Receiver operating characteristic (ROC) curve for predicting case fatality risk in 39 <i>V</i>. <i>vulnificus</i>-infected patients.

<p>The areas under the ROC curve (AOC) of the MELD and ΔMELD are 0.929 (95% CI = 0.818–1.000; <i>p</i> = 0.002) and 0.897 (95% CI = 0.772–1.000; <i>p</i> = 0.005), respectively. The diagonal reference line indicates no discrimination.</p

Laboratory findings on admission and the extreme data during hospitalization in 39 <i>V</i>. <i>vulnificus</i>-infected patients treated between 2007 and 2010.

<p>Data are presented as mean ± SE, unless otherwise indicated.</p><p>^† Wilcoxon rank sum test, unless otherwise indicated.</p><p>* The difference is significant (p < 0.05).</p><p>^a CRP, C-reactive protein.</p><p>^b WBC, white blood cells.</p><p>^c INR, international normalized ratio.</p><p>^d LRINEC, laboratory risk indicator for necrotizing fasciitis.</p><p>^e MELD, model for end-stage liver disease.</p><p>^f MELD-Na, modified model for end-stage liver disease including sodium.</p><p>Laboratory findings on admission and the extreme data during hospitalization in 39 <i>V</i>. <i>vulnificus</i>-infected patients treated between 2007 and 2010.</p

Area under the receiver operating characteristic (ROC) curve for predicting mortality risk in 39 <i>V</i>. <i>vulnificus</i>-infected patients treated between 2007 and 2010.

<p>* P value < 0.05 is significant and all analysis was done by logistic regression model in SPSS 17.0.</p><p>^a LRINEC, laboratory risk indicator for necrotizing fasciitis.</p><p>^b MELD, model for end-stage liver disease.</p><p>^c MELD-Na, modified model for end-stage liver disease including sodium.</p><p>^d Δ, difference between the admission and the extreme scores.</p><p>^e AUC, area under the receiver operating characteristic curve.</p><p>^f CI, confidence interval.</p><p>Area under the receiver operating characteristic (ROC) curve for predicting mortality risk in 39 <i>V</i>. <i>vulnificus</i>-infected patients treated between 2007 and 2010.</p

Odds ratio of the index variables in relation to the case fatality.

<p>* P value < 0.05 is significant and all analysis was done by logistic regression model in SPSS 17.0.</p><p>^a LRINEC, laboratory risk indicator for necrotizing fasciitis.</p><p>^b MELD, model for end-stage liver disease.</p><p>^c MELD-Na, modified model for end-stage liver disease including sodium.</p><p>^d Δ, difference between the admission and the extreme scores.</p><p>^e OR, odds ratio;</p><p>^f CI, confidence interval.</p><p>Odds ratio of the index variables in relation to the case fatality.</p

Selected variables in 28 RA patients with PJI treated with two-stage exchange.

<p><b>NOTE.</b> Data are no. (%) of joints, unless otherwise indicated.</p><p>NS: Not significant; CRP: C-reactive protein; ESR: erythrocyte sedimentation rate.</p>*<p>Statistical significance (p<0.05).</p

Group comparison of laboratory findings on admission and the extreme data during hospitalization.

<p>Data are presented as mean ± SE, unless otherwise indicated.</p><p>^† Wilcoxon rank sum test, unless otherwise indicated.</p><p>* The difference is significant (p < 0.05).</p><p>^a CRP, C-reactive protein.</p><p>^b WBC, white blood cells.</p><p>^c INR, international normalized ratio.</p><p>Group comparison of laboratory findings on admission and the extreme data during hospitalization.</p

Flow chart of treatment modalities for 46 episodes of PJI in RA patients treated between 2002 and 2008.

<p>Flow chart of treatment modalities for 46 episodes of PJI in RA patients treated between 2002 and 2008.</p

Additional file 1: of The effects of zoledronate on the survival and function of human osteoblast-like cells

Figure S1. Zoledronate (ZOL) at the ΟM level presents a dose-dependently inhibitory effect on cellular proliferation of rat stromal cells (R7500). (EPS 825 kb

Additional file 2: of The effects of zoledronate on the survival and function of human osteoblast-like cells

Figure S2. Zoledronate (ZOL) at the ΟM level presents a negative effect on matrix mineralization of rat stromal cells (R7500). (EPS 1961 kb

ERK activity independent of AMPK-Syk-Src signaling participates in PKC-mediated monocyte adhesion.

<p>(<b>A</b>) After pretreatment with 10 nM GF109203X for 30 min, followed by PMA (100 nM) treatment for 10 min, cell lysates were subjected to immunobloting (left panel). In some experiments, after pretreatment with U0126 and/or compound C for 30 min, THP-1 cells were stimulated with PMA (100 nM) for 4 h, and cell adhesion was determined (middle and right panels). (<b>B–D</b>) THP-1 cells were treated with PMA in the presence of vehicle or pharmacological agents for 10 min (lower panel of <b>B</b>, <b>D</b>) or indicated time periods (upper panel of <b>B</b>, <b>C</b>). Immunobloting with specific antibodies was conducted. FAK activation was determined by immunoprecipitation with FAK-specific antibody and immunoblotting with phospho-tyrosine antibody (<b>D</b>). (<b>E</b>) THP-1 cells pre-labeled with BCECF were treated with SykI, PP2, compound C, U0126 (each at 10 µM), or Ro318220 (3 µM) for 30 min prior to the addition of PMA (100 nM). After 1 h incubation, THP-1 cells were washed with complete medium twice, and then added to HUVEC monolayer grown in 96-well plate. After 1 h, adhesion of THP-1 cells to HUVEC was determined. (<b>F</b>) Human primary monocytes were similarly treated with inhibitors and PMA, and cell adhesion at 4 h was determined. (G) PMA-induced cell adhesion to matrix-coated culture plates, in the absence or presence of alpha5beta1 inhibitor and alphaVbeta3 blocking antibody (LM609), was determined (left panel). In some experiments, after pretreatment with integrin inhibitors for 30 min, THP-1 cells were stimulated with PMA (100 nM) for 4 h, and cell adhesion to either the culture plate or to HUVEC was determined (right panel).</p