87 research outputs found

    Emergent Endovascular vs. Open Surgery Repair for Ruptured Abdominal Aortic Aneurysms: A Meta-Analysis

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    <div><p>Objectives</p><p>To systematically review studies comparing peri-operative mortality and length of hospital stay in patients with ruptured abdominal aortic aneurysms (rAAAs) who underwent endovascular aneurysm repair (EVAR) to patients who underwent open surgical repair (OSR).</p><p>Methods</p><p>The Medline, Cochrane, EMBASE, and Google Scholar databases were searched until Apr 30, 2013 using keywords such as abdominal aortic aneurysm, emergent, emergency, rupture, leaking, acute, endovascular, stent, graft, and endoscopic<b>.</b> The primary outcome was peri-operative mortality and the secondary outcome was length of hospital stay.</p><p>Results</p><p>A total of 18 studies (2 randomized controlled trials, 5 prospective studies, and 11 retrospective studies) with a total of 135,734 rAAA patients were included. rAAA patients who underwent EVAR had significantly lower peri-operative mortality compared to those who underwent OSR (overall OR = 0.62, 95% CI = 0.58 to 0.67, P<0.001). rAAA patients with EVAR also had a significantly shorter mean length of hospital stay compared to those with OSR (difference in mean length of stay ranged from −2.00 to −19.10 days, with the overall estimate being −5.25 days (95% CI = −9.23 to −1.26, P = 0.010). There was no publication bias and sensitivity analysis showed good reliability.</p><p>Conclusions</p><p>EVAR confers significant benefits in terms of peri-operative mortality and length of hospital stay. There is a need for more randomized controlled trials to compare outcomes of EVAR and OSR for rAAA.</p></div

    Characteristics of studies included in the meta-analysis.

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    †<p>The peri-operative mortality for these studies was calculated on an intention to treat basis.</p>‡<p>Study quality assessment performed using the Newcastle-Ottawa Scale.</p><p>Abbreviation: EVAR, endovascular repair; OSR, open surgical repair; AAA, abdominal aortic aneurysm.</p

    Funnel plot for evaluating publication bias while reporting peri-operative mortality.

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    <p>White circles represent published article and white rhombuses represent the actual combined effect sizes, respectively.</p

    Preparation of Nitrogen Doped Biochar-Based Iron Catalyst for Enhancing Gasoline-Range Hydrocarbons Production

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    Developing catalysts to obtain high space time yield (STY) of gasoline-range hydrocarbons via Fischer–Tropsch synthesis (FTS) is a huge challenge due to the restriction of Anderson–Schulz–Flory distribution. Herein, a nitrogen doped biochar-based iron catalyst was synthesized by a one-step method using sugar cane bagasse as carbon precursor, which exhibited an excellent gasoline STY of 8.65 gC5–12 gFe–1 h–1, exceeding most reported catalysts. A strong positive relationship between the amount of pyrrolic N and long-chain hydrocarbons selectivity was displayed. The characterization results indicated that pyrrolic N configuration on anchor sites tuned effectively the dispersion of iron species and metal–support interaction as well as CO adsorption, improving the FTS performance

    DataSheet_1_A tumor microenvironment preoperative nomogram for prediction of lymph node metastasis in bladder cancer.zip

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    BackgroundGrowing evidence suggests that tumor metastasis necessitates multi-step microenvironmental regulation. Lymph node metastasis (LNM) influences both pre- and post-operative bladder cancer (BLCA) treatment strategies. Given that current LNM diagnosis methods are still insufficient, we intend to investigate the microenvironmental changes in BLCA with and without LNM and develop a prediction model to confirm LNM status.Method"Estimation of Stromal and Immune cells in Malignant Tumors using Expression data" (ESTIMATE) algorithm was used to characterize the tumor microenvironment pattern of TCGA-BLCA cohort, and dimension reduction, feature selection, and StrLNM signature construction were accomplished using least absolute shrinkage and selection operator (LASSO) regression. StrLNM signature was combined with the genomic mutation to establish an LNM nomogram by using multivariable logistic regression. The performance of the nomogram was evaluated in terms of calibration, discrimination, and clinical utility. The testing set from the TCGA-BLCA cohort was used for internal validation. Moreover, three independent cohorts were used for external validation, and BLCA patients from our cohort were also used for further validation.ResultsThe StrLNM signature, consisting of 22 selected features, could accurately predict LNM status in the TCGA-BLCA cohort and several independent cohorts. The nomogram performed well in discriminating LNM status, with the area under curve (AUC) of 75.1% and 65.4% in training and testing datasets from the TCGA-BLCA cohort. Furthermore, the StrLNM nomogram demonstrated good calibration with p >0.05 in the Hosmer-Lemeshow goodness of fit test. Decision curve analysis (DCA) revealed that the StrLNM nomogram had a high potential for clinical utility. Additionally, 14 of 22 stably expressed genes were identified by survival analysis and confirmed by qPCR in BLCA patient samples in our cohort.ConclusionIn summary, we developed a nomogram that included an StrLNM signature and facilitated the preoperative prediction of LNM status in BLCA patients.</p

    FTY720 alleviates ischemic brain damage and improves functional recovery following cerebral ischemia.

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    <p><b>A,</b> Representative MRI images for the ischemia+vehicle treatment group and ischemia+FTY720 treatment group at 1 day (left) and 3 days (right) after photothrombotic ischemia. <b>B,</b> Reduced infarction volume was assessed by MRI examination after treatment with FTY720 at 1 day and 3 days post photothrombotic injury. <b>C,</b> Neurological deficiency was evaluated at 1, 3, 5, and 7 days post ischemia. Values are expressed as mean ± SEM and data were evaluated by the Student’s t test (n = 6, *p <0.05 vs. ischemia+vehicle group, **p <0.01 vs. ischemia+vehicle group).</p

    FTY720 attenuates neuronal apoptosis following ischemic stroke.

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    <p><b>A,</b> Schematic diagram of the photothrombotic stroke model (left) and ischemic lesions evaluated by Nissl staining (right). <b>B,</b> Nissl staining (B1-3) and TUNEL assays (B4-9) were performed to assess effects of FTY720 on neuronal survival and apoptosis in the boundary of the ischemic lesion core at 1 day post injury. Sham mice (without ischemia induction) were also tested in parallel. The scale bar represents 50 μm. <b>C,</b> Quantification of the results from panels B1-3. <b>D,</b> Quantification of the results from panels B4-6. (n = 4 for each group, #p < 0.05 vs. sham group, *p < 0.05 vs. ischemia+vehicle group, **p < 0.01 vs. ischemia+vehicle group, one-way ANOVA followed with Tukey post hoc test).</p

    FTY720 attenuates activation of autophagy following ischemic stroke in a dose-dependent manner.

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    <p><b>A</b>, The impact of increasing concentrations of FTY720 on the expression of Beclin1 and LC3 was evaluated by western blotting. Results are representative of 4 independent experiments. <b>B,</b> Quantification of the results in panel A. (n = 4 for each group, *p < 0.05 vs. sham group, **p < 0.01 vs. sham group, one-way ANOVA with Tukey post hoc test). <b>C,</b> Top, Representative electron microphotographs in neurons in the sham, ischemia+vehicle, and ischemia+FTY720 treated groups at 3 days post photothrombic ischemic stroke (A1-A3). Higher magnification images of the square area in A1-A3 showed abundant lysosomes and autophagosomes (arrows) in the ischemia+vehicle group, which was reversed by treatment with FTY720 (A4-A6). D. Representative images of LC3 and Beclin1 staining in sham treated, ischemia+vehicle, and ischemia+FTY720 groups.</p

    FTY720 reverses activation of autophagy induced by mTOR inhibitor, rapamycin.

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    <p>A, The impact of FTY720 and rapamycin on the expression of Beclin1 and LC3 was evaluated by western blotting. Results are representative of 4 independent experiments. <b>B,</b> Quantification of the results in panel A. (n = 4 for each group, *p < 0.05 vs. sham group, *p < 0.01 vs. ischemia+rapamycin group, one-way ANOVA with Tukey post hoc test).</p
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