Solid-Liquid Phase Equilibria in the Quinary System NaCl + NaOH + Na2CO3 + Na2SO4 + H2O at 363.15 K.

Solid-liquid equilibria in the quinary system NaCl + NaOH + Na2CO3 + Na2SO4 + H2O at 363.15 K were measured by the wet residue method, and the equilibrium solid phases and solubilities of saturated solutions were determined experimentally. Using the experimental results, dry-salt phase diagrams and water diagrams versus composition diagrams were plotted (saturated with saturated sodium chloride, sodium hydroxide, sodium carbonate, and sodium sulfate). The experimental results show that there are a solid solution (γ-salt, mNa2SO4·nNa2CO3) and co-saturation complex salts (S3, Na2SO4·NaCl·NaOH and S1, NaOH·Na2SO4) formed in this quinary system. Based on Xu's activity coefficient model, the solubilities of the quinary system NaCl + NaOH + Na2CO3 + Na2SO4 + H2O at 363.15 K were calculated with corresponding parameters. Comparing the experimental and calculated results, it was shown that the calculated values had a good agreement with the experimental ones.

Phase Equilibria in the Quaternary Systems NaOH + Na2CO3 + Na2SO4 + H2O, Na2CO3 + NaOH + NaCl + H2O, and NaOH + Na2SO4 + NaCl + H2O at 363.15 K.

The solid-liquid equilibrium data of the aqueous NaOH-Na2CO3-Na2SO4-H2O, NaOH-Na2CO3-NaCl-H2O, and NaOH-Na2SO4-NaCl-H2O quaternary systems at 363.15 K were measured. The equilibrium solid phases and solubilities of salts in the three systems and its subsystems were determined. The densities of the saturated solutions were also determined. The experimental data are used to plot the solubility diagrams and water content diagrams of the systems. It was found that the NaOH-Na2CO3-Na2SO4-H2O system contains the solid solution of γ-salt (mNa2SO4·nNa2CO3) and the other two systems Na2CO3-NaOH-NaCl-H2O and NaOH-Na2SO4-NaCl-H2O have the complex salts S1 (Na2SO4·NaOH) and S3 (Na2SO4·NaCl·NaOH). On the basis of Xu's activity coefficient model, a model was constructed for the correlation of solid-liquid equilibrium in electrolyte solutions to calculate the solubilities of salts in these systems at 363.15 K. The calculated solubilities are in agreement with the experimental values.

Variable effects of the co-administration of a GM-CSF-expressing plasmid on the immune response to flavivirus DNA vaccines in mice.

As a cytokine adjuvant, granulocyte-macrophage colony-stimulating factor (GM-CSF) has been demonstrated to play central roles in the enhancement of the immune response and protection elicited by experimental vaccines. However, in our previous work, the co-administration of GM-CSF produced untoward effects on the immune response induced by a Japanese encephalitis virus DNA vaccine candidate. This study aimed to elucidate the adjuvant roles of GM-CSF in several Flaviviridae virus DNA vaccine candidates. Our results showed that the effects of GM-CSF were diverse: co-inoculated GM-CSF caused significant suppression to the dengue virus type 1 and type 2 prM-E DNA vaccinations and influenced protective efficiency against virus challenge. In contrast, GM-CSF showed little effect or an enhancement on the immune response elicited by hepatitis C virus C or E1 DNA vaccine candidates. Notably, these effects of GM-CSF were highly durable. Our results suggested that the adjuvant roles of the GM-CSF plasmid were complex and diverse, ranging from enhancement to suppression, depending on the immunogen of Flaviviridae virus DNA vaccine candidates. Therefore, the application of GM-CSF as a vaccine adjuvant or a therapeutic agent should be evaluated carefully.

Inhibitory effect of glutathione on oxidative liver injury induced by dengue virus serotype 2 infections in mice.

The pathogenesis of dengue virus (DV) infection has not been completely defined and change of redox status mediated by depletion of glutathione (GSH) in host cell is a common result of viral infection. Our previous study has demonstrated that DV serotype 2 (DV2) infection alters host intracellular GSH levels, and exogenous GSH inhibits viral production by modulating the activity of NF-κB in HepG2 cells. GSH is the most powerful intracellular antioxidant and involved in viral infections. Thus, this study was to investigate whether DV2 infection can induce alteration in redox balance and effect of GSH on the disease in HepG2 xenografts SCID mice. Our results revealed that mice infected with DV2 showed alterations in oxidative stress by increasing the level of malondialdehyde (MDA), an end product of lipid peroxidation, and GSSG/GSH ratio. DV2-infected mice also showed a decrease in the activity of catalase (CAT) and total superoxide dismutase (T-SOD) in the serum and/or observed organs, especially the liver. Moreover, DV2 infection resulted in elevated serum levels of the cytokines tumor necrosis factor-α and interlukin-6 and obvious histopathological changes in the liver. The administration of exogenous GSH significantly reversed all of the aforementioned pathological changes and prevented significant liver damage. Furthermore, in vitro treatment of HepG2 cells with antioxidants such as GSH inhibited viral entry as well as the production of reactive oxygen species in HepG2 cells. These results suggest that GSH prevents DV2-induced oxidative stress and liver injury in mice by inhibiting proinflammatory cytokine production, and GSH and may be a promising therapeutic agent for prevention of oxidative liver damage during DV infection.

[The adjuvant effect of granulocyte macrophage colony stimulating factor (GM-CSF) in dengue virus and hepatitis C virus DNA vaccines].

To investigate the adjuvant effect of granulocyte macrophage colony stimulating factor (GM-CSF) in Flaviviridae virus DNA vaccines. After DNA immunization, the antibody levels of serum from mice were detected by ELISA and indirect immunofluorescence assay. Co-immunization of GM-CSF suppressed the immune responses induced by DV1 and DV2 candidate vaccines whereas enhanced the immune response induced by HCV C and E1 DNA vaccines. As genetic adjuvant for DNA vaccines, GM-CSF might display complex diversity on the immune responses: an augmentation or suppression due to different immunogens. Therefore, GM-CSF should be used with some cautions in clinic.

Suppressive effects on the immune response and protective immunity to a JEV DNA vaccine by co-administration of a GM-CSF-expressing plasmid in mice.

As a potential cytokine adjuvant of DNA vaccines, granulocyte-macrophage colony-stimulating factor (GM-CSF) has received considerable attention due to its essential role in the recruitment of antigen-presenting cells, differentiation and maturation of dendritic cells. However, in our recent study of a Japanese encephalitis virus (JEV) DNA vaccine, co-inoculation of a GM-CSF plasmid dramatically suppressed the specific IgG response and resulted in decreased protection against JEV challenge. It is known that GM-CSF has been used in clinic to treat neutropenia for repopulating myeloid cells, and as an adjuvant in vaccine studies; it has shown various effects on the immune response. Therefore, in this study, we characterized the suppressive effects on the immune response to a JEV DNA vaccine by the co-administration of the GM-CSF-expressing plasmid and clarified the underlying mechanisms of the suppression in mice. Our results demonstrated that co-immunization with GM-CSF caused a substantial dampening of the vaccine-induced antibody responses. The suppressive effect was dose- and timing-dependent and likely related to the immunogenicity of the antigen. The suppression was associated with the induction of immature dendritic cells and the expansion of regulatory T cells but not myeloid-derived suppressor cells. Collectively, our findings not only provide valuable information for the application of GM-CSF in clinic and using as a vaccine adjuvant but also offer further insight into the understanding of the complex roles of GM-CSF.