for lung bud formation. The culture condition for epithelial tips was optimized by testing different concentrations of FGF10 and CHIR99021 and evaluating branching formation. The epithelial rudiments in self-renewing conditions formed spherical 3D structures with homogeneous Sox9 expression.ConclusionWe report efficient protocols for ex vivo culture systems of pseudoglandular stage mouse embryonic lungs. These models can be applied to human samples and could be useful to paediatric surgeons to investigate normal lung development, understand the pathogenesis of congenital lung diseases, and explore novel therapeutic strategies.
18
Cereda, Maurizio, Yi Xin, Hooman Hamedani, Justin Clapp, Stephen Kadlecek, Natalie Meeder, Johnathan Zeng, Harrilla Profka, Brian P. Kavanagh, and Rahim R. Rizi. "Mild loss of lung aeration augments stretch in healthy lung regions." Journal of Applied Physiology 120, no. 4 (February 15, 2016): 444–54. http://dx.doi.org/10.1152/japplphysiol.00734.2015.
Abstract:
Inspiratory stretch by mechanical ventilation worsens lung injury. However, it is not clear whether and how the ventilator damages lungs in the absence of preexisting injury. We hypothesized that subtle loss of lung aeration during general anesthesia regionally augments ventilation and distension of ventilated air spaces. In eight supine anesthetized and intubated rats, hyperpolarized gas MRI was performed after a recruitment maneuver following 1 h of volume-controlled ventilation with zero positive end-expiratory pressure (ZEEP), FiO20.5, and tidal volume 10 ml/kg, and after a second recruitment maneuver. Regional fractional ventilation (FV), apparent diffusion coefficient (ADC) of3He (a measurement of ventilated peripheral air space dimensions), and gas volume were measured in lung quadrants of ventral and dorsal regions of the lungs. In six additional rats, computed tomography (CT) images were obtained at each time point. Ventilation with ZEEP decreased total lung gas volume and increased both FV and ADC in all studied regions. Increases in FV were more evident in the dorsal slices. In each lung quadrant, higher ADC was predicted by lower gas volume and by increased mean values (and heterogeneity) of FV distribution. CT scans documented 10% loss of whole-lung aeration and increased density in the dorsal lung, but no macroscopic atelectasis. Loss of pulmonary gas at ZEEP increased fractional ventilation and inspiratory dimensions of ventilated peripheral air spaces. Such regional changes could help explain a propensity for mechanical ventilation to contribute to lung injury in previously uninjured lungs.
19
Keshavjee, Shaf. "Multiple cytokine mRNA analysis in donor lung predicts survival after lung transplantation." Journal of the Japanese Association for Chest Surgery 19, no. 3 (2005): 329. http://dx.doi.org/10.2995/jacsurg.19.329_1.
20
Kitterman, Joseph A. "Physiological factors in fetal lung growth." Canadian Journal of Physiology and Pharmacology 66, no. 8 (August 1, 1988): 1122–28. http://dx.doi.org/10.1139/y88-184.
Abstract:
Adequate pulmonary function at birth depends upon a mature surfactant system and lungs of normal size. Surfactant is controlled primarily by hormonal factors, especially from the hypophysis, adrenal, and thyroid; but these have little influence on fetal lung growth. In contrast, current data indicate that lung growth is determined by the following physical factors that permit the lungs to express their inherent growth potential. (a) Adequate intrathoracic space: lesions that decrease intrathoracic space impede lung growth, apparently by physical compression. (b) Adequate amount of amniotic fluid: oligohydramnios retards lung growth, possibly by lung compression or by affecting fetal breathing movements or the volume of fluid within the potential airways and airspaces. (c) Fetal breathing movements of normal incidence and amplitude: fetal breathing movements stimulate lung growth, possibly by stretching the pulmonary tissue, and do not affect mean pulmonary blood flow but do induce small changes in phasic flow; these changes are probably too slight to influence lung growth. (d) Normal balance of volumes and pressures within the potential airways and airspaces: in the fetus, tracheal pressure > amniotic pressure > pleural pressure. This differential produces a distending pressure which may promote lung growth. Disturbing the normal pressure relationships alters the volume of fluid in the lungs and distorts lung growth, which is stimulated by distending the lungs and is impeded by decreasing lung fluid volume. The mechanisms by which these factors affect lung growth remain to be defined. Fetal lung growth also depends on at least a small amount of blood flow through the pulmonary arteries. Although a modest reduction in flow (to 85% of control) does not affect lung growth, total obstruction of the pulmonary artery impairs lung growth. Thus, bronchial blood flow alone is insufficient to supply the nutritional demands of the growing fetal lung.
21
Barker, Kimberly A., Anukul T. Shenoy, Nicole Stauffer-Smith, Emad Isam Arafa, Carolina Lyon de Ana, Alex Barron, Fumiaki Aihara, et al. "Lung resident memory B cells are a common and functionally significant component of lung adaptive immunity." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 85.8. http://dx.doi.org/10.4049/jimmunol.204.supp.85.8.
Abstract:
Abstract Resident memory B cells (BRM) in influenza-recovered mouse lungs were recently described, but whether other types of infections elicit these cells is unknown. The relevance of BRM in human lungs and to lung immune defenses also remains unexplored. Using flow cytometry and immunofluorescence, we found that respiratory pneumococcal exposures in mice elicited lung BRM without concurrent tertiary lymphoid structure formation. Additionally, flow cytometry analysis of normal human lung tissue showed that human lungs are enriched compared to human blood for B cells bearing a resident memory phenotype. These findings indicate that lung BRM are a common feature of antigen-experienced lungs. Multiple mouse models were used to address the contributions of B cell immunity to anti-pneumococcal lung defenses. Mice exposed to a low virulence pneumococcal strain 4 weeks previously were well-protected from a serotype-mismatched pneumococcal challenge. When previously exposed mice were depleted of circulating B cells (but not lung B cells) with anti-CD20 treatment before the challenge infection, there was no effect on the acquired lung immunity. However, a genetically engineered mouse strain allowed effective depletion of lung B cells bearing PD-L2 (a mouse memory B cell marker) from previously exposed mice, and doing so before the virulent pneumococcal challenge resulted in substantial defects in bacterial clearance compared to mice with lung B cells intact. These results provide the first direct evidence of a role for lung BRM in anti-bacterial lung immunity. Notably, this defense was pneumococcal serotype-independent, distinguishing it from the serotype-specific immunity elicited by current pneumococcal vaccines.
22
Hirai, T., K. A. McKeown, R. F. M. Gomes, and J. H. T. Bates. "Effects of lung volume on lung and chest wall mechanics in rats." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 16–21. http://dx.doi.org/10.1152/jappl.1999.86.1.16.
Abstract:
To investigate the effect of lung volume on chest wall and lung mechanics in the rats, we measured the impedance (Z) under closed- and open-chest conditions at various positive end-expiratory pressures (0–0.9 kPa) by using a computer-controlled small-animal ventilator (T. F. Schuessler and J. H. T. Bates. IEEE Trans. Biomed. Eng. 42: 860–866, 1995) that we have developed for determining accurately the respiratory Z in small animals. The Z of total respiratory system and lungs was measured with small-volume oscillations between 0.25 and 9.125 Hz. The measured Z was fitted to a model that featured a constant-phase tissue compartment (with dissipation and elastance characterized by constants G and H, respectively) and a constant airway resistance (Z. Hantos, B. Daroczy, B. Suki, S. Nagy, and J. J. Fredberg. J. Appl. Physiol. 72: 168–178, 1992). We matched the lung volume between the closed- and open-chest conditions by using the quasi-static pressure-volume relationship of the lungs to calculate Z as a function of lung volume. Resistance decreased with lung volume and was not significantly different between total respiratory system and lungs. However, G and H of the respiratory system were significantly higher than those of the lungs. We conclude that chest wall in rats has a significant influence on tissue mechanics of the total respiratory system.
23
Cutillo, A. G., K. C. Goodrich, K. Ganesan, S. Watanabe, D. C. Ailion, K. H. Albertine, A. H. Morris, and C. H. Durney. "Lung water measurement by nuclear magnetic resonance: correlation with morphometry." Journal of Applied Physiology 79, no. 6 (December 1, 1995): 2163–68. http://dx.doi.org/10.1152/jappl.1995.79.6.2163.
Abstract:
Estimates of lung water content obtained from nuclear magnetic resonance (NMR) and morphometric and gravimetric measurements were compared in normal and experimentally injured rats. Average lung water density (rho H2O) was measured by an NMR technique in excised unperfused rat lungs (20 normal lungs and 12 lungs with oleic acid-induced edema) at 0 (full passive deflation) and 30 cmH2O lung inflation pressure and in vivo (4 normal rats and 8 rats with lung injury induced by oleic acid or rapid saline infusion). The rho H2O values were compared with morphometric measurements of lung tissue volume density (Vv) obtained from the same lungs fixed at corresponding liquid-instillation pressures. A close correlation was observed between rho H2O and Vv in normal and injured excised lungs [correlation coefficient (r) = 0.910, P < 0.01]. In vivo rho H2O was also closely correlated with Vv (r = 0.897, P < 0.01). The correlation coefficients between rho H2O and gravimetric lung water content (LWGr) were lower in the excised lung group (r = 0.663 and 0.692, respectively, for rho H2O at 0 and 30 cmH2O lung inflation pressure, P < 0.01) than in the in vivo study (r = 0.857, P < 0.01). Our results indicate that NMR techniques, which are noninvasive and nondestructive, provide reliable estimates of lung water density and that the influence of lung inflation on rho H2O is important (compared with the effect of lung water accumulation in lung injury) only in the presence of deliberately induced very large variations in the lung inflation level.
24
Pronych, Scott, and Richard Wassersug. "Lung use and development in Xenopus laevis tadpoles." Canadian Journal of Zoology 72, no. 4 (April 1, 1994): 738–43. http://dx.doi.org/10.1139/z94-099.
Abstract:
Shortly after hatching, Xenopus laevis tadpoles fill their lungs with air. We examined the role played by early lung use in these organisms, since they are able to respire with both their lungs and their gills. We investigated the effect on X. laevis development when the larvae were prevented from inflating their lungs, and whether early lung use influenced the size of the lungs or the tadpole's ability to metamorphose. Tadpoles that were denied access to air had lungs one-half the size of those of controls. This difference in lung size was too large to be explained merely by a stretching of the lung due to inflation. The longer tadpoles were denied access to air, the longer they took to metamorphose, and their probability of completing metamorphosis diminished. One tadpole raised throughout its larval life without access to air successfully metamorphosed but had abnormal, solidified lungs and an enlarged heart. Collectively, these experiments demonstrate that early lung use in tadpoles is important in determining both ultimate lung size and the probability of successfully metamorphosing. Lung use during early larval development in X. laevis is not absolutely necessary for survival through metamorphosis, but its absence severely handicaps growth.
25
Jackson, R. M., W. J. Russell, and C. F. Veal. "Endogenous and exogenous catalase in reoxygenation lung injury." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 858–64. http://dx.doi.org/10.1152/jappl.1992.72.3.858.
Abstract:
Reexpansion pulmonary edema parallels reperfusion (reoxygenation) injuries in other organs in that hypoxic and hypoperfused lung tissue develops increased vascular permeability and neutrophil infiltration after reexpansion. This study investigated endogenous lung catalase activity and H2O2 production during hypoxia (produced by lung collapse) and after reoxygenation (resulting from reexpansion), in addition to assessing the effects of exogenous catalase infusion on the development of unilateral pulmonary edema after reexpansion. Lung collapse resulted in a progressive increase in endogenous catalase activity after 3 (14%) and 7 days (23%), while activities in contralateral left lungs did not change (normal left lungs averaged 180 +/- 11 units/mg DNA). Tissue from control left lungs released H2O2 into the extracellular medium at a rate calculated to be 242 +/- 34 nmol.h-1.lung-1. No significant change in extracellular release of H2O2 occurred after 7 days of right lung collapse. However, after reexpansion of the previously collapsed right lungs for 2 h, H2O2 release from both reexpanded right and contralateral left lungs significantly increased (88 and 60%, respectively) compared with controls. Infusion of exogenous catalase significantly increased plasma and lung catalase activities. Exogenous catalase infusion prevented neither the increase in lung permeability nor the infiltration with neutrophils that typically occurs in reexpanded lungs. These data indicate that lung hypoxia/reoxygenation, induced by sequential collapse and reexpansion, has specific effects on endogenous lung catalase activity and H2O2 release. However, exogenous catalase does not prevent reexpansion pulmonary edema, eliminating extracellular (but not intracellular) H2O2 as an important mediator of unilateral lung injury in this model.
26
Naito, Noritsugu, Keith Cook, Yoshiya Toyoda, and Norihisa Shigemura. "Artificial Lungs for Lung Failure." Journal of the American College of Cardiology 72, no. 14 (October 2018): 1640–52. http://dx.doi.org/10.1016/j.jacc.2018.07.049.
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Maitra, Gayatri, Kevin Inchley, Richard J. Novick, Ruud A. W. Veldhuizen, James F. Lewis, and Fred Possmayer. "Acute lung injury and lung transplantation influence in vitro subtype conversion of pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 1 (January 1, 2002): L67—L74. http://dx.doi.org/10.1152/ajplung.2002.282.1.l67.
Abstract:
The effects of surfactant treatment on surfactant subtype conversion after lung injury were examined. Dogs were subjected to hyperventilation for 8 h with or without surfactant treatment. Lungs were stored for 17 h, and the right lung was transplanted and reperfused for 6 h. Conversion of large aggregate (LA) surfactant to small aggregates was investigated using in vitro surface area cycling. LA from transplanted lungs (Transplant-LA) from the nontreated group converted more rapidly than Transplant-LA from the treated group. Transplant-LA from both groups converted more rapidly than LA from normal lungs. Calculations based on [3H]dipalmitoylphosphatidylcholine in the administered surfactant [bovine lipid extract surfactant (BLES)] showed that the endogenous component of Transplant-LA converted more rapidly than the exogenous component. This indicates exogenous BLES did not equilibrate completely with endogenous surfactant. LA from hyperventilated, stored donor right lungs and from the recipients' native lungs from the nontreated group converted more rapidly than corresponding LA in the BLES-treated group. Similar relative conversions were observed with exogenous components from all lungs. Relative conversion of endogenous component from Transplant-LA was more rapid than that from LA from donor's stored right lung or from the recipient's native right lung. Low levels of phenylmethylsulfonyl fluoride inhibited conversion of Transplant-LA to a greater extent than normal LA. LA from all experimental groups had similar protein levels. These studies show acute lung injury, transplant, ischemia-reperfusion, and surfactant treatment have major effects on surfactant subtype integrity.
28
Szpinda, Michał, Waldemar Siedlaczek, Anna Szpinda, Alina Woźniak, Celestyna Mila-Kierzenkowska, and Mateusz Badura. "Quantitative Anatomy of the Growing Lungs in the Human Fetus." BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/362781.
Abstract:
Using anatomical, digital, and statistical methods we examined the three-dimensional growth of the lungs in 67 human fetuses aged 16–25 weeks. The lung dimensions revealed no sex differences. The transverse and sagittal diameters and the base circumference were greater in the right lungs while the lengths of anterior and posterior margins and the lung height were greater in the left lungs. The best-fit curves for all the lung parameters were natural logarithmic models. The transverse-to-sagittal diameter ratio remained stable and averaged0.56±0.08and0.52±0.08for the right and left lungs, respectively. For the right and left lungs, the transverse diameter-to-height ratio significantly increased from0.74±0.09to0.92±0.08and from0.56±0.07to0.79±0.09, respectively. The sagittal diameter-to-height ratio significantly increased from1.41±0.23to1.66±0.18in the right lung, and from1.27±0.17to1.48±0.22in the left lung. In the fetal lungs, their proportionate increase in transverse and sagittal diameters considerably accelerates with relation to the lung height. The lung dimensions in the fetus are relevant in the evaluation of the normative pulmonary growth and the diagnosis of pulmonary hypoplasia.
29
Joshua, Eali Stephen Neal. "LUNG NODULE SEMANTIC SEGMENTATION WITH BI-DIRECTION FEATURES USING U-INET." Journal of Medical pharmaceutical and allied sciences 10, no. 5 (October 15, 2021): 3494–99. http://dx.doi.org/10.22270/jmpas.v10i5.1454.
Abstract:
It's difficult to detect lung cancer and determine the severity of the disease without a CT scan of the lungs. The anonymity of nodules, as well as physical characteristics such as curvature and surrounding tissue, suggest that CT lung nodule segmentation has limitations. According to the study, a new, resource-efficient deep learning architecture dubbed U-INET is required. When a doctor orders a computed tomography (CT) scan for cancer diagnosis, precise and efficient lung nodule segmentation is required. Due to the nodules' hidden form, poor visual quality, and context, lung nodule segmentation is a challenging job. The U-INET model architecture is given in this article as a resource-efficient deep learning approach for dealing with the problem. To improve segmentation operations, it also includes the Mish non-linearity functions and mask class weights. Furthermore, the LUNA-16 dataset, which included 1200 lung nodules, was heavily utilized to train and evaluate the proposed model. The U-INET architecture outperforms the current U-INET model by 81.89 times and reaches human expert level accuracy.
30
Bryan, C. L., A. J. Patefield, D. Cohen, J. L. Nielsen, B. Emanuel, and J. H. Calhoon. "Assessment of injury in transplanted and nontransplanted lungs after 6 h of cold storage with glutathione." Journal of Applied Physiology 76, no. 3 (March 1, 1994): 1232–41. http://dx.doi.org/10.1152/jappl.1994.76.3.1232.
Abstract:
Single-lung transplantation after 3 h of hypothermic storage produces bilateral lung injury [pulmonary reimplantation response (PRR)]. We hypothesized that glutathione (GSH) hypothermic storage would protect both lungs from PRR for extended preservation times and that differences in injury and protection would be realized between the graft and the nontransplanted lung. Mongrel dogs underwent left single-lung autotransplantation after preservation for 5–6 h in Euro-Collins (EC) solution, EC plus exogenous GSH (EC+GSH), or Viaspan (VIA) at 4 degrees C. Lung injury was measured in both lungs after 1 h of reperfusion. EC dogs demonstrated significant increases in lung edema, lipid peroxidation, and alveolar neutrophil recruitment in the lung graft and to a less extent in the nontransplanted right lung compared with control dogs (P < 0.05). Edema, lipid peroxidation, and alveolar neutrophils were significantly reduced in both lungs from EC+GSH and VIA dogs compared with lungs from EC dogs (P < 0.05). An increase in large-pore permeability was measured in the lung graft from EC dogs compared with all other lungs. Bronchoalveolar lavage fluid lactate dehydrogenase and total protein concentrations were elevated in both lungs from all three groups of tranplanted dogs compared with those of control dogs (P < 0.05). These data suggest that GSH-containing solutions attenuate the PRR after 6 h of ischemic hypothermic storage but that the protection is incomplete. Mechanisms of injury affecting the lung graft during the PRR appear to differ from those affecting the nontransplanted lung.
31
Khubutiya, M. Sh, A. M. Gasanov, E. A. Tarabrin, T. V. Chernen’kaya, T. E. Kallagov, and E. I. Pervakova. "A comparison of airway microbiota in donors and recipients of lung transplants." Russian Pulmonology 29, no. 2 (July 1, 2019): 184–88. http://dx.doi.org/10.18093/0869-0189-2019-29-2-184-188.
Abstract:
This study was aimed at investigation of relationships between bronchial washing culture in post-transplant recipient and bronchial flora of the lung donor. Methods. A comparative analysis of bronchial washing cultures from 30 post-transplant lung recipients was performed. All lung donors were stratified to ideal, suboptimal and marginal donors according to the lung transplant suitability. Results. As a result, development of post-transplant pulmonary complications was directly related to bacterial flora of the donor lung. The incidence of pneumonia in post-transplant patients was 3.3% after transplantation of ideal donor lungs, 20% after transplantation of suboptimal donors lungs and 100% after transplantation of marginal donor lungs. Conclusion. The rate of pneumonia in transplanted lungs was directly related to bronchial flora in the donor lungs. This should be taken into account when planning antibacterial therapy after lung transplantation.
32
Pérez-Bravo, David, Despoina Myti, Ivana Mižíková, Tilman Pfeffer, David E. Surate Solaligue, Claudio Nardiello, István Vadász, et al. "A comparison of airway pressures for inflation fixation of developing mouse lungs for stereological analyses." Histochemistry and Cell Biology 155, no. 2 (December 29, 2020): 203–14. http://dx.doi.org/10.1007/s00418-020-01951-0.
Abstract:
AbstractThe morphometric analysis of lung structure using the principles of stereology has emerged as a powerful tool to describe the structural changes in lung architecture that accompany the development of lung disease that is experimentally modelled in adult mice. These stereological principles are now being applied to the study of the evolution of the lung architecture over the course of prenatal and postnatal lung development in mouse neonates and adolescents. The immature lung is structurally and functionally distinct from the adult lung, and has a smaller volume than does the adult lung. These differences have raised concerns about whether the inflation fixation of neonatal mouse lungs with the airway pressure (Paw) used for the inflation fixation of adult mouse lungs may cause distortion of the neonatal mouse lung structure, leading to the generation of artefacts in subsequent analyses. The objective of this study was to examine the impact of a Paw of 10, 20 and 30 cmH2O on the estimation of lung volumes and stereologically assessed parameters that describe the lung structure in developing mouse lungs. The data presented demonstrate that low Paw (10 cmH2O) leads to heterogeneity in the unfolding of alveolar structures within the lungs, and that high Paw (30 cmH2O) leads to an overestimation of the lung volume, and thus, affects the estimation of volume-dependent parameters, such as total alveoli number and gas-exchange surface area. Thus, these data support the use of a Paw of 20 cmH2O for inflation fixation in morphometric studies on neonatal mouse lungs.
33
Schaefers, Hans J. "Lung transplantation-current status." Journal of the Japanese Association for Chest Surgery 19, no. 3 (2005): 285. http://dx.doi.org/10.2995/jacsurg.19.285.
34
Dabak, Gül, and Ömer Şenbaklavacı. "History of Lung Transplantation." Turkish Thoracic Journal 17, no. 2 (June 10, 2016): 71–75. http://dx.doi.org/10.5578/ttj.17.2.014.
35
KIDO, Masamitsu. "Work-Related Lung Disorders." Journal of UOEH 10, no. 1 (1988): 133. http://dx.doi.org/10.7888/juoeh.10.133.
36
Verleden, Stijn E., Dragoş M. Vasilescu, John E. McDonough, David Ruttens, Robin Vos, Elly Vandermeulen, Hannelore Bellon, et al. "Linking clinical phenotypes of chronic lung allograft dysfunction to changes in lung structure." European Respiratory Journal 46, no. 5 (June 25, 2015): 1430–39. http://dx.doi.org/10.1183/09031936.00010615.
Abstract:
Chronic lung allograft dysfunction (CLAD) remains the major barrier to long-term success after lung transplantation. This report compares gross and microscopic features of lungs removed from patients receiving a redo-transplant as treatment for CLAD.Lungs donated by patients with either the bronchiolitis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS) phenotype of CLAD and appropriate control lungs (eight per group) were air-inflated, frozen solid and kept frozen while a multi-detector computed tomography (MDCT) was obtained. The lung was then cut into 2-cm thick transverse slices and sampled for micro-CT and histopathology.The MDCT showed reduced lung volume with increased lung weight and density in RAS versus BOS and control (p<0.05). Although pre-terminal bronchioles were obstructed in both phenotypes, RAS lungs showed a reduction of pre-terminal bronchioles (p<0.01). Micro-CT and matched histopathology showed that RAS was associated with reduced numbers of terminal bronchioles/lung compared to BOS and controls (p<0.01), with expansion of the interstitial compartment and obliteration of the alveolar airspaces by fibrous connective tissue.RAS is associated with greater destruction of both pre-terminal and terminal bronchioles. Additionally, the interstitial compartments are expanded and alveolar airspaces are obliterated by accumulation of fibrous connective tissue.
37
Balsara, Keki R., Varun Puri, and Daniel Kreisel. "Ex vivo lung perfusion: Perfusing less lung can yield more lungs." Journal of Thoracic and Cardiovascular Surgery 154, no. 5 (November 2017): e91-e92. http://dx.doi.org/10.1016/j.jtcvs.2017.07.007.
38
Abernathy, V. J., N. A. Pou, R. E. Parker, and R. J. Roselli. "Evaluation of perilla ketone-induced unilateral lung injury using external gamma scanning." Journal of Applied Physiology 76, no. 1 (January 1, 1994): 138–45. http://dx.doi.org/10.1152/jappl.1994.76.1.138.
Abstract:
We used a modified external gamma scanning technique to quantitate right and left lung permeability changes to iodinated sheep albumin before and after perilla ketone (PK)-mediated unilateral lung injury in seven anesthetized sheep. Three portable gamma scintillation probes containing 2-in. NaI crystals detected radioactivities of 51Cr-labeled red blood cells and 125I-labeled albumin over the right and left lungs and blood, respectively. Radioactivities were monitored for 1 h before and 3 h after infusion of 25 mg/kg PK into a single lung. Calculation of normalized slope index (NSI) (Roselli and Riddle, J. Appl. Physiol. 67: 2343–2350, 1989) over the 30-min interval before PK and over the 60- to 90-min interval after PK for each lung revealed a four- to five-fold NSI increase in lungs receiving PK (0.00237 +/- 0.00065 to 0.0109 +/- 0.0016 min-1) and no increase in contralateral control lungs (0.00214 +/- 0.00065 to 0.00201 +/- 0.00032 min-1). Observed changes in NSI were consistent with postmortem evaluations of each lung. Lungs receiving PK had significantly higher wet-to-dry lung weight ratios and extravascular lung water volumes than contralateral control lungs. Measured bloodless wet-to-dry lung weight ratios were 5.68 +/- 0.39 and 3.27 +/- 0.27 (P < 0.05) for PK and control lungs, respectively.
39
Okabe, Ryo, Toyofumi F. Chen-Yoshikawa, Akihiko Yoshizawa, Tsuyoshi Hirashima, Masao Saito, Hiroshi Date, and Takanori Takebe. "Orthotopic foetal lung tissue direct injection into lung showed a preventive effect against paraquat-induced acute lung injury in mice." European Journal of Cardio-Thoracic Surgery 58, no. 3 (April 7, 2020): 638–45. http://dx.doi.org/10.1093/ejcts/ezaa091.
Abstract:
Abstract OBJECTIVES Lung transplantation is the only effective therapy for patients with end-stage lung disease but an organ shortage crisis necessitates the development of alternative therapies. Recent studies have highlighted the potential of foetal tissue transplantation to facilitate the regeneration of vital organs such as liver that have been damaged by lethal diseases. Herein, with the aim of restoring pulmonary function, we hypothesized that allogenic foetal lung tissue implantation would attenuate severe respiratory failure. METHODS Lung tissue from the foetuses of pregnant green fluorescent protein-C57BL/6 mice at 13.5 days of gestation was injected into the left lungs of recipient mice. Severe lung injury was induced by paraquat, and we analysed the survival rate and pathohistological findings after 1 month. RESULTS The survival rate of the therapy group was 39%, which was significantly higher than the vehicle group at 5.9% (P = 0.034). Immunochemical staining showed that positive cytoplasmic stained cells with anti-interleukin-10 antibody were identified in the gland-like structure of embryonic day 13.5 foetal lung. At 4 weeks after orthotopic implantation, haematoxylin and eosin staining showed reduced lung inflammatory cells, reduced lung oedema and increased active cell proliferation of foetal lung cells. Lung injury score showed that the airway septal thickening revealed statistically significant differences between vehicle and foetal lung therapy (P < 0.001). CONCLUSIONS Immature foetal lungs improved the survival rate of mice with paraquat-induced severe lung injury, establishing the need for systematic follow-up studies. The anti-inflammatory cytokine in the tissue from embryonic day 13.5 foetal lung might suppress severe lung injury.
40
Chen, C. R., N. F. Voelkel, and S. W. Chang. "PAF potentiates protamine-induced lung edema: role of pulmonary venoconstriction." Journal of Applied Physiology 68, no. 3 (March 1, 1990): 1059–68. http://dx.doi.org/10.1152/jappl.1990.68.3.1059.
Abstract:
We studied the synergistic interaction between platelet-activating factor (PAF) and protamine sulfate, a cationic protein that causes pulmonary endothelial injury, in isolated rat lungs perfused with a physiological salt solution. A low dose of protamine (50 micrograms/ml) increased pulmonary artery perfusion pressure (Ppa) but did not increase wet lung-to-body weight ratio after 20 min. Pretreatment of the lungs with a noninjurious dose of PAF (1.6 nM) 10 min before protamine markedly potentiated protamine-induced pulmonary vasoconstriction and resulted in severe lung edema and increased lung tissue content of 6-keto-prostaglandin F1 alpha, thromboxane B2, and leukotriene C4. Pulmonary microvascular pressure (Pmv), measured by double occlusion, was markedly increased in lungs given PAF and protamine. These potentiating effects of PAF were blocked by WEB 2086 (10(-5) M), a specific PAF receptor antagonist. Pretreatment of the lungs with a high dose of histamine (10(-4) M) failed to enhance the effect of protamine on Ppa, Pmv, or wet lung-to-body weight ratio. Furthermore, PAF pretreatment enhanced elastase-, but not H2O2-, induced lung edema. To assess the role of hydrostatic pressure in edema formation, we compared lung permeability-surface area products (PS) in papaverine-treated lungs given either protamine alone or PAF + protamine and tested the effect of mechanical elevation of Pmv on protamine-induced lung edema. In the absence of vasoconstriction, PAF did not potentiate protamine-induced increase in lung PS. On the other hand, mechanically raising Pmv in protamine-treated lungs to a level similar to that measured in lungs given PAF + protamine did not result in a comparable degree of lung edema. We conclude that PAF potentiates protamine-induced lung edema predominantly by enhanced pulmonary venoconstriction. However, a pressure-independent effect of PAF on lung vasculature cannot be entirely excluded.
41
Wong, Aaron, Ricardo Zamel, Jonathan Yeung, Gary D. Bader, Claudia C. Dos Santos, Xiaohui Bai, Yubo Wang, Shaf Keshavjee, and Mingyao Liu. "Potential therapeutic targets for lung repair during human ex vivo lung perfusion." European Respiratory Journal 55, no. 4 (February 14, 2020): 1902222. http://dx.doi.org/10.1183/13993003.02222-2019.
Abstract:
IntroductionThe ex vivo lung perfusion (EVLP) technique has been developed to assess the function of marginal donor lungs and has significantly increased donor lung utilisation. EVLP has also been explored as a platform for donor lung repair through injury-specific treatments such as antibiotics or fibrinolytics. We hypothesised that actively expressed pathways shared between transplantation and EVLP may reveal common mechanisms of injury and potential therapeutic targets for lung repair prior to transplantation.Materials and methodsRetrospective transcriptomics analyses were performed with peripheral tissue biopsies from “donation after brain death” lungs, with 46 pre-/post-transplant pairs and 49 pre-/post-EVLP pairs. Pathway analysis was used to identify and compare the responses of donor lungs to transplantation and to EVLP.Results22 pathways were enriched predominantly in transplantation, including upregulation of lymphocyte activation and cell death and downregulation of metabolism. Eight pathways were enriched predominantly in EVLP, including downregulation of leukocyte functions and upregulation of vascular processes. 27 pathways were commonly enriched, including activation of innate inflammation, cell death, heat stress and downregulation of metabolism and protein synthesis. Of the inflammatory clusters, Toll-like receptor/innate immune signal transduction adaptor signalling had the greatest number of nodes and was central to inflammation. These mechanisms have been previously speculated as major mechanisms of acute lung injury in animal models.ConclusionEVLP and transplantation share common molecular features of injury including innate inflammation and cell death. Blocking these pathways during EVLP may allow for lung repair prior to transplantation.
42
Davydova, Zlata V., and Oraz D. Yagmurov. "Alcoholic lung injury." Pediatrician (St. Petersburg) 10, no. 5 (January 28, 2020): 67–72. http://dx.doi.org/10.17816/ped10567-72.
Abstract:
The article presents modern data on pathomorphological changesin lung tissue formed under the influence of acute and chronic intoxication with ethanol and its metabolites. At autopsy of the persons abusing alcohol, along with defeat ofabrain, heart, a liver note considerable changes in lungs. It was found that ethanol is excreted by the lungs and kidneys unchanged. The lungs are actively involved in the conversion of ethanol into carbon dioxide. The toxic effect ofethanol and its metabolites increases the permeability of the vascular wall, which leads to the accumulation of protein in the lung tissue with the development of pronounced dystrophic and destructive changes with the formation ofsubsequent pneumosclerosis. Alcohol negatively affects the function of alveolar macrophages, which have an important role inprotecting the lungs. Under the influence of ethanol in macrophages, biochemical processes are slowed down, expressed in a sharp decrease in their phagocytic activity and ability to move. In turn, it is necessary to note the studies that reflect the data on the influence of alcohol on the lung surfactant, which stabilizes the surface tension in the alveoli and counteracts the transudation of fluid into the alveoli. Alcohol adversely affects the phospholipids included in the surfactant and disrupts the process of its formation. Alcohol intoxication is the cause of 60% of comatose States, and obturation-aspiration complications are the leading form of respiratory disorders. Alcohol-induced disorders of the mucociliary apparatus contribute to the ingress of foreign particles into the respiratory tract. The defeat of these protective mechanisms in combination with a decrease in the overall immune reactivity of the body cause the development of anumber of pathological changes in the lungs. Thus, the study of morphological features of lung injuries in acute ethanol poisoning is of fundamental importance in elucidating the links of pathogenesis ofterminal States, their justified therapy.
43
Hinze, Alicia M., Cheng T. Lin, Amira F. Hussien, Jamie Perin, Aida Venado, Jeffrey A. Golden, Francesco Boin, Robert H. Brown, Robert A. Wise, and Fredrick M. Wigley. "Longitudinal assessment of interstitial lung disease in single lung transplant recipients with scleroderma." Rheumatology 59, no. 4 (August 27, 2019): 790–98. http://dx.doi.org/10.1093/rheumatology/kez341.
Abstract:
Abstract Objective To investigate the natural history of fibrotic lung disease in recipients of a single lung transplant for scleroderma-associated interstitial lung disease (ILD). Methods Global ILD (including ground glass, nodular opacities and fibrosis) was categorized into severity quintiles on first and last post-transplant CT scans, and percent fibrosis by manual contouring was also determined, in nine single lung transplant recipients. Quantitative mean lung densities and volumes for the native and allograft lungs were also acquired. Results In the native lung, global ILD severity quintile worsened in two cases and percent fibrosis worsened in four cases (range 5–28%). In the lung allograft, one case each developed mild, moderate and severe ILD; of these, new fibrotic ILD (involving <10% of lung) occurred in two cases and acute cellular rejection occurred in one. The average change in native lung density over time was +2.2 Hounsfield Units per year and lung volume +1.4 ml per year, whereas the allograft lung density changed by –5.5 Hounsfield Units per year and total volume +27 ml per year (P = 0.011 and P = 0.039 for native vs allograft density and volume comparisons, respectively). Conclusions While the course of ILD in the native and transplanted lungs varied in this series, these cases illustrate that disease progression is common in the native lung, suggesting that either the immune process continues to target autoantigens or ongoing fibrotic pathways are active in the native lung. Mild lung disease may occur in the allograft after several years due to either allograft rejection or recurrent mild ILD.
44
Sozo, Foula, Megan J. Wallace, Valerie A. Zahra, Caitlin E. Filby, and Stuart B. Hooper. "Gene expression profiling during increased fetal lung expansion identifies genes likely to regulate development of the distal airways." Physiological Genomics 24, no. 2 (February 2006): 105–13. http://dx.doi.org/10.1152/physiolgenomics.00148.2005.
Abstract:
Growth and development of the fetal lungs is critically dependent on the degree to which the lungs are expanded by liquid; increases in fetal lung expansion accelerate lung growth, whereas reductions in lung expansion cause lung growth to cease. The mechanisms mediating expansion-induced lung growth are unknown but likely include alterations in the expression of genes that regulate lung cell proliferation. Our aim was to isolate and identify genes that are up- or downregulated by increased fetal lung expansion. In chronically catheterized fetal sheep at 126 days gestational age (GA), the left lung was expanded for 36 h, while the right lung remained at a control level of expansion. Subtraction hybridization was used to isolate genes differentially expressed between the left and right lungs. Screening of ∼6,000 clones identified 1,138 and 118 cDNA fragments that were up- and downregulated by increased lung expansion, respectively. Northern blot analyses in separate groups of control fetuses and fetuses exposed to increased lung expansion were used to verify differential expression. Increased fetal lung expansion upregulated heat shock protein 47, thrombospondin-1, TROP2, tropoelastin, and tubulin-α3 in fetal lung tissue by ∼200–300%; connective tissue growth factor and cysteine-rich angiogenic inducer 61 were increased by 20–30%. Genes downregulated by increased fetal lung expansion included CCSP-related protein-1, elongation factor-1α and vitamin D3 upregulated protein 1. We conclude that an increase in fetal lung expansion differentially regulates the expression of numerous genes in lung tissue, many of which have important putative roles in lung development, while the functions of others are currently unknown.
45
Moores, H. K., C. J. Beehler, M. E. Hanley, P. F. Shanley, E. E. Stevens, J. E. Repine, and L. S. Terada. "Xanthine oxidase promotes neutrophil sequestration but not injury in hyperoxic lungs." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 941–45. http://dx.doi.org/10.1152/jappl.1994.76.2.941.
Abstract:
Neutrophil accumulation in alveolar spaces is a conspicuous finding in hyperoxia-exposed lungs. We hypothesized that xanthine oxidase (XO)-derived oxidants contribute to retention of neutrophils in hyperoxic lungs. Rats were subjected to normobaric hyperoxia (100% O2) for 48 h, and lungs were assessed for neutrophil sequestration (morphometry and lavage cell counts) and injury (lavage albumin levels and lung weights). In rats exposed to hyperoxia, we found increased (P < 0.05) lung neutrophil retention, lavage albumin levels, and lung weights compared with normoxia-exposed control rats. Suppression of XO activity by pretreatment with allopurinol decreased (P < 0.05) lung neutrophil retention but increased (P < 0.05) lavage albumin concentrations and lung weights in hyperoxic rats. Allopurinol treatment had no effect (P > 0.05) on the numbers of macrophages or lymphocytes recoverable by lung lavage. Depletion of XO activity by an independent method, tungsten feeding, also decreased (P < 0.05) lung lavage neutrophil counts and increased (P < 0.05) lavage albumin concentrations. We conclude that XO may be involved in lung neutrophil retention but not lung injury during exposure to hyperoxia.
46
Ramanathan, Kollengode, Hend Mohammed, Peter Hopkins, Amanda Corley, Lawrence Caruana, Kimble Dunster, Adrian G. Barnett, and John F. Fraser. "Single-Lung Transplant Results in Position Dependent Changes in Regional Ventilation: An Observational Case Series Using Electrical Impedance Tomography." Canadian Respiratory Journal 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/2471207.
Abstract:
Background. Lung transplantation is the optimal treatment for end stage lung disease. Donor shortage necessitates single-lung transplants (SLT), yet minimal data exists regarding regional ventilation in diseased versus transplanted lung measured by Electrical Impedance Tomography (EIT).Method. We aimed to determine regional ventilation in six SLT outpatients using EIT. We assessed end expiratory volume and tidal volumes. End expiratory lung impedance (EELI) and Global Tidal Variation of Impedance were assessed in supine, right lateral, left lateral, sitting, and standing positions in transplanted and diseased lungs. A mixed model with random intercept per subject was used for statistical analysis.Results. EELI was significantly altered between diseased and transplanted lungs whilst lying on right and left side. One patient demonstrated pendelluft between lungs and was therefore excluded for further comparison of tidal variation. Tidal variation was significantly higher in the transplanted lung for the remaining five patients in all positions, except when lying on the right side.Conclusion. Ventilation to transplanted lung is better than diseased lung, especially in lateral positions. Positioning in patients with active unilateral lung pathologies will be implicated. This is the first study demonstrating changes in regional ventilation, associated with changes of position between transplanted and diseased lung.
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Sakuma, Tsutomu, Keiji Takahashi, Nobuo Ohya, Osamu Kajikawa, Thomas R. Martin, Kurt H. Albertine, and Michael A. Matthay. "Ischemia-reperfusion lung injury in rabbits: mechanisms of injury and protection." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 1 (January 1, 1999): L137—L145. http://dx.doi.org/10.1152/ajplung.1999.276.1.l137.
Abstract:
To study the mechanisms responsible for ischemia-reperfusion lung injury, we developed an anesthetized rabbit model in which the effects of lung deflation, lung inflation, alveolar gas composition, hypothermia, and neutrophils on reperfusion pulmonary edema could be studied. Rabbits were anesthetized and ventilated, and the left pulmonary hilum was clamped for either 2 or 4 h. Next, the left lung was reperfused and ventilated with 100% oxygen. As indexes of lung injury, we measured arterial oxygenation, extravascular lung water, and the influx of a vascular protein (131I-labeled albumin) into the extravascular space of the lungs. The principal results were that 1) all rabbits with the deflation of the lung during ischemia for 4 h died of fulminant pulmonary edema within 1 h of reperfusion; 2) inflation of the ischemic lung with either 100% oxygen, air, or 100% nitrogen prevented the reperfusion lung injury; 3) hypothermia at 6–8°C also prevented the reperfusion lung injury; 4) although circulating neutrophils declined during reperfusion lung injury, there was no increase in interleukin-8 levels in the plasma or the pulmonary edema fluid, and, furthermore, neutrophil depletion did not prevent the reperfusion injury; and 5) ultrastructural studies demonstrated injury to both the lung endothelium and the alveolar epithelium after reperfusion in deflated lungs, whereas the inflated lungs had no detectable injury. In summary, ischemia-reperfusion injury to the rabbit lung can be prevented by either hypothermia or lung inflation with either air, oxygen, or nitrogen.
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Kelley, J., J. P. Fabisiak, K. Hawes, and M. Absher. "Cytokine signaling in lung: transforming growth factor-beta secretion by lung fibroblasts." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 2 (February 1, 1991): L123—L128. http://dx.doi.org/10.1152/ajplung.1991.260.2.l123.
Abstract:
Control of growth and phenotypic expression of interstitial fibroblasts is a critical determinant of lung architecture and physiology during processes of growth and remodeling. We examined the ability of lung fibroblasts to produce transforming growth factor-beta (TGF-beta), a cytokine that is known to modulate proliferation and phenotypic expression of mesenchymal cells. Cultures of fibroblasts isolated from rat lungs spontaneously secrete TGF-beta as measured in the standard bioassay of anchorage-independent growth of normal rat kidney (NRK) cells in soft agar. Rat lung fibroblasts secrete TGF-beta in an inactive precursor form. Fibroblasts cultured from adult and fetal rat lungs produced comparable amounts of TGF-beta. The ability of lung fibroblast supernatant fluids to induce colony formation in soft agar could be completely neutralized by preincubation of samples with anti-TGF-beta immunoglobulin (Ig). Anti-platelet-derived growth factor IgG had no effect on anchorage-independent growth of NRK cells driven by rat fibroblast culture supernatant samples. These results indicate that TGF-beta does not require the presence of and interaction with secondary cytokines for its activity. In contrast to the results obtained with rat cells, neither human fetal nor adult lung fibroblasts secreted detectable amount of active TGF-beta or its inactive precursor. This was not due to the presence of TGF-beta inhibitors in fibroblast culture media, because the addition of purified porcine TGF-beta to conditioned medium from human lung fibroblast cultures yielded the expected increase in NRK cell growth in soft agar. These results point to differing cytokine control patterns in the lungs of the two species.
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Liao, Zhengchang, Xiaocheng Zhou, Ziqiang Luo, Huiyi Huo, Mingjie Wang, Xiaohe Yu, Chuanding Cao, Ying Ding, Zeng Xiong, and Shaojie Yue. "N-Methyl-D-aspartate Receptor Excessive Activation Inhibited Fetal Rat Lung DevelopmentIn VivoandIn Vitro." BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/5843981.
Abstract:
Background. Intrauterine hypoxia is a common cause of fetal growth and lung development restriction. Although N-methyl-D-aspartate receptors (NMDARs) are distributed in the postnatal lung and play a role in lung injury, little is known about NMDAR’s expression and role in fetal lung development.Methods. Real-time PCR and western blotting analysis were performed to detect NMDARs between embryonic days (E) 15.5 and E21.5 in fetal rat lungs. NMDAR antagonist MK-801’s influence on intrauterine hypoxia-induced retardation of fetal lung development was testedin vivo, and NMDA’s direct effect on fetal lung development was observed using fetal lung organ culturein vitro.Results. All seven NMDARs are expressed in fetal rat lungs. Intrauterine hypoxia upregulated NMDARs expression in fetal lungs and decreased fetal body weight, lung weight, lung-weight-to-body-weight ratio, and radial alveolar count, whereas MK-801 alleviated this damagein vivo.In vitroexperiments showed that NMDA decreased saccular circumference and area per unit and downregulated thyroid transcription factor-1 and surfactant protein-C mRNA expression.Conclusions. The excessive activation of NMDARs contributed to hypoxia-induced fetal lung development retardation and appropriate blockade of NMDAR might be a novel therapeutic strategy for minimizing the negative outcomes of prenatal hypoxia on lung development.
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Walker, A. M., B. C. Ritchie, T. M. Adamson, and J. E. Maloney. "Effect of changing lung liquid volume on the pulmonary circulation of fetal lambs." Journal of Applied Physiology 64, no. 1 (January 1, 1988): 61–67. http://dx.doi.org/10.1152/jappl.1988.64.1.61.
Abstract:
During fetal life the lung develops as a liquid-filled structure with low blood flow compared with postnatal life. We studied the effects of liquid expansion of the fetal lung by measuring vascular conductance in perfused lungs in situ and arterial diameters in excised lungs of fetal lambs. Pulmonary vascular conductance invariably rose as the lung was deflated from its initial volume; maximal deflation to residual volume increased conductance 122%. With reexpansion, conductance fell progressively, culminating in cessation of flow at lung volumes of twice the initial volume. These changes persisted after vagotomy and thoracic sympathectomy and therefore were mechanical in character. Lung expansion from residual volume initially expanded 300- to 500-micron arteries but compressed arteries greater than 1,500 micron. Further expansion reduced the caliber of all arteries. Thus increasing lung liquid volume progressively constricts the pulmonary circulation in the fetus. Because the fetal pulmonary vascular resistance-lung volume relationship differs from that of the U-shaped form found in adult lungs, concepts based on the adult pulmonary circulation are not appropriate for liquid-filled fetal lungs.