Stretchable and Breathable Electroluminescent Displays Based on Ultrathin Nanocomposite Designs.

Stretchable electroluminescent devices represent an emerging optoelectronic technology for future wearables. However, their typical construction on sub-millimeter-thick elastomers has limited moisture permeability, leading to discomfort during long-term skin attachment. Although breathable textile displays may partially address this issue, they often have distinct visual appearances with discrete emissions from fibers or fiber junctions. This study introduces a convenient procedure to create stretchable, permeable displays with continuous luminous patterns. The design utilizes ultrathin nanocomposite devices embedded in a porous elastomeric microfoam to achieve high moisture permeability. These displays also exhibit excellent deformability, low-voltage operation, and excellent durability. Additionally, the device is decorated with fluorinated silica nanoparticles to achieve self-cleaning and washable capabilities. The practical implementation of these nanocomposite devices is demonstrated by creating an epidermal counter display that allows intimate integration with the human body. These developments provide an effective design of stretchable and breathable displays for comfortable wearing.

Ultrastretchable Electrically Self-Healing Conductors Based on Silver Nanowire/Liquid Metal Microcapsule Nanocomposites.

Stretchable conductive nanocomposites are essential for deformable electronic devices. These conductors currently face significant limitations, such as insufficient deformability, significant resistance changes upon stretching, and drifted properties during cyclic deformations. To tackle these challenges, we present an electrically self-healing and ultrastretchable conductor in the form of bilayer silver nanowire/liquid metal microcapsule nanocomposites. These nanocomposites utilize silver nanowires to establish their initial excellent conductivity. When the silver nanowire networks crack during stretching, the microcapsules are ruptured to release the encased liquid metal for recovering the electrical properties. This self-healing capability allows the nanocomposite to achieve ultrahigh stretchability for both uniaxial and biaxial strains, minor changes in resistance during stretching, and stable resistance after repetitive deformations. The conductors have been used to create skin-attachable electronic patches and stretchable light-emitting diode arrays with enhanced robustness. These developments provide a bioinspired strategy to enhance the performance and durability of conductive nanocomposites.

Nootkatone attenuates airway inflammation in asthmatic mice through repressing ROS-induced NLRP3 inflammasome activation.

Nootkatone (NKT) exhibits potential pharmacological activities including anti-oxidation and anti-inflammation. Nevertheless, little is known about the roles of NKT in asthmatic airway inflammation. In the study, mice were sensitized and challenged with ovalbumin (OVA) to establish experimental allergic asthma model. After treatment with NKT, lung tissues, peripheral blood, and bronchoalveolar lavage fluid (BALF) were collected to assess inflammatory cytokines, oxidative stress, and pathological alternations. The effects of NKT on regulating reactive oxygen species (ROS)-induced NLR family pyrin domain containing 3 (NLRP3) inflammasome activation was assessed in IL-13-treated BEAS-2B cell model. We found that NKT treatment decreased the production of Th2 inflammatory cytokines (IL-4, IL-5, and IL-13) in BALF and IgE levels in serum, and alleviated inflammatory cell penetration, goblet cell proliferation, collagen accumulation, and mucus hypersecretion in lung tissues. NKT treatment mitigated oxidative stress and NLRP3 inflammasome activation in asthmatic mice. IL-13 treatment induced oxidative stress and NLRP3-mediated pyroptosis in BEAS-2B bronchial epithelial cells, whereas these effects were blocked by NKT. NKT protected against airway remodeling, as indicated by decreased epithelial-mesenchymal transition. Taken together, these results demonstrate that NKT mitigates asthmatic airway inflammation by inhibiting ROS-triggered NLRP3 activation and may be a potential agent for treating asthma.

Long non-coding RNA PANDAR promoted radiation and cisplatin-induced DNA damage repair through ATR/CHK1 in NSCLC.

BACKGROUND: DNA-damaging agents, including radiation and platinum-based chemotherapy, are indispensable treatments for non-small cell lung cancer (NSCLC) patients. However, cancer cells tend to be resistant to both radiation and chemotherapy, thus resulting in treatment failure or recurrence. The purpose of this study was to explore the effect and mechanism of long non-coding RNA (lncRNA) PANDAR (promoter of CDKN1A antisense DNA damage-activated RNA) on NSCLC sensitivity to radiation and chemotherapy. METHODS: Cell counting kit (CCK-8), colony formation and flow cytometry were respectively performed to determine the cell cycle and apoptosis of NSCLC cells treated with γ-ray radiation and cisplatin. The extent of DNA damage was evaluated using a comet assay and immunofluorescence staining against γH2AX. In addition, we explored the role of PANDAR in DNA damage response pathways through western blot analysis. Finally, a nude mouse subcutaneous xenograft model was established to assess the sensitivity to radiation and chemotherapy in vivo. RESULTS: In cell experiments, PANDAR knockdown can increase the sensitivity of NSCLC cells to radiation and cisplatin. The CCK-8 results showed that cell viability was significantly increased in the overexpression group after radiation and cisplatin treatments. The overexpression group also showed more colonies, less apoptosis and DNA damage, and G2/M phase arrest was aggravated to provide the time necessary for DNA repair. Contrary to PANDAR overexpression, the trends were reversed in the PANDAR knockdown group. Furthermore, PANDAR knockdown inhibited radiation and cisplatin-activated phosphorylation levels of ATR and CHK1 in NSCLC cells. Finally, our in vivo model showed that targeting PANDAR significantly sensitized NSCLC to radiation and cisplatin. CONCLUSION: Our study showed that PANDAR knockdown promoted sensitivity to radiation and cisplatin in NSCLC by regulating the ATR/CHK1 pathway, thus providing a novel understanding as well as a therapeutic target for NSCLC treatment. In NSCLC cells, lncRNA PANDAR negatively regulates sensitivity to radiation and cisplatin. PANDAR can promote the repair of radiation and cisplatin-induced DNA damage and activation of the G2/M checkpoint through the ATR/CHK1 pathway. PANDAR knockdown results in defects in DNA damage repair accompanied by more cell apoptosis.

Ultrastretchable MXene Microsupercapacitors.

Stretchable microsupercapacitors represent emerging miniaturized energy-storage devices for next-generation deformable electronics. Two-dimensional (2D) transition metal carbides (MXenes) are considered attractive electrode materials due to their metallic conductivity, hydrophilic surfaces, and excellent processability. Here, an ultrastretchable microsupercapacitor of interdigitated MXene microelectrodes with crumpled surface textures is created. The microsupercapacitor shows a series of attractive properties including a high specific capacitance of ≈185 mF cm-2 , ultrahigh stretchability up to 800% area strain, and ≈89.7% retention of the initial capacitance after 1000 stretch-relaxation cycles. In addition to static strains, the microsupercapacitor demonstrates robust mechanical properties to retain stable charging-discharging capability under dynamic stretching at different strain rates. A self-powering circuit system utilizes four microsupercapacitor packs to power a light-emitting diode (LED) array, which exhibits stable operations under large tensile strain and skin-attached wearable settings. The developments offer a generic design strategy to enhance the deformability of microsupercapacitors based on 2D nanomaterials.

CD147 promotes breast cancer migration and invasion by inducing epithelial-mesenchymal transition via the MAPK/ERK signaling pathway.

BACKGROUND: CD147, a transmembrane glycoprotein, has been implicated in various cancer-related processes but its role in breast cancer remains poorly understood. Herein, we investigated the expression of CD147 in different breast cancer cell lines and explored its functional roles, including migration, invasion, drug resistance and modulation of key proteins associated with cancer progression. METHODS: The expression of CD147 was assessed in MCF-10 A, BT549, MDA-MB-231 and MCF-7 breast cancer cell lines using qRT-PCR and Western blotting, following which lyposome transfections were performed, leading overexpression of CD147 in BT549 cells and knockdown of CD147 in MCF-7 cells. Scratch assays and Transwell invasion and were performed to evaluate the cells' migration and invasion abilities. Sensitivity to 5-FU was determined via CCK-8 assays, and the expression of Snail1, E-cadherin, Vimentin, MMP-9 and the MAPK/ERK pathway were analyzed by qRT-PCR and Western blotting. RESULTS: Compared with normal beast epithelial cells, CD147 was highly expressed in all breast cancer cell lines, with the highest overexpression observed in MCF-7 cells and the lowest overexpression observed in BT549 cells. Overexpression of CD147 in BT549 cells increased, migration, invasion, viability and resistance to 5-FU of BT549 cells, while CD147 knockdown in MCF-7 cells reduced these properties of MCF-7 cells. Furthermore, CD147 influenced the expression of Snail1, Vimentin, E-cadherin, and MMP-9, suggesting its involvement in epithelial-mesenchymal transition (EMT) regulation. The MAPK/ERK pathway was activated by CD147 in BT549 cells, as indicated by increased p-MEK/MEK ratio and p-ERK/ERK ratio. In contrast, CD147 silencing in MCF-7 cells resulted in reduced p-MEK/MEK ratio and p-ERK/ERK ratio. CONCLUSION: In summary, our findings suggest CD147 as a potential therapeutic target in breast cancer treatment, particularly in cases where drug resistance and metastasis are concerns, worthy of further explorations.

Positron Emission-Computed Tomography, Cryobiopsy versus Bronchoalveolar Lavage and Computed Tomography Findings for Interstitial Lung Disease: A Long-Term Follow-Up.

Background and Objectives: Interstitial lung diseases have always been an issue for pulmonary and rheumatology physicians. Computed tomography scans with a high-resolution protocol and bronchoalveolar lavage have been used along with biochemical blood tests to reach a diagnosis. Materials and Methods: We included 80 patients in total. First, all patients had their diagnosis with computed tomography of the thorax, serological/ immunological blood tests and bronchoalveolar lavage. However; after 3 months, all were divided into 2 groups: those who had bronchoalveolar lavage again and those who had cryobiopsy instead of bronchoalveolar lavage (40/40). Positron emission-computed tomography was also performed upon the first and second diagnosis. The patients' follow-up was 4 years from diagnosis. Results: Patients suffered most from chronic obstructive pulmonary disease (56, 70%), while lung cancer was rarely encountered in the sample (7, 9.75%). Age distribution ranged between 53 and 68 years with a mean value of 60 years. The computed tomography findings revealed 25 patients with typical diagnosis (35.2%), 17 with interstitial pulmonary fibrosis (23.9%) and 11 with probable diagnosis (11%). The cryobiopsy technique led to a new diagnosis in 28 patients (35% of the total sample). Patients who had a new diagnosis with cryobiopsy had a mean survival time of 710 days (<1460). Positron emission-computed tomography SUV uptake was positively associated with the cryobiopsy technique/new disease diagnosis and improved all respiratory functions. Discussion: Positron emission-computed tomography is a tool that can be used along with respiratory functions for disease evaluation. Conclusions: Cryobiopsy is a safe tool for patients with interstitial lung disease and can assist in the diagnosis of interstitial lung diseases. The survival of patients was increased in the cryobiopsy group versus only bronchoalveolar lavage for disease diagnosis.

Dectin-2 promotes house dust mite-skewed Th2 response through the activation of cDC2s.

The role of Dectin-2 (gene symbol, Clec4n) in house dust mite (HDM) induced Th2 immune response and the exact mechanism remains controversial. In this study, we illustrated that, Clec4n-/- mice had decreased Th2 immune response following HDM challenge, which may ascribe to dramatically reduced type 2 conventional dendritic cells (cDC2s) in lung of Clec4n-/- mice, as cDC2s from lung of Clec4n-/- mice after challenging had less ability to induce Th2 response with decreased production of IL-4/IL-13. Further in vitro experiments showed the activation of Clec4n-/--BMDCs significantly decreased after HDM stimulation accompanied with decreased activation of Syk-NF-κB and Syk-JNK signal pathway. Importantly, Dectin-2 expression in PBMCs from asthmatic patients was significantly higher than that in healthy controls. Taken together, these results demonstrated that Dectin-2 could promote cDC2s activation in lung, which polarizes Th2 immune response outlining a novel mechanism of asthma development.

Galectin-1 secreted by bone marrow-derived mesenchymal stem cells mediates anti-inflammatory responses in acute airway disease.

The hallmarks of allergic airway disease (AAD) include infiltration of inflammatory cells into the bronchoalveolar space. Bone marrow derived mesenchymal stem cells (BMSCs) show anti-inflammatory properties in AAD. In addition, galectin-1 (Gal-1) is a lectin significantly upregulated upon inflammation and is also known to mediate potential anti-inflammatory responses. We hypothesized that BMSCs regulated inflammatory responses by secretion of Gal-1 during AAD pathogenesis. BMSCs were isolated from murine femurs and tibiae and adoptively transferred into an ovalbumin-induced AAD mouse model. Knockdown of Gal-1 in BMSCs was performed using shRNA. Flow cytometry, ELISAs, and immunohistology were performed to analyze inflammatory responses in mice, and a Transwell system was used to establish an in vitro co-culture system of lung epithelial cells (MLE-12) and BMSCs. Administration of BMSCs significantly upregulated Gal-1 expression upon inflammation and decreased infiltration of inflammatory cells and secretion of proinflammatory cytokines in vivo. In addition, we showed that this function was mediated by reduced activation of the MAPK p38 signaling pathway. Similar observations were found using an in vitro lipopolysaccharide-induced model when MLE-12 cells were co-cultured with BMSCs. Gal-1 secretion by BMSCs alleviated inflammatory responses observed in AAD and hence provides a promising therapeutic alternative to AAD patients insensitive to conventional drug treatments.

Nutritional deficiency induces nucleus pulposus cell apoptosis via the ATF4-PKM2-AKT signal axis.

BACKGROUND: The intervertebral disc is the largest avascular tissue in the human body. The nucleus pulposus (NP) consumes glucose and oxygen to generate energy to maintain cellular metabolism via nutrients that diffuse from the cartilage endplate. The microenvironment in the intervertebral disc becomes nutritionally deficient during degeneration, and nutritional deficiency has been shown to inhibit the viability and proliferation of NP cells. METHODS: To investigate the molecular mechanism by which nutritional deficiency reduces viability and decreases proliferation, we created an in vitro model by using decreasing serum concentration percentages. RESULTS: In this study, we found that nutritional deficiency reduced NP cell viability and increased cell apoptosis and that the upregulation of ATF4 expression and the downregulation of PKM2 expression were involved in this process. Moreover, we found that PKM2 inhibition can reduce the cell apoptosis induced by ATF4 silence under nutritional deficiency. CONCLUSION: Our findings revealed that PKM2 inhibition reduces the cell apoptosis induced by ATF4 silence under nutritional deficiency by inhibiting AKT phosphate. Revealing the function and mechanism of NP cell development under nutritional deficiency will provide new insights into the etiology, diagnosis, and treatment of intervertebral disc and related diseases.

Crumpled MXene Electrodes for Ultrastretchable and High-Area-Capacitance Supercapacitors.

In spite of the excellent electrical and electrochemical properties, two-dimensional transition metal carbide (MXene) is often limited by the high stiffness for the direct implementation in next-generation stretchable and wearable energy storage devices. The improved deformability has been achieved in ultrathin composite electrodes utilizing additives that substantially reduce the specific capacitance. Here, we demonstrate an ultrastretchable and high-performing supercapacitor based on MXene electrodes with crumpled textures. After screening on the thickness, the crumpled MXene film of ∼3 µm in thickness is identified as the optimal choice to mitigate the crack formations under large and repetitive mechanical strains. The as-prepared symmetric supercapacitor, therefore, demonstrates a high specific capacitance of ∼470 mF cm-2, ultrahigh stretchability up to 800% area strain, and >90% retention of the initial capacitance after 1000 stretch-relaxation cycles. The developments offer an attractive avenue to design stretchable electrodes based on various two-dimensional nanomaterials and their composites.

Treg-dependent immunosuppression triggers effector T cell dysfunction via the STING/ILC2 axis.

Lung cancer remains the leading cause of cancer-related deaths and despite extensive research, the survival rate of lung cancer patients remains significantly low. Recent data reveal that aberrant Kras signaling drives regulatory T cells (Tregs) present in lung tumor microenvironment to establish immune deregulation and immunosuppression but the exact pathogenic mechanism is still unknown. In this study, we investigate the role of oncogenic Kras in Treg-related immunosuppression and its involvement in tumor-associated metabolic reprogramming. Findings reveal Tregs to prompt GATA3/NOS2-related immunosuppression via STING inhibition which triggers a decline in CD4+ T infiltration, and a subsequent increase in lung metastatic burden. Enhanced Treg expression was also associated with low T/MDSC ratio through restriction of CD8+CD44+CD62L- T effector cells, contributing to a tumor-promoting status. Specifically, TIM3+/LAG3+ Tregs prompted Kras-related immunosuppressive chemoresistance and were associated with T cell dysfunction. This Treg-dependent immunosuppression correlated with CD8 T cell exhaustion phenotype and ILC2 augmentation in mice. Moreover, enhanced Treg expression promoted activation-induced cell death (AICD) of T lymphocytes and guided lymph node metastasis in vivo. Overall, these findings demonstrate the multifaceted roles of Tregs in sustaining lung immunosuppressive neoplasia through tumor microenvironment remodeling and provide new opportunities for effective metastasis inhibition, especially in chemoresistant tumors.

Molecular hydrogen alleviates asthma through inhibiting IL-33/ILC2 axis.

BACKGROUND: Asthma is one of the most common noninfectious chronic diseases characterized by type II inflammation. This study aimed to investigate the effects of molecular hydrogen on the pathogenesis of asthma. METHODS: OVA sensitized asthma mouse model and house dust mite treated 16HBE cellular model were established and hydrogen/oxygen mixture was used to treat asthmatic mice and 16HBE cells. Serum and BALF cytokines were measured with specific ELISA assays. E-cadherin and ZO-1 were detected by immunohistochemical staining and expression of caspase 3 and 9, NF-κB, IL-33 and ST2 was assessed by quantitative real-time PCR, western blot and/or immunofluorescence. IL-33 promoter activity was analyzed by dual-luciferase assay. ILC2 population was assayed by flow cytometry and differentially expressed miRNAs were detected using miRNA array. RESULTS: Serum and BALF levels of IL-33 and other alarmin and type II cytokines were greatly increased by OVA and inhibited by H2 in asthmatic mice. The expression of NF-κB (p65) and ST2 was upregulated by OVA and suppressed by H2. ILC2 population was markedly increased in OVA-induced asthmatic mice, and such increase was inhibited by H2. E-cadherin and ZO-1 levels in airway tissues of asthmatic mice were significantly lower than that of control mice, and the reduction was recovered by H2 treatment. H2 alleviated HDM induced apoptosis of 16HBE cells, upregulation of IL-33 and ST2, and elevation of IL-33 promoter activity. A group of miRNAs differentially expressed in HDM and HDM + H2 treated 16HBE cells were identified. CONCLUSIONS: These data demonstrated that H2 is efficient in suppressing allergen-induced asthma and could be developed as a therapeutics for asthma and other conditions of type II inflammation.

TIGIT presents earlier expression dynamic than PD-1 in activated CD8+ T cells and is upregulated in non-small cell lung cancer patients.

CD8+ T cells are considered a critical component of antitumor immunity. However, tumor-infiltrating CD8+ T cells may express more than one checkpoint molecules that have the potential to inhibit effector responses alone or cooperatively. Here, we focused on the expression dynamic of TIGIT and PD-1 in CD8+ T cells. TIGIT+ subset presented significantly higher PD-1 expression than TIGIT- subset in circulating CD8+ T cells. The expression dynamic of TIGIT and PD-1 was then tracked. In total CD8+ T cells, TIGIT mRNA increased more rapidly than PD-1 mRNA, and TIGIT+ CD8+ T cells upregulated PD-1 more rapidly than TIGIT- CD8+ T cells. Next, 24-h-stimulated CD8+ T cells were re-sorted into TIGIT+ and TIGIT- subsets, and the TIGIT+ cells that came from TIGIT- cells also presented significantly more rapid PD-1 induction than persistent TIGIT- CD8+ T cells. In non-small cell lung cancer (NSCLC) patients, the expression of PD-1 was more enriched in TIGIT+ cells than in TIGIT- cells in both circulating CD8+ T cells and tumor-infiltrating CD8+ T cells. Function analysis revealed that TIGIT+ CD8 T cells presented lower interferon-gamma, perforin 1, and granzyme B upregulation than TIGIT- CD8 T cells, especially in NSCLC patients. Overall, these data indicated that TIGIT presented earlier expression dynamic than PD-1 in activated CD8+ T cells and was upregulated in NSCLC patients.

Serum apolipoprotein B/apolipoprotein A1 ratio in relation to intervertebral disk herniation: a cross-sectional frequency-matched case-control study.

STUDY DESIGN: This was a cross-sectional frequency-matched case-control study. BACKGROUND AND AIM: The serum lipid profile of lipoprotein(a) [Lp(a)] level and apolipoprotein B/apolipoprotein A1 ratio (Apo B/Apo A1) ratio were found to be more representative for serum lipid level and were recognized as the independent risk factors for various diseases. Although the blood levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were found to be associated with symptomatic intervertebral disk herniation (IDH), no studies to date have evaluated the association of Apo AI, Apo B, Lp(a), and Apo B/Apo AI levels with symptomatic IDH. This study aimed to assess the link between blood lipid levels and symptomatic IDH. METHOD: The study included 1839 Chinese patients. Of these, 918 patients were diagnosed with IDH and enrolled in the experimental group. A control group of 921 patients underwent a physical examination during the same period. The serum lipid levels of TC, TG, LDL-C, HDL-C, Lp(a), Apo B, and Apo B/Apo AI were examined and analyzed. The control group comprised randomly selected patients who met the baseline levels of the aforementioned lipid molecules. RESULTS: Patients with IDH exhibited significantly higher TC, TG, LDL, Apo B, and Lp(a) levels than controls. The percentage of high TC, high TG, high LDL, high Apo B, and high Lp(a) were obviously higher in the IDH group than in the control group. However, hyperlipidemia had no relationship with the degenerated segment of the IDH (P = 0.201). The odds ratio (OR) for the incidence of IDH with elevated levels of LDL-C, TC, TG, Lp(a), Apo B, and Apo B/Apo AI was 1.583, 1.74, 1.62, 1.58, 1.49, and 1.39, respectively. The correlation analysis revealed the correlation between elevated LDL-C, TC, TG, Apo B, Lp(a), and incidence of IDH was significant (R2LDL = 0.017; R2TC = 0.004; R2TG = 0.015; R2Apo B = 0.004; R2Lp(a) = 0.021) (P < 0.05). CONCLUSION: This study suggested that elevated levels of serum TC, TG, LDL, Apo B, Lp(a), and Apo B/Apo AI were associated with a higher risk of IDH. This study provided useful information to identify a population that might be at risk of developing IDH based on elevated lipid levels.

Chinese Expert Recommendation for Diagnosis and Treatment of Massive Hemoptysis.

Massive hemoptysis is one of emergency and critical diseases of the respiratory system. The definition of massive hemoptysis has always been different in the literature, which often depends on the quantitative estimation of the amount of hemoptysis, such as the amount of hemoptysis being in the range of 300-600 mL within 24 h, or hemoptysis more than 3 times within 1 week. Each amount of hemoptysis that is greater than 100 mL can be considered as massive hemoptysis, but the amount of hemoptysis is difficult to accurately estimate. Therefore, massive hemoptysis can be defined as any life-threatening hemoptysis and any hemoptysis that may cause airway obstruction and asphyxia. Massive hemoptysis accounts for approximately 5% of all hemoptysis cases and usually indicates the presence of a potentially severe respiratory or systemic disease. The mortality rate of massive hemoptysis is about 6.5-38%. The cause of death is generally shock caused by airway obstruction or excessive bleeding, and asphyxia is the main cause of death. At present, due to insufficient understanding of massive hemoptysis, there are limited technical means in the etiological diagnosis and untimely or improper treatment, resulting in high mortality of massive hemoptysis. Therefore, the diagnosis and treatment of massive hemoptysis needs to be standardized.

Multiple intraventricular metastases from lung adenocarcinoma with EGFR G719X mutation: a case report.

BACKGROUND: Brain is one of the most common target organ of lung cancer metastasis, while descriptions of intraventricular carcinomatosis could hardly be found among previous cases. To date no cases from lung adenocarcinoma have been reported in the literature. CASE PRESENTATION: We report here a case of multiple intraventricular metastases from lung adenocarcinoma with EGFR G719X mutation. This 64-year-old woman was referred to our hospital with complaints of dizziness and vomiting. Target therapy with afatinib was initiated and the lesions in both lung and brain achieved good partial responses. CONCLUSIONS: This case report revealed a phenomenon of rare intraventricular metastasis from lung cancer, which should be carefully distinguished from primary ventricular tumors. Compared to brain parenchyma metastasis, intraventricular lesions would cause more severe symptoms which may be rapidly progressive. Target therapy could become a potential option in such patients with non-drugresistant EGFR mutations.

Management of Persistent Air Leaks Using Endobronchial Autologous Blood Patch and Spigot Occlusion: A Multicentre Randomized Controlled Trial in China.

BACKGROUND: Optimal management of persistent air leaks (PALs) in patients with secondary spontaneous pneumothorax (SSP) remains controversial. OBJECTIVE: To evaluate the efficacy and safety of endobronchial autologous blood plus thrombin patch (ABP) and bronchial occlusion using silicone spigots (BOS) in patients with SSP accompanied by alveolar-pleural fistula (APF) and PALs. METHODS: This prospective multicentre randomized controlled trial compared chest tube-attached water-seal drainage (CTD), ABP, and BOS that were performed between February 2015 and June 2017 in one of six tertiary care hospitals in China. Patients diagnosed with APF experiencing PALs (despite 7 days of CTD) and inoperable patients were included. Outcome measures included success rate of pneumothorax resolution at the end of the observation period (further 14 days), duration of air leak stop, lung expansion, hospital stay, and complications. RESULTS: In total, 150 subjects were analysed in three groups (CTD, ABP, BOS) of 50 each. At 14 days, 60, 82, and 84% of CTD, ABP, and BOS subjects, respectively, experienced full resolution of pneumothorax (p = 0.008). All duration outcome measures were significantly better in the ABP and BOS groups than in the CTD group (p < 0.016 for all). The incidence of adverse events, including chest pain, cough, and fever, was not significantly different. All subjects in the ABP and BOS groups experienced temporary haemoptysis. Spigot displacement occurred in 8% of BOS subjects. CONCLUSION: ABP and BOS resulted in clinically meaningful outcomes, including higher success rate, duration of air leak stop, lung expansion, and hospital stay, with an acceptable safety profile.

Interventional Bronchoscopy for the Treatment of Malignant Central Airway Stenosis: An Expert Recommendation for China.

Malignant central airway stenosis refers to airway stenosis caused by primary or metastatic malignant tumors which may lead to different levels of dyspnea or asphyxia in patients. With the rapid development of interventional pulmonology, therapeutic bronchoscopy has become one of the main methods for the diagnosis and treatment of malignant central airway stenosis. However, the level of diagnosis and treatment of respiratory intervention techniques in China is uneven at present, the treatment methods are not uniform, the treatment effects vary greatly, and some treatments even lead to serious complications. The interventional treatment technology for malignant central airway stenosis in China needs to be standardized. Therefore, the relevant experts of the Beijing Health Promotion Association Respiratory and Oncology Intervention and Treatment Alliance have formulated this consensus after several rounds of full discussion.

Validity of a Chinese version of the Mini Asthma Quality of Life Questionnaire (MiniAQLQ) and a comparison of completion by patients and relatives.

OBJECTIVE: To test the psychometric properties of the Chinese version of the Mini Asthma Quality of Life Questionnaire (MiniAQLQ) and to investigate the differences between the MiniAQLQ completed by patients (p-MiniAQLQ) and by their relatives (r-MiniAQLQ). METHODS: One hundred and two asthmatic patients and 45 relatives were recruited. The reliability was evaluated using Cronbach's alpha and intraclass correlation coefficient (ICC). The validity of the MiniAQLQ was assessed by comparing it with the Sydney Asthma Quality of Life Questionnaire (AQLQ-S) and lung function measurements. The mean quality of life scores were compared by gender and smoking history, and the p-MiniAQLQ scores were then compared with the r-MiniAQLQ scores. RESULTS: The MiniAQLQ showed high internal consistency (Cronbach's alpha = 0.901) and a high two-week reproducibility (ICC = 0.863). The cross-sectional correlations between the MiniAQLQ and the AQLQ-S were strong. Correlations between the MiniAQLQ and lung function (predicted FEV1% and PEF) ranged from poor to weak at the total or domain levels. The MiniAQLQ scores were not significantly associated with gender or smoking history. There was poor agreement between the p-MiniAQLQ and r-MiniAQLQ scores at the total or domain levels. CONCLUSIONS: The Chinese version of the MiniAQLQ showed good reliability and validity. It is reliable for evaluating the impact of asthma on patients' quality of life. Relatives of the patients did not have a comprehensive grasp of the patients' conditions. Physicians should be cautious when patients' relatives come to the hospital to seek a modified treatment when the patients are not present.