ABSTRACT
Pulmonary arterial hypertension (PAH) is a common clinical syndrome characterized by dysfunction of pulmonary arterioles leading to increased vascular resistance and elevated pulmonary artery pressure. Insulin resistance (IR) is recognized as a critical risk factor for cardiovascular disease, but recent evidence suggested an association between IR and PAH. The pathological consequences of IR, such as hyperinsulinemia, dyslipidemia, chronic inflammation, and oxidative stress can cause pulmonary vasoconstriction, endothelial dysfunction and vascular remodeling, which aggravate the progressive course of PAH. Therefore, addressing the molecular mechanisms by which IR promotes the development of pulmonary hypertension and searching for appropriate interventions are important in the management of PAH.
Subject(s)
Humans , Hypertension , Hypertension, Pulmonary , Inflammation , Insulin Resistance , Lung , Oxidative Stress , VasoconstrictionABSTRACT
<p><b>OBJECTIVE</b>To systematically review whether statins can reduce the risk of infection and infection-related mortality.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSION</b>Statins can significantly reduce the risk of infection but does not lower infection-related mortality.</p>
Subject(s)
Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Therapeutic Uses , Infections , Epidemiology , Mortality , Randomized Controlled Trials as Topic , Risk FactorsABSTRACT
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.
Subject(s)
Humans , Cell Proliferation , Hypertension, Pulmonary , Lung , Myocytes, Smooth Muscle , Cell Biology , Pulmonary Artery , Cell Biology , Signal Transduction , Vascular RemodelingABSTRACT
<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>Western 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.</p><p><b>RESULTS</b>Western 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.</p><p><b>CONCLUSIONS</b>pTSX2 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.</p>