Risk Factor For COPD Research Articles

Understanding the Risk Factors, Burden, and Interventions for Chronic Respiratory Diseases in Low- and Middle-Income Countries: A Scoping Review

ObjectiveThis scoping review aims to identify risk factors for COPD and asthma, examine the burden and intervention measures, and clarify the findings in the context of climate change, with a particular focus on LMICs.MethodsFollowing the PRISMA-ScR guidelines, we conducted a scoping review using PubMed, Embase, and Scopus, focusing on studies published from 2011 to 2024.ResultsOur review included 52 studies that encompassed 244,004 participants. Predominantly conducted in SSA (n = 43, 83%) and Asia (n = 16, 31%), they address indoor and ambient air pollution, occupational hazards, and environmental conditions. Climate change exacerbates risks, varying regionally. SSA faces severe household and occupational exposures, while other LMICs deal with industrial and urban pollution. Stigma, social exclusion and economic burden underscore the necessity for intervention strategies (e.g., educational programs, pulmonary rehabilitation, low-emission cookstoves).ConclusionOur research shows a strong link between air pollution, occupational and environmental exposures, and the prevalence of COPD and asthma in LMICs. It suggests that targeted interventions are effective ways to mitigate these diseases and also highlights the significant impact of climate change on respiratory health.

Prevalence and Risk Factors of COPD Among Smokers in the Philippines

Prevalence and Risk Factors of COPD Among Smokers in the Philippines

Tobacco introduced Perilla frutescens and Ocimum basilicum genes attenuates neutrophilic inflammation in lung tissues of COPD rats

The new-type tobacco varieties “Zisu” and “Luole” were obtained by distant hybridization between N. tabacum L. var. HHY and Perilla frutescens and Ocimum basilicum, with obviously different chemical composition. Smoking is the major risk factor for COPD, characterized by neutrophil-dominant inflammation. In the present study, rat COPD model was established by cigarette exposure, and the health hazard of three varieties was compared by general condition observation, pathological and morphological evaluation, total and differential cell numeration, and characterization of major inflammatory mediators and MAPK/NF-κB pathway, etc. Rats in “HHY” group developed obvious symptoms such as cough, dyspnea, mental fatigue, etc., but these symptoms were obviously mitigated in “Zisu” and “Luole” groups. H&E staining analysis, including score, MLI, MAN, wt% and WA%, showed that “Zisu” and “Luole” significantly alleviated lung injury and the degree of airway remodeling and emphysema compared to “HHY”. In BALF, the number of total leukocyte and the percent neutrophils in “Zisu” and “Luole” groups were evidently lower than “HHY” group. The levels of inflammatory mediators, such as IL-8, MPO, MIP-2, LTB4, TNF-α and neutrophil elastase, in “HHY” group were obviously higher than “Zisu” and “Luole” groups. The ROS-mediated NF-κB p65 and p38MAPK pathways may play an important role. Results indicated that tobacco introduced perilla and basil genes could remarkably attenuate recruitment, infiltration and activation of neutrophils and intervene in airway inflammation, retarding disease progression, especially “Zisu”. Changes in chemical composition via breeding techniques may be a novel way for tobacco harm reduction.

COPD in Never-Smokers: BOLD Australia Study.

Tobacco smoking is the major risk factor for COPD, and it is common for other risk factors in never-smokers to be overlooked. We examined the prevalence of COPD among never-smokers in Australia and identified associated risk factors. We used data from the Australia Burden of Obstructive Lung Disease (BOLD) study, a cross-section of people aged ≥40 years from six sites. Participants completed interviews and post-bronchodilator spirometry. COPD was primarily defined as an FEV1/FVC ratio <0.70 and secondarily as the ratio less than the lower limit of normal (LLN). The prevalence of COPD in the 1656 never-smokers who completed the study was 10.5% (95% CI: 9.1-12.1%) [ratio<LLN 4.6%]. The likelihood of having COPD increased with advancing age [odds ratio (OR) 4.11 in those 60-69 years and OR 8.73 in those 70 years and older], having attained up to 12 years of education (OR 1.75) compared to those with more than 12 years, having a history of asthma (OR 2.30), childhood hospitalization due to breathing problems before age 10 years (OR 2.50), or having a family history of respiratory diseases (OR 2.70). Being overweight or obese was associated with reduced prevalence of COPD compared with being normal weight. In males and females, advanced age, a history of asthma, and childhood breathing problems before age 10 were factors that elevated the likelihood of COPD. However, in males, additional factors such as a higher body mass index and a family history of respiratory diseases also contributed to increased odds of COPD. COPD was prevalent in this population of never-smokers aged 40 years and over. This finding highlights the significance of risk factors other than smoking in the development of COPD.

Factors contributing in non-adherence to inhaler therapy among patients with obstructive airway diseases in a tertiary care setting

Medication adherence is crucial for managing respiratory conditions effectively. This study aimed to explore the multifaceted factors influencing medication adherence among patients with respiratory illnesses. A comprehensive analysis was conducted, focusing on patient demographics, characteristics, clinical factors, beliefs about medications, and reasons for irregular medication use. A cross-sectional design assessed medication adherence and beliefs in COPD patients through questionnaires. The study identified a middle-aged population (average age: 48.5 years) with high smoking prevalence, aligning with established COPD risk factors. Medication adherence scores indicated moderate levels (average ARMS score: 62.7), but with significant individual variation. Financial burden emerged as the primary barrier, with nearly 28% of participants reporting cost-related non-adherence, particularly impacting lower socioeconomic status (SES) patients. Social stigma regarding respiratory illness, a novel factor, influenced adherence, especially in urban areas (19.8% reported experiencing stigma). The study found a positive correlation between positive medication beliefs and adherence, highlighting the importance of fostering trust in treatment effectiveness. Additionally, a confirmed COPD diagnosis and specific inhaler devices (DPI, PMDI with spacer) were linked to improved adherence. This study identified significant factors impacting medication adherence in COPD, including financial constraints, social stigma, medication beliefs, and inhaler device type.

Biomass-related PM2.5 induced inflammatory microenvironment via IL-17F/IL-17RC axis

Biomass exposure is a significant environmental risk factor for COPD, but the underlying mechanisms have not yet been fully elucidated. Inflammatory microenvironment has been shown to drive the development of many chronic diseases. Pollution exposure can cause increased levels of inflammatory factors in the lungs, leading to an inflammatory microenvironment which is prevalent in COPD. Our findings revealed that IL-17F was elevated in COPD, while exposure to biomass led to increased expression of IL-17F in both alveolar epithelial and macrophage cells in mice. Blocking IL-17F could alleviate the lung inflammation induced by seven days of biomass exposure in mice. We employed a transwell co-culture system to simulate the microenvironment and investigate the interactions between MLE-12 and MH-S cells. We demonstrated that anti-IL-17F antibody attenuated the inflammatory responses induced by BRPM2.5 in MLE-12 and MH-S co-cultured with BRPM2.5-MLE-12, which reduced inflammatory changes in microenvironment. We found that IL-17RC, an important receptor for IL-17F, played a key role in the interactions. Knockout of IL-17RC in MH-S resulted in inhibited IL-17F signaling and attenuated inflammatory response after MH-S co-culture with BRPM2.5-MLE-12. Our investigation suggests that BRPM2.5 induces lung epithelial-macrophage interactions via IL-17F/IL-17RC axis regulating the inflammatory response. These results may provide a novel strategy for effective prevention and treatment of biomass-related COPD.

Keratin 15 protects against cigarette smoke-induced epithelial mesenchymal transformation by MMP-9

BackgroundChronic obstructive pulmonary disease (COPD), a chronic inflammatory lung disease, is a leading cause of morbidity and mortality worldwide. Prolonged cigarette smoking (CS) that causes irreversible airway remodeling and significantly reduces lung function is a major risk factor for COPD. Keratin15+ (Krt15+) cells with the potential of self-renewal and differentiation properties have been implicated in the maintenance, proliferation, and differentiation of airway basal cells; however, the role of Krt15 in COPD is not clear.MethodsKrt15 knockout (Krt15−/−) and wild-type (WT) mice of C57BL/6 background were exposed to CS for six months to establish COPD models. Krt15-CrePGR;Rosa26-LSL-tdTomato mice were used to trace the fate of the Krt15+ cells. Hematoxylin and eosin (H&E) and Masson stainings were performed to assess histopathology and fibrosis, respectively. Furthermore, lentivirus-delivered short hairpin RNA (shRNA) was used to knock down KRT15 in human bronchial epithelial (HBE) cells stimulated with cigarette smoke extract (CSE). The protein expression was assessed using western blot, immunohistochemistry, and enzyme-linked immunosorbent assay.ResultsKrt15−/− CS mice developed severe inflammatory cell infiltration, airway remodeling, and emphysema. Moreover, Krt15 knockout aggravated CS-induced secretion of matrix metalloproteinase-9 (MMP-9) and epithelial–mesenchymal transformation (EMT), which was reversed by SB-3CT, an MMP-9 inhibitor. Consistent with this finding, KRT15 knockdown promoted MMP-9 expression and EMT progression in vitro. Furthermore, Krt15+ cells gradually increased in the bronchial epithelial cells and were transformed into alveolar type II (AT2) cells.ConclusionKrt15 regulates the EMT process by promoting MMP-9 expression and protects the lung tissue from CS-induced injury, inflammatory infiltration, and apoptosis. Furthermore, Krt15+ cells transformed into AT2 cells to protect alveoli. These results suggest Krt15 as a potential therapeutic target for COPD.

Relationship between depression severity and respiratory symptoms in US adults: A national cross-sectional study

The relationship between depression severity and cough, wheeze and exertional dyspnoea is unclear. The aim of this study was to explore this relationship. We used weighted logistic regression analysis and fitted curves to explore the relationship between depression severity and respiratory symptoms. In addition, we examined the relationship between depression and COPD and asthma. Stratified analyses were used to analyse specific populations. We weighted 10,142 subjects to reflect the entire US population. Using the population without depression as a reference, the risk of cough and asthma in the severely depressed population was 3.32 times (OR 3.324, 95% CI 1.567-7.050) and 2.84 times (OR 2.842, 95% CI 1.521-5.311) higher than that in the population without depressive symptoms, and the risk of asthma and COPD was 2.4 times and 2.6 times (OR 2.410, 95% CI 1.371-4.236; OR 2.566, 95% CI 1.236-4.921). In subgroup analyses, the correlation between depression scores and prevalence of cough and wheeze was corrected for gender level. In addition, smoking status and marital status were interaction factors between depression score and prevalence of cough. The prevalence of exertional dyspnoea by depression score was influenced by CVD. Depression severity was associated with respiratory symptoms, asthma, and COPD. Gender corrected the correlation between depression and cough and asthma, and depressive state was an independent risk factor for asthma and COPD. This finding provides new ideas for the management of respiratory symptoms and diseases.

COPD in Non-Smokers in South Asia: An Under Estimated and Unrecognized Condition

COPD is an acronym used for chronic obstructive pulmonary disease. Globally, it is one of the leading causes of morbidity and mortality. It is among the significant causes of death in the developing countries of the world too. A major established causal risk factor for COPD is tobacco smoking.

Pattern of Chronic Obstructive Pulmonary Disease Patients

Abstract Background Chronic obstructive pulmonary disease (COPD) is a widespread chronic respiratory disease with rising morbidity and death, resulting in enormous societal and economic costs. COPD is a widespread, avoidable, and curable condition characterised by usual symptoms such as dyspnea, coughing, and/or sputum production. The goal of this study was to use a COPD questionnaire to analyse clinical, demographic, and available prescription pattern for chronic obstructive pulmonary disease. Results Our findings suggest that patients' early knowledge of COPD risk factors and symptoms, as well as assistance in early illness detection and the provision of patient-centered treatment based on patients' unique requirements in disease management, are all necessary. Conclusion The major objective of COPD management is to control symptoms and limit the risk of exacerbation in order to enhance the quality of life of patients. In addition to pharmaceutical management, achieving these goals necessitates the adoption of a healthy lifestyle and the avoidance of risk factors.

Lung function, respiratory symptoms and incident venous thromboembolism during a 44-year follow-up

BackgroundChronic obstructive pulmonary disease (COPD) and infections are risk factors for venous thromboembolism (VTE), but the reasons behind the associations are not fully known. Few studies have investigated whether lung function and respiratory symptoms in individuals without COPD are associated with VTE. ObjectivesTo study the incidence of VTE in individuals without COPD and other major VTE risk factors, in relation to baseline lung function and respiratory symptoms, through a 44-year follow-up prospective cohort study. MethodsAs part of a health screening program, a total of 20,253 men and 7361 women underwent a baseline examination from 1974 to 1992, including a spirometry test and a self-administered questionnaire about respiratory symptoms, e.g., chronic bronchitis, cough, phlegm, and dyspnoea. Lung function was assessed through quartiles of forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC). Through linkage with national registers, all individuals were followed for incidence of VTE. ResultsRespiratory symptoms (cough and dyspnoea) at baseline were associated with an increased risk of incident VTE in women after adjustments for age, height, BMI, smoking status, varicose veins, and FEV1/FVC. The adjusted hazard ratio in relation to chronic bronchitis was 1.57 (95% confidence interval 1.17–2.11). Poor lung function was not associated with an increased risk of VTE after adjustments for potential confounders. ConclusionWomen with respiratory symptoms of cough and dyspnoea without COPD have an increased risk of VTE, independent of lung function and major VTE risk factors. Further studies are needed to confirm the association and to study the clinical applicability of the results.

Mechanisms of lung damage in tuberculosis: implications for chronic obstructive pulmonary disease.

Pulmonary tuberculosis is increasingly recognized as a risk factor for COPD. Severe lung function impairment has been reported in post-TB patients. Despite increasing evidence to support the association between TB and COPD, only a few studies describe the immunological basis of COPD among TB patients following successful treatment completion. In this review, we draw on well-elaborated Mycobacterium tuberculosis-induced immune mechanisms in the lungs to highlight shared mechanisms for COPD pathogenesis in the setting of tuberculosis disease. We further examine how such mechanisms could be exploited to guide COPD therapeutics.

Single Nucleotide Polymorphisms of FAM13A Gene in Chronic Obstructive Pulmonary Disease-A Case Control Study in Vietnam.

In 2018, GOLD addressed the issues of genotypes associated with risk factors for COPD. The genome-wide association study (GWAS) demonstrated an association between COPD and several genetic variants of single nucleotide polymorphisms (SNPs) of the FAM13A gene with the risk of COPD. To study the single nucleotide polymorphisms rs2869967 and rs17014601 of the FAM13A gene in chronic obstructive pulmonary disease. Subjects and research methods: 80 subjects diagnosed with COPD and 80 subjects determined not to have COPD according to GOLD 2020 criteria; the subjects were clinically examined, interviewed, and identified as possessing single nucleotide polymorphisms using the sanger sequencing method on whole blood samples. The male/female ratio of the patient group and the control group was 79/1 and 39/1, respectively. The percentages of C and T alleles of rs2869967 in COPD patients were 50.6% and 49.4%, respectively. The percentages of C and T alleles of rs17014601 in COPD patients were 31.9% and 68.1%, respectively. At rs17014601, the ratio values of alleles T and C in the disease group and the control group were markedly different, making them statistically reliable (p = 0.031). The rate of CT genotype in the group of patients was considerably higher than that of the control group. The TT homozygous genotype had a lower risk of COPD compared with the other genotypes in the dominant model (ORTT/(CC + CT) = 0.441; CI95% = 0.233-0.833); this difference was statistically significant (p = 0.012). With rs17014601, it is characteristic that the frequency of the T allele appears more than the C allele, and the CT heterozygous phenotype accounts for the highest proportion in rs17014601 and rs2869967 recorded in COPD patients. There is an association between the genetic variant of the SNP FAM13A-rs17014601 and the risk of COPD.

Exhaled volatile organic compounds associated with risk factors for obstructive pulmonary diseases: a systematic review.

Asthma and COPD are among the most common respiratory diseases. To improve the early detection of exacerbations and the clinical course of asthma and COPD new biomarkers are needed. The development of noninvasive metabolomics of exhaled air into a point-of-care tool is an appealing option. However, risk factors for obstructive pulmonary diseases can potentially introduce confounding markers due to altered volatile organic compound (VOC) patterns being linked to these risk factors instead of the disease. We conducted a systematic review and presented a comprehensive list of VOCs associated with these risk factors. A PRISMA-oriented systematic search was conducted across PubMed, Embase and Cochrane Libraries between 2000 and 2022. Full-length studies evaluating VOCs in exhaled breath were included. A narrative synthesis of the data was conducted, and the Newcastle-Ottawa Scale was used to assess the quality of included studies. The search yielded 2209 records and, based on the inclusion/exclusion criteria, 24 articles were included in the qualitative synthesis. In total, 232 individual VOCs associated with risk factors for obstructive pulmonary diseases were found; 58 compounds were reported more than once and 12 were reported as potential markers of asthma and/or COPD in other studies. Critical appraisal found that the identified studies were methodologically heterogeneous and had a variable risk of bias. We identified a series of exhaled VOCs associated with risk factors for asthma and/or COPD. Identification of these VOCs is necessary for the further development of exhaled metabolites-based point-of-care tests in these obstructive pulmonary diseases.

MCP-4 and Eotaxin-3 Are Novel Biomarkers for Chronic Obstructive Pulmonary Disease.

The aim of our study was to examine the production of monocyte chemoattractant protein (MCP-4) and eotaxin-3 during the onset and progression of COPD. The expression levels of MCP-4 and eotaxin-3 were evaluated in COPD samples and healthy controls using immunostaining and ELISA. The relationship between the clinic pathological features in the participants and the expression of MCP-4 and eotaxin-3 were evaluated. The association of MCP-4/eotaxin-3 production in COPD patients was also determined. The results revealed enhanced production of MCP-4 and eotaxin-3 in COPD patients especially the cases with AECOPD in both bronchial biopsies and bronchial washing fluid samples. Furthermore, the expression signatures of MCP-4/eotaxin-3 show high AUC values in distinguishing COPD patients and healthy volunteers and AECOPD and stable COPD cases, respectively. Additionally, the number of MCP-4/eotaxin-3 positive cases was notably increased in AECOPD patients compared to those with stable COPD. Moreover, the expression of MCP-4 and eotaxin-3 was positively correlated in COPD and AECOPD cases. In addition, the levels of MCP-4 and eotaxin-3 could be increased in HBEs stimulated with LPS, which is a risk factor of COPD. Moreover, MCP-4 and eotaxin-3 may exert their regulatory functions in COPD by regulating CCR2, 3, and 5. These data indicated that MCP-4 and eotaxin-3 were potential markers for the clinical course of COPD, which could provide guidance for accurate diagnosis and treatment for this disease in future clinical practice.

Spatial distribution of unscheduled hospital admissions for chronic obstructive pulmonary disease in the central area of Asturias, Spain

BackgroundChronic obstructive pulmonary disease (COPD) is one of the major causes of mortality worldwide and also reports high morbidity rates and the global burden COPD has continued to rise over the last several decades. The best-known COPD risk factors are tobacco smoke and air pollution, but genetics, age, sex, and socioeconomic status are additional factors. This study aimed to assess the spatial distribution of unscheduled COPD hospital admissions of men and women in the central area of Asturias during 2016–2018 and identify trends, spatial patterns, or clusters in the area.MethodsUnscheduled COPD hospital admissions in the central area of Asturias were registered, geocoded, and grouped by census tracts (CTs), age, and sex. Standardized admission ratio, smoothed relative risk, posterior risk probability, and spatial clusters between relative risks throughout the study area were calculated and mapped.ResultsThe spatial distribution of COPD hospital admissions differed between men and women. For men, high-risk values were located primarily in the northwestern area of the study, whereas for women the cluster pattern was not as clear and high-risk CTs also reached central and southern areas. In both men and women, the north-northwest area included the majority of CTs with high-risk values.ConclusionsThe present study showed the existence of a spatial distribution pattern of unscheduled COPD hospital admissions in the central area of Asturias that was more pronounced for men than for women. This study could provide a starting point for generating knowledge about COPD epidemiology in Asturias.

Levels of teacher smoking and copd awareness: The case of Sanliurfa

Objective: This study aims to investigate the smoking status of teachers, the relationship between smoking and COPD, and teachers' awareness of COPD. Material and Method: 504 teachers participated in this cross-sectional study. The data was obtained through an online questionnaire utilizing a 22-question form designed by the researchers. Results: The mean age of the participants was 38.677.70 years, 47.8% of them were female, and 81.5% worked in public schools. 28% of teachers reported smoking. 24.4% of teachers reported living with a COPD patient, with 86.5% citing smoking as the major risk factor for COPD. 88.3% of participants indicated that avoiding tobacco products is crucial in preventing COPD. The majority of participants (92.7%) provided the correct response when asked about the symptoms of COPD. While 67.7% responded that PFT is used for diagnosis, 50.6% reported that it is a treatable disease, and 25% reported that inhaler medicines are used for treatment. There was a statistically significant distinction between the frequency of hearing about COPD and the specialties of the teachers. It was shown that 91.1% of smokers were aware of COPD, however, no statistical correlation was found between smoking and awareness. Conclusion: This study revealed that the prevalence of smoking among teachers in Sanliurfa was lower than previously reported in the literature. The level of awareness that COPD is a lung disease was found to be higher than in previous studies of a similar sort. It was established that awareness of the risk factors for COPD, its symptoms, preventive strategies, and the fact that COPD is a treatable disease was high. We believe that this awareness will play a crucial role in protecting students from smoking and various smoking-related diseases, such as COPD.

Impact of Previous Pulmonary Tuberculosis on Chronic Obstructive Pulmonary Disease: Baseline Results from a Prospective Cohort Study.

Pulmonary tuberculosis (PTB) is a significant risk factor for COPD, and Xinjiang, China, has a high incidence of pulmonary tuberculosis. The effects of tuberculosis history on airflow restriction, clinical symptoms, and acute episodes in COPD patients have not been reported in the local population. Besides, the exact relationship between lung function changes in people with a history of tuberculosis and COPD risk is not clear. This study is based on the Xinjiang baseline survey data included in the Natural Population Cohort Study in Northwest China from June to December, 2018. Subjects' questionnaires, physical examination, and lung function tests were performed through a face-to-face field survey to analyze the impact of previous pulmonary tuberculosis on local COPD. Furthermore, we clarified the specific relationship between pulmonary function decline and the probability of developing COPD in people with a history of tuberculosis. A total of 3249 subjects were eventually enrolled in this study, including 87 with a history of tuberculosis and 3162 non-TB. The prevalence of COPD in the prior TB group was significantly higher than that in the control group (p-value = 0.005). First, previous pulmonary tuberculosis is an essential contributor to airflow limitation in the general population and patients with COPD. In all subjects included, pulmonary function, FEV1% predicted (p-value < 0.001), and FEV1/FVC (%) (p-value < 0.001) were significantly lower in the prior TB group than in the control group. Compared to non-TB group, FEV1% prediction (p-value = 0.019) and FEV1/FVC (%) (p-value = 0.016) were found to be significantly reduced, and airflow restriction (p-value = 0.004) was more severe in prior TB group among COPD patients. Second, COPD patients in the prior TB group had more severe clinical symptoms. Compared with no history of tuberculosis, mMRC (p-value = 0.001) and CAT (p-value = 0.002) scores were higher in the group with a history of tuberculosis among COPD patients. Third, compared with the non-TB group, the number of acute exacerbations per year (p-values=0.008), the duration of each acute exacerbation (p-values=0.004), and hospitalization/ patient/year (p-values<0.001) were higher in the group with a history of tuberculosis among COPD patients. Finally, a dose-response relationship between FEV1/FVC (%) and the probability of developing COPD in people with previous pulmonary TB was observed; when FEV1/FVC (%) was < 80.8, the risk of COPD increased by 13.5% per unit decrease in lung function [0.865(0.805, 0.930)]. COPD patients with previous pulmonary tuberculosis have more severe airflow limitations and clinical symptoms and are at higher risk for acute exacerbations. Furthermore, lung function changes in people with a history of tuberculosis were associated with a dose-response relationship with the probability of developing COPD.

Prevalence of Common Risk Factors of Adhesive Capsulitis in Abbottabad, Khyber Pakhtunkhwa, Pakistan

This study was conducted to determine the prevalence of common risk factors among known cases of adhesive capsulitis in Abbottabad. Study was done on 253 patients selected through non-probability convenient sampling technique. Data was collected from Shaheena Jameel (Frontier) Hospital, Abbottabad, Ayub Medical Complex, Abbottabad and Physiotherapy Clinic of WIRS, Abbottabad and data was analyzed using SPSS version 27.0 and MS Excel 2010. This study showed that common risk factors of adhesive capsulitis were DM (29.2%), cardiac disease (14.2%), Stroke (12.4%), history of immobilization of shoulder joint (13%), upper limb neuropathies (8.3%), thyroid disorders (7.1%), COPD (6.3%), having two or more comorbidities or risk factors (4%) and idiopathicity (5.5%). This study showed that 56.5% patients got PT treatment and 43% patients did not seek PT treatment for frozen shoulder. This study concluded that systemic conditions, neurological diseases and immobilization were more prevalent risk factors of adhesive capsulitis in patients attending hospitals of Abbottabad. In small number of people, adhesive capsulitis was labeled idiopathic. Prevalence of usage of physiotherapy treatment was quite high among the patients of adhesive capsulitis.

Identification of exercise-regulated genes in mice exposed to cigarette smoke.

Cigarette smoke (CS) is the major risk factor for COPD and is linked to cardiopulmonary dysfunction. Exercise training as part of pulmonary rehabilitation is recommended for all COPD patients. It has several physiological benefits, but the mechanisms involved remain poorly defined. Here, we employed transcriptomic profiling and examined lung endothelium to investigate novel interactions between exercise and CS on cardiopulmonary alterations. Mice were exposed to 20 weeks of CS, CS + 6 weeks of high-intensity interval training on a treadmill, or control. Lung and cardiac (left and right ventricle) tissue were harvested and RNA-sequencing was performed and validated with RT-qPCR. Immunohistochemistry assessed pulmonary arteriolar changes. Transcriptome analysis between groups revealed 37 significantly regulated genes in the lung, 21 genes in the left ventricle, and 43 genes in the right ventricle (likelihood-ratio test). Validated genes that showed interaction between exercise and CS included angiotensinogen (p=0.002) and resistin-like alpha (p=0.019) in left ventricle, with prostacyclin synthetase different in pulmonary arterioles (p=0.004). Transcriptomic profiling revealed changes in pulmonary and cardiac tissue following exposure to CS, with exercise training exerting rescue effects. Exercise-regulated genes included angiotensinogen and resistin-like alpha, however, it remains unclear if these represent potential candidate genes or biomarkers that could play a role during pulmonary rehabilitation.