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Cement is an important way to digest industrial waste. Semi‐dry gas desulfurized ash (SGDA) and granulated blast furnace slag (GBFS) as solid waste both have pozzolanic activity as well as small particle size and continuous particle size distribution, which allow their use as cement mixtures. In the present work, a cement matrix with 60% Portland cement, 20% SGDA, and 20% GBFS, including 3% nano‐TiO2 and 2% nano‐SiO2 as dopants, was produced via cement slurry mixing process. The obtained matrix was found to have the better 3‐ and 28‐day age compressive strength (by 104% and 116%, respectively) as compared with the pure Portland cement; the mortar compressive strength is also improved. The imaging and mineralogical analysis revealed that the nanomodified cement matrix had a more compact structure along with a well‐developed crystal form and the uniform micropore distribution. Furthermore, the doped cement mixture exhibited good fire resistance: Even after exposure to simulated fire conditions for 2.5 h at 450°C, the compressive strength of the composite was 98.27% of its initial value (57 MPa) and the microstructure remained undestroyed. The findings of this study open up new prospects for collaborative use of SGDA and GBFS as solid waste along with nano‐TiO2 and nano‐SiO2 as dopants, therefore providing outstanding fire stability of related composites. [ABSTRACT FROM AUTHOR]

Cement is an important way to digest industrial waste. Semi‐dry gas desulfurized ash (SGDA) and granulated blast furnace slag (GBFS) as solid waste both have pozzolanic activity as well as small particle size and continuous particle size distribution, which allow their use as cement mixtures. In the present work, a cement matrix with 60% Portland cement, 20% SGDA, and 20% GBFS, including 3% nano‐TiO2 and 2% nano‐SiO2 as dopants, was produced via cement slurry mixing process. The obtained matrix was found to have the better 3‐ and 28‐day age compressive strength (by 104% and 116%, respectively) as compared with the pure Portland cement; the mortar compressive strength is also improved. The imaging and mineralogical analysis revealed that the nanomodified cement matrix had a more compact structure along with a well‐developed crystal form and the uniform micropore distribution. Furthermore, the doped cement mixture exhibited good fire resistance: Even after exposure to simulated fire conditions for 2.5 h at 450°C, the compressive strength of the composite was 98.27% of its initial value (57 MPa) and the microstructure remained undestroyed. The findings of this study open up new prospects for collaborative use of SGDA and GBFS as solid waste along with nano‐TiO2 and nano‐SiO2 as dopants, therefore providing outstanding fire stability of related composites. [ABSTRACT FROM AUTHOR]

Background: High mobility group box-1 protein (HMGB1), a ubiquitous nuclear protein, which is recognized as a danger-associated molecular pattern (DAMP) triggering activation of the innate immune system. Previous studies have shown that HMGB1 also plays a role in T cell-mediated immunity, but the effect of HMGB1 on apoptosis of T cells and its precise mechanism remain to be determined. Methods: Two kinds of apoptosis assay techniques were used, i.e., Annexin V-FITC conjunction with PI to identify early apoptotic cells, Hoechst 33342 staining for double-stranded DNA to observe nuclear fragmentation or apoptotic body. The activation status of caspase-3, caspase-8, as well as caspase-9 was examined by colorimetric assay. The dynamic changes in intracellular calcium concentration ([Ca2+]i) was monitored by flow cytometry. Overexpression of Mfn2 was preformed by lentiviral vector transfection. The mRNA and protein levels of Mfn2 were determined by RT-PCR and Western-blotting. Results: Treatment of Jurkat T cells with recombinant human HMGB1 (rhHMGB1) causes a significant dose-dependent increase in percentage of apoptotic cells. When T cells are incubated with HMGB1 they express decreased mitochondria fusion-related protein mitofusin-2 (Mfn2) and activate mitochondrial apoptotic pathway via elevation of [Ca2+]i, Bax insertion, and activation of caspase. Furthermore, overexpression of Mfn2 ameliorates the apoptosis of T cells induced by HMGB1. This occurs at least partly through Mfn2 keeps Ca2+ homeostasis in T cells evidenced by monitoring [Ca2+]i dynamics. Conclusion: HMGB1 can trigger apoptosis of T lymphocytes through mitochondrial death pathway associated with [Ca2+]i elevation. Mfn2 plays a pivotal role in this process, and it might be a novel therapeutic target in T cell apoptosis related disorders. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The examination of anti-double stranded DNA (ds-DNA) IgG antibody is of great significance for the diagnosis, differential diagnosis, assessment of disease activity, and prognosis of disease recurrence in SLE., Methods: We used a chemiluminescence method to detect ds-DNA IgG and found that the levels of ds-DNA IgG antibody in the patient's serum were significantly increased and the indirect immunofluorescence (IIF) test result was negative. Laboratory tests show that the patient's RF level far exceeds the upper limit of their reference range., Results: RF 110.6 IU/mL, ds-DNA IgG 753 IU/mL; After PEG6000 treatment, the RF was 108.7 IU/mL, and then the ds-DNA IgG was measured at 23.5 IU/mL., Conclusions: The RF IgM subtype is the main cause of RF interference in IgG antibody detection, mainly due to the binding of the Fc region of RF to the Fab segment of IgG. Combining with capture antibodies and labeled antibodies leads to the formation of non-specific detection signals, or directly reacting with the detected substance, resulting in false positive test results.

Background: Heterophilic antibodies (HA) are one of the main substances that interfere with immunology, especially chemiluminescence immunoassay. Non-specific binding, labeling antibodies, bridging to capture antibodies, or labeling antigens can interfere with the detection process, leading to serious discrepancies between the measured results and clinical manifestations, and even delaying clinical diagnosis and treatment., Methods: This paper is a case of epidemic hemorrhagic fever causing pseudo CEA elevation caused by heterophagy induced antibodies in the body., Results: The patient's CEA detected on the ABBOTT detection platform was 51.1 ng/mL, and on the ROCHE detection platforms it was 4.66 ng/mL, and treated by PEG precipitation it was 45.2 ng/mL, after diluting the sample the CEA was 50.2 ng/mL, meanwhile the patient's platelets were 96 x 109/L and serum creatinine was 188.4 μmol/L, epidemic hemorrhagic fever IgM antibody was positive., Conclusions: When the test results do not match clinical symptoms, further confirmation is required through additional testing. Patients who use mouse monoclonal antibody preparations for diagnosis or treatment may have human anti-mouse antibodies in their serum, and the test results may falsely increase or decrease.

Background: TSH and ACTH are crucial hormones for diagnosing thyroid and adrenal diseases, and incorrect test reports can cause significant harm to patients., Methods: The TSH and ACTH levels on the testing system of our laboratory were measured using "sandwich" assays. The patient had heterophilic antibodies in their body, causing a false increase in TSH and ACTH levels., Results: TSH on the Abbott platform was 59.7 μIU/mL and on the Roche platform it was 4.33 μIU/mL. After pretreatment with HBR it was 3.95 μIU/mL; ACTH on the SIEMENS platform was 263.5 pg/mL, on the Abbott platform it was 47.6 pg/mL. After pretreatment with HBR it was 36.5 pg/mL., Conclusions: The patient's serum contains heterophilic antibodies, which interfere with the TSH and ACTH tested by this method.

Background: Mitofusin-2 (MFN2), a well-known mitochondrial fusion protein, has been shown to participate in innate immunity, but its role in mediating adaptive immunity remains poorly characterized. In this study, we explored the potential role of MFN2 in mediating the immune function of T lymphocytes., Methods: We manipulated MFN2 gene expression in Jurkat cells via lentiviral transduction of MFN2 small interfering RNA (siRNA) or full-length MFN2. After transduction, the immune response and its underlying mechanism were determined in Jurkat cells. One-way analysis of variance and Student's t-test were performed to determine the statistical significance between the groups., Results: Overexpression of MFN2 enhanced the immune response of T lymphocytes by upregulating Ca2+ (359.280 ± 10.130 vs. 266.940 ± 10.170, P = 0.000), calcineurin (0.513 ± 0.014 vs. 0.403 ± 0.020 nmol/L, P = 0.024), and nuclear factor of activated T cells (NFATs) activation (1.040 ± 0.086 vs. 0.700 ± 0.115, P = 0.005), whereas depletion of MFN2 impaired the immune function of T lymphocytes by downregulating Ca2+ (141.140 ± 14.670 vs. 267.060 ± 9.230, P = 0.000), calcineurin (0.054 ± 0.030 nmol/L vs. 0.404 ± 0.063 nmol/L, P = 0.000), and NFAT activation (0.500 ± 0.025 vs. 0.720 ± 0.061, P = 0.012). Furthermore, upregulated calcineurin partially reversed the negative effects of MFN2 siRNA on T cell-mediated immunity evidenced by elevations in T cell proliferation (1.120 ± 0.048 vs. 0.580 ± 0.078, P = 0.040), interleukin-2 (IL-2) production (473.300 ± 24.100 vs. 175.330 ± 12.900 pg/ml, P = 0.000), and the interferon-γ/IL-4 ratio (3.080 ± 0.156 vs. 0.953 ± 0.093, P = 0.000). Meanwhile, calcineurin activity inhibitor depleted the positive effects of overexpressed MFN2 on T cells function., Conclusions: Our findings suggest that MFN2 may regulate T cell immune functions primarily through the Ca2+-calcineurin-NFAT pathway. MFN2 may represent a potential therapeutic target for T cell immune dysfunction-related diseases.

Objective: To observe the effects of Nrf2 gene expression induced by RU486 at different doses on A549 cell damage induced by paraquat (PQ)., Methods: After A549 cells transfected with Ad-RUNrf2 were treated by RU486 at the doses of 10(-10), 10(-9), 10(-8) and 10(-7) mol/L for 6 h, A549 cell cultures were exposed to 10(-3) mol/L of PQ for 48 h. Then qRT-PCR and EMSA assays were used to detect the expression of Nrf2 gene, and qRT-PCR and ELISA assays were utilized to measure the effects of Nrf2 gene on the expression of the inflammatory cytokines IL-6, IL-10 and TNF-α, apoptotic factors Caspase-3, Caspase-9 and Cytochrome C. The oxidation factors (CAT and MDA protein contents) were observed by Chemical Colorimetric Analysis., Results: Nrf2 gene relative expression and protein contents increased with RU486 concentrations, and the above expression was the highest when the concentration of RU486 was 10(-7) mol/L, which was significantly higher than those in control and PQ exposure groups (P < 0.01 or P < 0.05). The relative gene expression and protein expression of IL-6 and TNF-α enhanced with the reduced concentrations of RU486, which were the lowest when RU486 concentration was 10(-7) mol/L, as compared with control and PQ exposure groups (P < 0.01 or P < 0.05), while the change of IL-10 content was the opposite. The relative expression of Caspase3, Caspase9 and Cytochrome C genes also increased with the reduced concentrations of RU486, which were the lowest when RU486 concentration was 10(-7) mol/L, as compared with control and PQ exposure groups (P < 0.01 or P < 0.05). The content of CAT enhanced with RU486 concentration, which was the highest when RU486 concentration was 10(-7) mol/L, as compared with control and PQ exposure groups (P < 0.05). But the change of MDA content was the contrary., Conclusion: Nrf2 expression induced by RU486 can promote the balance of oxidation-antioxidation system in A549 cells and inhibit the inflammation and apoptosis factors, which has a protective effect on A549 cell injury induced by PQ.