[Recent progress in the treatment of non-T2 asthma].

Non-T2 asthma, also known as non-eosinophilic asthma or low T2 asthma, does not have markers of type 2 inflammation and is often associated with hormone insensitivity and severe asthma. This article reviews the progress in drug therapy for non-T2 asthma.

Smoking Status Modifies the Relationship between Th2 Biomarkers and Small Airway Obstruction in Asthma.

Background: Cigarette smoking and Th2-inflammation are both crucial in the pathogenesis of asthma. However, it is unknown whether smoking can affect the association between Th2-inflammation and small airway obstruction in adults with asthma.

Methods: Adults diagnosed with asthma by a pulmonologist according to Global Initiative for Asthma guidelines were recruited from September 2016 to April 2018 to participate in this study.

Targeted resequencing showing novel common and rare genetic variants increases the risk of asthma in the Chinese Han population.

Background: Although studies have identified hundreds of genetic variants associated with asthma risk, a large fraction of heritability remains unexplained, especially in Chinese individuals.

Methods: To identify genetic risk factors for asthma in a Han Chinese population, 211 asthma-related genes were first selected based on database searches. The genes were then sequenced for subjects in a Discovery Cohort (284 asthma patients and 205 older healthy controls) using targeted next-generation sequencing.

A nonsynonymous polymorphism (rs117179004, T392M) of hyaluronidase 1 (HYAL1) is associated with increased risk of idiopathic pulmonary fibrosis in Southern Han Chinese.

Background: Idiopathic pulmonary fibrosis (IPF) is a genetic heterogeneous disease with high mortality and poor prognosis. Hyaluronidase 1 (HYAL1) was found to be upregulated in fibroblasts from IPF patients, and overexpression of HYAL1 could prevent human fetal lung fibroblast proliferation. However, the genetic correlation between the HYAL1 and IPF or connective tissue diseases related interstitial lung disease (CTD-ILD) has not been determined.

Osthole Attenuates Macrophage Activation in Experimental Asthma by Inhibitingthe NF-ĸB/MIF Signaling Pathway.

Inhibition of activated macrophages is an alternative therapeutic strategy for asthma. We investigated whether a coumarin compound, osthole, isolated from (L.) Cuss, alleviated macrophage activation and .

The Role of Macrophage Migration Inhibitory Factor (MIF) in Asthmatic Airway Remodeling.

Purpose: Recent studies have demonstrated that macrophage migration inhibitory factor (MIF) is of importance in asthmatic inflammation. The role of MIF in modulating airway remodeling has not yet been thoroughly elucidated to date. In the present study, we hypothesized that MIF promoted airway remodeling by intensifying airway smooth muscle cell (ASMC) autophagy and explored the specific mechanisms.

IL-24 deficiency protects mice against bleomycin-induced pulmonary fibrosis by repressing IL-4-induced M2 program in macrophages.

Idiopathic pulmonary fibrosis (IPF) is the most common type of idiopathic interstitial pneumonia and has one of the poorest prognosis. However, the molecular mechanisms underlying IPF progression remain largely unknown. In this study, we determined that IL-24, an IL-20 subfamily cytokine member, was increased both in the serum of IPF patients and the bronchoalveolar lavage fluid (BALF) of mice following bleomycin (BLM)-induced pulmonary fibrosis.

MicroRNA-16 inhibits the proliferation and metastasis of human lung cancer cells by modulating the expression of YAP1.

Purpose: Accounting for significant human morbidity and mortality across the globe, lung cancer is the most prevalent type of cancer as far as incidence and mortality is concerned. MicroRNAs (miRs) have shown an amazing potential to act as therapeutic agents for the management of several human diseases. This study investigated the function of miR-16 in lung cancer.

Fixed Ratio Versus Lower Limit of Normal: Health Status and Risk Factors for COPD Overdiagnosis.

Background: The threshold of the lower limit of the normal range of lung function has been suggested to be more accurate than the 0.7 fixed ratio (FEV/FVC < 0.7) for a diagnosis of COPD.

Airway reversibility in asthma and phenotypes of Th2-biomarkers, lung function and disease control.

Background: High bronchodilator reversibility in adult asthma is associated with distinct clinical characteristics. In this study, we aim to make a comparison with T-helper 2 (Th2)-related biomarkers, lung function and asthma control between asthmatic patients with high airway reversibility (HR) and low airway reversibility (LR).

Methods: Patients with asthma diagnosed by pulmonologist according to Global Initiative for Asthma guidelines were recruited from the outpatient department of our hospital from August 2014 to July 2017.

E4BP4 facilitates glucocorticoid sensitivity of human bronchial epithelial cells via down-regulation of glucocorticoid receptor-beta.

It has recently been recognized that a subset of asthma patients suffer from glucocorticoid (GC) insensitivity, and glucocorticoid receptor-β (GR-β) is associated with corticosteroid resistance, but the underlying mechanisms remain unknown. Here we demonstrated that Interleukin-17A induced glucocorticoid sensitivity in human bronchial epithelial cells (16HBE) is enhanced, which is depend on E4 promoter-binding protein 4 (E4BP4) mediated GR-β expression. Our data show that the expression of E4BP4 is significantly up-regulated in 16HBE cells, and the depletion of E4BP4 dramatically decreased glucocorticoid sensitivity in IL-17A induced 16HBE cells.

Targeted resequencing reveals genetic risks in patients with sporadic idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a genetic heterogeneous disease with high mortality and poor prognosis. However, a large fraction of genetic cause remains unexplained, especially in sporadic IPF (∼80% IPF). By systemically reviewing related literature and potential pathogenic pathways, 92 potentially IPF-related genes were selected and sequenced in genomic DNAs from 253 sporadic IPF patients and 125 matched health controls using targeted massively parallel next-generation sequencing.

Fast Constrained Spectral Clustering and Cluster Ensemble with Random Projection.

Constrained spectral clustering (CSC) method can greatly improve the clustering accuracy with the incorporation of constraint information into spectral clustering and thus has been paid academic attention widely. In this paper, we propose a fast CSC algorithm via encoding landmark-based graph construction into a new CSC model and applying random sampling to decrease the data size after spectral embedding. Compared with the original model, the new algorithm has the similar results with the increase of its model size asymptotically; compared with the most efficient CSC algorithm known, the new algorithm runs faster and has a wider range of suitable data sets.

[Serum levels of ANP signaling in different degree of allergic asthmatics and its role in the pathogenesis of allergic asthma].

Objective: To investigate the relationship between the severity of allergic asthma and the levels of atrial natriuretic peptide (ANP), and to analyze the potential role of ANP signaling in the pathogenesis of asthma.


Methods: We recruited 96 subjects, including 23 healthy volunteers, 25 stable allergic asthmatics, 21 mild allergic asthmatics and 27 moderate allergic asthmatics, from the Affiliated Hospital of Guilin Medical University. ANP, IFN-γ and IL-4 levels in serum were detected by enzyme-linked immunosorbent assay (ELISA), and the mRNA and protein expressions of natriuretic peptide receptor A (NPRA), transcription factor T-bet and GATA3 were measured by RT-PCR and Western blot.

[The role of SDF-1/CXCR4 on airway inflammation and airway remodeling in a rat asthma model].

Objective: To explore the roles of stromal cell-derived factor 1 (SDF-1) and C-X-C chemokine receptor 4 (CXCR4) on airway inflammation and airway remodeling in rat asthma models.

Methods: Eighteen female SD rats were randomly divided into 3 groups (n = 6): control group, asthmatic 4 weeks group and asthmatic 8 weeks group. The rats were sensitized and inhaled ovalbumin (OVA).

[The effect of LPS on airway inflammation, airway remodeling and TLR4 expression in asthmatic rat].

Objective: To investigate the effects of lipopolysaccharide (LPS) on airway inflammation, airway remodeling and the expression of Toll-like receptor 4 (TLR4) mRNA in asthmatic rats.

Methods: Twenty-four SPF level SD rats were randomly divided into four groups (n = 6): control group, low dose of LPS group, high dose of LPS group and asthma group. Using ovalbumin (OVA) to sensitize and challenge to establish asthmatic rat model.

Expression of seven stem-cell-associated markers in human airway biopsy specimens obtained via fiberoptic bronchoscopy.

Background: Previous reports have suggested that malignant transformations originate from adult stem cells, and may thus express the stem-cell-associated markers. The purpose of this study is to investigate the differential expression and clinical significance of seven stem-cell-associated markers (Bmi1, CD133, CD44, Sox2, Nanog, OCT4 and Msi2) in lung cancer, providing new targets for the diagnosis and treatment of lung cancer.

Methods: In this study, we evaluated the differential expression of mRNA levels seven stem-cell-associated markers by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) from 112 human lung cancer and 18 non-cancer tissues obtained by bronchoscopy.

[Effects of TOLL-like receptor 4 on passively sensitized human airway smooth muscle cells proliferation and synthesis and secretion function of TGF-beta1].

Objective: To investigate the activation of Toll like receptor 4 (TLR4) on passively sensitized human airway smooth muscle cells (HASMCs) proliferation and the synthesis and secretion function.

Methods: Through the cultivation of primary HASMCs, we studied TLR4 expression on cell surface, cell proliferation and transformation of parturient factor-beta1 (TGF-beta1) in asthma under the condition of synthesis and secretion level by passively sensitized HASMCs with asthma serum.

Results: Compared with the control group, in passive sensitized group and TNF-alpha group TLR4 expression were significantly increased (P < 0.

[Effect of TLR4 on the migration of asthmatic airway smooth muscle cells induced by airway epithelial cells].

Objective: To explore the effect of Toll-like receptor 4 (TLR4) activation on the migration of asthmatic airway smooth muscle cell (ASMCs) induced by airway epithelial cells.

Methods: Primary ASMCs were cultured by the method of cell digestion. Cell culture supernatant of RTE cells were collected by TNF-alpha stimulation of epithelial cells.

An improved authentication scheme for telecare medicine information systems.

The telecare medicine information system enables or supports health-care delivery services. In order to safeguard patients' privacy, such as telephone number, medical record number, health information, etc., a secure authentication scheme will thus be in demand.

[Role of toll-like receptor 4 in the asthmatic rat airway smooth muscle cells proliferation and apoptosis].

Objective: To explore the role of Toll like receptor 4(TLR4) in the asthmatic rat airway smooth muscle cell (ASMCs) proliferation and apoptosis.

Methods: Established rat model of asthma,isolated and cultured rat ASMCs in asthma, using methods of small molecule RNA interference technology and lipofection method, for small molecule RNA-TLR4 transfection, detected proliferation of ASMCs by MIT minim colorimetry, apoptosis of ASMCs by TUNNEL, the expression of TLR4 protein and mRNA were detected by Western blot and RT-PCR in cells.

Results: The proliferation of ASMCs in TNF-alpha group were significantly higher than that in control group and siRNA-TLR4 transfection group and TNF-alpha + siRNA-TLR4 transfection group respectively and the proliferation of ASMCs in siRNA-TLR4 transfction group was lower than that in control group.