Bibliografie tematiche / Lungs Inflammation

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Letteratura scientifica selezionata sul tema "Lungs Inflammation"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 27 gennaio 2023

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Articoli di riviste sul tema "Lungs Inflammation"

Kumar, Rajiv. "SARS-CoV-2, Inflammation, Allergy of the Lungs and Nanotherapeutics." International Journal of Clinical Case Reports and Reviews 11, no. 1 (April 4, 2022): 01–02. http://dx.doi.org/10.31579/2690-4861/208.

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Nanomaterials and nanotechnology are quite helpful in disease identification, prevention, treatment, scheming, and monitoring [4]. The properties of multifunctional nanomaterials altered by applying the strategies of nanotechnology and furnished for designing novel remedies for various medical applications. Furthermore, modified features of nanomaterials can influence their fate and also upgrade their claims in inhalation. Thus these types of nanoscale innovations achieved by adopting aforesaid strategies significantly. The nanotools and remedies treat viral infection and, in the end, also imp

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Le, Nguyen Phuong Khanh, Shankaramurthy Channabasappa, Mokarram Hossain, Lixin Liu, and Baljit Singh. "Leukocyte-specific protein 1 regulates neutrophil recruitment in acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 9 (November 1, 2015): L995—L1008. http://dx.doi.org/10.1152/ajplung.00068.2014.

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The mechanisms of excessive migration of activated neutrophils into inflamed lungs, credited with tissue damage, are not fully understood. We explored the hitherto unknown expression of leukocyte-specific protein 1 (LSP1) in human and mouse lungs and neutrophils and examined its role in neutrophil migration in acute lung inflammation. Autopsied septic human lungs showed increased LSP1 labeling in epithelium, endothelium, and leukocytes, including in their nuclei compared with normal lungs. We induced acute lung inflammation through intranasal administration of E. coli lipopolysaccharide (LPS)

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Lorenzo, Erica, Jacob Hopkins, Julie Lefebvre, and Laura Haynes. "Vaccination does not protect aged mice from influenza-induced lung inflammation (VAC9P.1062)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 145.2. http://dx.doi.org/10.4049/jimmunol.194.supp.145.2.

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Abstract Aging predisposes individuals to increased susceptibility to influenza infection and delays in viral clearance. Importantly, we show that age-related delays in viral clearance are correlated with lingering inflammation in the lungs of aged mice. This is critical since inflammation in the lungs is associated with an enhanced susceptibility to secondary bacterial infection, which is a significant sequela to flu infection and often causes death. Inflammation in young lungs following flu infection can be significantly reduced by prior flu immunity, such as that generated following vaccina

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Small, Donna M., Ryan R. Brown, Declan F. Doherty, Anthony Abladey, Zhe Zhou-Suckow, Rebecca J. Delaney, Lauren Kerrigan, et al. "Targeting of cathepsin S reduces cystic fibrosis-like lung disease." European Respiratory Journal 53, no. 3 (January 17, 2019): 1801523. http://dx.doi.org/10.1183/13993003.01523-2018.

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Cathepsin S (CatS) is upregulated in the lungs of patients with cystic fibrosis (CF). However, its role in CF lung disease pathogenesis remains unclear.In this study, β-epithelial Na+ channel-overexpressing transgenic (βENaC-Tg) mice, a model of CF-like lung disease, were crossed with CatS null (CatS−/−) mice or treated with the CatS inhibitor VBY-999.Levels of active CatS were elevated in the lungs of βENaC-Tg mice compared with wild-type (WT) littermates. CatS−/−βENaC-Tg mice exhibited decreased pulmonary inflammation, mucus obstruction and structural lung damage compared with βENaC-Tg mice.

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Ramos-Ramírez, Patricia, Carina Malmhäll, Kristina Johansson, Mikael Adner, Jan Lötvall, and Apostolos Bossios. "Lung Regulatory T Cells Express Adiponectin Receptor 1: Modulation by Obesity and Airway Allergic Inflammation." International Journal of Molecular Sciences 21, no. 23 (November 26, 2020): 8990. http://dx.doi.org/10.3390/ijms21238990.

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Regulatory T cells (Tregs) decrease in the adipose tissue upon weight gain, contributing to persistent low-grade inflammation in obesity. We previously showed that adipose tissue Tregs express the adiponectin receptor 1 (AdipoR1); however, the expression in lung Tregs is still unknown. Here, we aimed to determine whether Helios+ and Helios− Treg subsets expressed AdipoR1 in the lungs of obese mice and whether different obesity grades affected the expression upon allergic lung inflammation. For diet-induced obesity (DIO), mice were fed a high-fat diet (HFD) for up to 15 weeks (overweight), 21 w

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Chapoval, Svetlana P., Ann E. Kelly-Welch, Elizabeth Smith, and Achsah D. Keegan. "Complex role of STAT6 in allergic airway inflammation (39.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S27. http://dx.doi.org/10.4049/jimmunol.178.supp.39.11.

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Abstract STAT6 plays a critical role in Th2 cell differentiation and in allergic lung inflammation. Using a chimeric mouse model, we observed alternative lung pathology in STAT6 KO mice even when WT bone marrow or Th2 cells were provided. Thus, we hypothesized that STAT6 contributes to inflammation in a complex manner. To detail STAT6 function, WT and STAT6 KO mice were subjected to OVA priming and challenges. Broncho-alveolar lavage (BAL) cell composition, lung histology, and FACS analysis of digested lungs were assessed 48h after the last challenge. As expected, eosinophils composed a majori

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Herbein, Joel F., and Jo Rae Wright. "Enhanced clearance of surfactant protein D during LPS-induced acute inflammation in rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 1 (July 1, 2001): L268—L277. http://dx.doi.org/10.1152/ajplung.2001.281.1.l268.

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Pulmonary surfactant participates in the regulation of alveolar compliance and lung host defense. Surfactant homeostasis is regulated through a combination of synthesis, secretion, clearance, recycling, and degradation of surfactant components. The extracellular pool size of surfactant protein (SP) D fluctuates significantly during acute inflammation. We hypothesized that changes in SP-D levels are due, in part, to altered clearance of SP-D. Clearance pathways in rats were assessed with fluorescently labeled SP-D that was instilled into control lungs or lungs that had been treated with lipopol

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Ahn, So Yoon, Dong Kyung Sung, Yun Sil Chang, and Won Soon Park. "Intratracheal Transplantation of Mesenchymal Stem Cells Attenuates Hyperoxia-Induced Microbial Dysbiosis in the Lungs, Brain, and Gut in Newborn Rats." International Journal of Molecular Sciences 23, no. 12 (June 13, 2022): 6601. http://dx.doi.org/10.3390/ijms23126601.

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We attempted to determine whether intratracheal (IT) transplantation of mesenchymal stem cells (MSCs) could simultaneously attenuate hyperoxia-induced lung injuries and microbial dysbiosis of the lungs, brain, and gut in newborn rats. Newborn rats were exposed to hyperoxia (90% oxygen) for 14 days. Human umbilical cord blood-derived MSCs (5 × 105) were transplanted via the IT route on postnatal day (P) five. At P14, the lungs were harvested for histological, biochemical, and microbiome analyses. Bacterial 16S ribosomal RNA genes from the lungs, brain, and large intestine were amplified, pyrose

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Marín-Corral, Judith, Leticia Martínez-Caro, José A. Lorente, Marta de Paula, Lara Pijuan, Nicolas Nin, Joaquim Gea, Andrés Esteban, and Esther Barreiro. "Redox Balance and Cellular Inflammation in the Diaphragm, Limb Muscles, and Lungs of Mechanically Ventilated Rats." Anesthesiology 112, no. 2 (February 1, 2010): 384–94. http://dx.doi.org/10.1097/aln.0b013e3181c38bed.

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Background High tidal volume (VT) mechanical ventilation was shown to induce organ injury other than lung injury and systemic inflammation in animal models of ventilator-induced lung injury. The authors aimed to explore whether high VT mechanical ventilation per se induces early oxidative stress and inflammation in the diaphragm, limb muscles, and lungs of healthy rats exposed to ventilator-induced lung injury. Methods Protein carbonylation and nitration, antioxidants (immunoblotting), and inflammation (immunohistochemistry) were evaluated in the diaphragm, gastrocnemius, soleus, tibialis ante

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Bai, Jing, Shi-Lin Qiu, Xiao-Ning Zhong, Qiu-Ping Huang, Zhi-Yi He, Jian-Quan Zhang, Guang-Nan Liu, Mei-Hua Li, and Jing-Min Deng. "Erythromycin EnhancesCD4+Foxp3+Regulatory T-Cell Responses in a Rat Model of Smoke-Induced Lung Inflammation." Mediators of Inflammation 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/410232.

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Heavy smoking can induce airway inflammation and emphysema. Macrolides can modulate inflammation and effector T-cell response in the lungs. However, there is no information on whether erythromycin can modulate regulatory T-cell (Treg) response. This study is aimed at examining the impact of erythromycin on Treg response in the lungs in a rat model of smoking-induced emphysema. Male Wistar rats were exposed to normal air or cigarette smoking daily for 12 weeks and treated by gavage with 100 mg/kg of erythromycin or saline daily beginning at the forth week for nine weeks. The lung inflammation a

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Più fonti

Tesi sul tema "Lungs Inflammation"

McLennan, Geoffrey. "Oxygen toxicity and radiation injury to the pulmonary system." Title page, index and forward only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phm164.pdf.

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Bibliography: leaves 168-184. The work in this study encompasses oxygen free radical related inflammation in the peripheral lung and in lung cells. Animal and human studies have been used. Methods include cell culture with function studies, protein chemistry, animal and human physiology, and cell and lung structure through histopathology, and various forms of electron microscopy. The work resulting from this thesis has formed an important basis for understanding acute and chronic lung injury.

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Corsino, Betsy Ann 1962. "THE PULMONARY RESPONSE INDUCED BY GLASS FIBERS (INFLAMMATION, SILICOSIS, MURINE MODEL)." Thesis, The University of Arizona, 1986. http://hdl.handle.net/10150/291468.

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Dokka, Sujatha. "IL-10 gene therapy for the treatment of pulmonary inflammation." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1421.

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Thesis (Ph. D.)--West Virginia University, 2000.<br>Title from document title page. Document formatted into pages; contains ix, 132 p. : ill. (some col.) Vita. Includes abstract. Includes bibliographical references.

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Finlay, Alison. "Kinetics of pulmonary eosinophilia in a mouse model." Thesis, University of York, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245971.

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Karandashova, Sophia. "The Role of Ceramide in Neutrophil Elastase Induced Inflammation in the Lungs." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5468.

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Alterations to sphingolipid metabolism are associated with increased pulmonary inflammation, but the impact of inflammatory mediators, such as neutrophil elastase (NE), on airway sphingolipid homeostasis remains unknown. NE is a protease associated CF lung disease progression, and can be found in up to micromolar concentrations in patient airways. While sphingolipids have been investigated in the context of CF, the focus has been on loss of cystic fibrosis transmembrane conductance regulator (CFTR) function. Here, we present a novel observation: oropharyngeal aspiration of NE increases airway

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McDaniel, Dylan K. "Characterization of Biomedical and Incidental Nanoparticles in the Lungs and Their Effects on Health." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/86128.

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Nanomaterials are defined as any material with at least one external dimension less than 100 nm. Recently, nanomaterials have become more common in medicine, technology, and engineering. One reason for their increased interest is due to nanomaterials having unique properties that allow them to interact effectively with biological systems. In terms of drug delivery, the lungs are a highly desirable site to administer therapeutic nanoparticles. Indeed, inflammatory diseases such as asthma and emphysema could potentially benefit from nanoparticle-mediated delivery. However, the lungs are also in

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Zheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.

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Lewis, Joshua B. "Alterations in Tight Junctional Proteins and Their Effects on Pulmonary Inflammation." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6308.

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The lungs represent one of the earliest interfaces for pathogens and noxious stimuli to interact with the body. As such, careful maintenance of the permeability barrier is vital in providing homeostasis within the lung. Essential to maintaining this barrier is the tight junction, which primarily acts as a paracellular seal and regulator of ionic transport, but also contributes to establishing cell polarity, cell-to-cell integrity, and regulating cell proliferation and differentiation. The loss of these tight junctions has been documented to result in alterations in inflammation, and ultimat

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Lau, Kwok-wai, and 劉國威. "The involvement of serotoninergic system in cigarette smoke-induced oxidative stress and inflammation: relevantto chronic obstructive pulmonary disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47869616.

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Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD) with chronic airway inflammation as a key feature. Currently, no effective treatment can reduce the protracted inflammation in the lung of COPD. Further research on the inflammatory mechanisms would therefore be important in determining new potential therapeutic targets in COPD. Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter that plays an important role in pulmonary functions and inflammatory responses. The serotoninergic system including serotonin trans

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McNamara, Tracy Renee. "Chlamydia pneumoniae and airways inflammation : an investigation of the host cell-pathogen relationship /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phm4791.pdf.

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Più fonti

Libri sul tema "Lungs Inflammation"

1940-, Olivieri D., and Bianco S, eds. Airway obstruction and inflammation: Present status and perspectives. Basel: Karger, 1990.

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Criner, Gerard J., William D. Cornwell, and Thomas J. Rogers. Smoking and lung inflammation: Basic, pre-clinical, and clinical research advances. New York: Springer, 2013.

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L, Kradin Richard, and Robinson Bruce W. S, eds. Immunopathology of lung disease. Boston: Butterworth-Heinemann, 1996.

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Bertolini, Renzo. Animal and vegetable dusts as a cause of deep lung inflammation. Hamilton: CCOHS, 1988.

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Michel, Chignard, and Conference on Cytokines and Adhesion Molecules in Lung Inflammation (1995 : Paris, France), eds. Cytokines and adhesion molecules in lung inflammation. New York: New York Academy of Sciences, 1996.

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F, Donner C., ed. COPD is/is not a systemic disease? Hauppauge, NY: Nova Science, 2009.

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1952-, Strieter Robert M., Kunkel S. L, and Standiford Theodore J, eds. Chemokines in the lung. New York: Marcel Dekker, Inc., 2003.

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Rogers, Thomas J., Gerard J. Criner, and William D. Cornwell, eds. Smoking and Lung Inflammation. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0.

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Dubinett, Steven M., ed. Inflammation and Lung Cancer. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1.

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Alper, Scott, and William J. Janssen, eds. Lung Innate Immunity and Inflammation. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8.

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Capitoli di libri sul tema "Lungs Inflammation"

Marleau, S., C. Fortin, and P. Borgeat. "In Vivo Desensitization to LTB4-Induced Neutrophil Sequestration in Rabbit Lungs." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 261–63. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_51.

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Ulges, Alexander, Edgar Schmitt, Tobias Bopp, and Matthias Klein. "Messenger RNA Sequencing of Rare Cell Populations in the Lung and Lung-Draining Lymph Nodes." In Inflammation, 199–219. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6786-5_14.

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Sharma, Sherven, Siwen Hu-Lieskovan, Steven M. Dubinett, and Jay Moon Lee. "Inflammation and Lung Cancer: Addressing Inflammation with Immunotherapy." In Inflammation and Lung Cancer, 191–209. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_7.

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Porsbjerg, Celeste, and Unnur Björnsdóttir. "Biomarkers of eosinophilic inflammation." In Eosinophilic Lung Diseases, 37–50. Sheffield, United Kingdom: European Respiratory Society, 2022. http://dx.doi.org/10.1183/2312508x.10029520.

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Kennedy, Paul A., and Laurie E. Kilpatrick. "Neutrophil Inflammation in COPD." In Smoking and Lung Inflammation, 59–79. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0_3.

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Houghton, A. McGarry, and Steven D. Shapiro. "Inflammation and Lung Cancer: The Relationship to Chronic Obstructive Pulmonary Disease." In Inflammation and Lung Cancer, 1–21. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_1.

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Walser, Tonya C., Stacy J. Park, Jane Yanagawa, and Steven M. Dubinett. "Inflammation and Lung Cancer: The Role of Epithelial–Mesenchymal Transition." In Inflammation and Lung Cancer, 23–68. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_2.

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Kadara, Humam, Wilbur A. Franklin, and Ignacio I. Wistuba. "Inflammation and Lung Cancer: Molecular Pathology." In Inflammation and Lung Cancer, 69–93. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_3.

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Bauer, Alison K., York E. Miller, and Robert L. Keith. "Inflammation and Lung Cancer: Prevention." In Inflammation and Lung Cancer, 95–136. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_4.

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El Rayes, Tina, Raul Catena, Shahin Rafii, Nasser Altorki, and Vivek Mittal. "Inflammation and Lung Cancer: The Link to Angiogenesis." In Inflammation and Lung Cancer, 137–59. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1_5.

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Atti di convegni sul tema "Lungs Inflammation"

Kuroda, E., and KJ Ishii. "1707c Inhaled fine particles induce allergic inflammation in the lungs." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.145.

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Torres-Gonzalez, Edilson, Jeffrey D. Ritzenthaler, and Jesse Roman-Rodriguez. "Modulation Of Inflammation By Mid-Cervical Vagotomy In Murine Lungs." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5131.

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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 adopt

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Shirai, Atsushi, and Toshiyuki Hayase. "Effect of Neutrophils Retention Time in Capillaries on Increase in Their Concentration in a Lattice Capillary Network Model." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176717.

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Neutrophils are known as the most popular cells in leukocytes, and play important roles in immune system. They are retained in pulmonary capillary network even in normal lungs, causing higher concentration than in systemic circulation due to their low deformability [1]. The lungs can be a route for pathogenic substances to invade the host, since thickness of septa which separates blood and outer air is extremely thin. However, the highly concentrated neutrophils are thought to be effectively recruited to the sites of inflammation for the host defense. Therefore, it is essential to know how neu

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Glasser, Stephan W., Melissa D. Maxfield, Teah L. Witt, John E. Baatz, Henry T. Akinbi, and Tom Korfhagen. "LPS Exposure Increases Inflammation In The Lungs Of SP-C Deficient Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2454.

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Odom, C., Y. Kim, F. T. Korkmaz, E. Na, L. Baird, M. R. Jones, J. P. Mizgerd, K. Traber, and L. J. Quinton. "Liver Activity Reprograms the Lungs During Systemic Inflammation to Fortify Pulmonary Defense." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1262.

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Zhou, Haiying, Shawn He, Sean Gunsten, Steven Brody, Walter Akers, and Mikhail Y. Berezin. "NIR fluorescent contrast agents for detection of inflammation of lungs in vivo." In CLEO: Applications and Technology. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/cleo_at.2014.am2p.1.

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Chan, Y. L., B. Wang, H. Chen, K. F. Ho, and B. Oliver. "Impact of Traffic Related Air Pollutant Exposure on Lung Inflammation and Mitochondrial Wellbeing in Mouse Lungs." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1832.

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Titova, Olga, Natalya Kuzubova, Elena Lebedeva, Tatiana Preobrajenskaya, and Elizaveta Volchkova. "Influence of induced immunosupression on inflammation and lungs remodeling on the COPD model." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3853.

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Hamburg, Brian, Mei Hulver, Zeyu Xiong, Jeffrey Isenberg, and Janet S. Lee. "A Lack Of Thrombospondin-1 Predisposes The Lungs To Inflammation Following Exposure To Endotoxin." 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.a1087.

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Rapporti di organizzazioni sul tema "Lungs Inflammation"

Lin, Hongwei, Yanjun Gao, Kang Sun, and Faguang Jin. Association between PM2.5 pollution and outpatient visits for respiratory diseases in China: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0144.

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Review question / Objective: Previous epidemiological studies on the association between PM2.5 pollution and outpatient visits for respiratory diseases in China were mostly limited to one region， and the different papers have no coherent results. Our objective is to perform a systematic review and meta-analysis of the relevant literature in order to summarize the association between PM2.5 pollution and outpatient visits for respiratory diseases in multiple cities in China. Condition being studied: As an important component of air pollutants, particulate matter 2.5 (PM2.5) can float in the atmo

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Burgess, Jefferey L. Acute Lung Injury Following Smoke Inhalation: Predictive Value of Sputum Biomarkers and Time Course of Lung Inflammation. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada446886.

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Sun, Muzhen, Mei Cao, Yulian Zhang, and Xipeng Kang. Systemic immune inflammation index is a prognostic factor for small cell lung cancer: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0083.

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Czerwaty, Katarzyna, Karolina Dżaman, Krystyna Maria Sobczyk, and Katarzyna Irmina Sikrorska. The Overlap Syndrome of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0077.

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Abstract (sommario):

Review question / Objective: To provide the essential findings in the field of overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea, including prevalence, possible predictors, association with clinical outcomes, and severity compared to both chronic obstructive pulmonary disease and obstructive sleep apnea patients. Condition being studied: OSA is characterized by complete cessation (apnea) or significant decrease (hy-popnea) in airflow during sleep and recurrent episodes of upper airway collapse cause it during sleep leading to nocturnal oxyhemoglobin desatura

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Ma, He, Jifu Zhao, and Zhilei Wang. Efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0114.

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Abstract (sommario):

Review question / Objective: This study is the protocol for a systematic review to evaluate the efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease. we conducted a systematic review and meta-analysis of published randomized clinical trials (RCTs) of such combined therapy in the treatment of AECOPD, It provides a reliable scientific basis for clinicians to use this approach to treat AECOPD. Condition being studied: Chronic obstructive pulmonary disease is the third leading cause of death worldwide.

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