Relations Between Fractional-Order Model Parameters and Lung Pathology in Chronic Obstructive Pulmonary Disease

2009 ◽  
Vol 56 (4) ◽  
pp. 978-987 ◽  
Author(s):  
Clara M. Ionescu ◽  
Robin De Keyser
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Fractional Order ◽  
Chronic Obstructive ◽  
Model Parameters ◽  
Lung Pathology ◽  
Order Model ◽  
Obstructive Pulmonary Disease ◽  
Fractional Order Model

scholarly journals METABOLIC AND ADIPOCYTOKINE PRECONDITIONS FOR PROGRESSION OF NON-ALCOHOLIC STEATOHEPATITIS IN OBESITY PATIENTS DUE TO COMORBIDITY WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE

2020 ◽  
Vol 1 ◽  
pp. 28-35
Author(s):  
Olha Hryniuk ◽  
Oksana Khukhlina ◽  
Oksana Liakhovych ◽  
Viktoriia Hutsuliak ◽  
Snizhana Hnatkovych
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Total Cholesterol ◽  
Pulmonary Disease ◽  
Liver Steatosis ◽  
Blood Lipid ◽  
Atherogenic Index ◽  
High Density Lipoproteins ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Obstructive Pulmonary Disease

The increasing prevalence of chronic obstructive pulmonary disease (COPD) and nonalcoholic steatohepatitis (NASH) is a problem of high importance. Objective: to determine the state of blood lipid spectrum, glycemia, the degree of insulin resistance and their regulation by adipose tissue hormones in NASH patients against the background of obesity, depending on comorbidity with COPD. Methods. 130 patients were examined, including 35 NASH patients with obesity of the 1st stage (1 group), 60 NASH patients with obesity of the 1st stage and COPD 2-3 D (group 2), and 35 patients with COPD 2-3 D (group 3). Results: Blood lipid concentration in patients of the 1st and the 2nd groups exceeded the norm by 29.5% and 39.8% respectively (p<0.05). In the 3rd group - by 14.9% (p<0.05). The content of total cholesterol in the blood also points out its probable increase by 36.3%, 45.7% and 14.9% (p<0.05) in comparison with practically healthy individuals (PHI) in patients of the 1st, 2nd and 3rd groups. A probable increase in the concentration of triacylglycerols (TG) in blood (1.9 and 2.2 times, respectively (p<0.05)) was recorded in the 1st and 2nd groups of patients, while in patients of the 3rd group the changes were quite significant (1.6 times increase, p<0.05). Conclusions. Comorbidity of COPD in obese patients and NASH is an additional, powerful-inducing factor of lipid distress syndrome with significantly higher increase (compared with NASH without lung pathology) TG in blood, which form the basis of liver steatosis, total cholesterol, low density lipoproteins, with significantly higher decrease high density lipoproteins,  the atherogenic index, which are accompanied by hyperleptinemia, adiponectin deficiency, correlate with the degree of liver steatosis, fibrosis index, cytolytic activity, cholestatic, mesenchymal-inflammatory syndromes and are interrelated with hyperleptinemia, hypoadiponectinemia.

scholarly journals The EGFR-ADAM17 Axis in Chronic Obstructive Pulmonary Disease and Cystic Fibrosis Lung Pathology

2018 ◽  
Vol 2018 ◽  
pp. 1-22 ◽  
Author(s):  
Marta Stolarczyk ◽  
Bob J. Scholte
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Cystic Fibrosis ◽  
Pulmonary Disease ◽  
Molecular Mechanisms ◽  
Egf Receptor ◽  
Airway Epithelial Cells ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Obstructive Pulmonary Disease ◽  
Proinflammatory Mediators

Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF) share molecular mechanisms that cause the pathological symptoms they have in common. Here, we review evidence suggesting that hyperactivity of the EGFR/ADAM17 axis plays a role in the development of chronic lung disease in both CF and COPD. The ubiquitous transmembrane protease A disintegrin and metalloprotease 17 (ADAM17) forms a functional unit with the EGF receptor (EGFR), in a feedback loop interaction labeled the ADAM17/EGFR axis. In airway epithelial cells, ADAM17 sheds multiple soluble signaling proteins by proteolysis, including EGFR ligands such as amphiregulin (AREG), and proinflammatory mediators such as the interleukin 6 coreceptor (IL-6R). This activity can be enhanced by injury, toxins, and receptor-mediated external triggers. In addition to intracellular kinases, the extracellular glutathione-dependent redox potential controls ADAM17 shedding. Thus, the epithelial ADAM17/EGFR axis serves as a receptor of incoming luminal stress signals, relaying these to neighboring and underlying cells, which plays an important role in the resolution of lung injury and inflammation. We review evidence that congenital CFTR deficiency in CF and reduced CFTR activity in chronic COPD may cause enhanced ADAM17/EGFR signaling through a defect in glutathione secretion. In future studies, these complex interactions and the options for pharmaceutical interventions will be further investigated.

scholarly journals Comorbidity and thirty-day hospital readmission odds in chronic obstructive pulmonary disease: a comparison of the Charlson and Elixhauser comorbidity indices

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Russell G. Buhr ◽  
Nicholas J. Jackson ◽  
Gerald F. Kominski ◽  
Steven M. Dubinett ◽  
Michael K. Ong ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Standard Deviation ◽  
Pulmonary Disease ◽  
Model Fit ◽  
Sensitivity Analyses ◽  
Chronic Obstructive ◽  
Model Parameters ◽  
Standard Deviation Increase ◽  
Obstructive Pulmonary Disease ◽  
Comorbidity Index

Abstract Background Readmissions following exacerbations of chronic obstructive pulmonary disease (COPD) are prevalent and costly. Multimorbidity is common in COPD and understanding how comorbidity influences readmission risk will enable health systems to manage these complex patients. Objectives We compared two commonly used comorbidity indices published by Charlson and Elixhauser regarding their ability to estimate readmission odds in COPD and determine which one provided a superior model. Methods We analyzed discharge records for COPD from the Nationwide Readmissions Database spanning 2010 to 2016. Inclusion and readmission criteria from the Hospital Readmissions Reduction Program were utilized. Elixhauser and Charlson Comorbidity Index scores were calculated from published methodology. A mixed-effects logistic regression model with random intercepts for hospital clusters was fit for each comorbidity index, including year, patient-level, and hospital-level covariates to estimate odds of thirty-day readmissions. Sensitivity analyses included testing age inclusion thresholds and model stability across time. Results In analysis of 1.6 million COPD discharges, readmission odds increased by 9% for each half standard deviation increase of Charlson Index scores and 13% per half standard deviation increase of Elixhauser Index scores. Model fit was slightly better for the Elixhauser Index using information criteria. Model parameters were stable in our sensitivity analyses. Conclusions Both comorbidity indices provide meaningful information in prediction readmission odds in COPD with slightly better model fit in the Elixhauser model. Incorporation of comorbidity information into risk prediction models and hospital discharge planning may be informative to mitigate readmissions.

scholarly journals Bias away from the null due to miscounted outcomes? A case study on the TORCH trial

2017 ◽  
Vol 27 (10) ◽  
pp. 3151-3166 ◽  
Author(s):  
Stefanie Muff ◽  
Milo A Puhan ◽  
Leonhard Held
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Treatment Effect ◽  
Negative Binomial ◽  
Controlled Trial ◽  
Chronic Obstructive ◽  
Model Parameters ◽  
Unexpected Result ◽  
Validation Data ◽  
Obstructive Pulmonary Disease

Count outcomes occur in virtually all disciplines, such as medicine, epidemiology or biology, but they often contain error. Recently, it has been shown that self-reported numbers of exacerbations of Chronic Obstructive Pulmonary Disease patients can be considerably miscounted. Motivated by this result, we reanalysed data from the Towards a Revolution in Chronic Obstructive Pulmonary Disease Health trial, a large randomized controlled trial with the self-reported number of exacerbations of Chronic Obstructive Pulmonary Disease patients as outcome. To adjust for miscounting error in the response of Poisson and (zero-inflated) negative binomial models, we introduce novel, general methodology. The key idea is to formulate a zero-inflated negative binomial model to capture the error mechanism. This parametric approach automatically circumvents drawbacks of previously suggested methodology that treats miscounted outcomes in the misclassification framework. Prior information for the response error model parameters was elicited from validation data of an external study and adaptively weighted to account for potential prior-data conflict. The results of the Bayesian hierarchical modelling approach indicated that the treatment effect has been overestimated in the original study. However, closer inspection revealed that this unexpected result was an artefact of an unaccounted time dependency of the treatment effect.

scholarly journals Pulmonary infection with Mycobacterium szulgai: A case report

2019 ◽  
Vol 7 ◽  
pp. 2050313X1882344 ◽  
Author(s):  
Rex David S Gido ◽  
Amy L Wojciechowski ◽  
Rajinder PS Bajwa
Keyword(s):  
Risk Factors ◽  
Chronic Obstructive Pulmonary Disease ◽  
Case Report ◽  
Pulmonary Disease ◽  
Pulmonary Infection ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Obstructive Pulmonary Disease

Mycobacterium szulgai is a non-tuberculous mycobacterium that is an uncommon cause of infection in humans. Risk factors for infection include immunosuppression and pre-existing lung pathology. Herein, we present a case of a 42-year-old male with chronic obstructive pulmonary disease with pulmonary infection caused by M. szulgai that was successfully treated with a regimen of rifampin, isoniazid, pyrazinamide and ethambutol for 2 months, followed by rifampin, isoniazid and azithromycin for an additional 8 months. Symptomatic and radiographic resolutions were achieved.

scholarly journals Diminished ICAM-1 Expression and Impaired Pulmonary Clearance of Nontypeable Haemophilus influenzae in a Mouse Model of Chronic Obstructive Pulmonary Disease/Emphysema

2008 ◽  
Vol 76 (11) ◽  
pp. 4959-4967 ◽  
Author(s):  
Bing Pang ◽  
Wenzhou Hong ◽  
Shayla L. West-Barnette ◽  
Nancy D. Kock ◽  
W. Edward Swords
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Haemophilus Influenzae ◽  
Pulmonary Disease ◽  
Intercellular Adhesion Molecule ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Nontypeable Haemophilus Influenzae ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Clearance ◽  
Time Point

ABSTRACT The airways of patients with chronic obstructive pulmonary disease (COPD) are continually colonized with bacterial opportunists like nontypeable Haemophilus influenzae (NTHi), and a wealth of evidence indicates that changes in bacterial populations within the lung can influence the severity of COPD. In this study, we used a murine model for COPD/emphysema to test the hypothesis that COPD affects pulmonary clearance. Mice were treated with a pulmonary bolus of elastase, and as reported previously, the lungs of these mice were pathologically similar to those with COPD/emphysema at ∼1 month posttreatment. Pulmonary clearance of NTHi was significantly impaired in elastase-treated versus mock-treated mice. While histopathologic analysis revealed minimal differences in localized lung inflammation between the two groups, lower levels of intercellular adhesion molecule 1 (ICAM-1) were observed for the airway epithelial surface of elastase-treated mice than for those of control mice. Following infection, elastase-treated mice had lung pathology consistent with pneumonia for as long as 72 h postinfection, whereas at the same time point, mock-treated mice had cleared NTHi and showed little apparent pathology. Large aggregates of bacteria were observed within damaged lung tissue of the elastase-treated mice, whereas sparse individual bacteria were observed in lungs of mock-treated mice at the same time point postinfection. Additional infection studies showed that NTHi mutants with biofilm defects were less persistent in the elastase-treated mice than the parent strain. These findings establish a model for COPD-related infections and support the hypotheses that ICAM-1 promotes clearance of NTHi. Furthermore, the data indicate that NTHi may form biofilms within the context of COPD-related infections.

scholarly journals Association analysis between chronic obstructive pulmonary disease and polymorphisms in circadian genes

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9806
Author(s):  
Guo Chen ◽  
Jingwei Zhang ◽  
Lijuan Zhang ◽  
Xuan Xiong ◽  
Dongke Yu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Smoking Status ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Obstructive Pulmonary Disease ◽  
Circadian Genes ◽  
Significant Difference

Background Circadian genes have been suggested to play an important role in lung pathology. However, it remains unknown whether polymorphisms of these genes are associated with chronic obstructive pulmonary disease (COPD). Here, we aimed to investigate the association of circadian genes polymorphisms with COPD in a case-control study of 477 COPD patient and 323 control Han Chinese persons. Methods Genotyping assays were carried out for nine single nucleotide polymorphisms (SNPs) from five circadian genes (PER3, CLOCK, RORB, BMAL1 and CRY2) that were previously identified in lung pathology. Age, sex, BMI and smoking status and comorbidities were recorded for all subjects. Results No significant association was found in all SNP sites in overall subjects and no significant difference was found in age, sex, smoking status stratification analysis. Discussion The findings of this investigation indicated the effect of circadian genes polymorphisms on COPD susceptibility may only be small and possibly dependent on the subject factors, such as age and sex.

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