Relevant bibliographies by topics / Lung

Academic literature on the topic 'Lung'

Author: Grafiati
Published: 4 June 2021
Last updated: 22 June 2023

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Lung":

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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Lung":

1

Eriksson, Leif. "Lung transplantation clinical and experimental studies /." Lund : Depts. of Cardiothoracic Surgery, Respiratory Medicine and Clinical Physiology, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39068785.html.

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2

Johansson, Soller Maria. "Cytogenetic studies of lung tumors." Lund : Dept. of Clinical Genetics, University of Lund, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39068855.html.

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3

Wilson, Wendy Lee. "Xanthine oxidase in the lung." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26669.

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The generation of oxygen free radicals by the cytosolic enzyme, xanthine oxidase (XO), has been implicated in post-ischemic or reperfusion damage in several organs. XO catalyzes the conversion of hypoxanthine to urate with the concomitant production of superoxide anion free radical (0₂̅˙) and hydrogen peroxide (H₂O₂). Oxygen free radical-mediated injury has also been demonstrated in inflammatory lung disease. The possible involvement of XO in oxidative injury in the lung has not yet been studied. Therefore, this research project was designed to determine whether XO is present in the lung and to investigate its characteristics in porcine, bovine, rat and human lung and other tissues. Immunochemical analysis of xanthine oxidase in the tissues employed on polyclonal antibody raised to bovine milk XO. Proteins were separated by SDS-polyacrylamide gel electrophoresis of tissue homogenates. Proteins were transfered from the gels to nitrocellulose filters by Western blotting. After incubating the filters with a antisera containing the antibody to the purified bovine XO. XO on the filter was detected by its reaction with an enzyme-conjugated second antibody. XO was immunologically detectable in bovine lung and milk. Rat lung, kidney and liver all showed XO reactivity. XO was detectable in porcine liver but not detectable in porcine lung or kidney. Thus, the antibody to bovine XO was cross-reactive with porcine and rat XO. XO protein was not immunologically detectable in human lung possibly because the antibody was not cross reactive with the bovine antibody. In vivo, xanthine oxidase exists predominantly as a dehydrogenase rather than an oxidase. In this form as xanthine dehydrogenase (XDH) the enxyme does not produce either 0₂̅˙ or H₂O₂. The activity of both XDH and XO was measured in several tissues using a fluorometric assay which uses an artifical substrate, pterin which is catalytically converted to the fluorescent product isoxanthopterin (IXP). XO activity in porcine liver was of 1.1 x 10⁻³ µg IXP/mg protein/min although XO activity was not detectable in porcine lung and kidney, in rat lung of 1.7 x 10⁻² µg IXP/mg protein/min, rat kidney of 1.5 x 10⁻² µg IXP/mg protein/min, and rat liver of 2.2 x 10⁻² µg IXP/mg protein/min. Seven human lung biopsy samples were obtained after lung resection and initially tested for viability by determination of NADH oxidase activity and then assayed for XO-XDH. Three of these samples showed NADH oxidase activity indicating tissue viability, but only one of these three showed measurable XO activity of 5.35 x 10⁻⁶ µg IXP/mg protein/min. Irreversible conversion of XDH to XO is thought to be the result of limited proteolysis by a Ca²⁺/calmodulin activated protease, whereas reversible conversion of the enzyme occurs by oxidation of critical thiol groups. Studies on the rate and nature of fluorescence assay to detect catalytic activities of both enzyme forms. Incubation of lung homogenates with trypsin for 60 min caused irreverisble conversion of 90% of the XDH to XO. In contrast, incubation of homogenates at 15°C for 10 hours caused conversion of 100% of the XDH to XO. This conversion was reversible to the extent of 80% by reduction of thiol groups with dithiothreitol (DTT). The effects of free Ca²⁺ on the conversion of XDH to X0 was examined by using EDTA, a chelator of Ca²⁺ and other divalent cations; and EGTA, a more specific chelator of Ca²⁺. The presence of these chelating agents during homogenization of either normoxic or ischemic rat lung tissue did not inhibit reversible enzyme conversion. Increased XO activity was reversible by DTT. In the normoxic rat lung, homogenates prepared with EDTA and EGTA showed a similar conversion of 95% of XDH to XO which was reversible to 70% with DTT. In the ischemic rat lung, samples prepared with EDTA and EGTA showed a'conversion of 80% and 95% XDH to XO which was similar to control samples. The extent of reversibility to XDH was 75% with DTT incubation. In addition, perfusion of rat lungs with EDTA and DTT via a pulmonary artery cannula prior to 60 min of ischemia and homogenization did not affect the extent of XDH to XO conversion. These results indicate that irreversible Ca²⁺-mediated proteolytic conversion of XDH to XO does not occur to a great extent in the rat lung during either normoxia or ischemia. However, reversible conversion of XDH to XO does occur, suggesting that reversible thiol dependent conversion may play a role in the lung under both physiological and pathophysiological states.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
4

Bastin, Anthony John. "Modulation of lung injury after lung resection." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536026.

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5

Wolf, Samuel J., Alexander P. Reske, Sören Hammermüller, Eduardo L. V. Costa, Peter M. Spieth, Pierre Hepp, Alysson R. Carvalho, et al. "Correlation of lung collapse and gas exchange." Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-176099.

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Background: Atelectasis can provoke pulmonary and non-pulmonary complications after general anaesthesia. Unfortunately, there is no instrument to estimate atelectasis and prompt changes of mechanical ventilation during general anaesthesia. Although arterial partial pressure of oxygen (PaO2) and intrapulmonary shunt have both been suggested to correlate with atelectasis, studies yielded inconsistent results. Therefore, we investigated these correlations. Methods: Shunt, PaO2 and atelectasis were measured in 11 sheep and 23 pigs with otherwise normal lungs. In pigs, contrasting measurements were available 12 hours after induction of acute respiratory distress syndrome (ARDS). Atelectasis was calculated by computed tomography relative to total lung mass (Mtotal). We logarithmically transformed PaO2 (lnPaO2) to linearize its relationships with shunt and atelectasis. Data are given as median (interquartile range). Results: Mtotal was 768 (715–884) g in sheep and 543 (503–583) g in pigs. Atelectasis was 26 (16–47)% in sheep and 18 (13–23) % in pigs. PaO2 (FiO2 = 1.0) was 242 (106–414) mmHg in sheep and 480 (437–514) mmHg in pigs. Shunt was 39 (29–51)% in sheep and 15 (11–20) % in pigs. Atelectasis correlated closely with lnPaO2 (R2 = 0.78) and shunt (R2 = 0.79) in sheep (P-values<0.0001). The correlation of atelectasis with lnPaO2 (R2 = 0.63) and shunt (R2 = 0.34) was weaker in pigs, but R2 increased to 0.71 for lnPaO2 and 0.72 for shunt 12 hours after induction of ARDS. In both, sheep and pigs, changes in atelectasis correlated strongly with corresponding changes in lnPaO2 and shunt. Discussion and Conclusion: In lung-healthy sheep, atelectasis correlates closely with lnPaO2 and shunt, when blood gases are measured during ventilation with pure oxygen. In lung-healthy pigs, these correlations were significantly weaker, likely because pigs have stronger hypoxic pulmonary vasoconstriction (HPV) than sheep and humans. Nevertheless, correlations improved also in pigs after blunting of HPV during ARDS. In humans, the observed relationships may aid in assessing anaesthesia-related atelectasis.
6

Johnsson, Hans. "Lung hyaluronan and lung water in the perinatal period." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4989-1/.

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7

Cherukupalli, Kamala. "Studies on the normal and abnormal lung growth in the human and in the rat with emphasis on the connective tissue fibers of the lung." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/30607.

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Infants with bronchopulmonary dysplasia (BPD), showed impaired body growth when compared to control infants. In terms of changes in the biochemical composition of the lung, BPD infants had higher DNA, soluble protein, collagen and desmosine contents as well as increased concentrations of DNA, collagen and desmosine in their lungs when compared to the growth patterns obtained for the lungs of control infants. Pathologically BPD was classified into 4 grades. Grade I BPD, was a phase of acute lung injury, grades II and III were proliferative phases. In grade IV BPD, lung structure returned towards normal. Evidence of fibrosis was seen by a significant increase in collagen concentration in grades II and III while desmosine concentration was seen to increase in grades III and IV suggesting that the increase in collagen and desmosine contents in the lungs of BPD infants may be controlled by two different mechanisms. Collagen type I/III ratio was seen to decrease progressively from grade II to grade IV BPD in comparison to age matched controls, indicating a higher proportion of type III collagen in the lungs of infants with BPD. From the clinical analysis and the results obtained from discriminant analysis procedure, it was seen that there was a high degree of correlation between the continuation of the disease and collagen accumulation in the lungs suggesting that pulmonary fibrosis with excessive collagen accumulation is an integral part of BPD. This fibrotic process seemed to correlate significantly with assisted ventilation and high oxygen supplementation received by the infants, but it was difficult to assess the individual contribution of the two treatments in the pathogenesis of BPD. Other variables such as severity of the initial disease and the length of survival of the infants, made the assessment of individual contribution much more difficult.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
8

Trávníčková, Hana. "Implementace přenosového protokolu pro přenos dat mobilní cirkulační jednotky pro převoz plic." Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2014. http://www.nusl.cz/ntk/nusl-220838.

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The aim of this thesis is a data transfer protocol implementation for a mobile control unit for transporting lungs. Apart from this thesis the data transfer protocol is used in AlveoPic project. The introductory part is focused on an anatomical and physiological background of a human respiratory system. Consequently it describes the i-Lung module and the mobile circulation module (MCM). It deals with the healthcare informatics interoperability standards with an emphasis to the ISO/IEEE 11073 standard. The subsequent part is represented by MCM’s simulator realization and design of a monitoring application. The final part aims at an analysis of the test cases for a monitoring application’s and a protocol framework’s control.
9

Irving, Samantha. "Gas mixing in the lungs of children with obstructive lung disease." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/25402.

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Introduction: CF (cystic fibrosis) and PCD (primary ciliary dyskinesia) are obstructive airway diseases characterised by frequent infections and neutrophilic inflammation. However, PCD has a much milder course than CF. Pilot data showed that in PCD (n=8) the relationship between LCI (lung clearance index) derived from multiple breath washout (MBW), and FEV1 (forced expiratory volume in 1 second) differed from the established correlation in CF. This thesis sought to identify the reasons. Materials and Methods: Larger PCD (n=38) and CF cohorts (n=125), a non-CF bronchiectasis comparator group (n=28), and healthy controls (n=44) were recruited. All performed LCI and spirometry, and subgroups had more complex MBW parameters (conventional and modified phase III analysis and curvilinearity) calculated and HRCT scans scored. Results: As in the pilot data, there was no relationship between LCI and FEV1 in PCD, unlike in CF. PCD patients had fewer structural abnormalities than CF despite similar or worse spirometry and LCI, and the relationship between HRCT and spirometry or LCI in PCD was again different from that seen in CF. MBW analyses showed that Scond* is near-normal in PCD, suggesting less flow asynchrony, compared with CF. Conclusions: There are differences in the nature of distal airway disease between PCD and CF. As the non-CF bronchiectasis patients were similar to CF (rather than PCD), this likely results from the primary mucociliary clearance defect in PCD compared with secondary impairment in the other two conditions. This may be important as care of PCD patients is extrapolated from that of CF patients, which may not be appropriate. It is important not to extrapolate outcome measures uncritically between different disease groups, both clinically and when planning randomised controlled trials. Finally, a better understanding of what causes the better prognosis in PCD may help identify future new treatment avenues in CF.
10

Grewal, Amardeep Singh. "Prevalence and Outcome of Lung Cancer in Lung Transplant Recipients." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295910.

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Lung transplant is the only available therapy for patients with advanced lung disease. The goal of this study was to examine the prevalence, origin, management and outcome of lung cancer in recipients of lung transplant at the Brigham and Women’s Hospital. We conducted a retrospective chart review of all lung transplantations in our institution from January 1990 until June 2012. The prevalence of lung cancer in the explanted lung was 6 (1.2%) of 462 and all cases were in subjects with lung fibrosis. All 4 subjects with lymph node involvement died of causes related to the malignancy. Nine (1.9%) of 462 patients were found to have bronchogenic carcinoma after lung transplant. The median time to diagnosis after lung transplant was 28 months with a range from 9 months to 10 years. Median survival was 8 months, with tumors involving lymph nodes or distant metastases associated with a markedly worse prognosis (median survival 7 months) than stage I disease (median survival 27 months). While stage I disease is associated with improved survival in this cohort, survival is still not comparable to that of the general population, likely influenced by the need for aggressive immune suppression.
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Books on the topic "Lung":

1

R, Banner Nicholas, Polak Julia M, and Yacoub Magdi, eds. Lung transplantation. Cambridge: Cambridge University Press, 2003.

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1953-, Johnson Bruce E., and Johnson David H. 1948-, eds. Lung cancer. New York: Wiley-Liss, 1995.

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Perry, M. LaVora. Wu-lung & I-lung. East Cleveland, Ohio: Fortune Child Books, 2004.

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Matthay, Richard A. Lung cancer. Philadelphia: W.B. Saunders Co., 2002.

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M, McDowell Elizabeth, ed. Lung carcinomas. Edinburgh: Churchill Livingstone, 1987.

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Matthay, Richard A. Lung cancer. Philadelphia, PA: W.B. Saunders Co., 1993.

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Argiris, Athanassios. Lung cancer. New York, NY: Demos Medical Pub., 2012.

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Alexander, Patterson G., and Couraud Louis 1929-, eds. Lung transplantation. Amsterdam: Elsevier, 1995.

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M, Thurlbeck William, ed. Pathology of the lung. New York: Thieme Medical Publishers, 1988.

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V, Fossella Frank, Putnam J. B. 1953-, and Komaki Ritsuko, eds. Lung cancer. New York: Springer, 2003.

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Book chapters on the topic "Lung":

1

Magalhães, Giselle S., Maria Jose Campagnole-Santos, and Maria da Glória Rodrigues-Machado. "Lung." In Angiotensin-(1-7), 131–52. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22696-1_9.

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Mulholland, Kathleen M. "Lung." In Histopathology Specimens, 391–402. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-673-3_39.

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Lemos, Monica B., and Roberto Barrios. "Lung." In Atlas of Anatomic Pathology, 83–87. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20839-4_8.

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Mulholland, Kathleen M. "Lung." In Histopathology Specimens, 435–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57360-1_39.

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Farver, Carol F., Andrea V. Arrossi, and Henry D. Tazelaar. "Lung." In Essentials of Anatomic Pathology, 915–64. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-60327-173-8_22.

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Carr, Shamus R. "Lung." In Metastatic Bone Disease, 65–69. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-5662-9_6.

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Merrick, Malcolm V. "Lung." In Essentials of Nuclear Medicine, 57–79. London: Springer London, 1998. http://dx.doi.org/10.1007/978-1-4471-0907-5_3.

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Kelsey, Christopher R., Zeljko Vujaskovic, Isabel Lauren Jackson, Richard F. Riedel, and Lawrence B. Marks. "Lung." In ALERT • Adverse Late Effects of Cancer Treatment, 255–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-75863-1_11.

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Guerrieri, Patrizia, Paolo Montemaggi, Volker Budach, Carmen Stromberger, Volker Budach, Volker Budach, Anthony E. Dragun, et al. "Lung." In Encyclopedia of Radiation Oncology, 460–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_127.

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Braunstein, Steve E., Sue S. Yom, and Alexander R. Gottschalk. "Lung." In Handbook of Evidence-Based Stereotactic Radiosurgery and Stereotactic Body Radiotherapy, 109–44. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-21897-7_7.

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Conference papers on the topic "Lung":

1

Schinstock, Emma, Alex Deakyne, Tinen Iles, Andrew Shaffer, and Paul A. Iaizzo. "Lung Allocation Pipeline: Machine Learning Approach to Optimized Lung Transplant." In 2020 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/dmd2020-9030.

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Abstract Lung donation is the most risky transplant procedures. With low survival rates, and poor acceptance of donated lungs, those in need of a lung transplant are at high risk of dying. One reason for poor outcomes is the lack of optimal match between donor and recipient when it comes to lung size and shape. Lungs that do not properly fit in the recipient’s chest cavity can fail to inflate fully and quickly start to deteriorate. In such patients, lung contusions can form, edema occurs in healthy lung tissue, and overall lung function declines. To improve patient outcomes after lung transplant, we describe here a developed a computational pipeline which enables donor lungs to be properly matched to recipients. This tool uses CT scans from both the donor and potential recipients to calculate how anatomically different the sets of lungs are, and therefore provide improved matches in both size and shape for the donor lungs.
2

Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.
3

Nadybal, Ryan, Andrew Wang, and Paul A. Iaizzo. "DETECTING PULMONARY EDEMA THROUGHOUT EX VIVO LUNG PERFUSION." In 2023 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2023. http://dx.doi.org/10.1115/dmd2023-4133.

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Abstract Ex Vivo Lung Perfusion (EVLP) is now a powerful clinical technique that has facilitated the increase in successful human lung transplantation procedures. By having the abilities to assess marginal lungs, extend preservation times, and expand geographical distances for donations, EVLP has effectively both expanded the human lung transplantation donor pool and shortened times on the transplant waitlist. While clinical usage has expanded, preclinical research on EVLP has not. EVLP can be utilized as a preclinical research model, i.e., to investigate pharmacological responses (e.g., post-conditioning agents), organ preservation, device testing and/or methodology development. To facilitate the use of EVLP as a research tool, we have developed a low-cost testing system with ever increasing capabilities e.g., the use of a novel continuous weight sensor to evaluate lung edema. Real time tracking of edema allows us to hone in on potential causes of lung damage, and investigate techniques to rehabilitate and mitigate damage on a short time scale (&lt;8 hours). This system enhances our abilities to accurately test medical devices, lung physiology, and potential treatment impacts on lungs.
4

Amelon, Ryan, Kai Ding, Kunlin Cao, Gary E. Christensen, Joseph M. Reinhardt, and Madhavan Raghavan. "Comparison of Regional Lung Deformation Between Dynamic and Static CT Imagery Using Inverse Consistent Registration." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206689.

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The mechanics of lung deformation is traditionally assessed at a whole-lung or lobar level. We submit that key aspects of lung mechanics maybe better understood by studying regional patterns of lung deformation by leveraging recent developments in tomographic imaging and image processing techniques. Our group has developed an inverse consistent registration technique for estimating local displacement distributions from paired lung CT volumes [1,2]. This facilitates the estimation of strain distributions and consequently, the regional patterns in volume change and its preferential directionalities (anisotropy in deformation). In this study, we use this novel method to compare regional deformation in the lungs between static and dynamic inflations in an adult sheep. Much of our research has focused on registration of static lung images at different positive end-expiratory pressures (PEEP). More recently, respiratory-gated CT scans of supine, positive-pressure inflated sheep lungs have been gathered in order to compare the displacement fields of a dynamically inflating lung to the static lung scans. The theory is that scanning a dynamically inflating lung will more accurately reflect natural deformation during breathing by realizing time-dependent mechanical properties (viscoelasticity). The downside to human dynamic lung imaging is the increased radiation dose necessary to acquire the image data across the respiratory cycle, though low-dose CT scans are an option [3]. This experiment observed the difference in strain distribution between dynamically inflated lungs versus static apneic lungs using the inverse consistent image registration developed in our lab.
5

Dai, Zoujun, Ying Peng, Hansen A. Mansy, and Thomas J. Royston. "Sound Transmission in a Lung Phantom Model." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-63766.

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Alterations in the structure and function of the pulmonary system that occur in disease or injury often give rise to measurable changes in lung sound production and transmission. A better understanding of sound transmission and how it is altered by injury and disease might improve interpretation of lung sound measurements, including new lung imaging modalities that are based on an array measurement of the acoustic field on the torso surface via contact sensors or are based on a 3-dimensional measurement of the acoustic field throughout the lungs and torso using magnetic resonance elastography. It is beneficial to develop a computational acoustic model that would accurately simulate generation, transmission and noninvasive measurement of sound and vibration within the pulmonary system and torso caused by both internal and external sources. In the present study, sound transmission in the airway tree and coupling to and transmission through the surrounding lung parenchymal tissue were investigated on a mechanical lung phantom with a built-in bifurcating airway tree through airway insonification. Sound transmission in the airway tree was studied by applying the Horsfield self-consistent model of asymmetric dichotomy for the bronchial tree. The acoustics of the bifurcating airway segments and lung phantom surface motion were measured by microphones and scanning laser Doppler vibrometty respectively. Finite element simulations of sound transmission in the lung phantom were performed. Good agreement was achieved between experiments and finite element simulations. This study validates the computational approach for sound transmission and provides insights for simulations on real lungs.
6

Mussa, J., A. M. Al-Jumaily, and G. Ijpma. "An Investigation Into Quantifying Pressure Wave Oscillation in the Lung." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-38234.

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Understanding pressure wave propagation in the lung is of importance for a number of medical devices including those for diagnostics and treatments. The main objective of this research is to quantify the transmitability of the airway tree with respect to pressure oscillations. Ovine lungs are casted to produce a hollow airway tree. Variable pressure oscillations and airflow are supplied at the trachea of the casted model and pressure oscillations are measured at the bronchioles. The study indicates that pressure waves with different frequencies can be delivered to different locations of the lung by controlling the pressure oscillation source to the lung.
7

Isabekov, N. R. "METHOD OF RESPIRATORY SUPPORT FOR ACUTE CHEMICAL LUNG LESIONS OF PROFESSIONAL GENESIS." In The 4th «OCCUPATION and HEALTH» International Youth Forum (OHIYF-2022). FSBSI «IRIOH», 2022. http://dx.doi.org/10.31089/978-5-6042929-6-9-2022-1-87-90.

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Introduction: Currently, the problem of chemical defeats at work continues to be relevant. According to the Federal Center for Hygiene and Epidemiology of Rospotrebnadzor, diseases (intoxication) caused by chemical factors exposure averaged 5.74–6.39% of occupational diseases per year all registered cases. As result of toxic substances inhalation, direct damage to lungs occurs with the further development of acute respiratory distress syndrome (ARDS). According to the national intensive care guide in the treatment of ARDS, the following main areas are distinguished - respiratory therapy and drug treatment. The latter includes infusion therapy, the use of glucocorticoids, surfactant preparations, narcotic analgesics and diuretics. Respiratory support consists in the use of mechanical ventilation (MV), and if the latter is not effective, extracorporeal membrane oxygenation (ECMO). Methods: literature data analyzes of acute chemical lung lesions treatment, as well as data on types, methods of liquid ventilation lung use. Results: It was found that the use of lungs both partial and total liquid ventilation using perfluorocarbon (PFC) compounds not only improved gas exchange in the lungs, but reduced the severity of the inflammatory response also. It was shown that the method of lung liquid ventilation (LVL) is promising. In turn, the increase in oxygenation we received, the increase in partial blood pressure during the alveolar phase of oedema, shows the advantage of liquid ventilation over existing ventilation regimes MV, thereby reflecting the potential of LAVL as a new method of respiratory support in acute lung lesions.
8

Lazko, Alexey, Larisa Udochkina, and Nina Losovskaya. "Histochemical changes of the lung tissue in experimental chronic alcoholic intoxication." In Innovations in Medical Science and Education. Dela Press Publishing House, 2022. http://dx.doi.org/10.56199/dpcsms.nrjc3772.

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Among organ systems in the human body affected by alcohol abuse, the lungs are particularly vulnerable to infections and injury. Chronic alcoholism causesalterations in host defence of the upper and lower airways, disruption of alveolar epithelial barrier integrity, alcohol-induced ciliary lesions and alveolar macrophages dysfunction. Currently with a spread of SARS-COV 2 infections which instantly destroys the lung tissue, the alcohol-induced lung damage issues acquire vital importance, as they might further increase severity of lesions of lung tissue in the infected alcohol abusers.Recent investigations suggest that the effect of the chronic excessive alcohol consumption and SARS-COV 2 infection on the lungs might have similar and thus synergizing mechanisms. Therefore the mechanism of the lung tissue lesions in chronic alcohol intoxication need to be scrutinized, including the time-line of their development, to be able to develop more effective preventive measures. The objective of the study is to assess histochemical changes in the lung tissue of laboratory animals with chronic alcohol intoxication of different duration. Total of 48 outbred male white mice weighing 18-22 g were enrolled in the study. The experimental animals were exposed to alcohol for 1, 2 and 3 months by the semi-voluntary intake, using 20% alcohol as the only source of fluid, while control animals were getting drinking water. At the end of experiment the lung tissue of the mice was processed histologically and histochemically for alcoholic dehydrogenase (ADH), glucose-6-phasphate-dehydrogenae (G6PDH), alkaline (ALP) and acidic (AP) phosphatases, nonspecific esterase (NE) and succinate dehydrogenase (SDH). Image analysis of the histological slides was performed using Image Pro Plus software. Statistical differences were assessed using paired t-test. Chronic alcohol consumption causes metabolic lesions in the alveolar epithelium and endothelium of alveolar capillaries revealed by an increase in the activity of ADH, G6PD and NE paralleled with a decrease in the total SDH activity of the respiratory portion of the lungs in a time-related pattern. High activity of alkaline phosphatase was noted in endothelial cells of lung capillaries. Thus, under conditions of chronic intoxication, ethanol disturbs cell metabolism, as evidenced by the changes of the enzymatic activity in the lung tissue which leads to inhibition of oxygen-dependent metabolic processes and activation of reserve mechanisms for compensating of energy deficits.
9

Ludeke, D. Taylor, and Maj Dedin Mirmirani. "The Pulling Device for a Flexible Bronchoscope." In ASME 2006 Frontiers in Biomedical Devices Conference. ASMEDC, 2006. http://dx.doi.org/10.1115/nanobio2006-18045.

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The flexible bronchoscope, used both to directly visualize and biopsy lesions, is an important tool for diagnosing lung cancer [1]. Presented here is a conceptual design for a device that increases the depth to which the scope can be fed into the lungs. This allows doctors to find and accurately diagnose more cases of lung cancer first occurring deeper in the lungs.
10

Wall, Wolfgang A., Andrew Comerford, Lena Wiechert, and Sophie Rausch. "Coupled and Multi-Scale Building Blocks for a Comprehensive Computational Lung Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206407.

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Mechanical ventilation is a vital supportive therapy for critical care patients suffering from Acute Respiratory Distress syndrome (ARDS) or Acute Lung Injury (ALI) in view of oxygen supply. However, a number of associated complications often occur, which are collectively termed ventilator induced lung injuries (VILI) [1]. Biologically, these diseases manifest themselves at the alveolar level and are characterized by inflammation of the lung parenchyma following local overdistension or high shear stresses induced by frequent alveolar recruitment and derecruitment. Despite the more recent adoption of protective ventilation strategies based on the application of lower tidal volumes and a positive end-expiratory pressure (PEEP), patient mortality rates are with approximately 40% still very high. Understanding the reason why the lungs still become damaged or inflamed during mechanical ventilation is a key question sought by the medical community. In this contribution, an overview on recently developed building blocks of a comprehensive lung model will be given, with a main focus on lower airways.

Reports on the topic "Lung":

1

Fine, Alan. Acute Lung Injury: Making the Injured Lung Perform Better and Rebuilding Healthy Lungs. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566981.

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Fine, Alan. Acute Lung Injury: Making the Injured Lung Perform Better and Rebuilding Healthy Lungs. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada585102.

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Fine, Alan. Acute Lung Injury: Making the Injured Lung Perform Better and Rebuilding Healthy Lungs. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada561229.

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Fine, Alan. Acute Lung Injury: Making Injured Lungs Perform Better and Rebuilding Healthy Lungs. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada538317.

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Garland, Frank C., Edward D. Gorham, Kevin Kaiser, William D. Travis, Jose A. Centeno, Jerrold L. Abraham, and Franky Hasibuan. Navy Lung Disease Assessment Program. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada454560.

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Danny Colombara, Danny Colombara. Viral Causes of Lung Cancer. Experiment, December 2012. http://dx.doi.org/10.18258/0065.

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Fahlman, Andreas, Michael Moore, and Darlene Ketten. Imaging the Lung Under Pressure. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada531208.

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Tyack, Peter L., Andreas Fahlman, Michael Moore, and Darlene Ketten. Imaging the Lung Under Pressure. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada541723.

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Fahlman, Andreas, Bill Van Bonn, and Stephen Loring. Lung Mechanics in Marine Mammals. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada573475.

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Freeman, Carl A., Thomas E. Dahms, Jeffery A. Bailey, Kathryn Lindsay, Sally Tricomi, and Craig Dedert. Predictors of Acute Lung Injury. Fort Belvoir, VA: Defense Technical Information Center, February 2013. http://dx.doi.org/10.21236/ada583589.

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