The evolving landscape of IL-10, IL-22 and IL-26 in pleurisy especially in tuberculous pleurisy.

Pleurisy can be categorized as primary or secondary, arising from immunological, tumorous, or microbial conditions. It often results in lung structure damage and the development of various respiratory issues. Among the different types, tuberculous pleurisy has emerged as a prominent focus for both clinical and scientific investigations.

The epidemiology of traumatic brain injuries in the fastest-paced city in China: a retrospective study.

Introduction: Traumatic brain injury (TBI) seriously affects the quality of human health and the prognosis of the patient, but the epidemiological characteristics of TBI can vary among populations. Numerous changes have occurred in the epidemiological characteristics of individuals with TBI in the fast-paced city of Shenzhen, China. However, little is known about these characteristics.

Knockdown of rno_circRNA_009194 Improves Outcomes in Traumatic Brain Injury Rats through Inhibiting Voltage-Gated Sodium Channel Nav1.3.

Excessive activation of voltage-gated sodium channel Nav1.3 has been recently reported in secondary traumatic brain injury (TBI). However, the molecular mechanisms underlying regulating voltage-gated sodium channel (Nav1.

Retraction Note: Hsa-miR-623 suppresses tumor progression in human lung adenocarcinoma.

The authors have retracted the article [Hsa-miR-623 suppresses tumor progression in human lung adenocarcinoma, Cell Death & Disease volume 7, page e2388 (2016), doi 10.1038/cddis.2016.

Correction to: Hsa-miR-623 suppresses tumor progression in human lung adenocarcinoma.

Following publication of their article, the authors noticed that there were minor errors in Figs. 3, 7 and S5. The errors had no effect on the scientific content or conclusions.

A hypothesis study on a four-period prevention model for high altitude disease.

Background: High altitude disease (HAD) can reduce combat effectiveness and damage the health of soldiers at high altitudes. The objective of this hypothesis study is to build a four-period prevention model for high altitude disease that can be applied at high altitudes of over 3000 m.

Presentation Of The Hypothesis: We divided the time at high altitude into nine periods, with three stages from the ascent preparation to the descent to the plain, and applied a continuous dynamic and systematic four-period prevention model across the nine periods.

Hsa-miR-623 suppresses tumor progression in human lung adenocarcinoma.

This corrects the article DOI: 10.1038/cddis.2016.

Hsa-miR-623 suppresses tumor progression in human lung adenocarcinoma.

Our previous study revealed that Ku80 was overexpressed in lung cancer tissues and hsa-miR-623 regulated the Ku80 expression; however, the detailed function of hsa-miR-623 in lung cancer was unclear. We identified that hsa-miR-623 bound to the 3'-UTR of Ku80 mRNA, thus significantly decreasing Ku80 expression in lung adenocarcinoma cells. Hsa-miR-623 was downregulated in lung adenocarcinoma tissues compared with corresponding non-tumorous tissues, and its expression was inversely correlated with Ku80 upregulation.

Impact of village-based health education of tobacco control on the current smoking rate in Chinese rural areas.

The number of smokers in Chinese rural areas is more than 200 million, which is twice that in cities. It is very significant to carry out tobacco control interventions in rural areas. We performed this community intervention study to evaluate the efficacy of village-based health education of tobacco control on the male current smoking rate in rural areas.

Expression of Nitric Oxide Synthase Isoenzyme in Lung Tissue of Smokers with and without Chronic Obstructive Pulmonary Disease.

Background: It has been demonstrated that only 10%-20% cigarette smokers finally suffer chronic obstructive pulmonary disease (COPD). The underlying mechanism of development remains uncertain so far. Nitric oxide (NO) has been found to be closely associated with the pathogenesis of COPD, the alteration of NO synthase (NOS) expression need to be revealed.

CD8(+) Tc-lymphocytes immunodeviation in peripheral blood and airway from patients of chronic obstructive pulmonary disease and changes after short-term smoking cessation.

Background: Cigarette smoke induces an acute but persisting inflammation in peripheral blood and airway in chronic obstructive pulmonary disease (COPD), and CD8(+) Tc-lymphocytes are considered as a key role in this process. We aimed to investigate the Tc-lymphocytes immunodeviation in system and local airway of COPD patients and changes of the immunodeviation after short-term smoking cessation.

Methods: Peripheral blood (PB) and bronchoalveolar lavage fluid (BALF) were collected from 42 patients (14 COPD patients, 16 smokers with normal lung function and 12 nonsmokers), while PB and induced sputum (IS) were obtained from other 19 patients (10 quitting smokers and 9 continuing smokers) at baseline and follow-up respectively of 4-week smoking cessation.

ERK1/2 promotes cigarette smoke-induced rat pulmonary artery smooth muscle cells proliferation and pulmonary vascular remodeling via up-regulating cycline1 expression.

This study investigated the potential role of ERK1/2-cyclinE1 signaling pathway in rat pulmonary artery smooth muscle cells (rPASMCs) proliferation and pulmonary vascular remodeling induced by cigarette smoke exposure. A total of 24 male Wistar rats were randomly divided into 4 groups: control group (C group), S-1M, S-3M and S-6M groups (animals in the groups were exposed to smoke for 1, 3, and 6 months, respectively). HE staining and anti-α-smooth muscle actin antibody staining were performed to observe the degree of pulmonary vascular remodeling.

Change of extracellular signal-regulated kinase expression in pulmonary arteries from smokers with and without chronic obstructive pulmonary disease.

Background: Cigarette smoking may contribute to pulmonary hypertension in chronic obstructive pulmonary disease (COPD) by resulting in pulmonary vascular remodeling that involves pulmonary artery smooth muscle cell (PASMC) proliferation. However, the molecular mechanism underlying this process remains poorly understood.

Objectives: The purpose of this study was to investigate the role of extracellular signal-regulated kinase (ERK) in pulmonary arteries from smokers with normal lung function and smokers with mild to moderate COPD.

Mannose-binding lectin two gene polymorphisms and tuberculosis susceptibility in Chinese population: a meta-analysis.

Numerous studies have been done to explore the association between mannose-binding lectin two (MBL2) gene polymorphisms and the risk of tuberculosis (TB). However, the results are inconsistent. We performed a meta-analysis to investigate whether polymorphisms in the MBL2 gene were associated with TB risk.

[The expression of macrophage migration inhibition factor in pulmonary tissues of smokers with or without chronic obstructive pulmonary disease].

Objective: To investigate the expression of macrophage migration inhibition factor (MIF) in pulmonary tissues of the smokers with and without chronic obstructive pulmonary disease (COPD).

Methods: The subjects were assigned into three groups: non-smokers without COPD (control group, n = 12), smokers without COPD (smoker group, n = 13) and smokers with COPD (COPD group, n = 16). The specimens were obtained from lung tissues as far away from cancer focus as possible (> 5 cm).

[Expression of β-catenin in human pulmonary tissues of smokers with and without chronic obstructive pulmonary disease].

Objective: To investigate the expression of β-catenin in pulmonary tissues of smokers with and without chronic obstructive pulmonary disease (COPD).

Methods: Pulmonary tissues were obtained from patients who had underwent pneumonectomy in Tongji Hospital. The subjects were assigned into non-smokers without COPD (control group), smokers without COPD (smoker group) and smokers with COPD (smoker + COPD group) based on their pulmonary functions and smoking history, with 12 subjects each group.

Relationship between the microsatellite D2S388-5 and D2S2232 polymorphisms and chronic obstructive pulmonary disease in the Chinese Kazakh population.

Background And Objective: Chronic obstructive pulmonary disease (COPD) is influenced by multiple genetic and environmental factors. The role of genetic susceptibility in the pathogenesis of COPD has recently gained more attention. The surface lung surfactant protein B plays an important role in COPD pathogenesis.

NADPH oxidase activation: a mechanism of erectile dysfunction in a rat model of sleep apnea.

Erectile dysfunction (ED) is a frequent occurrence in male patients with obstructive sleep apnea syndrome (OSAS). Long-term intermittent hypoxia (LTIH), one of the hallmarks of OSAS, could mediate ED. The objective of this study was to test the hypothesis that increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity contributes to ED in rat responses to LTIH.

[The effect of cigarette smoke extract on the proliferation of human airway smooth muscle cells sensitized by serum from bronchial asthmatic patients].

Objective: To study the effect of cigarette smoke extract (CSE) on the proliferation of human airway smooth muscle cells (HASMCs) sensitized by serum from asthmatic patients and the underlying mechanisms.

Methods: HASMCs were cultured from primary generation. Cells between passage 4 and 8 were used in the study.

Cigarette smoke extract promotes human pulmonary artery smooth muscle cells proliferation through protein kinase C alpha-dependent induction of cyclin D1.

Background: Exposure to cigarette smoke stimulates the proliferation of human pulmonary artery smooth muscle cells (HPASMCs) in vivo and in vitro. However, the molecular mechanism remains unclear. This study aimed at investigating the role of signaling pathways involving protein kinase C alpha (PKCα) and cyclin D1 in the cigarette smoke extract (CSE)-induced HPASMCs proliferation.

CCN2 promotes cigarette smoke-induced proliferation of rat pulmonary artery smooth muscle cells through upregulating cyclin D1 expression.

Cigarette smoke has been demonstrated to induce pulmonary vascular remodeling, which is characterized by medial thickening of the pulmonary arteries mainly resulting from the abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs). However, the molecular mechanism underlying this process is still unclear. In the present study, we investigated whether CCN2 regulated rat PASMCs (rPASMCs) proliferation induced by cigarette smoke extract (CSE) and nicotine by upregulating cyclin D1 in vitro.

Cigarette smoke extract induced rat pulmonary artery smooth muscle cells proliferation via PKCα-mediated cyclin D1 expression.

Cigarette smoke could induce pulmonary smooth muscle cells (PASMCs) proliferation. Although our previous study had implied the involvement of protein kinase Cα (PKCα), the molecular mechanism underlying PKCα pathway in this process is still unknown. In this study, rat PASMCs were stimulated by cigarette smoke extract (CSE) or PMA (a special activator to PKCα).

Knockdown of connective tissue growth factor by plasmid-based short hairpin RNA prevented pulmonary vascular remodeling in cigarette smoke-exposed rats.

Cigarette smoking may contribute to pulmonary hypertension in chronic obstructive pulmonary disease by resulting in pulmonary vascular remodeling that involves pulmonary artery smooth muscle cell proliferation. Connective tissue growth factor (CTGF) is a cysteine-rich peptide implicated in several biological processes such as cell proliferation, survival, and migration. This study investigated the potential role of CTGF in pulmonary vascular remodeling.

[The expression variations of connective tissue growth factor and cyclinD1 in pulmonary vascular remodeling induced by cigarette smoke in rats].

Objective: To investigate the expression variations of connective tissue growth factor (CTGF) and cyclin D1 in pulmonary vasculature in rats exposed to cigarette smoke and their roles in pulmonary vascular remodeling.

Methods: Twenty-four male Wistar rats were randomly divided into 4 groups: 1 control group (C group) and 3 smoke exposure groups (S2w, S4w, S8w group). Arterial partial pressure of oxygen was measured.

[Effect of extracellular signal-regulated kinase antisense oligodeoxynucleotides on the proliferation of passively sensitized human airway smooth muscle cells].

Objective: Airway smooth muscle (ASM) cell proliferation is a key feature of airway remodeling in asthma. The extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is one of the most important transduction pathways involved in the proliferation of ASM of asthmatic rats. However, its role in the human ASMCs proliferation remains unclear.