Passivation of Sponge Iron and GAC in Fe⁰/GAC Mixed-Potential Corrosion Reactor

The Fe⁰/GAC mixed-potential corrosion reactor was used to treat the complicated, toxic, and refractory ABS resin wastewater. In the 100 days continuous run, the effect of the packing particles passivation on the treatment efficiency of the Fe⁰/GAC mixed-potential corrosion reactor was investigated seriously. The formation mechanism of the compounds in passive film was investigated first by SEM, EDS, and X-ray dot-mapping, which was the precondition for the control of the passivation of packing particles. The results show that the passive film consisted of five kinds of compounds such as Fe₃(PO)₂·8H₂O, FePO₄ ·3H₂O, Fe₂O₃, Fe₃O₄, and FeS, which obstructed the formation of macroscopic galvanic cells between sponge iron (Fe⁰) and GAC and decreased the COD treatment efficiency of the Fe⁰/GAC mixed-potential corrosion reactor from 45 to 55% to 0%. The formation of passive film mainly resulted from the elements of S and P, which were from the SO₄^2– and PO₄^3– in ABS resin wastewater. Therefore, the inorganic ions in wastewater, especially for SO₄^2– and PO₄^3–, should be removed first before the treatment of the Fe⁰/GAC mixed-potential corrosion reactor

Real-time quantitative PCR was performed to determine the AT2 receptor mRNA levels.

<p>After the addition of 0.1 µmol/L ghrelin, 0.1 µmol/L Ang II, 0.1 µmol/L ghrelin + 0.1 µmol/L Ang II, or culture medium (control), the cardiomyocytes were cultured for 24 hours. Real-time quantitative PCR was performed to determine the mRNA levels. The data are presented as the means ± SD. *P<0.05 vs. the control group.</p

Characteristics of patients with CHF and the control group.

<p>Characteristics of patients with CHF and the control group.</p

Ghrelin inhibited cardiomyocyte apoptosis both in vivo and in vitro.

<p>(A) TUNEL analysis was performed after the end of the ghrelin treatment. The TUNEL-positive cells (apoptotic cells) are indicated by arrows. The data are presented as the means ± SD. <b>**</b>P<0.01 vs. SO group, ^##P<0.01 vs. MI group. (B) Ang II-induced DNA fragmentation in cardiomyocytes with or without ghrelin. Cultured cardiomyocytes from neonatal rats were stimulated with or without Ang II and ghrelin for 24 hours. The cardiomyocyte lysate was first incubated with RNase and then with proteinase K. By this method, only fragmented DNA was extracted. The DNA was separated by electrophoresis on a 1.5% agarose gel and stained with ethidium bromide. Lane A, vehicle-treated cardiomyocytes; lane B, cardiomyocytes incubated with 0.1 µmol/L Ang II; lane C, cardiomyocytes incubated with 1 µmol/L Ang II; lane D, cardiomyocytes incubated with 0.1 µmol/L ghrelin and 0.1 µmol/L Ang II; lane E, cardiomyocytes incubated with 0.1 µmol/L ghrelin. (C) Apoptosis of cardiomyocytes treated with Ang II and ghrelin. Cardiomyocytes were incubated in culture medium (control), 0.1 µmol/L Ang II, 0.1 µmol/L ghrelin, or 0.1 µmol/L ghrelin + 0.1 µmol/L Ang II for 24 hours. Magnification: ×200. The graph presents the percentage of TUNEL-positive cells determined from 100 cells in 3 independent experiments. The data are presented as the means ± SD. **P<0.01 vs. the control group;^##P<0.01 vs. the Ang II group.</p

Primer sequences used in real-time PCR.

<p>Primer sequences used in real-time PCR.</p

Ghrelin inhibits Ang II-induced cell apoptosis by down-regulating AT1R and thereby preventing HF.

<p>(A) The expression of AT1R mRNA by real-time quantitative PCR. The total RNA of noninfarcted left ventricular tissue was extracted using TRIzol Reagent, and real-time quantitative PCR was performed to determine the AT1R mRNA levels. The data are presented as the means ± SD. **P<0.01 vs. SO group, ^##P<0.01 vs. MI group. (B) The expression of cardiac AT1R in rat cardiac tissues by immunohistochemical staining (×200). (C) Real-time quantitative PCR was performed to determine the AT1 receptor mRNA levels in cardiomyocytes. After the addition of 0.1 µmol/L ghrelin, 0.1 µmol/L Ang II, 0.1 µmol/L ghrelin + 0.1 µmol/L Ang II, or culture medium (control), the cardiomyocytes were cultured for 24 hours. Real-time quantitative PCR was performed to determine the mRNA levels. The data are presented as the means ± SD. **P<0.01 vs. the control group; ^##P<0.01 vs. the Ang II group. (D) Western blotting was performed to determine AT1 receptor expression. Proteins were extracted from cardiomyocytes, separated by SDS-PAGE, and immunoblotted sequentially with anti-AT1 receptor antibody. The graph shows the result of densitometric quantification of the AT1 receptor protein relative to GAPDH as an internal control. The data are presented as the means ± SD. *P<0.05, **P<0.01 vs. the control group; ^##P<0.01 vs. the Ang II group.</p

Ghrelin mediated myocardium protection by down-regulating caspase-3.

<p>(A) The expression of caspase-3 mRNA by real-time quantitative PCR. The total RNA of noninfarcted left ventricular tissue was extracted using TRIzol Reagent, and real-time quantitative PCR was performed to determine the caspase-3 mRNA levels. The data are presented as the means ± SD. **P<0.01 vs. SO group, ^##P<0.01 vs. MI group. (B) The expression of caspase-3 in rat cardiac tissues examined by immunohistochemical staining (×200). (C) Analysis of caspase-3 mRNA levels in cardiomyocytes by quantitative real-time RT-PCR. After the addition of 0.1 µmol/L ghrelin, 0.1 µmol/L Ang II, 0.1 µmol/L ghrelin + 0.1 µmol/L Ang II, or culture medium (control), the cardiomyocytes were cultured for 24 hours. Real-time quantitative PCR was performed to determine the mRNA levels. The data are presented as the means ± SD. **P<0.01 vs. control group; ^##P<0.01 vs. Ang II group. (D) Detection of caspase-3 protein expression in rat cardiomyocytes by immunocytochemical staining. After the addition of 0.1 µmol/L ghrelin, 0.1 µmol/L Ang II, 0.1 µmol/L ghrelin + 0.1 µmol/L Ang II, or culture medium (control), the cardiomyocytes were cultured for 24 hours. Magnification: ×200.</p

The effect of ghrelin on HF.

<p>(A) Representative images of hearts. Four weeks after ghrelin administration, the heart was removed, and the tissue sections were stained with H&E (×200 magnification). (B) Hemodynamic index, including ±dp/dt_max, LVEDP, and LVSP. +dp/dt_max, maximal rate of the rise in blood pressure in the ventricular chamber; -dp/dt_max, maximal rate of the decline in blood pressure in the ventricular chamber; LVEDP, left ventricular end diastolic pressure; LVSP, left ventricular systolic pressure. (C) The levels of plasma BNP. The data are presented as the means ± SD. <b>**</b>P<0.01 vs. SO group; ^#P<0.05, ^##P<0.01 vs. MI group.</p

Additional file 1 of Machine learning for the prediction of sepsis-related death: a systematic review and meta-analysis

Supplementary Material 1: Table S1 Search strategy. Table S2 Overview of key characteristics per study. Table S3 Risk of bias assessment results. Table S4 Modeling variable

The selection of reliable samples and the corresponding accuracy of BLDA.

<p>The number of selected reliable samples and the corresponding classification accuracy when probability threshold is kept to be 0.90 for the 5 subjects. The plot is derived from one of 5×10-fold cross validation for the five subjects. The red bar using the scale of the left axis represents the number of trials selected for expanding training set; the gray one using the scale of the right axis is the classification accuracy when the reliable samples are used for classifier training.</p