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Articoli di riviste sul tema "Lungs Pathophysiology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 28 gennaio 2023

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1

Bland, Richard D. "Pathophysiology of Neonatal Lung Injury." International Journal of Technology Assessment in Health Care 7, S1 (January 1991): 56–60. http://dx.doi.org/10.1017/s0266462300012514.

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Abstract (sommario):

Respiratory distress in newborn and young infants often develops as a result of acute lung injury, in which disruption of the normal barrier function of the pulmonary endothelium and epithelium causes protein-rich interstitial and alveolar edema. Several conditions may initiate acute lung injury, including aspiration of meconium or gastric contents, bacterial or viral infection, overzealous resuscitation, and birth associated with incomplete lung development that requires ventilatory support with positivepressure mechanical ventilation and high concentrations of inspired oxygen. The latter con

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2

Sundar, Isaac K., Hongwei Yao, Michael T. Sellix, and Irfan Rahman. "Circadian molecular clock in lung pathophysiology." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 10 (November 15, 2015): L1056—L1075. http://dx.doi.org/10.1152/ajplung.00152.2015.

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Disrupted daily or circadian rhythms of lung function and inflammatory responses are common features of chronic airway diseases. At the molecular level these circadian rhythms depend on the activity of an autoregulatory feedback loop oscillator of clock gene transcription factors, including the BMAL1:CLOCK activator complex and the repressors PERIOD and CRYPTOCHROME. The key nuclear receptors and transcription factors REV-ERBα and RORα regulate Bmal1 expression and provide stability to the oscillator. Circadian clock dysfunction is implicated in both immune and inflammatory responses to enviro

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van Zanden, Judith E., Henri G. D. Leuvenink, Erik A. M. Verschuuren, Michiel E. Erasmus, and Maximilia C. Hottenrott. "A translational rat model for ex vivo lung perfusion of pre-injured lungs after brain death." PLOS ONE 16, no. 12 (December 2, 2021): e0260705. http://dx.doi.org/10.1371/journal.pone.0260705.

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The process of brain death (BD) detrimentally affects donor lung quality. Ex vivo lung perfusion (EVLP) is a technique originally designed to evaluate marginal donor lungs. Nowadays, its potential as a treatment platform to repair damaged donor lungs is increasingly studied in experimental models. Rat models for EVLP have been described in literature before, yet the pathophysiology of BD was not included in these protocols and prolonged perfusion over 3 hours without anti-inflammatory additives was not achieved. We aimed to establish a model for prolonged EVLP of rat lungs from brain-dead dono

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Levvey, Bronwyn, Kovi Levin, Miranda Paraskeva, Glen Westall, and Gregory Snell. "Donation after Brain Death versus Donation after Circulatory Death: Lung Donor Management Issues." Seminars in Respiratory and Critical Care Medicine 39, no. 02 (March 26, 2018): 138–47. http://dx.doi.org/10.1055/s-0037-1615820.

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AbstractLung transplantation (LTx) has traditionally been limited by a lack of suitable donor lungs. With the recognition that lungs are more robust than initially thought, the size of the donor pool of available lungs has increased dramatically in the past decade. Donation after brain death (DBD) and donation after circulatory death (DCD) lungs, both ideal and extended are now routinely utilized. DBD lungs can be damaged. There are important differences in the public's understanding, legal and consent processes, intensive care unit strategies, lung pathophysiology, logistics, and potential-to

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5

Naramala, Srikanth, Sharmi Biswas, Sreedhar Adapa, Vijay Gayam, Romeo C. Castillo, Srinadh Annangi, and Venu Madhav Konala. "Pleomorphic Pulmonary Manifestations of IgG4-Related Disease." Case Reports in Rheumatology 2019 (August 20, 2019): 1–4. http://dx.doi.org/10.1155/2019/7572869.

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Immunoglobulin G4-related disease (IgG4-RD) is a fibroinflammatory disorder which has been first reported in 2001 by Hamano and colleagues in a patient with autoimmune sclerosing pancreatitis. Almost every organ in the human body can be affected by IgG4-RD from infiltration with IgG4-positive plasma cells. Involvement of lungs with IgG4 is reported previously, but still, there is no clear picture of the pathophysiology behind lung involvement. Here, we are presenting a patient who has IgG4-RD presenting as pseudotumor of the lungs.

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Agraval, Hina, and Hong Wei Chu. "Lung Organoids in Smoking Research: Current Advances and Future Promises." Biomolecules 12, no. 10 (October 12, 2022): 1463. http://dx.doi.org/10.3390/biom12101463.

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Tobacco smoking has been established to contribute to the pathogenesis of various respiratory diseases including chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. However, major hurdles in mechanistic studies on the role of smoking in human lungs remain in part due to the lack of ex vivo experimental models and ambiguous data from animal models that can best recapitulate the architecture and pathophysiology of the human lung. Recent development of the lung organoid culture system has opened new avenues for respiratory disease research as organoids are proving to be a sophi

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7

Das, Mita, W. Michael Zawada, James West, and Kurt R. Stenmark. "JNK2 regulates vascular remodeling in pulmonary hypertension." Pulmonary Circulation 8, no. 3 (May 2, 2018): 204589401877815. http://dx.doi.org/10.1177/2045894018778156.

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Pulmonary arterial (PA) wall modifications are key pathological features of pulmonary hypertension (PH). Although such abnormalities correlate with heightened phosphorylation of c-Jun N-terminal kinases 1/2 (JNK1/2) in a rat model of PH, the contribution of specific JNK isoforms to the pathophysiology of PH is unknown. Hence, we hypothesized that activation of either one, or both JNK isoforms regulates PA remodeling in PH. We detected increased JNK1/2 phosphorylation in the thickened vessels of PH patients’ lungs compared to that in lungs of healthy individuals. JNK1/2 phosphorylation parallel

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8

Frétaud, Maxence, Delphyne Descamps, Daphné Laubreton, Marie-Anne Rameix-Welti, Jean-François Eléouët, Thibaut Larcher, Marie Galloux, and Christelle Langevin. "New Look at RSV Infection: Tissue Clearing and 3D Imaging of the Entire Mouse Lung at Cellular Resolution." Viruses 13, no. 2 (January 28, 2021): 201. http://dx.doi.org/10.3390/v13020201.

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Background: Respiratory Syncytial Virus (RSV) is the major cause of severe acute respiratory tract illness in young children worldwide and a main pathogen for the elderly and immune-compromised people. In the absence of vaccines or effective treatments, a better characterization of the pathogenesis of RSV infection is required. To date, the pathophysiology of the disease and its diagnosis has mostly relied on chest X-ray and genome detection in nasopharyngeal swabs. The development of new imaging approaches is instrumental to further the description of RSV spread, virus–host interactions and r

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9

Raredon, Micha Sam Brickman, Taylor Sterling Adams, Yasir Suhail, Jonas Christian Schupp, Sergio Poli, Nir Neumark, Katherine L. Leiby, et al. "Single-cell connectomic analysis of adult mammalian lungs." Science Advances 5, no. 12 (December 2019): eaaw3851. http://dx.doi.org/10.1126/sciadv.aaw3851.

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Efforts to decipher chronic lung disease and to reconstitute functional lung tissue through regenerative medicine have been hampered by an incomplete understanding of cell-cell interactions governing tissue homeostasis. Because the structure of mammalian lungs is highly conserved at the histologic level, we hypothesized that there are evolutionarily conserved homeostatic mechanisms that keep the fine architecture of the lung in balance. We have leveraged single-cell RNA sequencing techniques to identify conserved patterns of cell-cell cross-talk in adult mammalian lungs, analyzing mouse, rat,

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Meyerowitz, Glen, and Igor Barjaktarevic. "369 The impact of asymmetric lung injury on gas and pressures distribution in a mechanical ventilation model with implementation of compartmentalized inspiratory hold." Journal of Clinical and Translational Science 6, s1 (April 2022): 69. http://dx.doi.org/10.1017/cts.2022.209.

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OBJECTIVES/GOALS: Asymmetries in lung pathophysiology can result in a maldistribution of gas between regions of the lungs which may generate dangerous pressures that are not observable by clinicians. Our study aims to demonstrate and quantify this through use of high-fidelity simulators to represent a range of commonly encountered clinical pathologies. METHODS/STUDY POPULATION: A benchtop study was performed with two high-fidelity breathing simulators, each representing one lung. This system allows for real-time monitoring of pressure and lung dynamics in a two-lung asymmetric injury model. On

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Chacón-Aponte, Ariana Alejandra, Érika Andrea Durán-Vargas, Jaime Adolfo Arévalo-Carrillo, Iván David Lozada-Martínez, Maria Paz Bolaño-Romero, Luis Rafael Moscote-Salazar, Pedro Grille, and Tariq Janjua. "Brain-lung interaction: a vicious cycle in traumatic brain injury." Acute and Critical Care 37, no. 1 (February 28, 2022): 35–44. http://dx.doi.org/10.4266/acc.2021.01193.

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The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respi

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12

Greenspan, Jay, Thomas Miller, and Thomas Shaffer. "The Neonatal Respiratory Pump: A Developmental Challenge with Physiologic Limitations." Neonatal Network 24, no. 5 (September 2005): 15–22. http://dx.doi.org/10.1891/0730-0832.24.5.15.

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Newborn lungs are particularly susceptible to pathophysiology. Respiratory distress commonly brings infants to the intensive care nursery. Premature birth compromises the infant’s ability to respond to early lung dysfunction because of the reduced functional reserve available at younger gestational ages. The respiratory pump consists of respiratory musculature and the chest wall. The respiratory pump is the physiologic “machine” that responds to lung pathology. From gestation onward, components of the pump undergo developmental changes that influence its compensatory ability in the neonate. Ca

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13

Armstead, Valerie E., Irina L. Opentanova, Alexander G. Minchenko, and Allan M. Lefer. "Tissue Factor Expression in Vital Organs during Murine Traumatic Shock." Anesthesiology 91, no. 6 (December 1, 1999): 1844. http://dx.doi.org/10.1097/00000542-199912000-00039.

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Background Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats. Methods Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger

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14

Romero-Lopez, Maria del Mar, Marc Oria, Miki Watanabe-Chailland, Maria Florencia Varela, Lindsey Romick-Rosendale, and Jose L. Peiro. "Lung Metabolomics Profiling of Congenital Diaphragmatic Hernia in Fetal Rats." Metabolites 11, no. 3 (March 18, 2021): 177. http://dx.doi.org/10.3390/metabo11030177.

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Congenital diaphragmatic hernia (CDH) is characterized by the herniation of abdominal contents into the thoracic cavity during the fetal period. This competition for fetal thoracic space results in lung hypoplasia and vascular maldevelopment that can generate severe pulmonary hypertension (PH). The detailed mechanisms of CDH pathogenesis are yet to be understood. Acknowledgment of the lung metabolism during the in-utero CDH development can help to discern the CDH pathophysiology changes. Timed-pregnant dams received nitrofen or vehicle (olive oil) on E9.5 day of gestation. All fetal lungs expo

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15

Reddy, R. Chandramouli, Basavaraj Devaranavadagi, and Kusal K. Das. "Nickel Induced Alteration of Pathophysiology of Lungs in Experimental Rats." Indian Journal of Public Health Research & Development 10, no. 8 (2019): 145. http://dx.doi.org/10.5958/0976-5506.2019.01867.9.

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Peterson, Steven. "Understanding the Sequence of Pulmonary Injury in the Extremely Low Birth Weight, Surfactant-Deficient Infant." Neonatal Network 28, no. 4 (July 2009): 221–29. http://dx.doi.org/10.1891/0730-0832.28.4.221.

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Human lung development begins around day 26 postconception and continues throughout early childhood. Many crucial events can affect this delicate tissue as it develops, leading to altered and abnormal growth and development of the lungs, thereby yielding a variety of morbidities and sometimes even mortality. Understanding the pathophysiology of lung injury in the extremely low birth weight neonate is essential when caring for these infants, especially during the first hours of life. This article provides bedside clinicians with foundational information related to acute lung injury and the sequ

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Amariei, Diana E., Neal Dodia, Janaki Deepak, Stella E. Hines, Jeffrey R. Galvin, Sergei P. Atamas, and Nevins W. Todd. "Combined Pulmonary Fibrosis and Emphysema: Pulmonary Function Testing and a Pathophysiology Perspective." Medicina 55, no. 9 (September 10, 2019): 580. http://dx.doi.org/10.3390/medicina55090580.

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Combined pulmonary fibrosis and emphysema (CPFE) has been increasingly recognized over the past 10–15 years as a clinical entity characterized by rather severe imaging and gas exchange abnormalities, but often only mild impairment in spirometric and lung volume indices. In this review, we explore the gas exchange and mechanical pathophysiologic abnormalities of pulmonary emphysema, pulmonary fibrosis, and combined emphysema and fibrosis with the goal of understanding how individual pathophysiologic observations in emphysema and fibrosis alone may impact clinical observations on pulmonary funct

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Kosutova, P., and P. Mikolka. "Aspiration syndromes and associated lung injury: incidence, pathophysiology and management." Physiological Research, S4 (December 30, 2021): S567—S583. http://dx.doi.org/10.33549//physiolres.934767.

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Aspiration is a common condition affecting healthy or sick patients which could create an acute or chronic inflammatory reaction in the lungs. Aspiration syndromes could be categorized according to a content entering the respiratory system into bacterial aspiration pneumonia with the gastric or oropharyngeal bacteria entering, aspiration chemical pneumonitis with bacteria-freegastric acid aspiration, or aspiration of a foreign body which causes an acute pulmonary emergency. There are differences in the clinical presentation of volume-dependent aspirations (microaspiration and macroaspiration):

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19

Marčetić, Dejan, Miroslav Samaržija, Andrea Vukić Dugac, and Jelena Knežević. "Angiotensin-Converting Enzyme 2 (ACE2) as a Potential Diagnostic and Prognostic Biomarker for Chronic Inflammatory Lung Diseases." Genes 12, no. 7 (July 9, 2021): 1054. http://dx.doi.org/10.3390/genes12071054.

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Chronic inflammatory lung diseases are characterized by uncontrolled immune response in the airways as their main pathophysiological manifestation. The lack of specific diagnostic and therapeutic biomarkers for many pulmonary diseases represents a major challenge for pulmonologists. The majority of the currently approved therapeutic approaches are focused on achieving disease remission, although there is no guarantee of complete recovery. It is known that angiotensin-converting enzyme 2 (ACE2), an important counter-regulatory component of the renin–angiotensin–aldosterone system (RAAS), is exp

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20

Arrigo, Mattia, Lars Christian Huber, Stephan Winnik, Fran Mikulicic, Federica Guidetti, Michelle Frank, Andreas J. Flammer, and Frank Ruschitzka. "Right Ventricular Failure: Pathophysiology, Diagnosis and Treatment." Cardiac Failure Review 5, no. 3 (November 4, 2019): 140–46. http://dx.doi.org/10.15420/cfr.2019.15.2.

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The prognostic significance of the right ventricle (RV) has recently been recognised in several conditions, primarily those involving the left ventricle, the lungs and their vascular bed, or the right-sided chambers. Recent advances in imaging techniques have created new opportunities to study RV anatomy, physiology and pathophysiology, and contemporary research efforts have opened the doors to new treatment possibilities. Nevertheless, the treatment of RV failure remains challenging. Optimal management should consider the anatomical and physiological particularities of the RV and include appr

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Barron, Luke, Amber Smith, Karim El Kasmi, Joseph Qualls, Xiaozhu Huang, Thomas Wynn, and Peter Murray. "Genetic analysis of arginase 1 in Th2-dominated lung inflammation (163.12)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 163.12. http://dx.doi.org/10.4049/jimmunol.186.supp.163.12.

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Abstract Arginase 1 (Arg1) expression in myeloid lineage cells, and especially alternatively-activated macrophages, increases dramatically in the lungs of mice with acute and chronic Th2-driven inflammation. Arg1 has been proposed to contribute to asthma pathogenesis by regulating at least four pathways: inhibiting the production of nitric oxide by substrate competition, regulating fibrosis and polyamine supply, regulating the bioavailability of arginine in the lung, and inhibiting T cell proliferation. Here we used mice lacking Arg1 in myeloid lineage cells, to investigate the contribution of

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Kelsey, Ryan, Fiona N. Manderson Koivula, Neville H. McClenaghan, and Catriona Kelly. "Cystic Fibrosis–Related Diabetes: Pathophysiology and Therapeutic Challenges." Clinical Medicine Insights: Endocrinology and Diabetes 12 (January 2019): 117955141985177. http://dx.doi.org/10.1177/1179551419851770.

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Cystic fibrosis–related diabetes (CFRD) is among the most common extrapulmonary co-morbidity associated with cystic fibrosis (CF), affecting an estimated 50% of adults with the condition. Cystic fibrosis is prevalent in 1 in every 2500 Caucasian live births and is caused by a mutation in the cystic fibrosis transmembrane conductance regulator ( CFTR) gene. Mutated CFTR leads to dehydrated epithelial surfaces and a build-up of mucus in a variety of tissues including the lungs and pancreas. The leading cause of mortality in CF is repeated respiratory bacterial infections, which prompts a decline

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Misra, Vikas, Hannah Lee, Anju Singh, Kewu Huang, Rajesh K. Thimmulappa, Wayne Mitzner, Shyam Biswal, and Clarke G. Tankersley. "Global expression profiles from C57BL/6J and DBA/2J mouse lungs to determine aging-related genes." Physiological Genomics 31, no. 3 (November 2007): 429–40. http://dx.doi.org/10.1152/physiolgenomics.00060.2007.

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This study identified gene expression profiles that provided evidence for genomic mechanisms underlying the pathophysiology of aging lung. Aging lungs from C57BL/6 (B6) and DBA/2 (D2) mouse strains differ in physiology and morphometry. Lungs were harvested from B6 mice at 2, 18, and 26 mo and from D2 mice at 2 and 18 mo of age. Purified RNA was subjected to oligonucleotide microarray analyses, and differential expression analyses were performed for comparison of various data sets. A significant majority of differentially expressed genes were upregulated with aging in both strains. Aging D2 lun

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Lindsey, Ashley S., Lydia M. Sullivan, Nicole A. Housley, Anna Koloteva, Judy A. King, Jonathon P. Audia, and Diego F. Alvarez. "Analysis of pulmonary vascular injury and repair during Pseudomonas aeruginosa infection-induced pneumonia and acute respiratory distress syndrome." Pulmonary Circulation 9, no. 1 (January 2019): 204589401982694. http://dx.doi.org/10.1177/2045894019826941.

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Herein we describe lung vascular injury and repair using a rodent model of Pseudomonas aeruginosa pneumonia-induced acute respiratory distress syndrome (ARDS) during: 1) the exudative phase (48-hour survivors) and 2) the reparative/fibro-proliferative phase (1-week survivors). Pneumonia was induced by intratracheal instillation of P. aeruginosa strain PA103, and lung morphology and pulmonary vascular function were determined subsequently. Pulmonary vascular function was assessed in mechanically ventilated animals in vivo (air dead space, PaO2, and lung mechanics) and lung permeability was dete

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Wagers, Scott, Lennart K. A. Lundblad, Mari Ekman, Charles G. Irvin, and Jason H. T. Bates. "The allergic mouse model of asthma: normal smooth muscle in an abnormal lung?" Journal of Applied Physiology 96, no. 6 (June 2004): 2019–27. http://dx.doi.org/10.1152/japplphysiol.00924.2003.

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Mice with allergically inflamed airways are widely used as animal models of asthma, but their relevance for human asthma is not understood. We, therefore, examined the time course of changes in respiratory input impedance during induced bronchoconstriction in BALB/c mice sensitized and challenged with ovalbumin. Our results indicate that bronchoconstriction in mice is accompanied by complete closure of substantial regions of the lung and that closure increases markedly when the lungs are allergically inflamed. With the aid of an anatomically accurate computational model of the mouse lung, we s

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Galaris, Apostolos, Dionysios Fanidis, Elli-Anna Stylianaki, Vaggelis Harokopos, Alexandra-Styliani Kalantzi, Panagiotis Moulos, Antigone S. Dimas, Pantelis Hatzis, and Vassilis Aidinis. "Obesity Reshapes the Microbial Population Structure along the Gut-Liver-Lung Axis in Mice." Biomedicines 10, no. 2 (February 19, 2022): 494. http://dx.doi.org/10.3390/biomedicines10020494.

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The microbiome is emerging as a major player in tissue homeostasis in health and disease. Gut microbiome dysbiosis correlates with several autoimmune and metabolic diseases, while high-fat diets and ensuing obesity are known to affect the complexity and diversity of the microbiome, thus modulating pathophysiology. Moreover, the existence of a gut-liver microbial axis has been proposed, which may extend to the lung. In this context, we systematically compared the microbiomes of the gut, liver, and lung of mice fed a high-fat diet to those of littermates fed a matched control diet. We carried ou

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Lindholm, Peter, and Claes EG Lundgren. "The physiology and pathophysiology of human breath-hold diving." Journal of Applied Physiology 106, no. 1 (January 2009): 284–92. http://dx.doi.org/10.1152/japplphysiol.90991.2008.

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This is a brief overview of physiological reactions, limitations, and pathophysiological mechanisms associated with human breath-hold diving. Breath-hold duration and ability to withstand compression at depth are the two main challenges that have been overcome to an amazing degree as evidenced by the current world records in breath-hold duration at 10:12 min and depth of 214 m. The quest for even further performance enhancements continues among competitive breath-hold divers, even if absolute physiological limits are being approached as indicated by findings of pulmonary edema and alveolar hem

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Hirleman, E., and DF Larson. "Cardiopulmonary bypass and edema: physiology and pathophysiology." Perfusion 23, no. 6 (November 2008): 311–22. http://dx.doi.org/10.1177/0267659109105079.

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Edema is a common morbidity following cardiopulmonary bypass (CPB) and can result in injury to many organs, including the heart, lungs, and brain. Generalized edema is also common and can lead to increased post-operative hospital stay and other morbidities. Pediatric patients are more susceptible to post-CPB edema and the consequences are more severe for this population. Hemodilution and systemic inflammatory responses are two suspected causes of CPB-related edema; however, the mechanisms involved are far from understood. Also, the common strategies to improve edema have not been completely su

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Wright, Joseph K., Lawrence T. Kim, Thomas E. Rogers, and Richard H. Turnage. "Prostaglandins potentiate U-46619-induced pulmonary microvascular dysfunction." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1167–74. http://dx.doi.org/10.1152/jappl.2000.88.4.1167.

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The induction of cyclooxygenase is an important event in the pathophysiology of acute lung injury. The purpose of this study was to examine the synergistic effects of various cyclooxygenase products (PGE2, PGI2, PGF2α) on thromboxane A2(TxA2)-mediated pulmonary microvascular dysfunction. The lungs of Sprague-Dawley rats were perfused ex vivo with Krebs-Henseleit buffer containing indomethacin and PGE2 (5 × 10− 8 to 1 × 10− 7 M), PGF2α (7 × 10− 9 to 5 × 10− 6 M), or PGI2 (5 × 10− 8 to 2 × 10− 5 M). The TxA2-receptor agonist U-46619 (7 × 10− 8 M) was then added to the perfusate, and then the cap

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Ambrosetti, Maria-Chiara, Giulia Battocchio, Stefania Montemezzi, Filippo Cattazzo, Tissjana Bejko, Evelina Tacconelli, Pietro Minuz, Ernesto Crisafulli, Cristiano Fava, and Giancarlo Mansueto. "The Caliber of Segmental and Subsegmental Vessels in COVID-19 Pneumonia Is Enlarged: A Distinctive Feature in Comparison with Other Forms of Inflammatory and Thromboembolic Diseases." Journal of Personalized Medicine 12, no. 9 (September 7, 2022): 1465. http://dx.doi.org/10.3390/jpm12091465.

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Background: The purpose of this study was to compare COVID-19 patients’ vessel caliber with that of normal lungs and lungs affected by other inflammatory and thromboembolic processes. Methods: between March and April 2020, 42 patients affected by COVID-19 pneumonia (COV-P) underwent CT scans of the lungs at Verona University Hospital for clinical indications. The lung images of four different groups of patients were compared (normal lung (NL), distal thromboembolism (DTE), and bacterial and fungal pneumonia (Bact-P, Fung-P)) by a radiologist with four years of experience. Results: The COV-P pa

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Nielsen, O. S., A. J. Munro, and I. F. Tannock. "Bone metastases: pathophysiology and management policy." Journal of Clinical Oncology 9, no. 3 (March 1991): 509–24. http://dx.doi.org/10.1200/jco.1991.9.3.509.

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The pathophysiology and options for management of bone metastases as well as criteria for determining response to therapy are reviewed. Bone metastases are frequently one of the first signs of disseminated disease in cancer patients. In the majority of patients, the primary tumor is in the breast, prostate, or lungs. Although almost all patients will die of their disease, a proportion of the patients will survive for several years. Treatment is primarily palliative: the intention is to relieve pain, prevent fractures, maintain activity and mobility, and, if possible, to prolong survival. Thera

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Marney, Samuel R. "Pathophysiology of Reactive Airway Disease and Sinusitis." Annals of Otology, Rhinology & Laryngology 105, no. 2 (February 1996): 98–100. http://dx.doi.org/10.1177/000348949610500203.

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The association between asthma and sinusitis was recognized more than a century ago. Since 1980, several studies have documented that severe asthma improved after coexisting sinusitis was effectively treated either medically or surgically. Because the mechanism relating sinusitis to asthma is not known, several theories have been proposed: 1) aspiration of infected sinus secretions into the lungs during sleep, 2) enhanced vagal stimulation in the infected sinus producing direct bronchospasm, 3) bronchospasm from excessive airway drying from mouth breathing, 4) production of bacterial toxins th

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Poloni, Tino Emanuele, Matteo Moretti, Valentina Medici, Elvira Turturici, Giacomo Belli, Elena Cavriani, Silvia Damiana Visonà, et al. "COVID-19 Pathology in the Lung, Kidney, Hearts and Brain: The Different Roles of T-Cells, Macrophages, and Microthrombosis." Cells 11, no. 19 (October 4, 2022): 3124. http://dx.doi.org/10.3390/cells11193124.

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Here, we aim to describe COVID-19 pathology across different tissues to clarify the disease’s pathophysiology. Lungs, kidneys, hearts, and brains from nine COVID-19 autopsies were compared by using antibodies against SARS-CoV-2, macrophages-microglia, T-lymphocytes, B-lymphocytes, and activated platelets. Alzheimer’s Disease pathology was also assessed. PCR techniques were used to verify the presence of viral RNA. COVID-19 cases had a short clinical course (0–32 days) and their mean age was 77.4 y/o. Hypoxic changes and inflammatory infiltrates were present across all tissues. The lymphocytic

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Roque, Willy, Alexandra Boni, Jose Martinez-Manzano, and Freddy Romero. "A Tale of Two Proteolytic Machines: Matrix Metalloproteinases and the Ubiquitin–Proteasome System in Pulmonary Fibrosis." International Journal of Molecular Sciences 21, no. 11 (May 29, 2020): 3878. http://dx.doi.org/10.3390/ijms21113878.

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Pulmonary fibrosis is a chronic and progressive lung disease characterized by the activation of fibroblasts and the irreversible deposition of connective tissue matrices that leads to altered pulmonary architecture and physiology. Multiple factors have been implicated in the pathogenesis of lung fibrosis, including genetic and environmental factors that cause abnormal activation of alveolar epithelial cells, leading to the development of complex profibrotic cascade activation and extracellular matrix (ECM) deposition. One class of proteinases that is thought to be important in the regulation o

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Aghali, Arbi, Maunick Lefin Koloko Ngassie, Christina M. Pabelick, and Y. S. Prakash. "Cellular Senescence in Aging Lungs and Diseases." Cells 11, no. 11 (May 29, 2022): 1781. http://dx.doi.org/10.3390/cells11111781.

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Abstract (sommario):

Cellular senescence represents a state of irreversible cell cycle arrest occurring naturally or in response to exogenous stressors. Following the initial arrest, progressive phenotypic changes define conditions of cellular senescence. Understanding molecular mechanisms that drive senescence can help to recognize the importance of such pathways in lung health and disease. There is increasing interest in the role of cellular senescence in conditions such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) in the context of understanding pathophysiology and ide

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Giucă, Adrian, Tea Gegenava, Carmen Marina Mihai, Ciprian Jurcuţ, Adrian Săftoiu, Diana Monica Gȋrniţă, Bogdan Alexandru Popescu, Nina Ajmone Marsan, and Ruxandra Jurcuț. "Sclerodermic Cardiomyopathy—A State-of-the-Art Review." Diagnostics 12, no. 3 (March 9, 2022): 669. http://dx.doi.org/10.3390/diagnostics12030669.

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Abstract (sommario):

Systemic sclerosis (SSc) is a chronic autoimmune disorder with unknown triggering factors, and complex pathophysiologic links which lead to fibrosis of skin and internal organs, including the heart, lungs, and gut. However, more than 100 years after the first description of cardiac disease in SSc, sclerodermic cardiomyopathy (SScCmp) is an underrecognized, occult disease with important adverse long-term prognosis. Laboratory tests, electrocardiography (ECG) and cardiovascular multimodality imaging techniques (transthoracic 2D and 3D echocardiography, cardiac magnetic resonance (CMR), and novel

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Sucre, Jennifer M. S., Dan Wilkinson, Preethi Vijayaraj, Manash Paul, Bruce Dunn, Jackelyn A. Alva-Ornelas, and Brigitte N. Gomperts. "A three-dimensional human model of the fibroblast activation that accompanies bronchopulmonary dysplasia identifies Notch-mediated pathophysiology." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 10 (May 15, 2016): L889—L898. http://dx.doi.org/10.1152/ajplung.00446.2015.

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Bronchopulmonary dysplasia (BPD) is a leading complication of premature birth and occurs primarily in infants delivered during the saccular stage of lung development. Histopathology shows decreased alveolarization and a pattern of fibroblast proliferation and differentiation to the myofibroblast phenotype. Little is known about the molecular pathways and cellular mechanisms that define BPD pathophysiology and progression. We have developed a novel three-dimensional human model of the fibroblast activation associated with BPD, and using this model we have identified the Notch pathway as a key d

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Bera, Monali, Bao Lu, Thomas Martin, Shun Cui, Craig Gerard, and Norma Gerard. "The C3a anaphylatoxin receptor is critical in the pathophysiology of RSV infection (49.2)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 49.2. http://dx.doi.org/10.4049/jimmunol.186.supp.49.2.

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Abstract Respiratory syncytial virus (RSV) is linked to severe lung disease and may lead to wheezing in infants. RSV infection in mice demonstrates infiltration of inflammatory cells, mucus cell metaplasia, and airway hyperresonsiveness (AHR) to methacholine. Previous studies demonstrated activation of complement by RSV. Other studies showed a requirement for C3 or C3a in AHR associated with antigen sensitization as well as inhalation of particulate matter. We hypothesized, therefore, that C3a is a critical component for the AHR associated with RSV infection. We found that mice lacking the C3a

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Weinberg, Frank, Robert P. Dickson, Deepak Nagrath, and Nithya Ramnath. "The Lung Microbiome: A Central Mediator of Host Inflammation and Metabolism in Lung Cancer Patients?" Cancers 13, no. 1 (December 22, 2020): 13. http://dx.doi.org/10.3390/cancers13010013.

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Abstract (sommario):

Lung cancer is the leading cause of cancer-related death. Over the past 5–10 years lung cancer outcomes have significantly improved in part due to better treatment options including immunotherapy and molecularly targeted agents. Unfortunately, the majority of lung cancer patients do not enjoy durable responses to these new treatments. Seminal research demonstrated the importance of the gut microbiome in dictating responses to immunotherapy in melanoma patients. However, little is known regarding how other sites of microbiota in the human body affect tumorigenesis and treatment responses. The l

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Hadjicharalambous, Marina R., and Mark A. Lindsay. "Idiopathic Pulmonary Fibrosis: Pathogenesis and the Emerging Role of Long Non-Coding RNAs." International Journal of Molecular Sciences 21, no. 2 (January 14, 2020): 524. http://dx.doi.org/10.3390/ijms21020524.

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Abstract (sommario):

Idiopathic pulmonary fibrosis (IPF) is a progressive chronic disease characterized by excessing scarring of the lungs leading to irreversible decline in lung function. The aetiology and pathogenesis of the disease are still unclear, although lung fibroblast and epithelial cell activation, as well as the secretion of fibrotic and inflammatory mediators, have been strongly associated with the development and progression of IPF. Significantly, long non-coding RNAs (lncRNAs) are emerging as modulators of multiple biological processes, although their function and mechanism of action in IPF is poorl

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Kim, Suhee, Hee Jin Park, and Sang-Il Lee. "The Microbiome in Systemic Sclerosis: Pathophysiology and Therapeutic Potential." International Journal of Molecular Sciences 23, no. 24 (December 18, 2022): 16154. http://dx.doi.org/10.3390/ijms232416154.

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Abstract (sommario):

Systemic sclerosis (SSc), also known as scleroderma, is an autoimmune disease with unknown etiology characterized by multi-organ fibrosis. Despite substantial investigation on SSc-related cellular and molecular mechanisms, effective therapies are still lacking. The skin, lungs, and gut are the most affected organs in SSc, which act as physical barriers and constantly communicate with colonized microbiota. Recent reports have documented a unique microbiome signature, which may be the pathogenic trigger or driver of SSc. Since gut microbiota influences the efficacy and toxicity of oral drugs, ev

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Hirata, Kazuto, Hiroshi Kanazawa, and Hiroshi Kamoi. "IV. Clinical aspects of delayed hypersensitivity in lungs: Pathophysiology of hypersensitivity disorders in clinics." Microscopy Research and Technique 53, no. 4 (2001): 307–12. http://dx.doi.org/10.1002/jemt.1097.

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Forgie, Keir A., Nicholas Fialka, Darren H. Freed, and Jayan Nagendran. "Lung Transplantation, Pulmonary Endothelial Inflammation, and Ex-Situ Lung Perfusion: A Review." Cells 10, no. 6 (June 7, 2021): 1417. http://dx.doi.org/10.3390/cells10061417.

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Abstract (sommario):

Lung transplantation (LTx) is the gold standard treatment for end-stage lung disease; however, waitlist mortality remains high due to a shortage of suitable donor lungs. Organ quality can be compromised by lung ischemic reperfusion injury (LIRI). LIRI causes pulmonary endothelial inflammation and may lead to primary graft dysfunction (PGD). PGD is a significant cause of morbidity and mortality post-LTx. Research into preservation strategies that decrease the risk of LIRI and PGD is needed, and ex-situ lung perfusion (ESLP) is the foremost technological advancement in this field. This review ad

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Renteria, L. S., E. Cruz, and B. O. Ibe. "Platelet-activating factor synthesis and receptor-mediated signaling are downregulated in ovine newborn lungs: relevance in postnatal pulmonary adaptation and persistent pulmonary hypertension of the newborn." Journal of Developmental Origins of Health and Disease 4, no. 6 (July 22, 2013): 458–69. http://dx.doi.org/10.1017/s2040174413000366.

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Abstract (sommario):

Platelet-activating factor (PAF) is a phospholipid with a wide range of biological activities. We studied PAF metabolism and PAF receptor (PAFR) signaling in perinatal ovine lungs to understand PAF's role in transition of the perinatal pulmonary hemodynamics and pathophysiology of persistent pulmonary hypertension of the newborn. We hypothesized that downregulation of PAF synthesis with upregulation of PAF catabolism by acetylhydrolase (PAF-Ah) in the newborn lung is needed for fetus-to-newborn pulmonary adaptation. Studies were conducted on fetal and newborn lamb pulmonary arteries (PA), vein

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Lilburn, David M. L., Clémentine Lesbats, Joseph S. Six, Eric Dubuis, Liang Yew-Booth, Dominick E. Shaw, Maria G. Belvisi, Mark A. Birrell, Galina E. Pavlovskaya, and Thomas Meersmann. "Hyperpolarized 83 Kr magnetic resonance imaging of alveolar degradation in a rat model of emphysema." Journal of The Royal Society Interface 12, no. 107 (June 2015): 20150192. http://dx.doi.org/10.1098/rsif.2015.0192.

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Abstract (sommario):

Hyperpolarized 83 Kr surface quadrupolar relaxation (SQUARE) generates MRI contrast that was previously shown to correlate with surface-to-volume ratios in porous model surface systems. The underlying physics of SQUARE contrast is conceptually different from any other current MRI methodology as the method uses the nuclear electric properties of the spin I = 9/2 isotope 83 Kr. To explore the usage of this non-radioactive isotope for pulmonary pathophysiology, MRI SQUARE contrast was acquired in excised rat lungs obtained from an elastase-induced model of emphysema. A significant 83 Kr T 1 relax

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Hsia, Connie C. W., and Merryn H. Tawhai. "What can imaging tell us about physiology? Lung growth and regional mechanical strain." Journal of Applied Physiology 113, no. 6 (September 15, 2012): 937–46. http://dx.doi.org/10.1152/japplphysiol.00289.2012.

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Abstract (sommario):

The interplay of mechanical forces transduces diverse physico-biochemical processes to influence lung morphogenesis, growth, maturation, remodeling and repair. Because tissue stress is difficult to measure in vivo, mechano-sensitive responses are commonly inferred from global changes in lung volume, shape, or compliance and correlated with structural changes in tissue blocks sampled from postmortem-fixed lungs. Recent advances in noninvasive volumetric imaging technology, nonrigid image registration, and deformation analysis provide valuable tools for the quantitative analysis of in vivo regio

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Høy Marbjerg, Lis, Christina Jacobsen, Jannik Fonager, Claus Bøgelund, Morten Rasmussen, Anders Fomsgaard, Jytte Banner, and Veronika Vorobieva Solholm Jensen. "Possible Involvement of Central Nervous System in COVID-19 and Sequence Variability of SARS-CoV-2 Revealed in Autopsy Tissue Samples: A Case Report." Clinical Pathology 14 (January 2021): 2632010X2110060. http://dx.doi.org/10.1177/2632010x211006096.

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Abstract (sommario):

The case presented here illustrates that interdisciplinary teamwork can be essential for the understanding of the COVID-19 disease presentation and enlightening of the pathophysiology. A 60-year-old woman without any comorbidities, apart from overweight, was found dead in her apartment after 14 days of home isolation due to suspicion of COVID-19. A forensic autopsy was performed. This revealed severely condensed, almost airless, firm lungs, and the cause of death was severe acute respiratory distress syndrome-associated with COVID-19 (SARS-CoV-2). In addition, SARS-CoV-2 was detected with reve

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Shrivastava, Bijal M., Kunal Kumar Jaiswal, Siddharth Budhreja, and Abhinav Tiwari. "Home environmental fungus: the hidden killer." International Journal of Contemporary Pediatrics 5, no. 2 (February 22, 2018): 667. http://dx.doi.org/10.18203/2349-3291.ijcp20180578.

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Abstract (sommario):

Hypersensitivity pneumonitis is generally attributed to inhalational organic dust, commonly due to exposure to dust at occupation or hobbies. Hypersensitivity pneumonitis or extrinsic allergic alveolitis is an inflammatory syndrome of lungs resulting from immunologically induced inflammation secondary to various airborne allergens. It is relatively rare in childhood. Knowledge of classical HRCT finding of lungs and use of antigen specific IgG and IgM antibodies (despite the false positive and false negative) analysis can act as supportive evidence for making diagnosis of Hypersensitivity pneum

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OBERT, MARTIN, STEFANIE HAGNER, GABRIELE A. KROMBACH, SELCUK INAN, and HARALD RENZ. "FRACTAL GEOMETRY ENABLES CLASSIFICATION OF DIFFERENT LUNG MORPHOLOGIES IN A MODEL OF EXPERIMENTAL ASTHMA." Fractals 23, no. 03 (July 31, 2015): 1550024. http://dx.doi.org/10.1142/s0218348x15500243.

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Abstract (sommario):

Animal models represent the basis of our current understanding of the pathophysiology of asthma and are of central importance in the preclinical development of drug therapies. The characterization of irregular lung shapes is a major issue in radiological imaging of mice in these models. The aim of this study was to find out whether differences in lung morphology can be described by fractal geometry. Healthy and asthmatic mouse groups, before and after an acute asthma attack induced by methacholine, were studied. In vivo flat-panel-based high-resolution Computed Tomography (CT) was used for mic

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Shiri Aghbash, Parisa, Hamed Ebrahimzadeh Leylabadlo, Hamidreza Fathi, Mohaddeseh Bahmani, Rojin Chegini, and Hossein Bannazadeh Baghi. "Hepatic Disorders and COVID-19: From Pathophysiology to Treatment Strategy." Canadian Journal of Gastroenterology and Hepatology 2022 (December 8, 2022): 1–15. http://dx.doi.org/10.1155/2022/4291758.

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Abstract (sommario):

Following the SARS-CoV-2 outbreak and the subsequent development of the COVID-19 pandemic, organs such as the lungs, kidneys, liver, heart, and brain have been identified as priority organs. Liver diseases are considered a risk factor for high mortality from the COVID-19 pandemic. Besides, liver damage has been demonstrated in a substantial proportion of patients with COVID-19, especially those with severe clinical symptoms. Furthermore, antiviral medications, immunosuppressive drugs after liver transplantation, pre-existing hepatic diseases, and chronic liver diseases such as cirrhosis have a

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