Anti-neutrophil cytoplasmic antibody-negative microscopic polyangiitis: A case report and literature review.

The aim of this study was to investigate the clinical characteristics, diagnosis and treatment of anti-neutrophil cytoplasmic antibody (ANCA)-negative microscopic polyangiitis (MPA). We described the case of a patient with ANCA-negative MPA and conducted analyses and a review of the relevant literature. Based on the collected data, the epidemiology, diagnosis and treatment of ANCA-negative MPA were discussed.

Expression variations of connective tissue growth factor in pulmonary arteries from smokers with and without chronic obstructive pulmonary disease.

Cigarette smoking contributes to the development of pulmonary hypertension (PH) complicated with chronic obstructive pulmonary disease (COPD), and the pulmonary vascular remodeling, the structural basis of PH, could be attributed to abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs).In this study, morphometrical analysis showed that the pulmonary vessel wall thickness in smoker group and COPD group was significantly greater than in nonsmokers. In addition, we determined the expression patterns of connective tissue growth factor (CTGF) and cyclin D1 in PASMCs harvested from smokers with normal lung function or mild to moderate COPD, finding that the expression levels of CTGF and cyclin D1 were significantly increased in smoker group and COPD group.

Expression of IL-17A and IL-17F in lipopolysaccharide-induced acute lung injury and the counteraction of anisodamine or methylprednisolone.

Th17 cytokines IL-17A and IL-17F as pro-inflammatory cytokines played an important role in triggering inflammatory responses. However, little was known about the expression of IL-17A and IL-17F in acute lung injury (ALI). Therefore, the present study investigated the expression of IL-17A and IL-17F in lipopolysaccharide (LPS)-induced ALI in rats and rat pulmonary microvascular endothelial cells (PMVEC) by enzyme-linked immunosorbant assay or reverse transcription-polymerase chains reaction.

[Role of caveolin-1 in pulmonary microvascular endothelial cells injury induced by lipopolysaccharide in rat].

Objective: To investigate the role of caveolin-1 (Cav-1) in the modulation of rat pulmonary microvascular endothelial cells (RPMVEC) injury induced by lipopolysaccharide (LPS).

Methods: Cultured RPMVEC were randomly divided into time-dependent injury group induced by LPS and intervention group in which cells were pretreated by protein kinase A inhibitor (PKI). In the time-dependent injury group, monolayers of cells were constructed to determine permeability changes after 10 μg/mL LPS challenge for 0, 1, 3, 6, 12 and 24 hours with the method of Evans blue-labeled albumin flux across the monolayer (Pd).

[Effect of tumor necrosis factor-α on expression of interleukin-17 receptor C in pulmonary microvascular endothelial cells in rats].

Objective: To explore the effects of tumor necrosis factor-alpha (TNF-α) or methylprednisolone on the expression of interleukin-17 receptor C (IL-17RC) in rat pulmonary microvascular endothelial cells (RPMVEC).

Methods: Culture RPMVEC were randomly divided into dose-dependent and time-dependent groups. In dose-dependent group, cells were cultured with TNF-α (0, 0.

Caveolin-1 regulates Rac1 activation and rat pulmonary microvascular endothelial hyperpermeability induced by TNF-α.

A multiplicity of vital cellular and tissue level functions are controlled by caveolin-1 and it is considered to be an important candidate for targeted therapeutics. Rac1-cortactin signaling plays an important role in maintaining the functions of the endothelial barrier in microvascular endothelial cells. The activity of Rac1 has been shown to be regulated by caveolin-1.

[Methods for measurement of permeability coefficient of pulmonary microvascular endothelial cells in rat].

Objective: To explore an optimal method for the measurement of pulmonary microvascular endothelial cell (PMVEC) permeability coefficient.

Methods: A monolayer of rat PMVEC model was constructed by culturing a cell suspension on transwell filter or polycarbonate filter membrane. After the state of confluence of cells was affirmed with epithelial volt-ohm meter or inverted microscope, the permeability coefficient was determined by means of transendothelial electrical resistance (TER), fluoresceinisothiocyanate-dextran (Pd), and permeation of Hanks solution (Lp) across monolayers.

Role of src-suppressed C kinase substrate in rat pulmonary microvascular endothelial hyperpermeability stimulated by inflammatory cytokines.

Objective: The aim of the study was to investigate the role of src-suppressed C kinase substrate (SSeCKS) in the modulation of rat pulmonary microvascular endothelial cells (RPMVEC) permeability elicited by interleukin (IL)-1β and tumor necrosis factor (TNF)-α.

Methods: The gene expression of SSeCKS was analyzed by reverse transcription-polymerase chain reaction. Immunoblotting was used to determine the SSeCKS protein expression and the activation of the protein kinase C (PKC) signaling pathway.

[Induction effect of platelet-activating factor on Src-suppressed C kinase substrate gene expression in rat pulmonary microvascular endothelial cells].

Objective: To investigate the effect of platelet-activating factor (PAF) on the production of Src-suppressed C kinase substrate (SSeCKS) mRNA in rat pulmonary microvascular endothelial cell (RPMVEC) and its signal transduction pathways.

Methods: Cellular in situ hybridization was performed to reveal changes in SSeCKS mRNA expression in the cultured RPMVECs after giving PAF stimulation.

Results: Normal RPMVECs expressed SSeCKS mRNA at a low level, which appeared throughout the cytoplasm with specific hybridization signals.

[The effect of intrapleural pingyangmycin administration on activity of fibrinolytic system and transforming growth factor-beta1 in malignant pleural effusion].

Objective: To observe the changes of the concentrations of plasminogen activator inhibitor-1(PAI-1), tissue-type plasminogen activator(t-PA), transforming growth factor-beta(1)(TGF-beta(1)) in peripheral blood and pleural effusion before and after intrapleural pingyangmycin administration, and therefore to investigate the mechanism by which pingyangmycin produces pleurodesis.

Methods: Since February to September 2008, a total of 26 patients with malignant pleural effusion (MPE) underwent intrapleural pingyangmycin administration. The concentrations of PAI-1, t-PA, TGF-beta(1) and the number of leucocytes in peripheral blood and pleural effusion before and after treatment were detected.

Interleukin-17F-induced pulmonary microvascular endothelial monolayer hyperpermeability via the protein kinase C pathway.

Background: Interleukin (IL)-17F is involved in lung inflammation, but the effect of IL-17F on endothelial permeability and its signaling pathway remain ill-defined. The current study sought to investigate the effect of IL-17F on endothelium and assess the role of protein kinase C (PKC) and src-suppressed C kinase substrate (SSeCKS) in this process.

Methods: Rat pulmonary microvascular endothelial monolayers were constructed to determine changes of permeability as measured by means of FITC-dextran and Hank's solution flux across monolayers and transendothelial electrical resistance with or without IL-17F and PKC inhibitors.

[Effect of endotoxin on expression of angiotensin converting enzyme-2 in cultured rat pulmonary microvascular endothelial cells].

Objective: To observe the effects of endotoxin on angiotensin converting enzyme-2 (ACE2) expression in rat pulmonary microvascular endothelial cells (RPMVECs) in vitro, and discuss the role of ACE2 in endotoxin-induced acute lung injury (ALI).

Methods: In vitro, cultured RPMVECs were incubated with endotoxin (10 mg/L), the expression of ACE2 mRNA and protein were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting techniques at time points of 3, 6, 12, and 24 hours respectively after incubation with endotoxin.

Results: After the treatment of RPMVECs with endotoxin (10 mg/L), the levels of ACE2 mRNA and protein decreased significantly, and then they increased slightly at 6 hours, followed by a continuous decrease until 24 hours.

[Studies on the expression of Src-suppressed C kinase substrate mRNA in pulmonary microvascular endothelial cells induced by lipopolysaccharide].

Objective: To study the expression of Src-suppressed C kinase substrate (SSeCKS) mRNA in pulmonary microvascular endothelial cells(PMVEC) induced by lipopolysaccharide, and the interfering effect of methylprednisolone sodium succinate.

Methods: Rat PMVEC (RPMVEC) were isolated and cultured in vitro, then grouped randomly according to different culture time and different dosage of LPS, and the expression of SSeCKS mRNA in RPMVEC of different groups were determined by reverse transcription polymerase chain reaction (RT-PCR).

Results: Normally, the expression of the SSeCKS mRNA in RPMVEC was maintained on a low level, and it could be elevated by stimulation of LPS, and the changes in the expression exhibited in dosage and time dependent manner.

[Effect of sodium hyaluronate on pleural adhesions and fibrosis in a rabbit model of empyema].

Objective: To study the effect of sodium hyaluronate (SH) on pleural adhesions and fibrosis in experimental empyema.

Methods: Twenty rabbits were randomly divided into two groups: a treatment group and a control group, 10 rabbits in each group. Chest tubes were placed into the right pleural cavity of the rabbits.

Diagnostic accuracy of human telomerase reverse transcriptase mRNA in malignant pleural effusions: A preliminary report for in situ hybridization detection.

Background: Detection of human telomerase reverse transcriptase (hTERT) mRNA by in situ hybridization (ISH) may be valuable in the diagnosis of cancer. We assessed the diagnostic performance of hTERT mRNA in cells from pleural fluid in malignant pleural effusions (PEs).

Methods: We used a 2-step ISH with digoxin-labelled oligonucleotide probes to detect hTERT mRNA in a blinded prospective study of cells from 103 unselected pleural fluid specimens.

Expression and regulation of AT1 receptor in rat lung microvascular endothelial cell.

Background: The renin-angiotensin system is thought to be involved in the development and progression of vascular endothelium inflammation, thereby contributing to vascular endothelium injury. To clarify the role of angiotensin II (Ang II) in rat pulmonary microvascular endothelial cells (RPMVECs), we examined the expression and functional significance of angiotensin II (Ang II) receptors in normal and lipopolysacchride (LPS) treated RPMVECs.

Methods: The expressions of Ang II type 1(AT(1)) and Ang II type 2 (AT(2)) receptors in cultured RPMVECs were identified by the reverse transcription-polymerase chain reaction (RT-PCR) technique, Western blot and (125)I-labeled [Sar(1),Ile(8)] Ang II binding assays.

LPS induces permeability injury in lung microvascular endothelium via AT(1) receptor.

Lipopolysaccharide (LPS) is known to stimulate the circulation and local production of angiotensin II (Ang II). To assess whether Ang II plays a role in LPS-induced acute lung injury, rats were injected with LPS, the microvascular endothelial permeability injury was evaluated by histological changes, increased pulmonary wet/dry weight ratio, and pulmonary microvascular protein leak. Besides, increased rat pulmonary microvascular endothelial cell monolayer permeability coefficient (K(f)) was measured after treatment with LPS and/or Ang II, respectively.

[Inflammatory injurious effect of angiotensin II on pulmonary microvascular endothelium in rat].

Objective: To investigate the effects of angiotensin II (AngII) and its receptors on monolayer permeability of pulmonary microvascular endothelial cells in rat.

Methods: The following examinations were done on cultured rat pulmonary microvascular endothelial cells (RPMVECs). 1.

[Effect of S-2-(3-aminopropylamino) ethyl phosphorothioic acid on apoptosis and proliferation inhibition of HL-60 cell line].

To study the effects of S-2-(3-aminopropylamino) ethyl phosphorothioic acid (WR-2721, amifostine) on proliferation inhibition and apoptosis of HL-60 human leukemia cell line, the cell apoptosis rate of HL-60 was determined by annexin V/PI double staining method. Cell proliferation and chemotherapy sensitivity were analyzed with XTT assay, and the changes of cell cycle were observed through flow cytometry. The results showed that WR-2721 could significantly inhibit HL-60 cell proliferation.

[Detection of human telomerase reverse transcriptase mRNA of cells in pleural fluid by two-step in situ hybridization using digoxin-labeled oligonucleotide probes].

Objective: To establish an method for detecting human telomerase reverse transcriptase (hTERT) mRNA of cells in pleural fluid by in situ hybridization (ISH), and to evaluate preliminarily the efficacy of this new method in recognizing neoplastic cells in the pleural fluid.

Methods: Fresh pleural fluid specimens were collected in 23 patients with pleural effusions and cell smears were prepared and after pretreatment, ISH between hTERT mRNA of the cells and digoxin-labelled oligonucleotide probes was performed. The signals of hTERT mRNA were detected by the sequential treatment with antigen, antibody, enzyme, and staining.