Gotowe bibliografie tematyczne / Emphysema

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Gotowa bibliografia na temat „Emphysema”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 9 czerwca 2025

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Artykuły w czasopismach na temat "Emphysema"

Griva, N. A., P. V. Gavrilov, I. A. Nikitina, L. D. Kiryukhina, A. N. Narkevich, and E. G. Sokolovich. "Impact of Emphysema Subtypes and Volume on Lung Ventilation and Gas Exchange Functions as Evidenced by Computed Tomography." Journal of radiology and nuclear medicine 102, no. 6 (February 3, 2022): 349–58. http://dx.doi.org/10.20862/0042-4676-2021-102-6-349-358.

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Objective: to characterize the relationship between the subtype and volume of pulmonary emphysema on the indicators of lung ventilation and gas exchange functions. Material and methods. The data of radiation and functional studies were analyzed in 50 patients. The inclusion criteria were chronic obstructive pulmonary disease and emphysema, which had been diagnosed by computed tomography (CT) and confirmed by two radiologists; comprehensive pulmonary function studies, including spirometry and body plethysmography, were performed; diffusion capacity was measured using a single-breath method, involving inhalation of carbon monoxide, and a breath hold. Patients with primary pulmonary emphysema, any history of pulmonary surgery, and emphysema concurrent with other lung X-ray syndromes (consolidation, cavity) were excluded. CT was performed with a 1-mm thick slice and standard scanning parameters on Toshiba tomographs (Japan). Pulmonary function was tested using a MasterScreen Body Diffusion expert diagnostic unit (VIASYS Healthcare, Germany) in accordance with the criteria for correct pulmonary functional tests proposed by a joint group of experts from the American Thoracic Society and the European Respiratory Society. Volumetric analysis of emphysema was performed using the Lung Volume Analysis software package (Toshiba, Japan). In the study, there was a predominance of male patients (n = 42 (84%)), mainly in the 61-70 age group. Results. The isolated type of emphysema was rare: centrilobular and paraseptal emphysemas were seen in 3 (6%) and 2 (4%) patients, respectively. The mixed type of emphysema was detected in 90% of cases; 33 (66%) patients having a predominant centrilobular component constituted a large proportion. It was determined that as the volume of emphysema increased, the patency of the airways worsened, the static pulmonary volumes increased, the lungs were hyperinflated, pulmonary gas exchange worsened, the bronchial resistance slightly increased during calm breathing. No statistically significant results were found from the point of view of correlations between the volume of emphysema and other parameters of pulmonary function. Conclusion. An increase in the volume of emphysema deteriorates pulmonary function; the greatest contribution to the overall picture is made by the patients with a mixed type of emphysema with a predominance of the centrilobular component.

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Sirpuram Milind Joshi, Varundev. "Congenital Lobar Emphysema." International Journal of Science and Research (IJSR) 12, no. 1 (January 5, 2023): 676–78. http://dx.doi.org/10.21275/mr23120200847.

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Petty, Thomas L. "Emphysema." Postgraduate Medicine 86, no. 6 (November 1989): 212–13. http://dx.doi.org/10.1080/00325481.1989.11704489.

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Slebos, Dirk-Jan, Karin Klooster, and Michiel Erasmus. "Emphysema!" American Journal of Respiratory and Critical Care Medicine 186, no. 2 (July 15, 2012): 197. http://dx.doi.org/10.1164/rccm.201201-0067im.

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Mahta, Ali, Alexander E. Merkler, Michael E. Reznik, Jaclyn E. Burch, Shadi Yaghi, Frank W. Sellke, Karen L. Furie, and Hooman Kamel. "Emphysema." Stroke 50, no. 4 (April 2019): 992–94. http://dx.doi.org/10.1161/strokeaha.118.024660.

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Background and Purpose— Protease/antiprotease imbalance is implicated in the pathogenesis of emphysema and may also lead to vessel wall weakening, aneurysm development, and rupture. However, it is unclear whether emphysema is associated with cerebral and aortic aneurysm rupture. Methods— We performed a retrospective cohort study using outpatient and inpatient claims data from 2008 to 2014 from a nationally representative sample of Medicare beneficiaries ≥66 years of age. Our predictor variable was emphysema, and our outcome was hospitalization for either aneurysmal subarachnoid hemorrhage or a ruptured aortic aneurysm. All predictors and outcomes were defined using previously reported International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis code algorithms. Survival statistics and Cox regression were used to compare risk between patients with and without emphysema. Results— We identified 1 670 915 patients, of whom 133 972 had a diagnosis of emphysema. During a mean follow-up period of 4.3 (±1.9) years, we identified 4835 cases of aneurysm rupture, 433 of which occurred in patients with emphysema. The annual incidence of aneurysm rupture was 6.5 (95% CI, 6.4–6.8) per 10 000 in patients without emphysema and 14.6 (95% CI, 13.3–16.0) per 10 000 in patients with emphysema. After adjustment for demographics and known risk factors for aneurysmal disease, emphysema was independently associated with aneurysm rupture (hazard ratio, 1.7; 95% CI, 1.5–1.9). Emphysema was associated with both aneurysmal subarachnoid hemorrhage (hazard ratio, 1.5; 95% CI, 1.3–1.7) and ruptured aortic aneurysm (hazard ratio, 2.3; 95% CI, 1.9–2.8). Conclusions— Patients with emphysema face an increased risk of developing subarachnoid hemorrhage and aortic aneurysm rupture, potentially consistent with shared pathways in pathogenesis.

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Subramanyam, Rajeev, Andrew Costandi, and Mohamed Mahmoud. "Congenital lobar emphysema and tension emphysema." Journal of Clinical Anesthesia 29 (March 2016): 17–18. http://dx.doi.org/10.1016/j.jclinane.2015.10.008.

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Parag, Sharma, Gupta Piyush, Sharma Prerna, and Shrivastava Nishant. "Differential Patterns of Cough and Sputum in Patients with Asthma and COPD in Tertiary Care Hospital of Central India." International Journal of Pharmaceutical and Clinical Research 14, no. 4 (April 30, 2022): 527–35. https://doi.org/10.5281/zenodo.13838473.

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Introduction: The evolution of knowledge concerning COPD and its components Emphysema, Chronic bronchitis, and Asthmatic bronchitis take us long back in to the history over 200 years. Since then there not a single terminology have been established to clearly demarcate difference between these components. Confusion still persists between chronic bronchitis and Emphysema. In this study, we aim to assess using the preexisting clinical, pathological, and radiological knowledge, whether these phenotypes can be distinguished or not. Material methods: The present study is a prospective, observational, hospital based study conducted on 110 pre diagnosed patients on basis of complete clinical evaluation including a detailed preformatted directed history, detailed and thorough clinical examination were considered. Results: 31 of asthma patients (100%) had episodic cough, while 29 (76.3%) of Emphysema patients and 18 (94.7%) of chronic bronchitis patients had constant cough. Our study showed that 30(96.8%) asthma had worsening at night time, while 13(34.1%) of Emphysema patients and 13(68.4%) of chronic bronchitis patients had worsening at both day and night. Cough was aggravated by dust, pollen and cold in 25(80.7%) of asthma patients. All chronic bronchitis patients19 (100%) had sticky sputum, whereas non sticky sputum was present in majority of Emphysema31 (93.9) and asthma 30(100%) patients. Sputum cytology in majority of asthma patients 26(83.9%) showed predominant eosinophils, whereas 18(94.8%) patients of chronic bronchitis and 18(50 %) patients of Emphysema had predominant neutrophils. Conclusion:Thus a clear demarcating pictures of COPD and asthma can be found over coughing and sputum patterns of the patients.

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Putri, Ayu Vidya, Seto Adiantoro, and Harmas Yazid Yusuf. "Subcutaneuous emphysema as a complication of tooth extraction: Case Report." International Journal of Oral Health Dentistry 8, no. 1 (March 15, 2022): 67–71. http://dx.doi.org/10.18231/j.ijohd.2022.014.

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Subcutaneous emphysema is an uncommon complication of dental procedures. This complication arises when air forced beneath the tissue. In dentistry it may appear with the use of high-speed bur and could cause a serious complication including airway obstruction. This case report highlights a complication during dental procedure to give information for the clinician the factors, diagnosis, and management of subcutaneous emphysema.A 33 years old male patient with difficulty in breathing and swelling at right lower jaw, neck and chest region. The swelling occurred about 2 hours before admission during tooth extraction of second right lower molar using a high-speed bur about 30 minutes, then he started to feel difficulty in breathing with swelling at right lower jaw, neck and chest region occurred and pain. Then he was transferred to Hasan Sadikin Emergency Department for further treatment. The patient was diagnosed with subcutaneous emphysema at right lower jaw, neck and chest region due to suspect iatrogenic. The management of this patient was conservative treatment with oxygenation 3 lpm, close observation vital sign and wide emphysema, IVFD ringer lactate 1500 cc/ 24 hours, medication with Ceftriaxone 1 gr, Ketorolac 30 mg, Omeprazole 20 mg intravenous and being hospitalized for 4 days. After general condition stable he was performed tooth extraction.Iatrogenic subcutaneous emphysema could be a serious and potentially life-threatening, so dentist has to be more careful while using high-speed bur for tooth extraction.

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Yane, Katsunari, Osamu Tanaka, and Takashi Matsunaga. "A Case of Spontaneous Mediastinal Emphysema with Subcutaneous Emphysema and Pharyngeal Emphysema." Practica oto-rhino-laryngologica. Suppl. 1990, Supplement37 (1990): 183–87. http://dx.doi.org/10.5631/jibirinsuppl1986.1990.supplement37_183.

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Meier-Schroers, Michael, Alois Sprinkart, Manuel Becker, Rami Homsi, and Daniel Thomas. "Quantitative and Qualitative Assessment of Pulmonary Emphysema with T2-Weighted PROPELLER MRI in a High-Risk Population Compared to Low-Dose CT." RöFo - Fortschritte auf dem Gebiet der Röntgenstrahlen und der bildgebenden Verfahren 190, no. 08 (March 7, 2018): 733–39. http://dx.doi.org/10.1055/a-0577-5619.

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Purpose To determine the suitability of T2-weighted PROPELLER MRI for the assessment of pulmonary emphysema. Materials and Methods 60 participants in a lung cancer screening program (30 subjects with pulmonary emphysema, and 30 control subjects without emphysema) were included for this retrospective study. All subjects were examined with low-dose CT (LDCT) and MRI within the screening program. The use of a T2-weighted PROPELLER sequence for the assessment of emphysema was analyzed and correlated with the results of LDCT. The presence and the extent of pulmonary emphysema were first assessed qualitatively using a three-point score, and then quantitatively with a semi-automated software program to obtain emphysema indices. Results All 30 cases with pulmonary emphysema were accurately detected by MRI. There were 3 cases with emphysema according to MRI without emphysematous changes on LDCT (false-positive results). The qualitative scores as well as the emphysema indices were significantly higher in the emphysema group compared to the control group for MRI and LDCT (p < 0.001). Both the scores and the indices correlated significantly between MRI and LDCT (qualitative score of severity: r = 0.912/p < 0.001 in the emphysema group and r = 0.668/p < 0.001 in the control group; emphysema index: r = 0.960/p < 0.001 in the emphysema group and r = 0.746/p < 0.001 in the control group). Conclusion The presence and the extent of pulmonary emphysema may be assessed qualitatively and quantitatively by T2-weighted PROPELLER MRI with very good correlation to LDCT. Key Points: Citation Format

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Rozprawy doktorskie na temat "Emphysema"

Turcotte, Antony. "Description of emphysema in mice with different susceptibilities to cigarette smoke-induced emphysema." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82444.

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The inflammatory response due to chronic smoking in COPD patients has been well characterized with increases in CD3+ T lymphocytes. A murine model was chosen in our laboratory as a good model of human emphysema. The first part of my project was to characterize the lung inflammatory response via immunocytochemistry in each mouse strain exposed to chronic smoke inhalation for a six-month period. Several T lymphocyte subsets (i.e. naive, central memory and effector memory) have been characterized in the immune system both in humans and mice. These subsets have different homing potentials and effector functions, and can be identified with cell surface markers. The second part of my project was to determine these T-cell subset ratios in the lungs of each strain after chronic smoke exposure. The third part of my project was to assess apoptosis in each strain after smoke exposure.

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Jörgensen, Kirsten. "Lung emphysema and cardiac function /." Göteborg : Dept. of Anaesthesiology and Intensive Care Medicine. Institute of Clinical Sciences, The Sahlgrenska Academy at Göteborg University, 2008. http://hdl.handle.net/2077/9635.

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Jones, Jennifer Grace. "A mathematical model of emphysema." Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269229.

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Haruna, Akane. "CT emphysema predicts mortality in COPD." Kyoto University, 2010. http://hdl.handle.net/2433/123335.

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Kariisa, Mbabazi M. "Measuring the Effects of Air Pollution among Persons with Severe Emphysema: The National Emphysema Treatment Trial (NETT)." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1357157519.

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Walsh, Robert Leo. "Leukocyte elastase and anti-elastases in pulmonary emphysema." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phw2261.pdf.

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Includes bibliographical references (leaves 218-249) The preferred theory to explain the aetiology of emphysema points to an imbalance in the protease-antiprotease systems within the lung with human leukocyte elastase and [alpha]1-protease inhibiter being the main candidates. Examines some aspects of this theory.

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Chrusciel, Sandra. "Rôle de P53 dans les macrophages alvéolaires en réponse à diverses agressions environnementales." Thesis, Paris Est, 2014. http://www.theses.fr/2014PEST1187.

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Il existe plusieurs types d’agressions environnementales : biologiques (virus, bactéries…), chimiques (gaz, fumées, métaux…), physiques (bruits, rayonnements…), et d’autres telles que le stress par exemple. L’appareil respiratoire, qui représente une interface majeure avec l’environnement, est particulièrement vulnérable vis-à-vis de ces agressions, qui ont souvent des conséquences pulmonaires, pouvant parfois conduire au décès. Le tabac notamment est la cause de près de 100 millions de décès au cours du XXème siècle d’après l’Organisation Mondiale de la Santé (OMS), et sera la cause d’environ un milliard de décès au prochain siècle. L’exposition à la fumée de cigarette engendre une inflammation chronique et est souvent corrélée au développement de cancers (1), mais induit aussi de nombreuses autres pathologies pulmonaires telles que la broncho-pneumopathie chronique obstructive (BPCO) There are several types of environmental attacks: biological (viruses, bacteria …), chemical (gases, smokes, metals …), physical appearances (rumours, brilliances …), and others such as the stress for example. The respiratory system, which represents a major interface with the environment, is particularly vulnerable towards these attacks, which often have lung consequences, being able to sometimes lead to the death. The tobacco in particular is the cause of about 100 million deaths during the XXth century according to the World Health Organization (WHO), and will be the cause about a billion deaths in the next century. The exhibition in the smoke of cigarette engenders a chronic inflammation and is often correlated in the development of cancers (1), but also leads of numerous

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Macnee, W. "Right ventricular function in chronic bronchitis and emphysema." Thesis, University of Glasgow, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383973.

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Carter, Richard Ian. "Biomarkers of disease activity in COPD and emphysema." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4071/.

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The flaws of current methods of assessing disease severity in patients with COPD and emphysema are increasingly recognised, and new methods of assessing disease activity are urgently required. Although many potential biomarkers have been suggested to fulfil this role, few have been effectively validated, and furthermore any biomarker should be based on our current understanding of the pathophysiology the disease process. This is poorly understood, however it is apparent that neutrophil proteases (particularly neutrophil elastase (NE) and proteinase 3 (Pr3)) may represent a final common pathway leading to tissue destruction. The current thesis describes the development and validation of a new marker of NE activity (Aα-Val360), and the identification of a marker of Pr3 activity, as potential biomarkers of COPD and emphysema disease activity. Methods Following in vitro validation, the performance of Aα-Val360 was assessed in a series of patient populations. Mass spectrometry was used to identify a specific marker of Pr3 activity. Results and Conclusion Aα-Val360 demonstrated acceptable in vitro and in vivo variability; related to physiological, radiological and patient reported outcomes in subjects with (or at risk of developing) COPD and emphysema (both with and without A1AT deficiency); increased during acute exacerbations; decreased in response to treatment; and partly related to disease progression in some populations. Also, a Pr3 specific cleavage product was identified which could be used to develop a new specific assay of Pr3 activity. These potential biomarkers of disease activity may be important in the assessment of patients with COPD and emphysema (or who are at risk of developing these conditions), particularly in early phase clinical trials.

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Gagliolo, Jean-Marie. "Rôle de la sénescence des fibroblastes dans la physiopathologie de la bronchopneumopathie chronique obstructive." Thesis, Paris Est, 2013. http://www.theses.fr/2013PEST1065.

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La sénescence, perte irréversible des capacités réplicatives des cellules associée à la sécrétion de médiateurs inflammatoires, pourrait participer au développement de l'atteinte pulmonaire dans la bronchopneumopathie chronique obstructive (BPCO) en initiant, maintenant et propageant un état inflammatoire. L'objectif de ce travail était d'évaluer les mécanismes de la sénescence impliqués dans l'induction et le maintien de l'inflammation au cours de la BPCO. Ainsi, des fibroblastes pulmonaires de témoins et de patients atteints de BPCO ont été mis en culture à long terme. Un phénotype sénescent majoré associée à un sécrétome pro-inflammatoire était détectée dans les fibroblastes de patients avec BPCO par rapport aux témoins. Par ailleurs, ces fibroblastes présentaient une expression accrue des récepteurs à la PGE2 (EP2 /4)au stade non sénescent et une production accrue de PGE2, un médiateur lipidique pro-inflammatoire, au stade sénescent. Dans cette optique, une partie du travail a consisté à déterminer si la PGE2 pouvait induire la sénescence et l'inflammation des fibroblastes pulmonaires de sujets atteints ou non de BPCO. Nous avons pu démontrer que la PGE2 synthétisée par les fibroblastes sénescents induisait, maintenait (effet autocrine) et propageait (effet paracrine) la sénescence et l'inflammation associée via une voie EP2/4 / COX-2 / oxydants / p53. L'implication des oxydants dans l'induction de la sénescence nous a conduit à étudier les effets de l'hème oxygénase (HO)-1, un système anti-oxydant et anti-inflammatoire sur la prévention de la sénescence des fibroblastes pulmonaires. Ainsi, des fibroblastes pulmonaires ont été traités chroniquement avec des substances pharmacologiques modulant l'activité d'HO-1. Des résultats préliminaires nous ont permis d'observer que l'activation de HO-1 prévenait l'induction de la sénescence chez des fibroblastes pulmonaires de témoins et de BPCO. Au total, la modulation des voies de la PGE2 et de l'HO-1 pourrait contribuer à limiter la sénescence des fibroblastes pulmonaires dans la BPCO Cellular senescence, a state of irreversible loss of replicative capacity associated with the secretion of inflammatory mediators, could participate in the development of chronic obstructive pulmonary disease (COPD) by initiating, maintaining and propagating an inflammatory state. The aim of this PhD project was to evaluate the mechanisms involved in senescence induction in COPD lung fibroblasts. COPD fibroblasts exhibited an increased senescent phenotype as compared to control cells. In addition, COPD fibroblasts showed an increased PGE2 receptors (EP2 /4) expression at non senescent stage and PGE2 production, apro-inflammatory lipid mediator at senescent stage. In this context, one part of the study was devoted to determine whether PGE2 could induce senescence of lung fibroblasts of subjects with and without COPD. We have shown that PGE2 synthesized by senescent fibroblasts induced, maintained (autocrine effect) and propagated (paracrine effect) senescence and associated inflammation via EP2 /4 / COX-2 / oxidants / p53 pathway. The essential role of oxidants production in the induction of senescence in COPD led us to study the effects of heme oxygenase (HO)-1, an antioxidant and anti-inflammatory system on the prevention of senescence in COPD fibroblasts. Pharmacological activation of HO-1 by hemin prevented the induction of senescence in lung fibroblasts from COPD patients probably in relation with an anti -oxidant effect. The modulation of PGE2 and HO-1 pathways may contribute to attenuate fibroblasts senescence in COPD

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Książki na temat "Emphysema"

Losso, Luis Carlos, Pallav L. Shah, Gerald J. Criner, Walter Weder, and José R. Jardim. Severe Pulmonary Emphysema:. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003251439.

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Grassi, C., J. Travis, L. Casali, and M. Luisetti, eds. Biochemistry of Pulmonary Emphysema. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3771-9.

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1926-, Grassi Carlo, and Workshop "Update in Biochemistry of Pulmonary Emphysema" (1990 : Pavia, Italy), eds. Biochemistry of pulmonary emphysema. London: Springer-Verlag, 1992.

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M, Nett Louise, ed. Enjoying life with emphysema. 2nd ed. Philadelphia: Lea & Febiger, 1987.

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Renkema, Tine Elisabeth Juliana. Pathogenesis and treatment of emphysema. [S.l: s.n.], 1996.

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C, Taylor Joseph, and Mittman Charles, eds. Pulmonary emphysema and proteolysis, 1986. Orlando: Academic Press, 1987.

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Haas, Francois. The chronic bronchitis and emphysema handbook. New York: Wiley, 1990.

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1956-, Fessler Henry E., Reilly John J. 1956-, and Sugarbaker David J, eds. Lung volume reduction surgery for emphysema. New York: Marcel Dekker, 2004.

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S, Banerjee, and Canadian Coordinating Office for Health Technology Assessment., eds. Lung volume reduction surgery for emphysema. Ottawa: Canadian Coordinating Office for Health Technology Assessment, 2005.

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Workshop, on Elastase Inhibitors for Treatment of Emphysema Approaches to Synthesis and Biological Evaluation (1985 Rockville Md ). Report of Workshop on Elastase Inhibitors for Treatment of Emphysema Approaches to Synthesis and Biological Evaluation, June 10-11, 1985. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1985.

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Części książek na temat "Emphysema"

Ye, Siqin. "Emphysema." In Encyclopedia of Behavioral Medicine, 755–57. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1292.

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Eisenberg, Ronald L. "Emphysema." In What Radiology Residents Need to Know: Chest Radiology, 153–59. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16826-1_12.

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LaCaille, Lara, Anna Maria Patino-Fernandez, Jane Monaco, Ding Ding, C. Renn Upchurch Sweeney, Colin D. Butler, Colin L. Soskolne, et al. "Emphysema." In Encyclopedia of Behavioral Medicine, 678–80. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1292.

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Cooley, Laura A., Daniel G. Bausch, Marija Stojkovic, Waldemar Hosch, Thomas Junghanss, Marija Stojkovic, Waldemar Hosch, et al. "Emphysema." In Encyclopedia of Intensive Care Medicine, 840. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1527.

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Al-Tubaikh, Jarrah Ali. "Emphysema." In Internal Medicine, 131–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03709-2_22.

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Inai, Kei, Alexander K. C. Leung, Jouni Uitto, Gerhard-Paul Diller, Michael A. Gatzoulis, John-John B. Schnog, Victor E. A. Gerdes, et al. "Emphysema." In Encyclopedia of Molecular Mechanisms of Disease, 572. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7260.

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Coomarasamy, Arri. "Surgical Emphysema." In Gynecologic and Obstetric Surgery, 208–9. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118298565.ch68.

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Cheng, Andy C. O. "Orbital Emphysema." In Emergencies of the Orbit and Adnexa, 157–58. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-1807-4_20.

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Shapiro, Steven D., and Robert M. Senior. "Pulmonary Emphysema." In Principles of Molecular Medicine, 339–47. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_38.

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Croake, Alexander, and Mary Frances Croake. "Subcutaneous Emphysema." In Essential Radiology Review, 147–49. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-26044-6_41.

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Streszczenia konferencji na temat "Emphysema"

San Jose Estepar, R., J. Kijewski, N. Wies, and G. R. Washko. "Emphysema Subtype Density Latent Metrics Predict Emphysema Progression." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6424.

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Zhang, Y. H., P. J. Castaldi, R. P. Bowler, C. P. Hersh, M. H. Cho, J. D. Morrow, and E. K. Silverman. "Multi-omics Analysis of Emphysema Predominant and Non-emphysema Predominant COPD." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4397.

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Carotenuto, Carlo, Francesco Orlandi, Luca Montorsi, and Massimo Milani. "CFD With Fluid Structure Interaction Analysis of Lung Alveolar Sacs and its Applications in Emphysema Study." In ASME 2023 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2023. http://dx.doi.org/10.1115/imece2023-109534.

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Abstract Emphysema, a chronic lung disease characterized by respiratory distress and reduced lung function, poses significant challenges. Computational Fluid Dynamics (CFD) coupled with fluid structure interaction (FSI) is a highly effective simulation technique that offers valuable insights into the mechanics of lung function and the influence of diseases like emphysema. The intricate lung alveolar sacs play a vital role in gas exchange, and CFD with FSI enables the simulation of mechanical forces that shape and impact their functionality. By employing CFD with FSI, we can simulate the fluid dynamics of emphysema and acquire a comprehensive understanding of disease progression. These simulations allow us to explore the contributions of tidal breathing and surface tension forces. This study has demonstrated through FSI that a lung alveolus affected by pulmonary emphysema, and therefore collapsed, causes reduced air intake with each breath. This is due to the significantly compromised deformability of the alveolar wall. Ultimately, this technique plays a critical role in developing therapeutic interventions to improve patient outcomes.

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Werz, J., J. Hahn, TK Hoffmann, and R. Riepl. "Emphysema after tooth problem." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1710900.

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Werz, J., J. Hahn, T. Hoffmann, and R. Riepl. "Emphysema after dental problems." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727746.

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Chen, C., L. Sørensen, F. Lauze, C. Igel, M. Loog, A. Feragen, M. de Bruijne, and M. Nielsen. "Towards exaggerated emphysema stereotypes." In SPIE Medical Imaging, edited by Bram van Ginneken and Carol L. Novak. SPIE, 2012. http://dx.doi.org/10.1117/12.911398.

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Tedrow, John, Brenda Juan-Guardela, David Gur, Joseph K. Leader, David A. Schwartz, Avrum Spira, Mark W. Geraci, et al. "Emphysema Gene Expression Signatures." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2271.

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Singh, H. "Pneumothorax With Extensive Subcutaneous Emphysema in Combined Pulmonary Fibrosis Emphysema (CPFE) Syndrome." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3217.

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Rivera Robles, J. D., I. Ahmad, D. Pendlebury, L. Sakr, A. P. Van, G. A. Heresi, J. P. Mehta, F. N. Rahaghi, and F. F. Rahaghi. "COPD Phenotypes: Out-of-Proportion Pulmonary Hypertension in Emphysema Vs. Non-emphysema COPD." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1146.

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Oakes, Jessica M., Alison L. Marsden, Celine Grandmont, Chantal Darquenne, and Irene E. Vignon-Clementel. "Multiscale Model of Airflow in Healthy and Emphysema Rat Lungs." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80418.

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An investigation of airflow is essential in understanding the fate of aerosol particles in healthy and diseased lungs. Emphysema is a heterogeneous disease that results in destroyed pulmonary tissue, alveolar space enlargement and oxygen delivery impairment. A numerical model of the entire lung will assist in understanding the ventilation and aerosol deposition changes that occur with emphysema. The pulmonary airflow cannot realistically be solved in 3D for the entire lung, therefore multiscale techniques must be used to simulate dynamics by coupling 3D and 0D models.

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Raporty organizacyjne na temat "Emphysema"

Wang, Yan, and Guowei Che. Prognostic impact of quantitative CT-defined emphysema in lung cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2024. http://dx.doi.org/10.37766/inplasy2024.6.0124.

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Hu, Yuqi, Chenyang Lv, Xiaonan Wang, Xiaowan Zhao, and Ai Cui. The prognosis and its clinical predictors of combined pulmonary fibrosis and emphysema comparison with idiopathic pulmonary fibrosis: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0081.

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CT Lung Densitometry, Consensus QIBA Profile. Chair Charles Hatt and Miranda Kirby. • The Publisher is Radiological Society of North America (RSNA)/Quantitative Imaging Biomarkers Alliance (QIBA), September 2020. https://doi.org/10.1148/qiba/20200904.

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The goal of a QIBA Profile is to achieve a repeatable and useful level of performance for measures of lung density from quantitative CT using the RA-950 HU and Perc15 biomarkers of emphysema. Please see Appendix C for more detailed information on the calculation of and rationale for RA-950 HU and Perc15 as the biomarkers of choice. The Claim (Section 2) describes the performance in terms of bias and precision of RA-950 HU and Perc15 for detecting change in lung density. The Activities (Section 3) describe how to generate RA-950 HU and Perc15 for longitudinal studies of the change in lung density. Requirements are placed on the Actors that participate in those activities as necessary to achieve the Claim in Section 2. Assessment Procedures (Section 4) for evaluating specific requirements are defined as needed. This QIBA Profile (CT: Lung Densitometry) addresses RA-950 HU and Perc15 for longitudinal studies which are often used as biomarkers of emphysema progression in chronic obstructive pulmonary disease (COPD) or as a response to cessation of smoking and possible future treatment approaches. It places requirements on Acquisition Devices, Physicists, Technologists, Clinicians, Statisticians, Reconstruction Software and Image Analysis Software involved in Product Qualification, Staff Qualification, Periodic Quality Assurance, Subject Handling, Protocol Design, Image Data Acquisition, Image Data Reconstruction, Image QA, Image Distribution and Image Analysis. The requirements are focused on achieving negligible bias and avoiding unnecessary variability of the RA-950 HU and Perc15 measurements by compensating for variations in CT number due to inconsistency of lung inflation volume and calibration of the CT scanner, and vendor-specific bias due to CT scanner make and model. To meet the claims, scanner calibration is performed using a well characterized imaging phantom ideally containing lung equivalent density foams as described in Section 4.1. The clinical performance targets are to achieve bias and repeatability such that a change in RA950 HU of ≥ 3.7% of the normalized lung volume, or a change in Perc15 of ≥ 11 HU after lung volume adjustment can be accepted as indicative of a true change (with 95% confidence). This document is intended to help clinicians basing decisions on these biomarkers, imaging staff generating these biomarkers, vendor staff developing related products, purchasers of such products and investigators designing trials with imaging endpoints. Note that this document only states requirements to achieve the claim, not “requirements for standard of care.” Conformance to this Profile is less important than providing appropriate patient care. The compilation of this document represents the efforts of many individuals over a several years of effort, some but not all of whom are acknowledged in Appendix A. QIBA Profiles addressing other imaging biomarkers using CT, MRI, PET and Ultrasound can be found at qibawiki.rsna.org.

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