Real-world tobacco cessation practice in China: findings from the prospective, nationwide multicenter China National Tobacco Cessation Cohort Study (CNTCCS).

Background: Tobacco cessation is proven to be the most effective and cost-effective strategy for smokers to reduce their risk of smoking-related disease and premature death. Providing effective, efficient, safe, and patient-centred tobacco cessation treatment to reach those who need them is a significant challenge. To date, only a few nationwide studies in China have assessed the overall clinical care practice and treatment outcome of tobacco cessation.

Polysaccharide H-1-2 Ameliorates High Glucose-Induced Podocyte Dysfunction by Suppressing Epithelial-to-Mesenchymal Transition via Restoration of SIRT1 in Vivo and in Vitro.

Renal interstitial fibrosis, a pathological feature of diabetic nephropathy, is closely related to endothelial-to-mesenchymal transition (EMT). This study aimed to explore the effect of H-1-2, a polysaccharide of Pseudostellaria heterophylla, on high glucose (HG) induced-podocyte EMT in vivo and ex vivo. DBA/2 mice were given five consecutive days of streptozotocin injection to induce the diabetic nephropathy model.

Effects of bone morphogenetic protein 4 on TGF-1-induced cell proliferation, apoptosis, activation and differentiation in mouse lung fibroblasts ERK/p38 MAPK signaling pathway.

Fibroblasts, in particular myofibroblasts, are the critical effector cells in idiopathic pulmonary fibrosis (IPF), a deadly lung disease characterized by abnormal lung remodeling and the formation of "fibroblastic foci". Aberrant activation of TGF-1 is frequently encountered and promotes fibroblast proliferation, activation, and differentiation in pulmonary fibrosis. Hence, the inhibition of TGF-1-induced lung fibroblast activation holds promise as a therapeutic strategy for IPF.

Integrated Analysis of Mutations, miRNA and mRNA Expression in Glioblastoma.

Background: Glioblastoma multiforme (GBM) is a common, malignant brain tumor in adults, with a median survival of only 15-23 months. Organisms respond to disease stress through sophisticated mechanisms at the physiological, transcriptional and metabolic levels. However, the molecular regulatory networks responsible for occurrence, progression and recurrence of glioma have yet to be elucidated.

Sodium Tanshinone IIA Sulfonate Attenuates Cigarette Smoke Extract-Induced Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Alveolar Epithelial Cells by Enhancing SIRT1 Pathway.

Emphysema is one of the most important phenotypes for chronic obstructive pulmonary disease (COPD). Apoptosis in alveolar epithelial cells (AECs) causes the emphysematous alterations in the smokers and patients with COPD. Sirtuin 1 (SIRT1) is able to attenuate mitochondrial dysfunction, oxidative stress, and to modulate apoptosis.

Mitomycin C induces pulmonary vascular endothelial-to-mesenchymal transition and pulmonary veno-occlusive disease via Smad3-dependent pathway in rats.

Background And Purpose: Pulmonary veno-occlusive disease (PVOD) is a rare disease characterized by the obstruction of small pulmonary veins leading to pulmonary hypertension. However, the mechanisms underlying pulmonary vessel occlusion remain largely unclear.

Experimental Approach: A mitomycin C (MMC)-induced PVOD rat model was used as in vivo animal model, and primarily cultured rat pulmonary microvascular endothelial cells (PMVECs) were used as in vitro cell model.

Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats.

Background And Purpose: Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling pathway, in this subtype of pulmonary hypertension.

Experimental Approach: Male Sprague Dawley rats were used to establish a model of pulmonary hypertension with pulmonary fibrosis, induced by bleomycin.

Altered Airway Microbiota Composition in Patients With Pulmonary Hypertension.

Alteration in microbiota composition of respiratory tract has been reported in the progression of many chronic lung diseases, yet, the correlation and causal link between respiratory tract microbiota and the disease development of pulmonary hypertension (PH) remain largely unknown. This study aims to define and compare the respiratory microbiota composition in pharyngeal swab samples between patients with PH and reference subjects. A total of 118 patients with PH and 79 reference subjects were recruited, and the pharyngeal swab samples were collected to sequence the 16S ribosomal RNA (16S rRNA) V3-V4 region of respiratory microbiome.

A novel rat model of pulmonary hypertension induced by mono treatment with SU5416.

Pulmonary hypertension (PH) is responsible for premature death caused by progressive and severe heart failure. A simple, feasible, and reproducible animal model of PH is essential for the investigation of the pathogenesis and treatment of this condition. Previous studies have demonstrated that the vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor SU5416 combined with hypoxia could establish an animal model of PH.

Tetramethylpyrazine: A promising drug for the treatment of pulmonary hypertension.

Background And Purpose: Tetramethylpyrazine (TMP) was originally isolated from the traditional Chinese herb ligusticum and the fermented Japanese food natto and has since been synthesized. TMP has a long history of beneficial effects in the treatment of many cardiovascular diseases. Here we have evaluated the therapeutic effects of TMP on pulmonary hypertension (PH) in animal models and in patients with pulmonary arterial hypertension (PAH) or chronic thromboembolic pulmonary hypertension (CTEPH).

Transplantation of Mesenchymal Stem Cells Attenuates Pulmonary Hypertension by Normalizing the Endothelial-to-Mesenchymal Transition.

For decades, stem cell therapies for pulmonary hypertension (PH) have progressed from laboratory hypothesis to clinical practice. Promising preclinical investigations have laid both a theoretical and practical foundation for clinical application of mesenchymal stem cells (MSCs) for PH therapy. However, the underlying mechanisms are still poorly understood.

Author Correction: Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.

Standardized Uptake Value Using Thyroid Quantitative SPECT/CT for the Diagnosis and Evaluation of Graves' Disease: A Prospective Multicenter Study.

The clinical applications of the quantitative single photon emission computed tomography (SPECT)/computed tomography (CT) are being expanded to a variety of fields of nuclear medicine. However, clinical application of quantitative SPECT/CT for the evaluation of Graves' disease (GD) still needs further investigation. Our aim was to investigate the feasibility of standard uptake value (SUV) of the thyroid for the clinical diagnosis and evaluation of GD.

Divergent changes of p53 in pulmonary arterial endothelial and smooth muscle cells involved in the development of pulmonary hypertension.

The tumor-suppressive role of p53, a transcription factor that regulates the expression of many genes, has been linked to cell cycle arrest, apoptosis, and senescence. The noncanonical function or the pathogenic role of p53 has more recently been implicated in pulmonary vascular disease. We previously reported that rapid nuclear accumulation of hypoxia-inducible factor (HIF)-1α in pulmonary arterial smooth muscle cells (PASMCs) upregulates transient receptor potential channels and enhances Ca entry to increase cytosolic Ca concentration ([Ca]).

Measurement and Evaluation of Quantitative Performance of PET/CT Images before a Multicenter Clinical Trial.

To ensure the reliability of the planned multi-center clinical trial, we assessed the consistence and comparability of the quantitative parameters of the eight PET/CT units that will be used in this trial. PET/CT images were scanned using a PET NEMA image quality phantom (Biodex) on the eight units of Discovery PET/CT 690 from GE Healthcare. The scanning parameters were the same with the ones to be used in the planned trial.

Long non-coding RNA expression patterns in lung tissues of chronic cigarette smoke induced COPD mouse model.

Long non-coding RNAs (lncRNAs) have critical regulatory roles in protein-coding gene expression. Aberrant expression profiles of lncRNAs have been observed in various human diseases. In this study, we investigated transcriptome profiles in lung tissues of chronic cigarette smoke (CS)-induced COPD mouse model.

Roles of IL-4 genetic polymorphisms and haplotypes in the risk of gastric cancer and their interaction with environmental factors.

Gastric cancer (GC) is the fifth most common cancer and imposes a global cancer burden. IL-4 is a typical cytokine of Th2 cells. IL-4 genetic polymorphisms have multiple functions in many cancers.

Bortezomib alleviates experimental pulmonary hypertension by regulating intracellular calcium homeostasis in PASMCs.

The ubiquitin-proteasome system is considered to be the key regulator of protein degradation. Bortezomib (BTZ) is the first proteasome inhibitor approved by the US Food and Drug Administration for treatment of relapsed multiple myeloma and mantle cell lymphoma. Recently, BTZ treatment was reported to inhibit right ventricular hypertrophy and vascular remodeling in hypoxia-exposed and monocrotaline-injected rats.

Sodium tanshinone IIA sulfonate inhibits hypoxia-induced enhancement of SOCE in pulmonary arterial smooth muscle cells via the PKG-PPAR-γ signaling axis.

Our laboratory previously showed that sodium tanshinone IIA sulfonate (STS) inhibited store-operated Ca(2+) entry (SOCE) through store-operated Ca(2+) channels (SOCC) via downregulating the expression of transient receptor potential canonical proteins (TRPC), which contribute to the formation of SOCC (Wang J, Jiang Q, Wan L, Yang K, Zhang Y, Chen Y, Wang E, Lai N, Zhao L, Jiang H, Sun Y, Zhong N, Ran P, Lu W. Am J Respir Cell Mol Biol 48: 125-134, 2013). The detailed molecular mechanisms by which STS inhibits SOCE and downregulates TRPC, however, remain largely unknown.

Heat shock protein 70 induction by glutamine increases the α-synuclein degradation in SH-SY5Y neuroblastoma cells.

Functional defects in heat shock proteins (HSPs), e.g. Hsp70, have been reported to have a key role in Parkinson's disease (PD).

Peroxisome Proliferator-Activated Receptor γ-Mediated Inhibition on Hypoxia-Triggered Store-Operated Calcium Entry. A Caveolin-1-Dependent Mechanism.

Our previous publication demonstrated that peroxisome proliferator-activated receptor γ (PPARγ) inhibits the pathogenesis of chronic hypoxia (CH)-induced pulmonary hypertension by targeting store-operated calcium entry (SOCE) in rat distal pulmonary arterial smooth muscle cells (PASMCs). In this study, we aim to determine the role of a membrane scaffolding protein, caveolin-1, during the suppressive process of PPARγ on SOCE. Adult (6-8 weeks) male Wistar rats (200-250 g) were exposed to CH (10% O2) for 21 days to establish CH-induced pulmonary hypertension.

inhibitor reduces the proliferation and migration in osteosarcoma MG-63 cells.

As the most common malignant primary bone tumor in childhood, osteosarcoma (OS) maintains a high recurrence, despite the significant improvements in the overall survival rate of high-grade OS patients during the recent decades. Therefore, a novel therapy strategy is required for OS treatment. Recently, various microRNAs (miRNAs or miRs) have been confirmed as deregulated in OS, and the dysregulation in OS has been discovered by the microarray analysis.