Ambient fine particulate matter and allergic symptoms in the middle-aged and elderly population: results from the PIFCOPD study.

BACKGROUND: The associations between short- and long-term exposure to ambient fine particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) and allergic symptoms in middle-aged and elderly populations remain unclear, particularly in China, where most cities have severe air pollution. METHODS: Participants (n = 10,142; age = 40-75 years) were recruited from ten regions in China from 2018 to 2021 for the Predictive Value of Inflammatory Biomarkers and Forced Expiratory Volume in 1 s (FEV1) for Chronic Obstructive Pulmonary Disease (PIFCOPD) study. Short-term (lag0 and lag0-7 day) and long-term (1-, 3- and 5-year) PM2.5 concentrations at residences were extracted from the air pollutant database known as Tracking Air Pollution (TAP) in China. Multivariate logistic regression models were used to estimate associations for short- and long-term PM2.5 exposure concentrations and long-term exposure models were additionally adjusted for short-term deviations. RESULTS: A 10 µg/m3 increase in PM2.5 on the day the allergic symptoms questionnaire was administered (lag0 day) was associated with higher odds of allergic nasal (1.09, 95% CI 1.05, 1.12) and eye symptoms (1.08, 95% CI 1.05, 1.11), worsening dyspnea caused by allergens (1.06, 95% CI 1.02, 1.10), and ≥ 2 allergic symptoms (1.07, 95% CI 1.03, 1.11), which was similar in the lag0-7 day concentrations. A 10 µg/m3 increase in the 1-year average PM2.5 concentration was associated with an increase of 23% for allergic nasal symptoms, 22% for eye symptoms, 20% for worsening dyspnea caused by allergens, and 21% for ≥ 2 allergic symptoms, similar to the 3- and 5-year average PM2.5 concentrations. These associations between long-term PM2.5 concentration and allergic symptoms were generally unchanged after adjustment for short-term deviations. CONCLUSIONS: Short- and long-term exposure to ambient PM2.5 was associated with an increased risk of allergic nasal and eye symptoms, worsening dyspnea caused by allergens, and ≥ 2 allergic symptoms. TRIAL REGISTRATION: Clinical trial ID: NCT03532893 (29 Mar 2018).

A severe case of human coronavirus 229E pneumonia in an elderly man with diabetes mellitus: a case report.

BACKGROUND: With pandemic of coronavirus disease 2019 (COVID-19), human coronaviruses (HCoVs) have recently attached worldwide attention as essential pathogens in respiratory infection. HCoV-229E has been described as a rare cause of lower respiratory infection in immunocompetent adults. CASE PRESENTATION: We reported a 72-year-old man infected by HCoV-229E with rapid progression to acute respiratory distress syndrome, in conjunction with new onset atrial fibrillation, intensive care unit acquired weakness, and recurrent hospital acquired pneumonia. Clinical and radiological data were continuously collected. The absolute number of peripheral T cells and the level of complement components diminished initially and recovered after 2 months. The patient was successfully treated under intensive support care and discharged from the hospital after 3 months and followed. CONCLUSION: HCoV-229E might an essential causative agent of pulmonary inflammation and extensive lung damage. Supportive treatment was essential to HCoVs infection on account of a long duration of immunological recovery in critical HCoV-229E infection.

PM2.5-related cell death patterns.

With the increasingly serious problem of environmental pollution, the health problems caused by PM2.5 are gradually coming into our line of sight. Previous researches have indicated that air pollution is nearly related to various diseases, but few studies have focused on the exact function mediated by particulate matter less than 2.5 (PM2.5) in these diseases. PM2.5 is known to induce multiple ways of cell death, including autophagy, necrosis, apoptosis, pyroptosis and ferroptosis. Therefore, it is of much importance to understand the different ways of cell death caused by PM2.5 in the pathogenesis and treatment of PM2.5-related diseases. This present review is an insight of multiple ways of PM2.5­induced cell death in different diseases.

Identification of exosome miRNAs in bronchial epithelial cells after PM2.5 chronic exposure.

Numerous epidemiological studies have demonstrated that chronic PM2.5 exposure was associated with the lung carcinogenesis without known potential mechanisms. Exosomes-derived non-coding RNAs, including miRNAs, are proposed to play critical role in the occurrence and development of malignant diseases. So identification of exosomes-derived miRNAs could help us to better understand the molecular toxicity of PM2.5-induced lung cancer. Establishment chronic exposure animal and cell model with PM2.5 was conducted as before. HE staining was used for estimating the histological alternations of lungs in vivo. The expressions of EMT markers in vivo and vitro were quantified by Western blot. Then the exosomes in cell culture supernatant were extracted and the involved miRNAs were extracted and sequenced. The different expression level of miRNAs were verified by RT-PCR. Chronic PM2.5 exposure induced bronchial epithelial cell atypical hyperplasia and massive macrophage infiltration. PM2.5 exposure induce EMT event in vivo and vitro indicated as increased expression of Vimentin and decreased expression of E-cadherin. And five passages of PM2.5 stimulation also induced the release of rich and extractable exosomes in the cell culture supernatant in vitro. Through sequencing, there were differentially expressed 36 miRNAs between PM2.5 chronic exposed and control groups with 1.5-fold and greater differences. Among them, there were 30 exosome-miRNAs upregulated and 6 downregulated expression by PM2.5 exposure. The downregulated expression of miR-29b-2-5p, miR-193b-5p and miR-320c and upregulated expression of miR-100-5p, 125b-5p and unconservative_2_45093 in PM2.5 group were identified and reconfirmed by qRT-PCR. Chronic PM2.5 exposure causes bronchial epithelial cells atypical hyperplasia and induces EMT event in vivo, and it also induce the expression differences of miRNAs in exosome in vitro. Meanwhile, the identified differentially expressed exosome-miRNAs may partially associate with tumorigenesis. To sum up, the identified exosome-miRNAs may play role in the development of lung cancer induced by chronic PM2.5 exposure.

PM2.5 Upregulates MicroRNA-146a-3p and Induces M1 Polarization in RAW264.7 Cells by Targeting Sirtuin1.

Background: Fine particulate matter (PM2.5) exposure is proved to be associated with illnesses, but the mechanism is not clear. Potential effects of PM2.5 on innate immunity have become a hotspot recently. Confronting PM2.5, macrophages are able to be activated and induce inflammatory responses. Whether PM2.5 exposure affects macrophage polarization and associated mechanisms remains to be further explored. Afterwards, whether Sirtuin1 (SIRT1) an important intermediate regulator in various physiological processes takes part in the macrophage polarization induced by PM2.5 is unknown. MiRNAs are acknowledged as key regulator in posttranscriptional modification and our previous study found that miR-146a is a novel biomarker of PM2.5 exposure. Thus, we propose a hypothesis, PM2.5 exposure induces M1 polarization and miR-146a-3p is a potential upstream regulator by targeting SIRT1. Methods: RAW264.7 cells were treated with different concentrations of PM2.5 for 24h. The expressions of cytokines and key molecular markers were detected by qRT-PCR, Western blotting and ELISA. The activation degree of TLRs and NF-κB was assessed by Western blotting. The specific agonist and antagonist of SIRT1 were used to explore the potential role of SIRT1 in M1 polarization induced by PM2.5. MiR-146a-3p mimic and inhibitor were pre-transfected into RAW264.7 cells and the effects on M1 polarization induced by PM2.5 were evaluated. Luciferase analysis was used to identify the binding site of miR-146a-3p and SIRT1. Results: PM2.5 increased the mRNA and protein expression of M1 markers including interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α) and inducible nitric oxide synthase (iNOS) in RAW264.7 cells. The protein level of TLR4 was significantly increased and the ratio of phosphorylated NF-κB p65 versus p65 subunit was also elevated in PM2.5 group. PM2.5 decreased the protein level of SIRT1 but not the mRNA expression in vitro and in vivo experiments. Pre-treatment with SIRT1 agonist SRT1720 rescued the PM2.5 induced M1 response. Whereas, SIRT1 antagonist EX527 augment the effect. MiR-146a-3p was upregulated in PM2.5 treated RAW264.7 cells. Luciferase experiments reported that SIRT1 was directly targeted by miR-146a-3p. Overexpression of miR-146a-3p downregulated the expression of SIRT1 protein in untreated RAW264.7 cells. Importantly, inhibition of miR-146a-3p upregulated SIRT1 protein and suppressed M1 polarization in PM2.5 treated RAW264.7 cells. Conclusions: These results suggested that PM2.5 induces the inflammatory M1 polarization and TLR4/NF-κB signal transduction pathway might be involved in the process. MiR-146a-3p is a novel regulator of PM2.5 exerted M1 polarization by targeting SIRT1.

A prospective study of salvational intervention with ICS/LABA for reducing chronic obstructive pulmonary disease exacerbation under severe air pollution (SIRCAP) in Beijing: protocol of a multi-center randomized controlled trial.

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) is a major cause of morbidity and mortality all over the world. Acute exacerbation of COPD (AECOPD) not only accelerates the progression of disease, but also causes hospital administration and death events. Epidemiologic studies have shown air pollution is a high risk factor of AECOPD. However, there are rare technics or treatment strategies recommended to reduce severe air pollution related AECOPD. METHODS: This is a multi-center, prospective, randomized and standard treatment parallel control clinical trial. Seven hundred sixty-four stable COPD patients in group B, C and D according to GOLD 2017 will be recruited and equally divided into two parallel groups, salvational intervention (SI group) and control group (CT group). Original treatments for participants include tiotropium (18µg once q.d), budesonide/formoterol (160µg/4.5µg once or twice b.i.d) or budesonide/formoterol (160µg/4.5µg once or twice b.i.d) with tiotropium (18µg once q.d). The savational intervention for SI group is routine treatment plus budesonide/formoterol (160µg/4.5µg once b.i.d) from the first day after severe air pollution (air quality index, AQI ≥200) to the third day after AQI < 200. CT group will maintain the original treatment. The intervention will last for 2 years. Primary outcome is the frequency of AECOPD per year and the secondary outcomes include the incidence of unplanned outpatient visits, emergency visits, hospitalization, medical cost and mortality associated with AECOPD per year. DISCUSSION: The salvational intervention is a novel strategy for COPD management under severe air pollution. Results of the present study will provide reference information to guide clinical practice in reducing the air pollution related exacerbation of COPD. TRIAL REGISTRATION: This study has been registered at www.ClinicalTrials.gov (registration identifier: NCT03083067 ) in 17 March, 2017.

PM2.5 induces EMT and promotes CSC properties by activating Notch pathway in vivo and vitro.

Fine particulate matter (PM2.5) has been closely linked to increased morbidity and mortality of lung cancer worldwide. However, the role of PM2.5 in the etiology of lung cancer and the mechanism involved in PM2.5 induced lung cancer are largely unknown. In this study, we performed chronic exposure animal model to investigate the carcinogenetic mechanisms of PM2.5 by targeting the induction of epithelial-mesenchymal transition (EMT) and cancer stem cells (CSC) properties through Notch1 signal pathway. The antagonism of Notch1 signal pathway was carried out in vitro cell lines of A549 and BEAS-2B to block EMT and CSC. We found that chronic PM2.5 exposure mice lung tissue pathology showed atypical hyperplasia of bronchiolar epithelium. Then, we discovered that chronic PM2.5 exposure induced notable EMT event and obvious CSC properties indicating the developing process of cell malignant behaviors. EMT characterized with decreased protein expression of E-cadherin and increased protein expression of Vimentin. CSC properties induced by chronic PM2.5 exposure characterized with increased cell-surface markers (ABCG2 and ALDH1A1) and self-renewal genes (SOX2 and OCT4). Furthermore, PM2.5 exposure activate Notch signal pathway by increasing expression of Notch1 and Hes1. At last, we blocked Notch signal pathway by inhibitor RO4929097 in vitro to explore the underlying mechanism mediating PM2.5 induced EMT and CSC. We found that blocking Notch1 could prevent PM2.5 induced malignant behaviors including EMT and CSC in A549 and BEAS-2B. These data revealed that the induction of EMT and CSC properties were involved in the lung cancer risk of PM2.5 in vivo, and blocking-up Notch1 may negatively regulate EMT and CSC to suppress the invasion and migration in vitro, thereby putatively serving as a novel therapeutic target for PM2.5 induced lung cancer.

Severe pneumonia caused by adenovirus 7 in pregnant woman: Case report and review of the literature.

We report a rare case of adenoviral pneumonia in a previously healthy pregnant woman at 26(+4) weeks' gestation. She presented with persistent high fever, cough for 5 days, and developed progressive dyspnea with hypoxemic respiratory failure and bilateral pulmonary infiltrates with pleural effusions. Aggressive supportive care and timely obstetrical management saved the mother and prevented preterm delivery and fetal anomaly.

COVID-19 surveillance based on consumer wearable devices.

Background: Consumer wearable devices such as wristbands and smartwatches have potential application value in communicable disease surveillance. Objective: We investigated the ability of wearable devices to monitor COVID-19 patients of varying severity. Methods: COVID-19 patients with mobile phones supporting wearable device applications were selected from Dalian Sixth People Hospital. Physiological parameters from the wearable devices and electronic questionnaires were collected from the device wearing until 14 days post-discharge. Clinical information during hospitalization was also recorded. Based on imaging data, the patients were categorized into the milder group without pneumonia and the more severe group with pneumonia. We plotted the curves of the physiological parameters of the two groups to compare the differences and changes. Results: Ninety-eight patients were included in the analysis. The mean age was 39.6 ± 10.5 years, including 45 males (45.9%). There were 24 asymptomatic patients, 10 mild patients, 60 moderate patients, and 4 severe patients. Compared with the milder group, the more severe group had higher heart rate-related parameters, while the heart rate variability (HRV) was the opposite. In the more severe group, the heart rate-related parameters showed a downward trend from 0 to 7 days after the fever resolution. Among them, the resting heart rate and sleep heart rate decreased on the 25th day after the onset and were close to the milder group 1 week after discharge. Conclusions: Consumer wearable devices have the potential to monitor respiratory infections. Heart rate-related parameters obtained from these devices can be sensitive indicators of COVID-19 severity and correlate with disease evolution. Trial registration: ClinicalTrials.gov NCT04459637.

Correlation of morning dry mouth with clinical features of OSA in a community population: a cross-sectional study.

OBJECTIVES: Morning dry mouth, commonly seen in Obstructive Sleep Apnea (OSA) patients, is absent in current OSA screening tools. This study evaluated the link between morning dry mouth and OSA's clinical symptoms and complications, aiming to determine its viability as a screening indicator. METHODS: This research analyses baseline data from a prospective cohort study (the PIFCOPD study). Demographic information, medical history, and the presence of morning dry mouth symptoms were collected. The STOP-Bang questionnaire was performed for OSA screening. Logistic regression analyses were employed to establish the correlations between morning dry mouth and the clinical symptoms and comorbidities of OSA. RESULT: 1291 participants (62.1±7.5 years; 501 males, 790 females) were included, of which 416 reported morning dry mouth (32.2%). 42.6% in the high-risk OSA group and 22.1% in the low-risk group reported morning dry mouth. Individuals with morning dry mouth also showed higher STOP-Bang scores (3.3±1.6 vs. 2.3±1.4, P<0.01). Significant associations were found between morning dry mouth and loud snoring, observed sleep apnea, daytime fatigue, and hyperlipidemia (P<0.01), but not with alcohol consumption, tea consumption, diabetes, or hypertension. CONCLUSION: Morning dry mouth is associated with increased OSA risk and its clinical signs, suggesting its potential as an OSA screening symptom. CLINICAL TRIAL REGISTRATION: This study has been registered at www.ClinicalTrials.gov (registration identifier: NCT03532893) on 21 May 2018.

Association of high-sensitivity CRP and FEV1%pred: a study on non-pulmonary disease in a population in Beijing, China.

BACKGROUND: No studies have investigated whether high-sensitivity C reactive protein (hsCRP) can be used to predict the forced expiratory volume in 1 s (FEV1)/estimated value of FEV1 (FEV1%pred). This study aimed to assess the association between hsCRP and FEV1%pred in middle-aged and elderly individuals without underlying lung disease. METHODS: The data for this study were obtained from a prospective cohort study that included 1047 middle-aged and elderly citizens from Beijing aged 40-75 years without any evidence of underlying lung diseases with FEV1 >70% after receiving inhalational bronchodilators. The baseline analysis of the participants was performed from 30 May 2018 to 31 October 2018. Restricted cubic spline regression and multivariate linear regression models were used to assess the non-linear association and linear association between hsCRP and FEV1/FEV in 6 s (FEV6) and FEV1%pred, respectively. RESULTS: The hsCRP values of 851 participants were recorded; the values were normal in 713 (83.8%) participants. The remaining 196 participants (18.7%) had missing data. A non-linear association was observed between normal hsCRP values and FEV1/FEV6. hsCRP was linearly and negatively correlated with FEV1%pred, and each 1 SD increase in hsCRP was significantly associated with a 2.4% lower in FEV1%pred. Significantly higher FEV1/FEV6 differences were observed in the female subgroup than those in the male subgroup (p=0.011 for interaction). CONCLUSIONS: hsCRP had a non-linear association with FEV1/FEV6 and a linear negative association with FEV1%pred in individuals with normal hsCRP values. hsCRP can be used to predict FEV1%pred, which can be used to predict the development of chronic obstructive pulmonary disease. hsCRP has a stronger association with lung function in women than that in men. TRIAL REGISTRATION NUMBER: NCT03532893.

Light dose effect of photodynamic therapy on growth inhibition and apoptosis induction in non-small cell lung cancer: A study in nude mouse model.

BACKGROUND: Photodynamic therapy (PDT) is receiving increasing attention in treating non-small cell lung cancer (NSCLC) worldwide, but in clinical practice, the relationship between treatment effect and PDT light dose in NSCLC remains unclear. Therefore, we aimed to determine the optimal light dose for PDT by exploring molecular biomarkers and evaluating tumor growth data. METHODS: We applied bioinformatics to identify promising genes and pathways in NSCLC and PDT. Then, the human lung adenocarcinoma cell line A549-bearing BALB/c nude mice were treated with hematoporphyrin derivative (HPD, 3 mg/kg) that is currently used widely for lung cancer treatment in the world even with photosensitization issues. After 48 h, tumor-bearing mice were irradiated superficially at doses of 100, 200, 300, 400, and 500 J/cm2. The tumor growth data and apoptotic molecules were assessed and calculated. RESULTS: Bioinformatics results indicated that the apoptosis pathway was significantly enriched and caspase 3 was the most promising biomarker on prognosis in NSCLC-PDT. Compared to the untreated group, there was no difference in the relative tumor volume (RTV) of the 100 J/cm2 group, while the RTV of the other treatment groups (200-500 J/cm2) was significantly lower. In the 100 J/cm2 group, there were significant differences in the complete remission (CR, 0 %) and the percentage of tumor growth inhibition rate (TGI%) over 75 % (20 %) compared with the other treatment groups, especially the 300 and 400 J/cm2 groups (CR 70 %; TGI% 90 %). In the 300 and 400 J/cm2 groups, the expression of caspase 3, cleaved-caspase 3, PARP1, and Bax was increased significantly, while Bcl-2 expression was significantly lower. CONCLUSIONS: Moderate doses of PDT (300 or 400 J/cm2) are more effective than low (100 or 200 J/cm2) or high doses (500 J/cm2) in the A549 tumor-bearing mice model. Since the A549 tumor is more akin to human tumors in pathological behavior, these experimental data may contribute to improving HPD-PDT illumination protocols for favorable clinical outcomes.

Association between preserved ratio impaired spirometry and sleep apnea in a Chinese community.

OBJECTIVE: This study investigated the association between obstructive sleep apnea (OSA) and preserved ratio impaired spirometry (PRISm) in a community population. METHODS: Baseline data from a prospective cohort study, the Predictive Value of Combining Inflammatory Biomarkers and Rapid Decline of FEV1 for COPD (PIFCOPD), were used for cross-sectional analysis. Participants aged 40-75 years were recruited from the community and their demographic information and medical history were collected. The STOP-Bang questionnaire (SBQ) was used to assess the risk of OSA. Pulmonary function tests were performed using a portable spirometer (COPD-6) and forced expiratory volume in 1 s (FEV1) and 6 s (FEV6) were measured. Routine blood, biochemical, high-sensitivity C-reactive protein (hs-CRP), and interleukin-6 tests were also performed. The pH of the exhaled breath condensate was determined. RESULTS: A total of 1183 participants were enrolled, of which 221 with PRISm and 962 with normal lung function. The neck circumference, waist-to-hip ratio, hs-CRP concentration, proportion of males, cigarette exposure, number of current smoker, high risk of OSA, and prevalence of nasal and ocular allergy symptoms were significantly higher in the PRISm group than in the non-PRISm group (p < .05). Logistic regression showed that the risk of OSA (odds ratio, 1.883; 95% confidence interval, 1.245-2.848), waist-to-hip ratio, current smoking, and prevalence of nasal allergy symptoms were independently associated with PRISm after correcting for age and sex. CONCLUSION: These findings showed that OSA prevalence is independently associated with PRISm prevalence. Further studies should confirm the relationship between systemic inflammation in OSA, localized inflammation of the airways, and impaired lung function.

Severe pigeon paramyxovirus 1 infection in a human case with probable post-COVID-19 condition.

Pigeon paramyxovirus 1 (PPMV-1) is an antigenic host variant of avian paramyxovirus 1. Sporadic outbreaks of PPMV-1 infection have occurred in pigeons in China; however, few cases of human PPMV-1 infection have been reported. The purpose of this article is to report a case of severe human PPMV-1 infection in an individual with probable post-COVID-19 syndrome (long COVID) who presented with rapidly progressing pulmonary infection. The patient was a 66-year-old man who was admitted to the intensive care unit 11 days after onset of pneumonia and recovered 64 days after onset. PPMV-1 was isolated from the patient's sputum and in cloacal smear samples from domesticated pigeons belonging to the patient's neighbour. Residual severe acute respiratory syndrome coronavirus 2 was detected in respiratory and anal swab samples from the patient. Sequencing analyses revealed that the PPMV-1 genome belonged to genotype VI.2.1.1.2.2 and had the 112RRQKRF117 motif in the cleavage site of the fusion protein, which is indicative of high virulence. This case of cross-species transmission of PPMV-1 from a pigeon to a human highlights the risk of severe PPMV-1 infection in immunocompromised patients, especially those with long COVID. Enhanced surveillance for increased risk of severe viral infection is warranted in this population.

Involvement of TLR2 and TLR4 and Th1/Th2 shift in inflammatory responses induced by fine ambient particulate matter in mice.

Epidemiologic studies have reported the association between fine particles (aerodynamic diameter ≤ 2.5 µm; PM2.5) and health effects, but the immunological mechanisms are not clear. To investigate the dose and time-dependent role of toll-like receptor (TLR) and Th1/Th2 shift in local and systemic inflammation induced by PM2.5, mice were subjected to intratracheal instillation of 2.5, 5, or 10 mg/kg PM2.5 in this study. After 24 h, 72 h, 7 days, and 14 days, mice were sacrificed to measure TLR2 and TLR4 expressions and Th1/Th2 related cytokines in bronchoalveolar lavage fluid (BALF) and peripheral blood. Histopathological changes in lung were also examined. Inflammatory infiltration and macrophages with engulfed particles were found by lung histopathology after PM2.5 exposure. TLR4 positive cells decreased in BALF but increased in blood at 24 h after the exposure. The low percentage of TLR4 positive cells continued to day 14 in BALF, but recovered at day 7 and decreased further to lower than the control value at day 14 in blood. TLR2 positive cell changed similar to TLR4 in BALF on the dose effects. In BALF at 24 h after the exposure, the Th2 related cytokines IL-5 and IL-10 increased dose-dependently; and in blood, the Th2 related cytokines IL-4, IL-5, and IL-10 also increased. These results suggest that acute exposure of PM2.5 leads to acute inflammatory responses locally and systemically in mice. TLR2 and TLR4 are involved in this process and PM2.5 can drive a Th2-biased immune response.

An online survey of primary care physicians' knowledge of common respiratory diseases in China.

China has a huge population with respiratory diseases, these diseases should be managed well in primary care, however, primary care physicians' knowledge level of these diseases were unknown. The aim of the study was to assess primary care physicians' knowledge of asthma, CAP, COPD, and influenza in China. An e-questionnaire was distributed to attendees of respiratory diseases academic conferences in China from July, 2017 to December, 2018. 7391 questionnaires were returned and 4815 valid questionnaires were analyzed, 3802 (79.0%) from community health service centers and 1013 (21.0%) from township hospitals. The average score of the questionnaire was 83.3 (±20.397) and 72.1 (±20.898) in township and community hospitals, respectively (P < 0.05). 61.4%, 48.7%, and 42.5% of the primary care physicians were aware of clinical manifestations of COPD, asthma, and simple influenza. 85.7%, 8.1%, 16.1%, and 1.0% knew how to diagnose COPD, asthma, CAP and influenza, respectively. 94.4% of the physicians lacked the knowledge of treating COPD with bronchodilators; 53.7% knew non-pharmacological treatments for COPD. 73.6% were unable to deal with asthma attacks. 65.1% did not know what the most essential and important treatment for influenza was. 92% of physicians did not know the management for stable COPD; 3.0% knew all prevention and management measures for asthma. 37.9% knew all the preventive measures for CAP. 44.9% did not know the important role of influenza vaccine in preventing influenza and its complications. Primary care physicians in China had a poor knowledge of CAP, asthma, Influenza, COPD. There is a need for improved training of common respiratory diseases.

Clinical outcomes and quantitative CT analysis after bronchoscopic lung volume reduction using valves for advanced emphysema.

Background: Bronchoscopic lung volume reduction (BLVR) using Zephyr endobronchial valve (EBV) and intrabronchial valve (IBV) has been shown to improve lung function and exercise capacity in severe emphysema. However, changes in airway structures and whether these are related to the clinical improvements remain unclear. Methods: A retrospective study was performed on patients treated with BLVR. We compared changes in 2nd-, 3rd-, and 4th-generation bronchial structures after therapy, including wall thickness (WT), percentage of wall thickness (WT%), intraluminal area (LA), wall area (WA), and WA%. Responder and non-responder subgroup analysis according to minimum clinically important difference (MCID) which was defined as an improvement of 15% in forced expiratory volume in 1 s (FEV1) and 26 m in 6 min walk distance (6MWD) was conducted. Results: Of the 19 patients, 11 were treated with EBV and 8 with IBV. In ipsilateral non-target lobes, WT% decreased significantly in 3rd-generation bronchi at 1 month, 3, and 6 months, as well as their WA% at 1 month and 6 months. Non-responders, who were unable to achieve MCID, showed no consistent bronchial wall changes. And their LA of 3rd-generation bronchi decreased especially at 1 month. After BLVR, the target lobe volume decreased significantly until 12 months of follow-up. The volume of ipsilateral lobes could increase correspondingly and achieve the best improvements at 6 months. The contralateral lung volume showed slight amelioration but there was no statistical significance. Conclusions: Both airway structures and lung volumes showed changes after BLVR. The 3rd- and 4th-bronchial walls tend to be thinner, which were consistent with clinical improvements. Further studies are needed to prove this conclusion and find detect potential mechanics.

The Current Status of Vaccine Uptake and the Impact of COVID-19 on Intention to Vaccination in Patients with COPD in Beijing.

Background: SARS-CoV-2 tends to cause more severe disease in patients with COPD once they are infected. We aimed to investigate the rates of influenza, pneumococcal and COVID-19 vaccination uptake in patients with COPD and to determine whether the COVID-19 pandemic and widespread vaccination against COVID-19 had any impact on the intention to accept influenza vaccines in these patients. Methods: We conducted a multi-center and cross-sectional survey in seven tertiary hospitals in Beijing and consecutively recruited outpatients with COPD from June 1st to July 30th, 2021. The survey included patient's clinical characteristics, uptake of influenza, pneumococcal and COVID-19 vaccination, vaccine knowledge, attitude towards vaccines, and the change of intention to receive influenza vaccination after COVID-19 epidemic and COVID-19 vaccination in Beijing. Results: A total of 264 patients were enrolled. The rate of COVID-19 vaccination during the study period was 39.0%. The rates of influenza vaccination in the past season and pneumococcal vaccination in the past year were 22.7% and 5.7%, respectively. Of the patients who had not received COVID-19 vaccination (n = 161), only 16.2% reported that COVID-19 vaccination was recommended by clinicians, while 23.5% had no knowledge regarding COVID-19 vaccination. About 51.1% of the patients reported that their intention to receive influenza vaccination was influenced by the COVID-19 pandemic. COVID-19 vaccination was independently associated with a positive change in intention to receive influenza vaccination. Conclusion: The coverage rate of COVID-19 vaccination among patients with COPD in Beijing was 39.0%, and that of influenza and pneumococcal vaccination was very low. The COVID-19 pandemic and the COVID-19 vaccination campaign showed a significant, positive impact on patients with COPD in terms of influenza vaccination. Improving awareness of the effectiveness and safety of vaccines among both healthcare professionals and patients could increase vaccination coverage in patients with COPD.

Serum surfactant protein D, lung function decline, and incident chronic obstructive pulmonary disease: a longitudinal study in Beijing.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) has become a major public-health problem in China. Surfactant protein D (SP-D) is a very promising biomarker and therapeutic target for COPD. To assess whether baseline serum SP-D is associated with lung function decline and incident COPD. METHODS: This longitudinal study was initiated in 2009 in a community in Beijing. Data were collected on spirometry, and the baseline level of serum SP-D was measured in 772 non-COPD subjects aged 40-70 years old. In 2012, spirometry was repeated in 364 individuals, 37 of whom subjects had incident COPD. RESULTS: From 2009 to 2012, subjects with incident COPD had a more rapid decline in FEV1 (MD 98.27 vs. MD 43.41 mL) compared with those without COPD. There was no association between baseline serum SP-D and the COPD incidence. Smoking (OR =2.72; P=0.002) and age (OR =1.06; P=0.000) were risk factors for COPD. The rate of FEV1 decline varies widely in the general population, and the univariate analysis showed that baseline serum SP-D levels (R=-0.169; P=0.003), income level, home-road distance, and statin use were inversely correlated with the decline in FEV1. After multivariable analyses, only smoking was consistently associated with the decline in FEV1. CONCLUSIONS: There was no correlation between baseline serum SP-D levels and incident COPD in a general population. Smoking and age were major risk factors for COPD. The effect of serum SP-D levels on the decline in FEV1 needs further investigation.

PM2.5 downregulates MicroRNA-139-5p and induces EMT in Bronchiolar Epithelium Cells by targeting Notch1.

PM2.5 was closely linked to lung cancer worldwide. However, the mechanism involved in PM2.5 induced lung cancer is still largely unknown. In this study, we performed chronic PM2.5 stimulation animal and cells model to investigate the carcinogenetic mechanisms of PM2.5 by targeting EMT through Notch1 signal pathway. Next, we focused on the miRNA involved in PM2.5 induced Notch1 pathway activation. We found chronic PM2.5 could induce EMT event in vivo and in vitro, while reducing miR-139-5p expression and activating Notch1 pathway meanwhile. And blocking Notch1 signal pathway by specific small molecule inhibitor could reverse PM2.5 induced EMT. Then, overexpression of miR-139-5p downregulated the expression of Notch1 protein in untreated 16HBE cells. Importantly, overexpression of miR-139-5p blocked Notch1 pathway activation and inhibited EMT event in PM2.5 treated cells. These results indicate that PM2.5 induces EMT event through Notch1 signal pathway and miR-139-5p is a novel regulator of PM2.5-induced EMT by targeting Notch1. Our conclusion is that overexpression of miR-139-5p can down-regulate the expression of Notch1 and reverse the occurrence of malignant lung events induced by chronic exposure to PM2.5.