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Purpose As stated in the Global Initiative for Asthma, there are still some asthmatic patients who have not achieved asthma control. Mobile is a useful tool for asthma management. We aimed to compare the advantages of mobile management with traditional management in improving adherence and control of asthma. Methods In this prospective, multicentre, randomized, controlled and parallel-group study, we enrolled patients with poor adherence and uncontrolled asthma at 32 hospitals in 28 provinces in China. Patients were randomly assigned to the mobile management or traditional management groups for 12 months. The primary endpoint was the proportion of patients with good adherence (Medication Adherence Report Scale for Asthma [MARS-A] score ≥ 45) for 6 months. This study is registered at ClinicalTrials.gov ( NCT02917174 ). Results Between April 2017 and April 2018, 923 patients were eligible for randomization (mobile group, n = 461; traditional group, n = 462). Dropout was 84 (18.2%) in the mobile management group and 113 (24.4%) patients in the traditional management group. The proportion of patients with good adherence was significantly higher in the mobile management group than in the traditional management group (66.0% vs. 58.99%, P = 0.048). The mobile management group showed higher mean MARS-A score (at 1, 6, 9, and 12 months) and asthma control test scores (at 6 and 9 months), and lower total lost rate to follow-up within 12 months than the traditional management group. Conclusions Mobile asthma management can improve adherence and asthma control compared to traditional management. Trial Registration ClinicalTrials.gov Identifier: NCT02917174

Background Although many studies have indicated that Psoriasis (PsO) could contribute to the risk of lung cancer, no study has reported a clear causal association between them. Our aim was to explore the potential causal association between PsO and the lung cancer risk using Mendelian randomization (MR) design. Methods To explore a causal association between the PsO and lung cancer, we used large‐scale genetic summary data from genome‐wide association study (GWAS), including PsO (n = 337 159) and lung cancer (n = 361 586), based on previous observational studies. Our main analyses were conducted by inverse‐variance weighted (IVW) method with random‐effects model, with a complementary with the other two analyses: weighted median method and MR‐Egger approach. Results The results of IVW methods demonstrated that genetically predicted PsO was significantly associated with higher odds of lung cancer, with an odds ratio (OR) of 1.06 (95%CI, 1.01–1.12; P = 0.02). Weighted median method and MR‐Egger regression also demonstrated directionally similar results (All P < 0.05). In addition, both funnel plots and MR‐Egger intercepts indicated no directional pleiotropic effects between PsO and lung cancer. Conclusions Our study provided potential evidence between genetically predicted PsO and lung cancer, which suggested that enhanced screening for lung cancer allows early detection of lung cancer.

Background A large proportion of pulmonary embolism (PE) heritability remains unexplained, particularly among the East Asian (EAS) population. Our study aims to expand the genetic architecture of PE and reveal more genetic determinants in Han Chinese. Methods We conducted the first genome-wide association study (GWAS) of PE in Han Chinese, then performed the GWAS meta-analysis based on the discovery and replication stages. To validate the effect of the risk allele, qPCR and Western blotting experiments were used to investigate possible changes in gene expression. Mendelian randomization (MR) analysis was employed to implicate pathogenic mechanisms, and a polygenic risk score (PRS) for PE risk prediction was generated. Results After meta-analysis of the discovery dataset (622 cases, 8853 controls) and replication dataset (646 cases, 8810 controls), GWAS identified 3 independent loci associated with PE, including the reported loci FGG rs2066865 (p-value = 3.81 × 10−14), ABO rs582094 (p-value = 1.16 × 10−10) and newly reported locus FABP2 rs1799883 (p-value = 7.59 × 10−17). Previously reported 10 variants were successfully replicated in our cohort. Functional experiments confirmed that FABP2-A163G(rs1799883) promoted the transcription and protein expression of FABP2. Meanwhile, MR analysis revealed that high LDL-C and TC levels were associated with an increased risk of PE. Individuals with the top 10% of PRS had over a fivefold increased risk for PE compared to the general population. Conclusions We identified FABP2, related to the transport of long-chain fatty acids, contributing to the risk of PE and provided more evidence for the essential role of metabolic pathways in PE development.