Additional file 6: of IFI44L is a novel tumor suppressor in human hepatocellular carcinoma affecting cancer stemness, metastasis, and drug resistance via regulating met/Src signaling pathway

Figure S5. Ectopic expression of Met significantly restored IFI44L expression-mediated inhibition of migration and invasion abilities. Left, overexpression of IFI44L reduced the phosphorylation of Met, which could be partially rescued by transfecting Met vector. The actin was used as an internal control. Relative band intensity was quantified by ImageJ 1.42 and was represented with normalized mean ± s.e. (n = 3) below each band. Right, the migration and invasion abilities affected by overexpression of IFI44L and ectopic expression of Met in Hep3B cell line. Quantitative data are shown by histograms and representative photographs of the migrated/invaded cells from different treatments are shown. Histograms represent means ± s.d. from 3 independent experiments (*, P < 0.05; **, P < 0.01). (TIF 437 kb

Additional file 4: of IFI44L is a novel tumor suppressor in human hepatocellular carcinoma affecting cancer stemness, metastasis, and drug resistance via regulating met/Src signaling pathway

Figure S3. Western blotting analysis of three different siRNAs against IFI44L in HepG2 and PLC cells. The actin was used as an internal control. Relative band intensity was quantified by ImageJ 1.42 and was represented with normalized mean ± s.e. (n = 3) below each band. (TIF 168 kb

Additional file 3: of IFI44L is a novel tumor suppressor in human hepatocellular carcinoma affecting cancer stemness, metastasis, and drug resistance via regulating met/Src signaling pathway

Figure S2. Dose-dependent growth inhibition of Hep3B and HepG2 cells upon continuous exposure to the indicated concentrations of doxorubicin for 48 h was measured by MTT assay. Cells were transfected with 20 nM of control (NC-siRNA) or IFI44L-siRNA (*, P < 0.05; **, P < 0.01). (TIF 160 kb

Low Potassium Dialysate as a Protective Factor of Sudden Cardiac Death in Hemodialysis Patients with Hyperkalemia

<div><p>Aim</p><p>Hyperkalemia increases the risk of sudden cardiac death (SCD) in hemodialysis patients. Our objective was to determine the association between administering low potassium dialysate to hyperkalemic hemodialysis patients and SCD.</p><p>Methods</p><p>We conducted a retrospective cohort study with patients undergoing maintenance hemodialysis from May 1, 2006, through December 31, 2013. The dialysate composition was adjusted over time according to monthly laboratory results. A 1.0 mEq/L potassium dialysate was applied in patients with predialysis hyperkalemia (>5.5 mEq/L) and was included as a time-dependent confounding factor. The clinical characteristics of enrolled patients, the incidence and timing of SCD and risk factors for all-cause mortality and SCD were analyzed.</p><p>Results</p><p>There were 312 patients on maintenance hemodialysis during the study period. One hundred and fifty-seven patients had been dialyzed against a 1.0 mEq/L potassium dialysate at least once. The rates of all-cause mortality and SCD were 48.17 and 20.74 per 1000 patient-years, respectively. A 1.12-fold increase in the risk of SCD in the 24-hour period starting with the hemodialysis procedure and a 1.36-fold increase in the 24 hours preceding a weekly cycle were found (<i>p</i> = 0.017). Multivariate Cox proportional hazards models showed that age, diabetes mellitus and predialysis hyperkalemia (>5.0 mEq/L) were significant predictors of all-cause mortality and SCD. Exposure to 1.0 mEq/L potassium dialysate, Kt/V, and serum albumin were independent protective factors against all-cause mortality. Only exposure to 1.0 mEq/L potassium dialysate significantly prevented SCD (hazard ratio = 0.33, 95% CI = 0.13–0.85).</p><p>Conclusions</p><p>Using low potassium dialysate in hyperkalemic hemodialysis patients may prevent SCD.</p></div

Baseline patient characteristics according to dialysate potassium concentration.

<p>Count data are expressed as number (percentage) and continuous values are expressed as mean ± SD if normally distributed or median (interquartile range) if skewed.</p><p>Abbreviations: K_D, potassium dialysate; Ca, calcium; EF, ejection fraction; ESRD, end-stage renal disease.</p><p>^†Patients who had at least one prescription of a 1.0 mEq/L potassium dialysate.</p><p>^‡Patients who had at least one prescription of a 2.5 mEq/L calcium dialysate.</p><p>^§Preserved EF refers to patients with an ejection fraction of 55% or more.</p><p>Baseline patient characteristics according to dialysate potassium concentration.</p

Flowchart of the patient selection process.

<p>Patients who had been exposed to a 1.0 mEq/L potassium dialysate at least once were defined as 1.0 mEq/L potassium dialysate users.</p

Additional file 2: Table S1. of The effects of the location of cancer stem cell marker CD133 on the prognosis of hepatocellular carcinoma patients

Relationship of the clinical parameters with cytoplasmic and nuclear CD133 in hepatocellular carcinoma patients. (DOC 53 kb

Additional file 1: Figure S1. of The effects of the location of cancer stem cell marker CD133 on the prognosis of hepatocellular carcinoma patients

CD133 is known to show both cytoplasmic and membranous staining from the Human Protein Atlas of a hepatocellular carcinoma sample. (DOC 2903 kb

OCT abnormalities in <i>rd16;Nrl^−/−</i> mice.

<p>(A) Upper panels: Representative OCT scans vertically across ∼2 mm of retina (centered at the ONH, optic nerve head) in a WT mouse and in two <i>rd16;Nrl^−/−</i> mice of different ages. Lower panels: Magnified parts of the superior region of the retinal sections with overlaid longitudinal reflectivity profiles (LRPs) to demonstrate the reflective abnormalities in the outer retinal region in <i>rd16;Nrl^−/−</i> mice (b and c) compared with C57BL6 WT (a). (B) Upper two panels: Vertical OCT sections quantified for ONL+ thickness in two age groups of <i>rd16;Nrl^−/−</i> mice. Regions of outer retina with pseudorosettes were excluded in the measurement. ONL+ profiles in the older (P83–89, n = 12 eyes) age group were thinner than those in younger (P31–41, n = 35 eyes) mice; gray bands in the P83–89 plot represent mean±2 SD for ONL+ thickness of the P31–41 mice. For reference, insets at lower right of the upper two plots show original raw data before suppression of pseudorosette regions. Third panel from top: Means of ONL+ data across the vertical meridian in two age groups (error bar: ± SD; P31–41, open circles; P83–89, filled triangles). Lowest panel: Histograms showing average ONL+ fraction across vertical meridian of two age groups (*represents <i>p</i><0.001). (C) Histological sections of <i>rd16;Nrl^−/−</i> retina at 4 different ages from P21 to P80, compared with a WT retinal section. Histograms show ONL fraction (based on the earlier age group) in <i>rd16;Nrl^−/−</i> mice from peripheral retina (n = 6 eyes in each of the two age groups, *represents <i>p</i> = 0.01).</p

Structure and function in the <i>rd16;Nrl^−/−</i> mouse retina.

<p>(A) ERG b-wave amplitudes of responses to UV- and M-cone stimuli as a function of age in <i>rd16;Nrl^−/−</i> mice from P34 to P83 (n = 95) with comparisons to data from previously recorded signals in <i>Nrl^−/−</i> (squares <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0092928#pone.0092928-Cheng1" target="_blank">[11]</a>; square with cross <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0092928#pone.0092928-Mears1" target="_blank">[19]</a>), and <i>rd16</i> (crosses <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0092928#pone.0092928-Cideciyan3" target="_blank">[7]</a>) mice. Upper: Cone b-wave responses to ultraviolet (UV, 360 nm peak) stimuli in the <i>rd16;Nrl^−/−</i> mice are severely reduced compared with those of <i>Nrl^−/−</i> mice at comparable ages. Amplitudes in <i>rd16</i> mice are low compared to the other mice. It is also notable that ERGs of the <i>Nrl^−/−</i> mice remain relatively stable throughout this age range, while ERGs of the <i>rd16; Nrl^−/−</i> and <i>rd16</i> mice decline in amplitude with age. Lower: Responses to green (510 nm) stimuli are substantially lower in amplitude than those from UV-cone stimuli. Again, <i>Nrl^−/−</i> mice have the largest amplitudes and do not decline with increasing age within this time period. The <i>rd16;Nrl^−/−</i> waveforms are lower in amplitude and there is a reduction with age. Only limited data were available for <i>rd16</i> mice and these fell within the range of <i>rd16;Nrl^−/−</i> amplitudes. Waveforms for representative <i>rd16;Nrl^−/−</i> mice at various ages (grey-filled circles) are illustrated in the panels at right. Grey lines: linear regression fit to log-converted data (dashes) and 95% prediction intervals (solid). Squares with cross at earliest age in graphs: <i>Nrl^−/−</i> data from Mears et al., 2001 (B) Photoreceptor structure (ONL+) as a function of the combined UV- and M-cone ERG b-wave amplitudes. ONL+ remains similar to the value at P31 (youngest age <i>rd16;Nrl^−/−</i> we studied) across various degrees of ERG amplitude reduction. Horizontal dashed line is the reference level for the lower limit of retinal structure thickness at P31 (−2SD from the mean at this age); photoreceptor structure above this lower limit indicates no difference compared to the data of P31 (error bars, +2SD from mean).</p