scholarly journals Dietary obesity in mice is associated with lipid deposition and metabolic shifts in the lungs sharing features with the liver

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
G. J. P. Rautureau ◽  
B. Morio ◽  
S. Guibert ◽  
C. Lefevre ◽  
J. Perrier ◽  
...  
Keyword(s):  
Pathological Process ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Respiratory Illnesses ◽  
Dietary Obesity ◽  
Obesity In Mice ◽  
Metabolite Quantification ◽  
A Minor ◽  
High Sucrose ◽  
Increased Susceptibility

AbstractObesity is associated with both chronic and acute respiratory illnesses, such as asthma, chronic obstructive pulmonary disease (COPD) or increased susceptibility to infectious diseases. Anatomical but also systemic and local metabolic alterations are proposed contributors to the pathophysiology of lung diseases in the context of obesity. To bring perspective to this discussion, we used NMR to compare the obesity-associated metabolomic profiles of the lung with those of the liver, heart, skeletal muscles, kidneys, brain and serum from male C57Bl/6J mice fed with a high-fat and high-sucrose (HFHSD) diet vs. standard (SD) chow for 14 weeks. Our results showed that the lung was the second most affected organ after the liver, and that the two organs shared reduced one-carbon (1C) metabolism and increased lipid accumulation. Altered 1C metabolism was found in all organs and in the serum, but serine levels were increased only in the lung of HFHSD compared to SD. Lastly, tricarboxylic acid (TCA)-derived metabolites were specifically and oppositely regulated in the serum and kidneys but not in other organs. Collectively, our data highlighted that HFHSD induced specific metabolic changes in all organs, the lung being the second most affected organ, the main alterations affecting metabolite concentrations of the 1C pathway and, to a minor extend, TCA. The absolute metabolite quantification performed in this study reveals some metabolic specificities affecting both the liver and the lung, that may reveal common metabolic determinants to the ongoing pathological process.

scholarly journals EVALUATION OF THE QUALITY OF LIFE IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE IN OVERWEIGHT PATIENTS

2020 ◽  
Vol 73 (8) ◽  
pp. 1668-1670
Author(s):  
Mykola M. Ostrovskyy ◽  
Nadiia V. Korzh
Keyword(s):  
Quality Of Life ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Body Mass ◽  
Pathological Process ◽  
The Body ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients

The aim: To evaluate the effect of overweight on the quality of life of chronic obstructive pulmonary disease (COPD) patients GOLD III. Materials and methods: 65 patients with chronic obstructive pulmonary disease (COPD GOLD III) were examined in different phases of pathological process. The pulmonary function (PF) test was performed by means of “SPIROKOM” device (Ukraine). The degree of overweight was determined by calculating the body mass index (BMI) using the formula І = m/h² (m – body mass in kilograms, h – height, square of the height in meters (kg/m²). Patients’ quality of life was evaluated with the help of standardized St.George’s Respiratory Questionnaire (SGRQ). Results: The study revealed changes in the PF indices and the decrease in quality of life in overweight patients, especially in case of destabilization of the pathological process. Conclusions: The obtained results show that overweight is the underlying condition for more severe course of the pathology and requires further study of its impact on the health and quality of life of patients in order to improve the effectiveness of treatment.

Chronic obstructive pulmonary disease and newly diagnosed tuberculosis: factors influencing outcome of the pathological process

Pharmateca ◽  
2018 ◽  
Vol 13_2018 ◽  
pp. 44-50
Author(s):  
N.V. Bagisheva () Bagisheva ◽  
V.V. Goltyapin () Goltyapin ◽  
A.V. Mordyk () Mordyk ◽  
D.I. Mordyk () Mordyk ◽  
◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Pathological Process ◽  
Chronic Obstructive ◽  
Newly Diagnosed ◽  
Obstructive Pulmonary Disease ◽  
Factors Influencing

scholarly journals Exploring Potential COPD Immunosuppression Pathways Causing Increased Susceptibility for MAC Infections among COPD Patients

2021 ◽  
Vol 11 (3) ◽  
pp. 619-630
Author(s):  
Shafaa Munjal ◽  
Shalok Munjal ◽  
Jingya Gao ◽  
Vishwanath Venketaraman
Keyword(s):  
Mycobacterium Avium ◽  
Opportunistic Pathogen ◽  
Developed Countries ◽  
The United States ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Susceptibility To Infection ◽  
Copd Patients ◽  
Respiratory Conditions ◽  
Increased Susceptibility

Although there has been a drastic decline in the cases of Tuberculosis in the United States, the prevalence of infections caused by Mycobacterium avium Complex (MAC) has steadily increased in the past decades. Mycobacterium avium (M. avium) is one of the most abundant microorganisms in the MAC species. The mycobacterium genus is divided into two major groups: tuberculosis causing mycobacteria and non-tuberculous mycobacteria. MAC is most prominent among the non-tuberculous mycobacteria. MAC is an opportunistic pathogen that is present in soil, water, and droplets in the air. MAC infections can result in respiratory disease and can disseminate in affected patients. MAC infections are especially prevalent in patients with preexisting respiratory conditions such as Chronic Obstructive Pulmonary Disease (COPD). COPD is one of the most common lung conditions in the world with the primary cause being smoking in developed countries. COPD involves chronic inflammation of lung tissue resulting in increased susceptibility to infection. There is a lack of research regarding the pathophysiology that leads COPD patients to be susceptible to MAC infection. Our review paper therefore aims to investigate how the pathogenicity of MAC bacteria and immune decline seen in COPD patients leads to a greater susceptibility to MAC infection among COPD patients.

scholarly journals Non-Malignant Respiratory Illnesses in Association with Occupational Exposure to Asbestos and Other Insulating Materials: Findings from the Alberta Insulator Cohort

2020 ◽  
Vol 17 (19) ◽  
pp. 7085
Author(s):  
Subhabrata Moitra ◽  
Ali Farshchi Tabrizi ◽  
Kawtar Idrissi Machichi ◽  
Samineh Kamravaei ◽  
Noushin Miandashti ◽  
...  
Keyword(s):  
Occupational Exposure ◽  
Pulmonary Function Tests ◽  
Prevalence Ratio ◽  
Cross Sectional Study ◽  
Chronic Obstructive ◽  
Ceramic Fibers ◽  
Cross Sectional ◽  
Obstructive Pulmonary Disease ◽  
Insulating Materials ◽  
Respiratory Illnesses

Many insulating materials are used in construction, although few have been reported to cause non-malignant respiratory illnesses. We aimed to investigate associations between exposures to insulating materials and non-malignant respiratory illnesses in insulators. In this cross-sectional study, 990 insulators (45 ± 14 years) were screened from 2011–2017 in Alberta. All participants underwent pulmonary function tests and chest radiography. Demographics, work history, and history of chest infections were obtained through questionnaires. Chronic obstructive pulmonary disease (COPD) was diagnosed according to established guidelines. Associations between exposures and respiratory illnesses were assessed by modified Poisson regression. Of those screened, 875 (88%) were males. 457 (46%) participants reported having ≥ 1 chest infection in the past 3 years, while 156 (16%) were diagnosed with COPD. In multivariate models, all materials (asbestos, calcium silicate, carbon fibers, fiberglass, and refractory ceramic fibers) except aerogels and mineral fibers were associated with recurrent chest infections (prevalence ratio [PR] range: 1.18–1.42). Only asbestos was associated with COPD (PR: 1.44; 95% confidence interval [CI]: 1.01, 2.05). Therefore, occupational exposure to insulating materials was associated with non-malignant respiratory illnesses, specifically, recurrent chest infections and COPD. Longitudinal studies are urgently needed to assess the risk of exposure to these newly implemented insulation materials.

The effect of CYP3A4 genetic variants on the susceptibility to chronic obstructive pulmonary disease in the Hainan Han population

2019 ◽  
Author(s):  
Huifang Shi ◽  
Jianguang Xu ◽  
Qiong Feng ◽  
Juan Sun ◽  
Yixiu Yang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Haplotype Analysis ◽  
Protective Role ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Han Population ◽  
Increased Risk ◽  
Control Study ◽  
Increased Susceptibility

Abstract PurposeGenetic polymorphisms act crucial role in chronic obstructive pulmonary disease (COPD) progression. This study was designed to investigate the correlation between CYP3A4 variants and COPD risk.MethodsWe carried out a case-control study of 821 individuals (313 patients and 508 healthy subjects) to identify the correlation of CYP3A4 SNPs with COPD risk in the Hainan Han population. The association was assessed by Odds ratios (OR) and 95% confidence intervals (CI).ResultsOur study showed that rs4646437 polymorphism was related to an increased susceptibility to COPD (OR = 1.45, 95% CI = 1.10-1.90, p = 0.008). Stratified analyses indicated that the rs4646437 polymorphism was significantly associated with an increased risk of COPD in males (OR = 1.95, 95% CI = 1.19-3.20, p = 0.008). However, rs4646440 played a protective role in females (OR = 0.54, 95% CI = 0.31-0.93, p = 0.024). The rs4646437 SNP was identified significantly improve the risk of COPD in smoking subjects (OR = 1.67, 95% CI = 1.12-2.48, p = 0.011). While rs4646440 had a significantly lower susceptibility to COPD with non-smoking individuals (OR = 0.64, 95% CI = 0.45-0.90, p = 0.010). Haplotype analysis revealed that Ars4646440Trs35564277 and Grs4646440Trs35564277 haplotypes of CYP3A4 were found to reduce the risk of COPD in non-smoking (OR = 0.61, 95% CI = 0.49-0.94, p = 0.024).ConclusionOur results would give some new understanding of the association between CYP3A4 gene and COPD in the Hainan Han population.

scholarly journals Drug-induced interstitial lung lesions

2018 ◽  
Keyword(s):  
General Condition ◽  
Morphological Changes ◽  
Beta Blockers ◽  
Lung Parenchyma ◽  
Pathological Process ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Drug Induced ◽  
Obstructive Pulmonary Disease ◽  
Lung Lesions

Drug-induced interstitial lung lesions (DIILL) are one of the most common forms of drug pneumopathy. DIILL account is about 3% in the structure of the entire interstitial lung pathology. Drugs induce various types of lesions of the lung parenchyma, often combining several histopathological patterns. Diagnostics of DIILL deals with many problems, since there are no specific clinical, morphological changes and specific markers. The diagnosis depends on the chronological dependence between taking the drug and the development of symptoms, and is confirmed by an improvement in the general condition of the patients after discontinuation of treatment. The aim of the work was to study the effect of various drugs on the development of DIILL, clinical diagnostic criteria, characteristic CT (computed tomography) and X-ray features, as well as the prognosis of the future course of the disease. We observed 12 patients with DIILL, which were divided into 2 groups: 1st group consisted of 4 patients with amiodarone lung, 2nd group of 8 patients, in which CT of the chest organs revealed an interstitial lesion of the lung tissue in the form of “frosted glass”. This gave us a reason to diagnose DIILL in patients who had CT scan in connection with suspected bronchocarcinoma in 3 patients, prolonged pneumonia in 3 patients and chronic obstructive pulmonary disease in 3 patients with fever. All patients took antibiotics of different groups a long time, ACE inhibitors, beta-blockers. The diagnosis of DIILL was made on the basis of the anamnesis of the patients, the CT data, as well as the positive dynamics of the general condition of the patients after the cancellation of the above medication. Diagnostic difficulties are often caused by late clinical and radiological manifestations or the lack of improvement after stopping the potentially “guilty” drug. However, timely diagnosis of DIILL is extremely important, since in many cases, the cancellation of the medication contributes to the resolution of the pathological process.

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