OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is a major health concern in northwest China; however, the impact of particulate matter (PM) exposure during sand-dust storms (SDS) remains poorly understood. Therefore, this study aimed to investigate the association between PM exposure on SDS days and COPD hospitalization risk in arid regions. METHODS: Data on daily COPD hospitalizations were collected from 323 hospitals from 2018 to 2022, along with the corresponding air pollutant and meteorological data for each city in Gansu Province. Employing a space-time-stratified case-crossover design and conditional Poisson regression, we analyzed 265,379 COPD hospitalizations. RESULTS: PM exposure during SDS days significantly increased COPD hospitalization risk [relative risk ( RR) for PM _2.5, lag 3:1.028, 95% confidence interval ( CI): 1.021-1.034], particularly among men and the elderly, and during the cold season. The burden of PM exposure on COPD hospitalization was substantially high in Northwest China, especially in the arid and semi-arid regions. CONCLUSION Our findings revealed a positive correlation between PM exposure during SDS episodes and elevated hospitalization rates for COPD in arid and semi-arid zones in China. This highlights the urgency of developing region-specific public health strategies to address adverse respiratory outcomes associated with SDS-related air quality deterioration.
Humans ; China/epidemiology* ; Pulmonary Disease, Chronic Obstructive/chemically induced* ; Particulate Matter/analysis* ; Hospitalization/statistics & numerical data* ; Male ; Female ; Middle Aged ; Aged ; Air Pollutants/analysis* ; Environmental Exposure/adverse effects* ; Spatio-Temporal Analysis ; Adult ; Sand ; Air Pollution

BACKGROUND: Glucocorticoids have been widely used to treat patients with chronic obstructive pulmonary disease (COPD). Nevertheless, corticosteroid insensitivity is a major barrier to the effective treatment of COPD and its mechanism remains unclear. This study aimed to evaluate the effect of cathelicidin LL-37 on corticosteroid insensitivity in COPD rat model, and to explore the involved mechanisms. METHODS: COPD model was established by exposing male Wistar rats to cigarette smoke combined with intratracheal instillation of lipopolysaccharide (LPS). Inhaled budesonide and LL-37 were consequently applied to COPD models separately or collectively to confirm the effects on inflammatory cytokines (tumor necrosis factor [TNF]-α and transforming growth factor [TGF]-β) by enzyme-linked immunosorbent assay (ELISA) and lung tissue histopathological morphology. Expression of histone deacetylase-2 (HDAC2) and phosphorylation of Akt (p-AKT) in lung were also measured. RESULTS: Briefly, COPD model rats showed an increased basal release of inflammatory cytokines (lung TNF-α: 45.7 ± 6.1 vs. 20.1 ± 3.8 pg/mL, P < 0.01; serum TNF-α: 8.9 ± 1.2 vs. 6.7 ± 0.5 pg/mL, P = 0.01; lung TGF-β: 122.4 ± 20.8 vs. 81.9 ± 10.8 pg/mL, P < 0.01; serum TGF-β: 38.9 ± 8.5 vs. 20.6 ± 2.3 pg/mL, P < 0.01) and COPD related lung tissue histopathological changes, as well as corticosteroid resistance molecular profile characterized by an increase in phosphoinositide 3-kinase (PI3K)/Akt (0.5 ± 0.1 fold of control vs. 0.2 ± 0.1 fold of control, P = 0.04) and a decrease in HDAC2 expression and activity (expression: 13.1 ± 0.4 μmol/μg vs. 17.4 ± 1.1 μmol/μg, P < 0.01; activity: 1.1 ± 0.1 unit vs. 1.4 ± 0.1 unit, P < 0.01), compared with control group. In addition, LL-37 enhanced the anti-inflammatory effect of budesonide in an additive manner. Treatment with combination of inhaled corticosteroids (ICS) and LL-37 led to a significant increase of HDAC2 expression and activity (expression: 15.7 ± 0.4 μmol/μg vs. 14.1 ± 0.9 μmol/μg, P < 0.01; activity: 1.3 ± 0.1 unit vs. 1.0 ± 0.1 unit, P < 0.01), along with decrease of p-AKT compared to budesonide monotherapy (0.1 ± 0.0 fold of control vs. 0.3 ± 0.1 fold of control, P < 0.01). CONCLUSIONS This study suggested that LL-37 could improve the anti-inflammatory activity of budesonide in cigarette smoke and LPS-induced COPD rat model by enhancing the expression and activity of HDAC2. The mechanism of this function of LL-37 might involve the inhibition of PI3K/Akt pathway.
Animals ; Antimicrobial Cationic Peptides ; pharmacology ; therapeutic use ; Glucocorticoids ; metabolism ; Histone Deacetylase 2 ; metabolism ; Humans ; Inflammation ; chemically induced ; drug therapy ; Lipopolysaccharides ; pharmacology ; Male ; Phosphatidylinositol 3-Kinases ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; metabolism ; Rats ; Rats, Wistar ; Smoking ; adverse effects ; Tumor Necrosis Factor-alpha ; metabolism

The aim of this study was to investigate the inhibitory effect of Cnidium monnieri fruit (CM) extracts on pulmonary inflammation induced in mice by cigarette smoke condensate (CSC) and lipopolysaccharide (LPS). Pulmonary inflammation was induced by intratracheal instillation of LPS and CSC five times within 12 days. CM extract was administered orally at a dose of 50 or 200 mg·kg(-1). The number of inflammatory cells in the bronchoalveolar lavage fluid was counted using a fluorescence activated cell sorter. Inflammatory mediator levels were determined by enzyme-linked immunosorbent assay. The administration of LPS and CSC exacerbated airway hyper-responsiveness (AHR) and induced an accumulation of inflammatory cells and mediators, and led to histological changes. However, these responses are modulated by treatment with CM, and the treatment with CM extract produces similar or more extensive results than the treatment with cyclosporin A (CSA). CM extract may have an inhibitory effect on pulmonary inflammation related with chronic obstructive pulmonary disease.
Animals ; Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Bronchoalveolar Lavage Fluid ; Cnidium ; Female ; Fruit ; Lipopolysaccharides ; Mice, Inbred BALB C ; Phytotherapy ; Plant Extracts ; pharmacology ; therapeutic use ; Pneumonia ; chemically induced ; drug therapy ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; pathology ; Smoke ; adverse effects ; Smoking ; adverse effects ; Tobacco Products ; adverse effects

OBJECTIVETo retrospectively investigate the clinical characteristics of sternal insufficiency fractures (SIFs) of post-menopausal women.

METHODSFindings on the clinical presentation, associated diseases, and imaging of SIFs in 17 postmenopausal women admitted to our hospital between February 1999 and January 2009 were reported.

RESULTSTwelve patients complained of severe pain in their anterior chest. Other symptoms included cough (5 cases), dyspnoea (3 cases), breathlessness (3 cases), and wheeze (2 cases). Four patients had no discomfort. The sternums of 11 cases were tender to palpation. Seventeen patients had osteoporosis. Other associated diseases were chronic obstructive pulmonary disease (7 cases), rheumatoid arthritis (3 cases), systemic lupus erythematosus (1 case), asthma (1 case), and thoracic vertebral fracture (13 cases). Nine patients had received glucocorticoid treatment. The fractures were located in the body of the sternum in 15 patients, in the manubrium in 1 patient, and in the manubriosternal junction in 1 patient. Displaced fracture was present in 13 cases. Lateral radiography of the sternum showed a fracture line in 14 patients. In the remaining 3 cases, other imaging examinations such as bone scan, computed tomography or magnetic resonance imaging demonstrated the presence of a fracture.

CONCLUSIONSOsteoporosis, glucocorticoid therapy, chronic obstructive pulmonary disease, and rheumatoid arthritis might be risk factors for SIFs. SIFs should be considered in the differential diagnosis of chest pain.

Aged ; Aged, 80 and over ; Arthritis, Rheumatoid ; complications ; epidemiology ; Cohort Studies ; Female ; Fractures, Bone ; diagnosis ; epidemiology ; etiology ; Fractures, Stress ; diagnosis ; epidemiology ; etiology ; Glucocorticoids ; adverse effects ; therapeutic use ; Humans ; Middle Aged ; Osteoporosis, Postmenopausal ; chemically induced ; complications ; epidemiology ; Postmenopause ; physiology ; Pulmonary Disease, Chronic Obstructive ; complications ; epidemiology ; Retrospective Studies ; Risk Factors ; Sternum ; injuries ; pathology

In clinical practice, we have found that cognitive impairment frequently occurs in chronic obstructive pulmonary disease (COPD) patients, but little is known about its pathophysiological mechanism. Given that brain-derived neurotrophic factor (BDNF) is affected by many factors such as smoking, infection, hypoperfusion and hypoxia, the present study was to explore the expression of BDNF in COPD rats. The rat COPD model was established by passive smoking and intratracheal instillation of lipopolysaccharide (LPS). Rats with the same age and gender ratios were divided into 4 groups: the control group (n = 6), the smoking group (n = 6), the LPS group (n = 6) and the smoking + LPS group (n = 6, COPD model). Level of BDNF in serum was measured by ELISA. And the expression of BDNF in the hippocampus was assessed using the immunohistochemistry and image analysis. The results showed that BDNF in the hippocampus and serum significantly increased in the smoking, LPS and smoking + LPS groups, compared to that in the control group. However, the expression of BDNF was less in the smoking + LPS group than that in the smoking or LPS group both in the hippocampus and serum. In conclusion, the expression of BDNF in the hippocampus and serum is highly increased in the COPD group. Smoking and intratracheal instillation of LPS induce the increase of BDNF level in the hippocampus and serum.
Animals ; Brain-Derived Neurotrophic Factor ; blood ; metabolism ; Disease Models, Animal ; Female ; Hippocampus ; metabolism ; Lipopolysaccharides ; Male ; Pulmonary Disease, Chronic Obstructive ; chemically induced ; metabolism ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Tobacco Smoke Pollution

The purpose of this study is to establish COPD animal model by intra-tracheal instillation of bleomycin (BLM) once and exposure to cigarette smoke for continuous 27 d, and to observe the effects of the inhalation on the model. At the 29th day, blood samples were taken from cervical artery for blood-gas analysis and parameters of lung function were recorded. Bronchoalveolar lavage fluid (BALF) was collected to measure intercellular adhesion molecule-1 (ICAM-1) concentration. The results showed that atomization inhaled resveratrol could alleviate rat COPD lung injury accompanied by amelioration of pathological changes, increase the ratio of forced expiratory volume in 0.3 s (FEV0.3) and forced vital capacity (FVC), and decrease the ICAM-1 level in BALF. The ultimate reduction of inflammatory factors was involved, at least in part, in the mechanism of resveratrol effects.
Animals ; Bleomycin ; Blood Gas Analysis ; Bronchoalveolar Lavage Fluid ; chemistry ; Disease Models, Animal ; Female ; Forced Expiratory Volume ; drug effects ; Intercellular Adhesion Molecule-1 ; metabolism ; Lung ; pathology ; Lung Compliance ; drug effects ; Male ; Maximal Midexpiratory Flow Rate ; drug effects ; Pulmonary Disease, Chronic Obstructive ; chemically induced ; metabolism ; pathology ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Smoking ; Stilbenes ; pharmacology