[Analysis of work stress and its influencing factors among nursing staff in Tianjin City].

Objective: To explore the current situation of work stress among nursing staff in Tianjin City and analyze its influencing factors. Methods: From August to October 2020, 26002 nursing staff from tertiary hospitals, secondary public hospitals, secondary private hospitals, primary hospitals, and other medical institutions in Tianjin City were selected as objects, and their general situation and working stress situation were surveyed by the general information questionnaire and the Nurse's Work Stressor Scale. Single factor analysis and multiple linear regression analysis were used to explore the influencing factors of work stress among nursing staff. Results: The average age of 26002 nursing staff was (33.86±8.28) years old, and the average working years were (11.84±9.12) years. There were 24874 women (95.66%) and 1128 men (4.34%). The total score of work stress was (79.82±21.69), and the average score of workload and time allocation dimension was the highest (2.55±0.79). The results of multiple linear regression analysis showed that marital status (ß=-0.015, P=0.014), employment form as contract system (ß=0.022, P=0.001), post as clinical nursing (ß=0.048, P<0.001), education level (ß=0.024, P<0.001), age (ß=0.050, P<0.001), working years (ß=0.075, P<0.001), and professional title (ß=0.036, P<0.001) were the influencing factors of work stress, which explained 22.8% of the total variation in work stress of nursing staff (F=24.25, P<0.001) . Conclusion: The work stress among nursing staff in Tianjin City is high, the corresponding departments and nursing managers should adopt scientific management methods to reduce the workload of nursing staff according to the influencing factors of work stress, so as to create a good atmosphere for further promoting the healthy development of nursing career and nursing industry in the new era.

Detection of Hole Pockets in the Candidate Type-II Weyl Semimetal MoTe_{2} from Shubnikov-de Haas Quantum Oscillations.

The bulk electronic structure of T_{d}-MoTe_{2} features large hole Fermi pockets at the Brillouin zone center (Γ) and two electron Fermi surfaces along the Γ-X direction. However, the large hole pockets, whose existence has important implications for the Weyl physics of T_{d}-MoTe_{2}, has never been conclusively detected in quantum oscillations. This raises doubt about the realizability of Majorana states in T_{d}-MoTe_{2}, because these exotic states rely on the existence of Weyl points, which originated from the same band structure predicted by density functional theory (DFT). Here, we report an unambiguous detection of these elusive hole pockets via Shubnikov-de Haas (SdH) quantum oscillations. At ambient pressure, the quantum oscillation frequencies for these pockets are 988 and 1513 T, when the magnetic field is applied along the c axis. The quasiparticle effective masses m^{*} associated with these frequencies are 1.50 and 2.77 m_{e}, respectively, indicating the importance of Coulomb interactions in this system. We further measure the SdH oscillations under pressure. At 13 kbar, we detected a peak at 1798 T with m^{*}=2.86m_{e}. Relative to the oscillation data at a lower pressure, the amplitude of this peak experienced an enhancement, which can be attributed to the reduced curvature of the hole pockets under pressure. Combining our experimental data with DFT+U calculations, where U is the Hubbard parameter, our results shed light on why these important hole pockets have not been detected until now.

Endobronchial valve for treatment of persistent air leak complicating spontaneous pneumothorax.

INTRODUCTION: Endobronchial one-way valves have been proposed as treatment for persistent air leak complicating spontaneous pneumothorax in which surgical intervention is not feasible. However, published data on efficacy, safety, and factors associated with success are scanty. METHODS: This is a retrospective study of 37 patients at a general hospital from 2008 to 2016. The impact of endobronchial valve implantation on the time to air-leak cessation after bronchoscopy was evaluated. RESULTS: The median patient age was 71 years. The majority of patients were males (92%), were ever-smokers (83%), had at least one co-morbidity (97%), and had secondary spontaneous pneumothorax (89%). Nineteen patients (51%) had a mean of 2.6 endobronchial valves implanted (range, 1-6). The air leak ceased within 72 hours for only eight patients (22% of the complete cohort), with immediate air-leak cessation after completion of endobronchial valve implantation. All six successful cases that had computed tomographic data of the thorax were shown to have bilateral intact interlobar fissures. The median (interquartile range) Charlson co-morbidity index was 1 (0.25-1) and 2 (1-3) for the success group and failure group, respectively (P=0.029). All patients in the no-endobronchial valve group survived, whereas three patients in the endobronchial valve group died within 30 days of endobronchial valve implantation. CONCLUSION: Only a small proportion of cases of endobronchial valve implantation for air leak complicating pneumothorax had unequivocal success. Intact bilateral interlobar fissures appear to be a necessary, though not sufficient, condition for success. Patients with fewer medical co-morbidities and immediate air-leak cessation after endobronchial valve implantation have a higher likelihood of success.

Optimising the utility of pleural fluid adenosine deaminase for the diagnosis of adult tuberculous pleural effusion in Hong Kong.

INTRODUCTION: Pleural fluid adenosine deaminase level can be applied to rapidly detect tuberculous pleural effusion. We aimed to establish a local diagnostic cut-off value for pleural fluid adenosine deaminase to identify patients with tuberculous pleural effusion, and optimise its utility. METHODS: We retrospectively reviewed the medical records of consecutive adults with pleural fluid adenosine deaminase level measured by the Diazyme commercial kit (Diazyme Laboratories, San Diego [CA], United States) during 1 January to 31 December 2011 in a cluster of public hospitals in Hong Kong. We considered its level alongside early (within 2 weeks) findings in pleural fluid and pleural biopsy, with and without applying Light's criteria in multiple scenarios. For each scenario, we used the receiver operating characteristic curve to identify a diagnostic cut-off value for pleural fluid adenosine deaminase, and estimated its positive and negative predictive values. RESULTS: A total of 860 medical records were reviewed. Pleural effusion was caused by congestive heart failure, chronic renal failure, or hypoalbuminaemia caused by liver or kidney diseases in 246 (28.6%) patients, malignancy in 198 (23.0%), non-tuberculous infection in 168 (19.5%), tuberculous pleural effusion in 157 (18.3%), and miscellaneous causes in 91 (10.6%). All those with tuberculous pleural effusion had a pleural fluid adenosine deaminase level of ≤100 U/L. When analysis was restricted to 689 patients with pleural fluid adenosine deaminase level of ≤100 U/L and early negative findings for malignancy and non-tuberculous infection in pleural fluid, the positive predictive value was significantly increased and the negative predictive value non-significantly reduced. Using this approach, neither additionally restricting analysis to exudates by Light's criteria nor adding closed pleural biopsy would further enhance predictive values. As such, the diagnostic cut-off value for pleural fluid adenosine deaminase is 26.5 U/L, with a sensitivity of 87.3%, specificity of 93.2%, positive predictive value of 79.2%, negative predictive value of 96.1%, and accuracy of 91.9%. Sex, age, and co-morbidity did not significantly affect prediction of tuberculous pleural effusion using the cut-off value. CONCLUSION: We have established a diagnostic cut-off level for pleural fluid adenosine deaminase in the diagnosis of tuberculous pleural effusion by restricting analysis to a level of ≤100 U/L, and considering early pleural fluid findings for malignancy and non-tuberculous infection, but not Light's criteria.

[Chinese expert consensus for non-antiinfective effects and clinical use of macrolides].

Important/potential value of macrolides has been proved in the management of chronic respiratory diseases by increasing basic and clinical trials.Through three face-to-face discussions, 10 experts examined important data and drafted this consensus related to macrolides: (1) mechanism of non-antiinfective effects; (2) clinical use in chronic respiratory diseases; (3) cautions of long-term use.The mechanism out of non-antiinfective effects includes anti-inflammatory effect, modifying airway secretion, immune-regulation related to antibacterial effect, corticoid saving effect and anti-viral effect.The efficacy of long-term use of low-dose macrolides is definitely confirmed in diffuse panbronchiolitis, chronic rhinosinusitis. It is considerably used in bronchiectasia, cystic fibrosis, severe asthma and chronic obstructive pulmonary disease. Further studies should be conducted in cryptogenic organizing pneumonia and respiratory viral infection. It should be paid attention to its possible adverse effects (including drug interactions, cardiac toxicity, ototoxicity and disturbance of intestinal flora) and drug resistance in long-term use.A Chinese consensus for non-antiinfective effects and clinical use of macrolides is developed for the first time, which aims to expand their rational use and the further research.

Mediastinal lymph node enlargement predicts progressive pulmonary fibrosis.

OBJECTIVE: To determine whether mediastinal lymph node enlargement (MLNE) predicts progressive pulmonary fibrosis (PPF).METHODS: A total of 800 patients hospitalised for interstitial lung diseases (ILDs) were included in our study. The clinical presentations, radiographic features and laboratory findings of the patients were reviewed.RESULTS: MLNE was present in 313 (39.1%) ILD patients and were associated with higher total fibrosis score and risk of death than ILD patients without MLNE. The risk factors for PPF were age (OR 1.044, 95% CI 1.020-1.069; P < 0.001), the total extent of fibrosis (OR 1.396, 95% CI 1.116-1.746; P = 0.003) and MLNE (OR 2.130, 95% CI 1.362-3.332; P = 0.001) compared to non-PPF. Multivariable analysis showed that age, the lactate dehydrogenase level, MLNE, the total fibrosis score and pulmonary arterial systolic pressure were risk/prognostic factors for ILD patients. The model was robust in patients with idiopathic pulmonary fibrosis. However, the only risk/prognostic factor common to other ILD subgroups was the total fibrosis score.CONCLUSIONS: MLNE is associated with higher total fibrosis score and worse prognosis in ILD patients and could predict the occurrence of PPF. The only risk/prognostic factor applicable to all subgroups of ILDs is the total pulmonary fibrosis score.

Outcome of adult critically ill patients mechanically ventilated on general medical wards.

OBJECTIVE. A significant number of critically ill mechanically ventilated patients are not admitted to the Intensive Care Unit but are cared for on general wards. This study looked at the outcome of these patients. DESIGN. Case series. SETTING. A 1100-bed tertiary hospital in Hong Kong. PATIENTS. All adult patients admitted in a 2.5-year period who received invasive mechanical ventilation on general medical wards without admission to Intensive Care Unit or other special care areas. INTERVENTIONS. Invasive mechanical ventilation. MAIN OUTCOME MEASURES. The observed number of deaths, the expected number of deaths as derived from the Mortality Probability Model II system admission model, and other morbidity measures. RESULTS. Among 755 patients studied, the observed number of deaths was 673, which amounts to a mortality of 89.1%. The expected number of deaths was 570. The risk-standardised mortality ratio was 1.18 (95% confidence interval, 1.09-1.28; P<0.0005). Patients with chronic obstructive pulmonary disease had the lowest mortality rate of 70.8% (P<0.005). The post-cardiac arrest subgroup had the highest mortality of 99.0%. CONCLUSIONS. There was a worse-than-predicted survival in the absence of Intensive Care Unit care for the critically ill patients who received mechanical ventilation on general wards. Patients with chronic obstructive pulmonary disease warranted more Intensive Care Unit admissions. Early discontinuation of invasive support should be seriously considered in the post-cardiac arrest patients.

Treatment of patients with chronic obstructive pulmonary disease as practised in a defined Hong Kong community: a cross-sectional pilot survey.

OBJECTIVES: To examine the characteristics of chronic obstructive pulmonary disease patients of the Kwai-Tsing area, Hong Kong, and the chronic treatments they received. DESIGN. Cross-sectional survey. SETTING: Four clinic settings in Hong Kong: Respiratory Specialist Clinic, Princess Margaret Hospital (group 1); Medical Specialist Clinics, Princess Margaret Hospital (group 2); General Outpatient Clinics, Princess Margaret Hospital (group 3); South Kwai Chung Chest Clinic, Department of Health (group 4). PATIENTS: Thirty physician-diagnosed chronic obstructive pulmonary disease patients in each of the above groups with post-bronchodilator 1-second forced expiratory volume/forced vital capacity ratios of less than 70% predicted values, who had been followed up at any of the participating clinics for at least 6 months. RESULTS: There were 111 male and nine female patients. The median age was 72.5 years and 79% had at least one medical co-morbidity. The mean duration of their chronic obstructive pulmonary disease was 9.8 years, and their mean post-bronchodilator 1-second forced expiratory volumes were 45% (for males) and 58% (for females) of predicted values. There were significantly fewer stage I and more stage IV patients in group 1. Influenza vaccination coverage within the previous 1 year was 54% and did not differ significantly between groups. Chronic obstructive pulmonary disease education was given significantly more often to group 1 patients. Short-acting beta agonists were used to treat all patients but long-acting bronchodilators and pulmonary rehabilitation were used almost exclusively in group 1. Overall, long-acting bronchodilators and pulmonary rehabilitation were offered to 16% and 5%, respectively, of those for whom these were indicated (according to international guidelines). CONCLUSION: In general there was insufficient education and under-treatment for chronic obstructive pulmonary disease patients. Management of such patients warrants improvements by way of increased accessibility to structured education programmes, pulmonary rehabilitation programmes, long-acting bronchodilator drugs, and respiratory specialist care.

Management of patients admitted with pneumothorax: a multi-centre study of the practice and outcomes in Hong Kong.

OBJECTIVE: To examine the management practice of pneumothorax in hospitalised patients in Hong Kong, especially the choice of drainage options and their success rates, as well as the factors associated with procedural failures. DESIGN: Retrospective study. SETTING: Multi-centre study involving 12 public hospitals in Hong Kong. PATIENTS: All adult patients admitted as an emergency in the year 2004 with a discharge diagnosis of 'pneumothorax' were included. Data on the management and outcomes of the various types of pneumothoraces were collected from their case records. RESULTS: Altogether these patients had 1091 episodes (476 primary spontaneous pneumothoraces, 483 secondary spontaneous pneumothoraces, 87 iatrogenic pneumothoraces, and 45 traumatic pneumothoraces). Conservative treatment was offered in 182 (17%) episodes, which were more common among patients with small primary spontaneous pneumothoraces (71%). Simple aspiration was performed to treat 122 (11%) of such episodes, and had a success rate of 15%. Aspiration failure was associated with having a pneumothorax of size 2 cm or larger (odds ratio=3.7; 95% confidence interval, 1.2-11.5; P=0.03) and a smoking history (4.1; 1.2-14.3; P=0.03). Intercostal tube drainage was employed in 890 (82%) episodes, with a success rate of 77%. Failure of intercostal tube drainage was associated with application of suction (odds ratio=4.1; 95% confidence interval, 2.8-5.9; P<0.001) and presence of any tube complications (1.55; 1.0-2.3; P=0.03). Small-bore catheters (<14 French) were used in 12 (1%) of the episodes only. Tube complications were encountered in 214 (24%) episodes. CONCLUSION: Notwithstanding recommendations from international guidelines, simple aspiration and intercostal tube drainage with small-bore catheters were not commonly employed in the management of hospitalised patients with the various types of pneumothoraces in Hong Kong.

Brachial-ankle vs carotid-femoral pulse wave velocity as a determinant of cardiovascular structure and function.

Carotid-femoral pulse wave velocity (cf-PWV) is a validated marker of arterial stiffening over the central arteries. Brachial-ankle pulse wave velocity (ba-PWV) integrates the mechanical properties from both the central and peripheral arteries and may be more representative than cf-PWV as arterial load for left ventricle (LV). We compared ba-PWV with cf-PWV for the association of cardiovascular structure and function in 320 subjects with various degrees of abnormality in cardiac structure and function. ba-PWV (by oscillometric technique) and cf-PWV (by tonometric technique) were measured simultaneously, and were highly correlated (r=0.79, P<0.001). Both ba-PWV and cf-PWV were significantly correlated with LV mass, but the correlation was better with ba-PWV (r=0.29 vs r=0.22, P=0.0219). While ba-PWV and cf-PWV were similarly significantly correlated with LV end-systolic elastance and mitral E/A ratio, ba-PWV had better correlation with isovolumic relaxation constant (r=0.34 vs r=0.27, P=0.0202) than cf-PWV. In addition, the correlation was also significantly stronger with ba-PWV than with cf-PWV for other indices of arterial stiffness, including carotid incremental modulus (r=0.59 vs 0.50, P=0.0013), effective arterial elastance (r=0.41 vs r=0.33, P=0.0081) and carotid augmentation index (r=0.38 vs r=0.32, P=0.0368). In conclusion, ba-PWV correlates better with LV mass and diastolic function and other indices of arterial function than cf-PWV, probably because ba-PWV encompasses a greater territory of arterial tree than cf-PWV.

Hypoxia is involved in hypoxic pulmonary hypertension through inhibiting the activation of FGF2 by miR-203.

OBJECTIVE: The aim of this study was to investigate whether hypoxia in vivo can induce hypoxic pulmonary hypertension by inhibiting the activation of FGF2 by miR-203. MATERIALS AND METHODS: We established a rat model of hypoxic pulmonary hypertension (HPH), and measured the right ventricular systolic pressure (RVSP) and right ventricular hypertrophy (right ventricular hypertrophy index). The ventricular hypertrophy index (RVHI) was calculated and HE staining of the lung tissue of HPH rats was performed. We extracted pulmonary arterial smooth muscle cells (PASMCs) from rats and identified them by immunofluorescence assay. The expression of miR-203 in hypoxic PASMCs was detected by quantitative Real time-polymerase chain reaction (qRT-PCR). The proliferation and migration of PASMCs were detected by EDU (5-Ethynyl-2'-deoxyuridine), cell counting kit-8 (CCK-8) and scratch assay, respectively. Dual Luciferase reporting assay and Western blot were used to detect the binding of miR-203 and FGF2. RESULTS: The results of qRT-PCR showed that miR-203 expression in rat PASMCs was significantly lower than that in normoxia control group at 24 h and 48 h after hypoxic treatment. EDU, CCK8 and scratch test results showed that proliferation and migration ability of PASMCs were weakened after overexpression of miR-203, and vice versa. Dual Luciferase reporter gene assays and Western blot experiments showed that miR-203 could target and combine with FGF2 to inhibit its expression. In vivo experiments showed that low expression of FGF2 could lead to decreased RVSP and RVHI, decreased FGF2 protein levels, and decreased WT% and (PM+FM)% in hypoxia-treated rats. CONCLUSIONS: Hypoxia in vivo is involved in the development of HPH by inhibiting the activation of FGF2 by miR-203. Meanwhile, specific inhibition of FGF2 can reduce hypoxia-induced pulmonary hypertension and improve pulmonary vascular remodeling.

Quasilinear quantum magnetoresistance in pressure-induced nonsymmorphic superconductor chromium arsenide.

In conventional metals, modification of electron trajectories under magnetic field gives rise to a magnetoresistance that varies quadratically at low field, followed by a saturation at high field for closed orbits on the Fermi surface. Deviations from the conventional behaviour, for example, the observation of a linear magnetoresistance, or a non-saturating magnetoresistance, have been attributed to exotic electron scattering mechanisms. Recently, linear magnetoresistance has been observed in many Dirac materials, in which the electron-electron correlation is relatively weak. The strongly correlated helimagnet CrAs undergoes a quantum phase transition to a nonmagnetic superconductor under pressure. Here we observe, near the magnetic instability, a large and non-saturating quasilinear magnetoresistance from the upper critical field to 14 T at low temperatures. We show that the quasilinear magnetoresistance may arise from an intricate interplay between a nontrivial band crossing protected by nonsymmorphic crystal symmetry and strong magnetic fluctuations.

KLF10 loss in the pancreas provokes activation of SDF-1 and induces distant metastases of pancreatic ductal adenocarcinoma in the KrasG12D p53flox/flox model.

Krüppel-like transcription factor 10 (KLF10), also named as TIEG1, plays essential roles in mediating transforming growth factor beta (TGFß) signaling and has been shown to function as a tumor suppressor in multiple cancer types. However, its roles in mediating cancer progression in vivo have yet to be fully characterized. Here, we have employed two well-characterized Pdx-1CreLSL-KrasG12D and Pdx-1CreLSL-KrasG12Dp53L/L pancreatic cancer models to ablate KLF10 expression and determine the impact of KLF10 deletion on tumor development and progression. We show that loss of KLF10 cooperates with KrasG12D leading to an invasive and widely metastatic phenotype of pancreatic ductal adenocarcinoma (PDAC). Mechanistically, loss of KLF10 in PDAC is shown to increase distant metastases and cancer stemness through activation of SDF-1/CXCR4 and AP-1 pathways. Furthermore, we demonstrate that targeting the SDF-1/CXCR4 pathway in the context of KLF10 deletion substantially suppresses PDAC progression suggesting that inhibition of this pathway represents a novel therapeutic strategy for PDAC treatment.

The placentas of patients with severe acute respiratory syndrome: a pathophysiological evaluation.

AIMS: The pathology of the placentas delivered from pregnant women who had severe acute respiratory syndrome (SARS) in Hong Kong was studied. METHODS: The pathology of the placentas was retrospectively studied in detail and compared with control sets. The clinical data of the women and neonates were also reviewed. RESULTS: A total of seven placentas were studied. The placentas from two women convalescent from SARS in the first trimester were normal. In three placentas delivered in the acute stage of SARS, there were increases in intervillous or subchorionic fibrin which might be related to disturbances in maternal placental blood flow due to the hypoxic respiratory disease. Extensive fetal thrombotic vasculopathy (FTV) with sharply demarcated zones of avascular fibrotic villi was noted in the placentas of two patients convalescent from SARS in the third trimester. Both pregnancies had intrauterine growth retardation, oligohydramnios and newborns small for gestation. The aetiology of the FTV might be related to thrombotic tendency due to SARS or placental hypoxia. CONCLUSIONS: This report highlights placental pathology that was probably the result of pathophysiological alteration of the maternal fetal unit during SARS. Further studies are required to delineate the relationship between severe maternal respiratory disease, placental pathology and pregnancy outcome.

Effects of 17 beta-estradiol on progesterone receptors and the uptake of thymidine in human breast cancer cell line CAMA-1.

Two sublines, CAMA-1R and CAMA-1N, were derived from the original CAMA-1 cells after continuous passages in our laboratory. 1R cells were supplemented in culture with estradiol and retained the properties of the original cell line, whereas 1N cells, not supplemented with estradiol, had a partial loss of estrogenic responsiveness. The doubling times for 1R and 1N cells were 2 and 2.4, respectively. These two sublines showed different effects on thymidine uptake after estradiol stimulation. Cells of 1R had a 2-fold greater thymidine incorporation than did the control without estradiol. In contrast, no difference of thymidine uptake was demonstrated in cells of 1N in the presence or absence of estradiol. Both cell lines contained cytoplasmic progesterone receptors with a Kd of 0.56 nM and a sedimentation coefficient of 6 to 7S on a 5 to 20% sucrose gradient. The progesterone receptor level in 1N was about 8-fold higher than in 1R cells. Both sublines exhibited a dose-dependent increase in progesterone receptor levels in response to estradiol with the maximal stimulation (8-fold increase) reached by using 5 nmol of estradiol. The rate of increase for estradiol-induced progesterone receptor appears to be the same for both sublines; a liner increase was demonstrated between Days 3 and 7 following plating. Our results show that estrogen regulation of thymidine uptake and progesterone receptor induction may be mediated through two separate mechanisms. Thus, following a chronically deficient supply of estradiol to 1N cells, there is apparent loss of responsiveness to estradiol-induced thymidine uptake, but the ability of these cells to respond to estradiol induction of progesterone receptor was retained.

Tamoxifen stimulates human papillomavirus type 16 gene expression and cell proliferation in a cervical cancer cell line.

The widely adopted use of tamoxifen as a chemotherapeutic agent is primarily based on its inhibition of cancer cell growth. However, we report that tamoxifen at low concentrations (10(-9) and 10(-11) M) causes stimulation of cell proliferation in a cervical cancer cell line, SFR. The facts that SFR cells do not contain estrogen receptors and are estrogen nonresponsive imply the existence of an antiestrogen-specific binding protein and suggest that the effect of tamoxifen is possibly mediated through a pathway other than estrogen receptors. Tamoxifen at low concentrations stimulated human papillomavirus type 16 (HPV-16) gene transcription and E7 protein production. Levels of HPV-16 mRNA and E7 protein reached a peak at approximately 2-4 h after tamoxifen treatment, persisted for several hours, and subsequently decreased to their prestimulation levels by about 24 h after treatment. Our results indicate for the first time that tamoxifen stimulates cell proliferation of cervical cancer cells, and we suggest that the enhanced HPV-16 mRNA and E7 protein levels are probably responsible.

Correlates of disease-specific knowledge in Chinese patients with COPD.

BACKGROUND: This study aimed to determine the associations of various sociodemographic factors with the level of disease-specific knowledge among Hong Kong Chinese patients with COPD. METHODS: A cross-sectional survey of 100 Chinese adults with COPD recruited from outpatient clinics was conducted from September 2009 to September 2010. Data on the knowledge specific to COPD and patients' sociodemographics were collected from face-to-face interviews. Primary outcome of disease-specific knowledge was measured using 65-item Bristol COPD Knowledge Questionnaire (BCKQ), summing up the 65 items as the BCKQ overall score. Associations of sociodemographic factors with the BCKQ overall score were evaluated using the linear regression model. RESULTS: The mean BCKQ overall score of our patients was 41.01 (SD: 10.64). The knowledge in topics of "Smoking" and "Phlegm" achieved the first (3.97, SD: 0.82) and second (3.91, SD: 1.17) highest mean scores, respectively, while the topic of "Oral steroids" returned the lowest mean score of 1.89 (SD: 1.64). The BCKQ overall score progressively declined (P<0.001) with increase in education level, with the highest BCKQ overall score of 46.71 at no formal education among all subgroups. Compared to nondrinkers, current drinkers were associated with lower total BCKQ score. CONCLUSION: We found that among COPD patients in outpatient clinics, impairments in the level of COPD knowledge were evident in patients who were current drinkers or had higher level of education.

Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava: electrophysiological characteristics and results of radiofrequency ablation.

BACKGROUND: The superior vena cava (SVC) has cardiac musculature extending from the right atrium. However, no previous study in humans has given details regarding the ectopic foci that initiate paroxysmal atrial fibrillation (PAF), which may originate from the SVC. METHODS AND RESULTS: A total of 130 patients with frequent attacks of PAF initiated by ectopic beats were included. Eight patients (6%) had spontaneous AF initiated by a burst of rapid ectopic beats from the SVC (located 19+/-7 mm above the junction of the SVC and right atrium), which was confirmed by multiplane angiographic and intracardiac echocardiographic visualization and was marked by a sharp SVC potential preceding atrial activity. During initial repetitive discharges, the group with SVC ectopy had a higher incidence of intravenous conduction block than the group with pulmonary vein ectopy (75% versus 37%; P=0.03). The activation time of the earliest intracardiac ectopic activities relative to ectopic P wave onset was significantly shorter in the SVC ectopy than the pulmonary vein ectopy group (37+/-15 versus 84+/-32 ms; P<0. 001). After 5+/-3 applications of radiofrequency energy, AF was eliminated. SVC angiography after ablation revealed a local indentation of the venous wall in one patient. Two patients manifested coexisting sinus rhythm and a "focal" fibrillating activity confined inside the SVC after radiofrequency ablation. During a follow-up period of 9+/-3 months, all 8 patients were free of antiarrhythmic drugs, without tachycardia recurrence or symptoms of SVC obstruction. CONCLUSIONS: Ectopic beats initiating PAF can originate from the SVC. A radiofrequency current delivered to eliminate these ectopies is a highly effective and safe way to prevent PAF.

Effect of verapamil on long-term tachycardia-induced atrial electrical remodeling.

BACKGROUND: The effect of verapamil on long-term tachycardia-induced atrial electrical remodeling has not been reported. METHODS AND RESULTS: Forty-eight dogs were randomly divided into verapamil and control groups. The dogs in the verapamil group received verapamil 120 mg every day, those in the control group did not receive verapamil. Atrial effective refractory period (AERP), inducibility of atrial fibrillation (AF), and duration of AF were assessed before and after complete atrioventricular junction ablation with 1-day, 1-week, or 6-week rapid atrial pacing (780 bpm). AERP shortening, AERP dispersion, AERP maladaptation, and inducibility of AF after 1-day pacing was significantly attenuated by verapamil. However, verapamil did not have any significant effect on these parameters in the dogs with 1-week or 6-week pacing. Verapamil did not have any significant effect on the conduction velocity in the dogs with 1-day, 1-week, or 6-week pacing. Before rapid atrial pacing, verapamil significantly prolonged the duration of AF. In the dogs with 1-day pacing, the duration of AF measured immediately after termination of pacing was similar between the control and verapamil groups. However, in the dogs with 1-week or 6-week pacing, the duration of AF after pacing was significantly longer in the verapamil group. CONCLUSIONS: Verapamil cannot prevent long-term (1 and 6 weeks, respectively) tachycardia-induced changes of atrial electrophysiological properties. Furthermore, verapamil increases the duration of AF in the dogs either before or after long-term rapid atrial pacing.

Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation.

BACKGROUND: Atrial fibrillation (AF) can be initiated by ectopic beats originating from the atrial or great venous tissues. This study investigated the anatomic characteristics and electrophysiological properties of pulmonary veins (PVs), as well as the possible mechanisms and response to drugs of ectopic foci, and assessed the effects of radiofrequency (RF) ablation on AF initiated by ectopic beats originating from PVs. METHODS AND RESULTS: Seventy-nine patients with frequent episodes of paroxysmal AF and 10 control patients were included. Distal PVs showed the shortest effective refractory periods (ERPs), and right superior PVs showed a higher incidence of intra-PV conduction block than left superior PVs. Superior and left PVs had longer myocardial sleeves than inferior and right PVs, respectively. These electrophysiological characteristics were similar between AF and control patients. Propranolol, verapamil, and procainamide suppressed ectopic beats that originated from the PVs. Of 116 ectopic foci that initiated AF, 103 (88.8%) originated from PVs. A mean of 7+/-3 RF applications completely eliminated 110 ectopic foci (94.8%). During the 6+/-2-month follow-up period, 68 patients (86. 1%) were free of AF without any antiarrhythmic drugs. Follow-up transesophageal echocardiogram showed 42.4% of ablated PVs had focal stenosis. One patient had mild exertional dyspnea after ablation, but it resolved 3 months later; 1 patient had onset of mild exertional dyspnea 5 months after ablation. CONCLUSIONS: Electrophysiological characteristics of PVs are different from those in the atria. Ectopic beats from PVs can initiate AF, and beta-adrenergic receptor blocker, calcium channel blockers, and sodium channel blockers can suppress these ectopic beats. Careful mapping and elimination of these ectopic foci can cure paroxysmal AF.