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1.
Int J Chron Obstruct Pulmon Dis ; 16: 1101-1107, 2021.
Article in English | MEDLINE | ID: mdl-33907396

ABSTRACT

Purpose: Previous research has indicated that female and male patients may experience different levels of symptoms. However, no studies of chronic obstructive pulmonary disease (COPD) patients have compared the number and types of symptom clusters identified in male and female patients. Therefore, the purpose of this study was to investigate gender differences in symptom clusters among COPD patients. Patients and Methods: A total of 371 eligible patients were enrolled in the study. We assessed nine COPD symptoms, namely, dyspnea, cough, sputum, chest tightness, sleep quality, fatigue, frailty, anxiety, and depression. Exploratory factor analyses were used to explore the underlying clusters of the COPD symptoms. Results: Underlying the nine symptoms, female patients had 2 clusters, and male patients had 3 clusters. Specifically, the three general symptoms poor sleep, fatigue, and frailty loaded on the same symptom cluster with anxiety and depression in female patients, while the same 3 general symptoms loaded on the same symptom cluster with chest tightness and dyspnea in male patients. Moreover, cough and sputum not only were more common in male patients but also loaded together on a separate symptom cluster. Conclusion: Our findings suggest that in order to improve fatigue, frailty, and poor sleep quality, symptom management strategies should more closely address anxiety and depression in female patients as well as chest tightness and dyspnea in male patients. Smoking cessation is particularly important in male COPD patients because they account for a much higher proportion of smokers and are more likely to have cough and sputum. These findings signify the importance of identifying and implementing gender-tailored symptom management strategies to relieve symptom burden in COPD patients to enhance their quality of life.


Subject(s)
Pulmonary Disease, Chronic Obstructive , Quality of Life , Dyspnea/diagnosis , Dyspnea/epidemiology , Dyspnea/etiology , Female , Humans , Male , Pulmonary Disease, Chronic Obstructive/diagnosis , Pulmonary Disease, Chronic Obstructive/epidemiology , Pulmonary Disease, Chronic Obstructive/therapy , Sex Factors , Syndrome
2.
J Cell Biochem ; 120(3): 3294-3305, 2019 03.
Article in English | MEDLINE | ID: mdl-30203496

ABSTRACT

The impact of particulate matter 2.5 (PM2.5) on the respiratory system is a worldwide concern. However, the mechanisms by which PM2.5 causes disease are still unclear. In this study, we investigated the effect of PM2.5 on autophagy and studied the effect of PM2.5-induced autophagy and 5'-adenosine monophosphate-activated protein kinase (AMPK) on cell proliferation, cell cycle, apoptosis, reactive oxygen species (ROS), and airway inflammation using human bronchial epithelial cells 16HBE140 cells. Results showed that exposure of cells to PM2.5 at a concentration of 100 µg/mL for 24 hours was most effective for inhibiting cell viability. PM2.5 induced cell arrest in the G0/G1 phase and increased mitochondrial membrane potential, ROS, and cell apoptosis with increasing concentration. PM2.5 downregulated cyclin D and matrix metallopeptidase-9 (MMP-9) expression but upregulated tissue inhibitor of metalloproteinases-1 (TIMP-1) expression, significantly promoted interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production, and enhanced the level and activation of AMPK. The levels of autophagy-related protein 5 (ATG5), Beclin-1, and LC3II/I were significantly increased by PM2.5. The activation of Unc-51-like autophagy activating kinase 1 was significantly inhibited by PM2.5. Moreover, ATG5 knockdown inhibited PM2.5-induced autophagy, ROS, and cell apoptosis significantly. The expression of cyclin D, MMP-9, and TIMP-1 was reversed by ATG5 suppression. PM2.5-induction of IL-6 and TNF-α was significantly inhibited by knockdown of ATG5. Thus, inhibition of autophagy protected the cells from PM2.5-induced injury. PM2.5 induced injury in human bronchial epithelial cells via activation of AMPK-mediated autophagy, suggesting possible therapeutic targets for the treatment of respiratory diseases.


Subject(s)
AMP-Activated Protein Kinases/metabolism , Autophagy/drug effects , Particulate Matter/toxicity , Apoptosis/drug effects , Autophagy-Related Protein 5/genetics , Autophagy-Related Protein 5/metabolism , Cell Line , Cell Survival/drug effects , Epithelial Cells/drug effects , Epithelial Cells/metabolism , Humans , Interleukin-6/metabolism , Membrane Potential, Mitochondrial/drug effects , Reactive Oxygen Species/metabolism , Tumor Necrosis Factor-alpha/metabolism
4.
Hip Int ; 22(2): 179-83, 2012.
Article in English | MEDLINE | ID: mdl-22547378

ABSTRACT

This study aimed to examine the association between hip joint effusion volume and osteonecrosis of the femoral head (ONFH) using the Association Research Circulation Osseous (ARCO) classification. Patients (n = 403) who were diagnosed with ONFH were enrolled between February 2005 and December 2008. Only patients (n = 109) with complete clinical and imaging data and at early to mid ARCO stage (I - III) were eligible for further analysis, including 94 males and 15 females. All the included patients had hip joint radiographic examinations (anteroposterior and frog-leg views) and magnetic resonance imaging scans (axial and coronal views). Out of 109 patients included in this study, 185 hip joints were involved (unilateral disease in 33 patients and bilateral diseases in 76 patients). The patients had a mean age of 39 ± 11 years (range, 13-70). All the affected hip joints exhibited effusion, classified as grade 1 (n = 70, 37.8%), grade 2 (n = 62, 33.5%), and grade 3 (n = 53, 28.7%). The volume of joint effusion varied significantly among stage I, II, and III (X2 = 29.210, P < 0.05). The effusion volume did not differ significantly among stage IIA, IIB, and IIC (X2 = 0.103, P > 0.05), whereas it differed significantly among stage IIIA, IIIB, and IIIC (X2 =11.556, P < 0.05). The volume of hip joint effusion was associated with the ARCO stage, and increased over the staging.


Subject(s)
Femur Head Necrosis/diagnosis , Femur Head/pathology , Hip Joint/pathology , Hydrarthrosis/pathology , Adolescent , Adult , Aged , Female , Femur Head/diagnostic imaging , Femur Head Necrosis/complications , Femur Head Necrosis/diagnostic imaging , Hip Joint/diagnostic imaging , Humans , Hydrarthrosis/diagnostic imaging , Hydrarthrosis/etiology , Magnetic Resonance Imaging , Male , Middle Aged , Radiography , Young Adult
5.
Zhongguo Fei Ai Za Zhi ; 13(5): 447-50, 2010 May.
Article in Chinese | MEDLINE | ID: mdl-20677640

ABSTRACT

BACKGROUND AND OBJECTIVE: Transbronchial needle aspiration (TBNA) and endobronchial ultrasound-guided TBNA (EBUS-TBNA) have been applied to the diagnosis for mediastinal lymph nodes. The aim of this study is to evaluate the clinical value and safety of TBNA and EBUS-TBNA on hilar and mediastinal lymph nodes of lung cancer patients. METHODS: Two hundred fifty patients with suspected lung cancer were enrolled. All petients with hilar and/or m lymphoadenopa-ediastinal thy found by CT scan received TBNA, biopsy and brushing. EBUS-TBNA was performed in 15 patients among them. RESULTS: Lung cancer were confirmed in 180 patients by TBNA, biopsy and brushing. The positive rates were 82.86%, 51.24% and 45.45%. Fifteen patients after EBUS-TBNA had a positive rate of 91.67%. CONCLUSION: TBNA and EBUS-TBNA were proved to be safe procedure with a high yield for the diagnosis ofhilar and mediastinal lymph nodes in lung cancer patients.


Subject(s)
Biopsy, Fine-Needle/methods , Bronchi/diagnostic imaging , Bronchi/pathology , Endosonography/methods , Lung Neoplasms/diagnosis , Lymph Nodes/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Female , Humans , Lung Neoplasms/diagnostic imaging , Lung Neoplasms/pathology , Male , Mediastinum/pathology , Middle Aged
6.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 21(3): 283-5, 2004 Jun.
Article in Chinese | MEDLINE | ID: mdl-15192839

ABSTRACT

OBJECTIVE: To investigate the relationship of angiotensin I-converting enzyme (ACE) gene polymorphism to diabetic retinopathy and diabetes myocardial infarction. METHODS: ACE insertion/deletion(I/D) polymorphism was determined by PCR. RESULTS: No evidence showed that ACE gene was associated with diabetic retinopathy. By comparison of the type 2 diabetes patients with myocardial infarction versus those without-myocardial infarction, it was found that the frequencies of homozygote DD (41.2% versus 33.2%) and of allele D (64.7% versus 55.0%) increased remarkably; the difference was statistically significant (P<0.05). CONCLUSION: Allele D(RR=1.50) and genotype DD(RR=1.33) seemed to be a genetic risk factor for type 2 diabetes myocardial infarction.


Subject(s)
Diabetes Mellitus, Type 2/complications , Diabetic Retinopathy/genetics , Myocardial Infarction/genetics , Peptidyl-Dipeptidase A/genetics , Polymorphism, Genetic , Adult , Aged , Diabetic Retinopathy/etiology , Female , Humans , Male , Middle Aged , Myocardial Infarction/etiology , Risk Factors
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