Effect of Aspirin on Fractalkine in Rats with Pulmonary Embolism

Purpose: To investigate the effect of aspirin on fractalkine (FKN) in rats with pulmonary embolism (PE).Methods: Sprague Dawley rats were divided into control group, sham operation group, PE model group and PE + aspirin group. PE was established by injecting self-embolus into the right jugular vein of the rats. Aspirin was administered orally 1 day and 40 min before PE surgery, and daily thereafter. At 4 and 72 h following embolism, the rat lung tissues were obtained for hematoxylin-eosin (HE) staining as well as measurement of mRNA expression of FKN, TNF-α and IL-1β. Additionally, serum FKN, IL-8, TNF-α, and IL-1β were measured by enzyme linked immunosorbent assay (ELISA).Results: The serum levels of FKN, IL-8, TNF-α and IL-1β were significantly decreased by treatment with aspirin compared with the PE group (p < 0.05). Furthermore, mRNA expressions of lung FKN, TNF- α and IL-1β in PE group were markedly decreased by treatment with aspirin compared with that in PE group. PE-induced lung injury was alleviated by treatment with aspirin based on the results of pathological examination..Conclusion: Aspirin has protective effects against PE-induced lung injuries, which is probably mediated by the suppression of the expression of IL-8, TNF-α, IL-1β, and FKN.Keywords: Aspirin, Pulmonary embolism, Lung injury, Fractalkine

Trafficking-Deficient G572R-hERG and E637K-hERG Activate Stress and Clearance Pathways in Endoplasmic Reticulum

Background: Long QT syndrome type 2 (LQT2) is the second most common type of all long QT syndromes. It is well-known that trafficking deficient mutant human ether-a-go-go-related gene (hERG) proteins are often involved in LQT2. Cells respond to misfolded and trafficking-deficient proteins by eliciting the unfolded protein response (UPR) and Activating Transcription Factor (ATF6) has been identified as a key regulator of the mammalian UPR. In this study, we investigated the role of ER chaperone proteins (Calnexin and Calreticulin) in the processing of G572R-hERG and E637K-hERG mutant proteins. Methods: pcDNA3-WT-hERG, pcDNA3-G572R-hERG and pcDNA3-E637K-hERG plasmids were transfected into U2OS and HEK293 cells. Confocal microscopy and western blotting were used to analyze subcellular localization and protein expression. Interaction between WT or mutant hERGs and Calnexin/Calreticulin was tested by coimmunoprecipitation. To assess the role of the ubiquitin proteasome pathway in the degradation of mutant hERG proteins, transfected HEK293 cells were treated with proteasome inhibitors and their effects on the steady state protein levels of WT and mutant hERGs were examined. Conclusion: Our results showed that levels of core-glycosylated immature forms of G572R-hERG and E637K-hERG in association with Calnexin and Calreticulin were higher than that in WT-hERG. Both mutant hERG proteins could activate the UPR by upregulating levels of active ATF6. Furthermore, proteasome inhibition increased the levels of core-glycosylated immature forms of WT and mutant hERGs. In addition, interaction between mutant hERGs and Calnexin/Calreticulin wa

Observation of a near-threshold enhancement in th p pbar mass spectrum from radiative J/psi-->gamma p pbar decays

We observe a narrow enhancement near 2mp in the invariant mass spectrum of ppbar pairs from radiative J/psi-->gamma ppbar decays. The enhancement can be fit with either an S- or P-wave Breit Wigner fuction. In the case of the S-wave fit, the peak mass is below the 2mp threshold and the full width is less than 30 MeV. These mass and width values are not consistent with the properties of any known meson resonance.Comment: 5 pages, 4 figures, submitted to Phys. Rev. Let

Respiratory syncytial virus infection induces higher Toll-like receptor-3 expression and TNF-α production than human metapneumovirus infection

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The association of APE1 −656T > G and 1349 T > G polymorphisms and cancer risk: a meta-analysis based on 37 case-control studies

<p>Abstract</p> <p>Background</p> <p>APE1 (apurinic/apyrimidinic endonuclease 1) is an important DNA repair protein in the base excision repair pathway. Polymorphisms in <it>APE1 </it>have been implicated in susceptibility to cancer; however, results from the published studies remained inconclusive. The objective of this study was to conduct a meta-analysis investigating the association between polymorphisms in <it>APE1 </it>and the risk for cancer.</p> <p>Methods</p> <p>The PubMed and Embase databases were searched for case-control studies published up to June, 2011 that investigated <it>APE1 </it>polymorphisms and cancer risk. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the associations.</p> <p>Results</p> <p>Two polymorphisms (−656 T > G, rs1760944 and 1349 T > G, rs1130409) in 37 case-control studies including 15, 544 cancer cases and 21, 109 controls were analyzed. Overall, variant genotypes (GG and TG/GG) of −656 T > G polymorphism were associated with significantly decreased cancer risk in homozygote comparison (OR = 0.81, 95%CI: 0.67-0.97), dominant model comparison (OR = 0.89, 95%CI: 0.81-0.97) and recessive model comparison (OR = 0.90, 95%CI: 0.82-0.98), whereas the 1349 T > G polymorphism had no effects on overall cancer risk. In the stratified analyses for −656 T > G polymorphism, there was a significantly decreased risk of lung cancer and among Asian populations.</p> <p>Conclusions</p> <p>Although some modest bias could not be eliminated, the meta-analysis suggests that <it>APE1 −</it>656 T > G polymorphism has a possible protective effect on cancer risk particularly among Asian populations whereas 1349 T > G polymorphism does not contribute to the development of cancer.</p

Measurements of the Mass and Full-Width of the ηc\eta_c Meson

In a sample of 58 million $J/\psi$ events collected with the BES II detector, the process J/$\psi\to\gamma\eta_c$ is observed in five different decay channels: $\gamma K^+K^-\pi^+\pi^-$, $\gamma\pi^+\pi^-\pi^+\pi^-$, $\gamma K^\pm K^0_S \pi^\mp$ (with $K^0_S\to\pi^+\pi^-$), $\gamma \phi\phi$ (with $\phi\to K^+K^-$) and $\gamma p\bar{p}$. From a combined fit of all five channels, we determine the mass and full-width of $\eta_c$ to be $m_{\eta_c}=2977.5\pm1.0 ({stat.})\pm1.2 ({syst.})$ MeV/$c^2$ and $\Gamma_{\eta_c} = 17.0\pm3.7 ({stat.})\pm7.4 ({syst.})$ MeV/$c^2$.Comment: 9 pages, 2 figures and 4 table. Submitted to Phys. Lett.

A Measurement of Psi(2S) Resonance Parameters

Cross sections for e+e- to hadons, pi+pi- J/Psi, and mu+mu- have been measured in the vicinity of the Psi(2S) resonance using the BESII detector operated at the BEPC. The Psi(2S) total width; partial widths to hadrons, pi+pi- J/Psi, muons; and corresponding branching fractions have been determined to be Gamma(total)= (264+-27) keV; Gamma(hadron)= (258+-26) keV, Gamma(mu)= (2.44+-0.21) keV, and Gamma(pi+pi- J/Psi)= (85+-8.7) keV; and Br(hadron)= (97.79+-0.15)%, Br(pi+pi- J/Psi)= (32+-1.4)%, Br(mu)= (0.93+-0.08)%, respectively.Comment: 8 pages, 6 figure