[Inhibition of 1,25-(OH)2D3 on passively sensitized human airway smooth muscle cells].

Objective: To investigate the effects of 1,25-(OH)(2)D(3) on the proliferation of passively sensitized human airway smooth muscle cells (HASMCs) and their expressions of MMP-9 and a disintegrin and metalloprotease 33(ADAM33).

Methods: HASMCs were passively sensitized with 10% serum from asthmatic patients. MTT colorimetry assay was used to examine the effect of 1,25-(OH)(2)D(3) on cell proliferation at different concentrations (10(-10) mol/L, 10(-9) mol/L, 10(-8) mol/L, 10(-7) mol/L).

[Respiratory syncytial virus infection enhances airway hyperresponsiveness in guinea pigs and the underlined mechanism].

Aim: To study the relation between Respiratory Syncytial Virus infection and asthma development by measuring airway responsiveness (AR) and M2R function.

Methods: Guinea pigs (n = 34) were randomly divided into 4 groups: Hep-2/NS group (group A, n = 9), RSV/NS group (group B, n =9), Hep-2/OVA group (group C, n = 8) and RSV/OVA group(group D, n = 8). On day 21 after infection we tested AR and M2R.

[To explore the mechanisms of neurogenic inflammation and airway hyperresponsiveness of rat by inhaled sulfur].

Aim: To explore the physiopathological mechanisms of airway injury and the effect on the airway responsiveness of rat by inhaled sulfur dioxide(SO2).

Methods: Sixteen SD male rats were divided randomly into 2 groups (n = 8): the control group and SO2 group. The control group was exposed o pure air.

Notch signaling regulates the FOXP3 promoter through RBP-J- and Hes1-dependent mechanisms.

Evidence has shown that Notch signaling modulates CD4(+)CD25(+) regulatory T-cells (Tregs). As transcription factor Foxp3 acts as a master molecule governing the development and function of Tregs, we investigated whether Notch signaling might directly regulate Foxp3 expression. Here, we provide evidence that Notch signaling can modulate the FOXP3 promoter through RBP-J- and Hes1-dependent mechanisms.

[CIAPIN1 expression in human lung cancer tissues and inhibitory effects of the gene on human pulmonary carcinoma NCI-H446 cells].

Aim: To explore CIAPIN1 gene expression in lung carcinoma tissues and its regulatory in the growth of NCI-H446.

Methods: Fifty-one formalin-fixed paraffin-embedded specimens of primary lung cancer and their non-cancerous counterparts were detected by SABC immunohistochemistry method. Adenoviral vector construction was recombined and the gene was transduced into NCI-H446 cells.

Effect of platelet-activating factor on cell proliferation & NF-kappaB activation in airway smooth muscle cells in rats.

Background & Objective: Despite the established pro-inflammatory actions of platelet activating factor (PAF) observed on chronic obstructive pulmonary disease (COPD), its action on airway remodeling has been still unclear. It has been reported that nuclear factor-kappa B (NF-kappaB) activity is necessary for ASMC proliferation. Further, PAF has been identified as the proximal inducer of NF-kappaB.

[Effect of IL-4 on ABCG2 expression in human lung adenocarcinoma cell lines].

Aim: To investigate the effect of IL-4 on the expression of ABCG2 in lung adencarcinoma cell lines.

Methods: The ABCG2 mRNA and protein expression was determined by semi-quantitative RT-PCR and Western blot respectively.

Results: The ABCG2 mRNA and protein was detectable in lung adencarcinoma cell lines A549 and SPC-A-1.

Inhibition of tumor angiogenesis by HMGB1 A box peptide.

High mobility group box 1 protein (HMGB1) is a highly conserved, ubiquitous non-histone nuclear protein, which participates in maintaining nucleosome structure, regulation of gene transcription, and modulating the activity of steroid hormone receptors. Substantial evidence demonstrated that HMGB1 could be secreted into the extracellular milieu, acts as a proinflammatory cytokine and mediates the downstream inflammatory responses in endotoxemia, arthritis and sepsis. Recently, several reports suggested that HMGB1 plays a key role in tumor angiogenesis through multiple mechanisms, including up-regulation of proangiogenic factors, promoting endothelial progenitor cells homing to ischemic tumor tissues and induction of endothelial cell migration and sprouting.

Comparative proteomic study of acute pulmonary embolism in a rat model.

Pulmonary embolism (PE) is a common, potentially fatal disease, whose blood clots originate from the deep venous system of the lower extremities. PE is of clinical importance because of the considerable mortality and morbidity. In this study, at first we established a rat PE model by injecting 3-4 emboli into the left jugular vein.

[Exploration of serum endothelin-1 as a marker of early radiation lung injury].

Aim: To explore the possibility of endothelin-1(ET-1) as a serological marker of early diagnosis and progression of radiation induced lung injury.

Methods: One hundred and ninety female rats were randomly divided into control group (group C) and experimental groups, namely, radiation group (group R), fluvastatin treatment group (group Flu), retinoic acid treatment group (group Ra) and dexemethasone treatment group (group Dex). The chests of rats in experimental groups were exposed to radiation by linear accelerator after anesthesia.

[The effects of rBCG expressing Der p2 in the form of lipoprotein on murine immune response].

Aim: To investigate the effects of rBCG vaccination containing foreign antigen Der p2 in the form of lipoprotein on murine immune response.

Methods: 6 to 8 weeks old and newborn BALB/c mice were vaccined intraperitoneally with 10(6) CFU rBCG or BCG. At the same time, the control group was injected with saline.

[Construction of antisense recombinant adenoviral vector for c-myc and its antiproliferative effect on rat lymphocytes].

Aim: To observe the antiproliferative effect of antisense recombinant adenoviral vector for c-myc on rat thymus lymphocytes.

Methods: Antisense and sense bacterial plasmids for c-myc were constructed. Bacterial plasmids and El detected adenoviral plasmid were cotransfected into 293 cells.

[The changes of expression level of matrix metalloprotease 9 and its inhibitor (TIMP-1) in murine pulmonary fibrosis model].

Aim: To evaluate the balance between matrix metalloprotease-9 (MMP-9) and its inhibitor, tissue inhibitor of metalloproteinases-1 (TIMP-1) in bleomycin-induced pulmonary fibrosis in mice.

Methods: Pulmonary fibrosis model was induced by bleomycin in mice. The histological images of lungs were studied by HE staining.

[NF-kappaB expression in lung tissue of acute lung injury rat model and the influence by antioxidant N-acetylcysteine].

Aim: To observe the NF-kappaB expression in the lung tissue of LPS-induced acute lung injury(ALI) rat model and the influence of N-acetylcysteine (NAC) on NF-kappaB expression.

Methods: The expression of NF-kappaB in lung tissue in ALI rat model and the influence of NAC on NF-kappaB expression were detected by immunohistochemical (ABC) staining and Western blot.

Results: There were a small amount of sporadic NF-kappaB cells in airway epithelium and interstitium in normal control group.

[Cloning and expression of the extracellular domain of calcium-activated chloride channel in mouse airway goblet cells].

Aim: To clone and express the extracellular domain of murine calcium-activated chloride channel (mCLCA3) in airway goblet cell of mouse.

Methods: According to the gene sequence of mCLCA3 the PCR primers for N-terminal, middle and C-terminal extracellular domains were designed. Using recombinant plasmid pcDNA3.

[Construction and identification of the E.coli-BCG shuttle vector expressing lipoprotein Der p2 on cell wall of mycobacterium vaccae].

Aim: To construct the E.coli-BCG shuttle vector carrying and expressing dust mite antigen gene Der p2 on cell wall of mycobacterium vaccae.

Methods: The gene fragment encoding 19 kDa antigen and the upstream control element (19-ss) was amplified by PCR from the mycobacteria tuberculosis H37Rv.

[Inhibitive effect on airway mucus overproduction with DNA vaccine based on xenogeneic homologous calcium-activated chloride channel in asthmatic mice].

Objective: To observe the inhibitive effect on airway mucus overproduction with DNA vaccine based on human calcium-activated chloride channel 1 (hCLCA1) in asthmatic mice, who own mCLCA3 being xenogeneic homology of hCLCA1 in airway goblet cell.

Methods: The DNA vaccine was made with hCLCA1 gene inserted into pSecTag2B, and then BALB/c mice were vaccinated by i.m.

[The inhibiting effect of niflumic acid on airway hyperresponsiveness in asthmatic mice].

Objective: To evaluate the inhibiting effect of niflumic acid (NFA), an inhibitor of calcium-activated chloride channel (ClCa) on airway epithelium, on the airway hyperresponsiveness in asthmatic mice.

Methods: BALB/c mice were randomly divided into an asthma group (A group), a NFA prevention asthmatic group (B group) and a sham-challenged group (C group). The airway pressure time index (APTI) and the content of ET-1 and NO in bronchoalveolar lavage fluid (BALF) in all groups were measured.