Objective To evaluate the efficacy and safety of sublingual immunotherapy (SLIT) in patients with allergic asthma in order to provide reliable evidence for clinical application of SLIT.Methods To search published articles of randomized controlled trials (RCTs) in allergic asthma from CNKI,WANFANG,Pubmed and Medline databases.The methodological quality of trials was assessed by Jadadscale.The heterogeneity was examined by using Stata 11.0 software.Fixed effect model or random effect model was used to pool the data.The articles which could not be pooled were carried out by descriptive analysis.The Egger's and Begg's test were used to evaluate the publication bias.Results There were total 6 RCTs included in this text.Compared with control group,SLIT could significantly reduce asthma symptom scores (SMD =-0.89,95％ CI-1.36--0.43,P =0.000) and asthma medication scores (SMD =-4.53,95％CI-6.97--2.08,P =0.000),but not forced expiratory volume (FEV1) of lung function (SMD =0.19,95％ CI-0.02-0.41,P =0.078),neither serum sIgE levels (SMD =0.05,95％ CI -0.58-0.69,P =0.870).There were no obvious adverse events reported after treatment of SLIT.No publication bias were indicated by Egger's and Begg's tests.Conclusion SLIT significantly reduces asthma symptom scores and medication scores,suggesting that SLIT is a safe and effective approach of immunotherapy.However,it still needs more highly qualified studies of RCTs to prove.

Objective To explore the diagnostic and score value of ultrasound on hemophiliac arthropathy referring to MRI on the diagnosis and score of hemophiliac arthropathy Methods The ultrasound and MRI examinations were performed on 42 joints of 42 hemophilia patients 14 knees 14 ankles and 14 elbows The consistency of ultrasound and magnetic resonance imaging in the detection and score of joint diseases was compared Finally inter-and intra-observer agreement of ultrasound scoring system were tested Results The consistency of ultrasound and magnetic resonance imaging was excellent κ=0 763-0 896 P < 0 001 in the detection of early soft tissue lesions effusion or hemarthrosis synovial hypertrophy hemosiderin excellent κ=0 793 P <0 001 in the detection of cartilage loss poor κ=0 133 P = 0 132 in the detection of erosions and poor κ= 0 100 P = 0 137 in the detection of subchondral cysts The consistency of ultrasound and magnetic resonance imaging was good to excellentκ=0 684-0 833 P < 0 001 in the score of early soft tissue lesions effusion or hemarthrosis synovial hypertrophy and hemosiderin and poor to good κ=0 145 -0 635 P <0 001 in the score of advanced osteochondral lesions cartilage loss and bone erosions The inter-observer agreement was good to excellent κ=0 676-0 870 P <0 001 for early soft tissue lesions and moderate to excellent κ=0 421- 0 75 1 P < 0 001 for advanced osteochondral lesions The intra-observer agreement was good to excellent κ=0 705-0 885 P <0 001 for early soft tissue lesions and moderate to good κ=0 532 -0 732 P <0 001 for advanced osteochondral lesions Conclusions Ultrasound plays an important role in detecting early soft tissue changes effusion or hemarthrosis synovial hypertrophy hemosiderin and cartilage loss which helps follow-up and guide clinical treatment.

OBJECTIVETo identify the immunological characteristics of the recombinant major pollen allergen pTSX2 of Humulus scandens and evaluate its safety in immunotherapy of allergic asthma in mice.

METHODSWestern blotting was used to characterize the immunological properties of pTSX2, and its immunogenicity in normal mice was evaluated by detecting sIgG and sIgE levels. The mouse models of allergic asthma were immunized with pTSX2 and examined for sIgE and sIgG levels, total cells and eosinophils percentage in BALF, interleukin-4 (IL-4) and interferon-γ (IFN-γ) levels in BALF and spleen homogenate, and changes in lung pathologies.

RESULTSWestern blotting showed that pTSX2 reacted with the majority (about 70%) of sera from patients allergic to Humulus pollen. In normal mice, pTSX2 mainly induced the production of sIgG. In mouse models of allergic asthma, intervention with pTSX2 caused a significant reduction of sIgE and an increase of sIgG (P<0.05), significantly decreased the total cells and eosinophils in BALF (P<0.05), obviously lowered IL-4 but increased IFN-γ in BALF and spleen homogenate (P<0.05), and diminished inflammatory cell infiltration and percentage of eosinophils in the lung tissues.

CONCLUSIONSpTSX2 shows a definite therapeutic effect and safety in the treatment of allergic asthma in mice possibly by inhibiting sIgE and inducing sIgG production, suppressing airway allergic inflammation and regulating the balance between Thl and Th2.

Allergens ; immunology ; Animals ; Asthma ; immunology ; therapy ; Bronchoalveolar Lavage Fluid ; immunology ; Disease Models, Animal ; Female ; Humans ; Humulus ; immunology ; Immunoglobulin E ; blood ; Immunoglobulin G ; blood ; Immunotherapy ; Interferon-gamma ; analysis ; Interleukin-4 ; analysis ; Mice ; Mice, Inbred BALB C ; Pollen ; immunology ; Th1 Cells ; cytology ; immunology ; Th2 Cells ; cytology ; immunology

Pulmonary hypertension (PAH) is a common clinical syndrome characterized by elevated pulmonary arterial pressure. The pathological changes in PAH include increased vasoconstrictor tone, thrombosis in situ and pulmonary vascular remodeling. Pulmonary arterial smooth muscle cell (PASMC) proliferation is a hallmark of pulmonary vascular remodeling, and exploration of the molecular mechanisms of PASMC proliferation and intervention of the involved signaling pathways is therefore of great importance for prevention and treatment of PAH. This review focus primarily on the current understanding of the molecular mechanisms involved in the proliferation of PASMCs.
Cell Proliferation ; Humans ; Hypertension, Pulmonary ; Lung ; Myocytes, Smooth Muscle ; cytology ; Pulmonary Artery ; cytology ; Signal Transduction ; Vascular Remodeling

OBJECTIVETo systematically review whether statins can reduce the risk of infection and infection-related mortality.

METHODSWe searched the Cochrane Library, MEDLINE, EMBASE, PubMed, Elsevier and CBM databases for randomized placebo-controlled trials of statins published by September 2013, and each trial enrolled at least 100 participants with follow-up for at least 4 weeks. Two reviewers independently assessed the quality of the included studies and extracted the relevant data for analysis using Stata 12.0 software.

RESULTSSixteen trails involving a total of 48973 patients were included in our meta-analysis. The results showed that statins significantly reduced the risk of infection (OR=0.93, 95% CI 0.89 to 0.98, P=0.004) compared to placebo but did not significantly lower infection-related mortality (OR=0.96, 95% CI 0.82 to 1.12, P=0.592).

CONCLUSIONStatins can significantly reduce the risk of infection but does not lower infection-related mortality.

Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; therapeutic use ; Infection ; epidemiology ; mortality ; Randomized Controlled Trials as Topic ; Risk Factors

Objective To systematically review whether statins can reduce the risk of infection and infection-related mortality. Methods We searched the Cochrane Library, MEDLINE, EMBASE, PubMed, Elsevier and CBM databases for randomized placebo-controlled trials of statins published by September 2013, and each trial enrolled at least 100 participants with follow-up for at least 4 weeks. Two reviewers independently assessed the quality of the included studies and extracted the relevant data for analysis using Stata 12.0 software. Results Sixteen trails involving a total of 48973 patients were included in our meta-analysis. The results showed that statins significantly reduced the risk of infection (OR=0.93, 95% CI 0.89 to 0.98, P=0.004) compared to placebo but did not significantly lower infection-related mortality (OR=0.96, 95% CI 0.82 to 1.12, P=0.592). Conclusion Statins can significantly reduce the risk of infection but does not lower infection-related mortality.

Pulmonary hypertension (PAH) is a common clinical syndrome characterized by elevated pulmonary arterial pressure. The pathological changes in PAH include increased vasoconstrictor tone, thrombosis in situ and pulmonary vascular remodeling. Pulmonary arterial smooth muscle cell (PASMC) proliferation is a hallmark of pulmonary vascular remodeling, and exploration of the molecular mechanisms of PASMC proliferation and intervention of the involved signaling pathways is therefore of great importance for prevention and treatment of PAH. This review focus primarily on the current understanding of the molecular mechanisms involved in the proliferation of PASMCs.

Objective To systematically review whether statins can reduce the risk of infection and infection-related mortality. Methods We searched the Cochrane Library, MEDLINE, EMBASE, PubMed, Elsevier and CBM databases for randomized placebo-controlled trials of statins published by September 2013, and each trial enrolled at least 100 participants with follow-up for at least 4 weeks. Two reviewers independently assessed the quality of the included studies and extracted the relevant data for analysis using Stata 12.0 software. Results Sixteen trails involving a total of 48973 patients were included in our meta-analysis. The results showed that statins significantly reduced the risk of infection (OR=0.93, 95% CI 0.89 to 0.98, P=0.004) compared to placebo but did not significantly lower infection-related mortality (OR=0.96, 95% CI 0.82 to 1.12, P=0.592). Conclusion Statins can significantly reduce the risk of infection but does not lower infection-related mortality.

Pulmonary hypertension (PAH) is a common clinical syndrome characterized by elevated pulmonary arterial pressure. The pathological changes in PAH include increased vasoconstrictor tone, thrombosis in situ and pulmonary vascular remodeling. Pulmonary arterial smooth muscle cell (PASMC) proliferation is a hallmark of pulmonary vascular remodeling, and exploration of the molecular mechanisms of PASMC proliferation and intervention of the involved signaling pathways is therefore of great importance for prevention and treatment of PAH. This review focus primarily on the current understanding of the molecular mechanisms involved in the proliferation of PASMCs.