116 research outputs found

    A Survey of the Knowledge of Venous Thromboembolism Prophylaxis among the Medical Staff of Intensive Care Units in North China

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    <div><p>Background</p><p>Guideline concordance for venous thromboembolism (VTE) prophylaxis in critically ill patients in intensive care units (ICUs) varies across different countries.</p><p>Objective</p><p>To explore how the medical staff of ICUs in China comprehend and practice VTE prophylaxis.</p><p>Method</p><p>Questionnaires comprising 39 questions and including 4 dimensions of thromboprophylaxis were administered in ICUs in North China.</p><p>Results</p><p>In all, 52 ICUs at 23 tertiary hospitals in 7 Chinese provinces and municipalities were surveyed. A total of 2500 questionnaires were sent, and 1861 were returned, corresponding to a response rate of approximately 74.4%. Of all surveyed medical staff, 36.5% of physicians and 22.2% of nurses were aware of the guidelines in China, and 19.0% of physicians and 9.5% of nurses comprehended the 9<sup>th</sup> edition of the guidelines of the American College of Chest Physicians (ACCP). Additionally, 37.6% of the medical staff chose a prophylaxis method based on the related guidelines, and 10.3% could demonstrate the exact indication for mechanical pattern application. Worries about skin injury, difficulty with removal and discomfort during mechanical thromboprophylaxis were cited by more than 30% of nurses, which was significantly more frequent than for physicians (graduated compression stockings: 54.3% VS 34.1%, 60.7% VS 49%, and 59.4% VS 54%, <i>p</i> = 0.000; intermittent pneumatic compression: 31% VS 22.2%, 19.2% VS 13.9%, and 37.8% VS 27.2%, <i>p</i> = 0.000).</p><p>Conclusions and Relevance</p><p>The knowledge of VTE prophylaxis among the medical staff of ICUs in North China remains limited, which may lead to a lack of standardization of VTE prophylaxis. Strengthened, standardized training may help medical staff to improve their comprehension of the relevant guidelines and may finally reduce the occurrence of VTE in ICUs and improve the prognosis of critically ill patients with VTE.</p></div

    Sn-dependent <i>trans</i> infection of reporter cells TZM-bl.

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    <p>(A) Sn-expressing cells, TSn and IFN-α-induced monocytes, bind HIV-1 and infect TZM-bl cells in <i>trans</i>. Cells were incubated with HIV-1<sub>NL4-3</sub> for 1 h, washed and then cocultured with TZM-bl cells for 48 h. HIV-1 infection of TZM-bl was defined by luciferase expression and quantified as relative light units (RLU). Cells pretreated with Sn mAb 7D2 showed significantly reduced capacity to facilitate <i>trans</i> infection of TZM-bl cells while mAb IgG1 isotype control had no effect. (B) HIV-1 receptor inhibitors block <i>trans</i> infection. Receptor and coreceptor requirements for <i>trans</i> infection of TZM-bl cells were tested by incubating TZM-bl cells with receptor inhibitors including mAbs to CD4, CXCR4 or CCR5, and small molecules AMD3100 or TAK779 prior to adding TSn with bound HIV-1<sub>NL4-3</sub>. The CD4, CXCR4, CCR5, AMD3100 and TAK779 receptor inhibitors were tested individually with TZM-bl and did not induce luciferase expression (data not shown). As a control, productive infection of TSn cells was prevented by addition of indinavir (100 µM). Data presented are the average of three separate experiments. Error bars represent SD.</p

    Sn-expressing cells capture HIV-1<sub>NL4-3</sub> and enhance infectivity.

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    <p>TZM-bl cell cultures were seeded with various concentrations of HIV-1<sub>NL4-3</sub> (800–8000 pg/ml). Monocytic cells, TSn or THP-1 cells, were added and cocultured for 48 h. The capacity of Sn to capture HIV-1<sub>NL4-3</sub> in the cell culture medium and <i>trans</i> infect TZM-bl cells was analyzed for TSn, THP-1 and cell-free virus. Luciferase expression in HIV-1<sub>NL4-3</sub>-infected TZM-bl cells was quantified as relative light units (RLU). Results were compiled from 3 separate experiments. Error bars represent SD.</p

    Dynamics of Ceramide Channels Detected Using a Microfluidic System

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    <div><p>Ceramide, a proapoptotic sphingolipid, has been shown to form channels, in mitochondrial outer membranes, large enough to translocate proteins. In phospholipid membranes, electrophysiological studies and electron microscopic visualization both report that these channels form in a range of sizes with a modal value of 10 nm in diameter. A hydrogen bonded barrel-like structure consisting of hundreds of ceramide molecules has been proposed for the structure of the channel and this is supported by electrophysiological studies and molecular dynamic simulations. To our knowledge, the mechanical strength and deformability of such a large diameter but extremely thin cylindrical structure has never been reported. Here we present evidence for a reversible mechanical distortion of the cylinder following the addition of La<sup>3+</sup>. A microfluidic system was used to repeatedly lower and then restore the conductance by alternatively perfusing La<sup>3+</sup> and EDTA. Although aspects of the kinetics of conductance drop and recovery are consistent with a disassembly/diffusion/reassembly model, others are inconsistent with the expected time scale of lateral diffusion of disassembled channel fragments in the membrane. The presence of a residual conductance following La<sup>3+</sup> treatment and the relationship between the residual conductance and the initial conductance were both indicative of a distortion/recovery process in analogy with a pressure-induced distortion of a flexible cylinder.</p> </div

    Tendencies in VTE prophylaxis pattern choices in various ICUs.

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    <p>Tendencies in VTE prophylaxis pattern choices in various ICUs.</p

    Sn binds HIV-1 <i>in vitro</i>.

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    <p>(A) TSn binds HIV-1 in an Sn-dependant manner. TSn and THP-1 were incubated with lab-adapted HIV-1<sub>NL4-3</sub>, an HIV-1 clade B primary isolate or clade C primary isolate for 1 h at 37°C, washed and then assayed for HIV-1 p24 by ELISA. HIV-1 binding to Sn was abrogated by pretreatment of cells with Sn mAb 7D2 or by pretreatment of HIV-1 with broad-spectrum sialidase. Pretreatment with IgG1 isotype control or CD4 mAbs did not reduce binding. Data presented are the average of 3 separate experiments. (B) IFN-α-treated CD14<sup>+</sup> monocytes bind HIV-1 in an Sn-dependant manner. HIV-1 binding assays were also performed on CD14<sup>+</sup> monocytes from seronegative controls treated with 500 U/ml IFN-α to induce Sn expression. Pretreatment with Sn mAb 7D2 and sialidase dramatically reduced HIV-1 binding while pretreatment with IgG1 isotype control or CD4 mAbs had little effect. Data represents monocytes from four separate donors. Error bars represent SD.</p

    Constitutive Sn expression in THP-1 by gene transduction (TSn).

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    <p>(A) Immunoblot analysis of Sn protein expression. THP-1 cell line was transduced with a plasmid encoding Sn cloned downstream of the high-level constitutive promoter CMV. Cell lysates were standardized, reduced with DTT and 10 µg of protein were loaded into each well: monocytes (lane 1), IFN-α-induced monocytes (lane2), THP-1 (lane 3) and TSn (lane 4) (M, molecular size marker). (B) Histogram of relative distribution of Sn on the cell surface of TSn clone. TSn (thick black line) and THP-1 cells (thin black line) were evaluated for Sn expression by flow cytometry using anti-Sn mAb 7D2 relative to the background isotype-matched control mAb (shaded region).</p

    Interferon-α and -γ induce Sn expression on CD14<sup>+</sup> monocytes and THP-1 cells.

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    <p>Cells were cultured in 500 U/ml IFN-α, 100 U/ml IFN-γ or 10 ng/ml TNF-α at 37°C for 48 h and analyzed for Sn expression by flow cytometry. Sn expression on IFN-α-, IFN -γ- or TNF-α-treated cells (thick black lines) and untreated cells (thin black line) were relative to an isotype-matched mAb control (shaded region). Results shown are representative histograms from three independent experiments using monocytes from three seronegative donors.</p
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