Effect of Anionic Surfactants on the Oil-Water-Rock Interactions by an Improved Washburn Method.

The complex and variable structure of subsurface oil reservoirs as well as the small pore throat size of reservoirs make it extremely important to investigate the effect of oil-water-rock interactions for enhancing oil recovery. In this paper, the powder wettability of oil sand with different polar solvents was investigated using the improved Washburn capillary rise method, and the surface free energy of oil sand was calculated in combination with the OWRK method. In addition, the wettability of anionic surfactants HABS and PS solutions on the surface of oil sand was determined, and it showed that their wetting rates showed different trends after CMC (critical micelle concentration). The C×cosθ value of HABS decreased significantly with increasing concentration, whereas PS showed little changes. This may be related to the aggregate structure formed by HABS on the oil sand surface. Meanwhile, the interfacial free energy between crude oil and oil sand was obtained by crude oil-to-oil sand wetting experiments, and found that the wetting rate of crude oil to oil sand was much lower than that of solvents and surfactants. In combination with the above results and the oil-water interfacial tension (IFT), the oil-water-rock three-phase contact angle and the work of adhesion between the crude oil and the solid were obtained by Young's equation. From the three-phase contact angle results, it can be found that the contact angle values of both HABS and PS are obviously higher than that of the simulated water, and both HABS and PS have the ability to significantly reduce the work of adhesion, which shows a strong ability to strip the oil film on the surface of the solid. The research results of this paper are helpful to understand the oil displacement mechanism of chemical flooding in reservoir pores, which is of great significance for improving oil recovery.

Study of Surface Wettability of Mineral Rock Particles by an Improved Washburn Method.

The surface wettability of rocks in underground reservoirs affects the distribution of fluids in the reservoir, so the wettability of reservoir minerals is a key factor for crude oil recovery from reservoirs. In this paper, the wettability of quartz sand with different particle sizes in different polar solvents was determined by Washburn's capillary rise method, and the C·cos θ values were calculated first. Next, the experimentally obtained macroscopic contact angle of water on the quartz surface of 15.0° was substituted into C·cos θ to obtain a linear equation between the particle size of quartz sand and the capillary constant C. The particle sizes of oil sand and mineral powder were then substituted into the equation to obtain their capillary constants C. Then, based on the Owens-Wendt-Rabel-Kaelbe (OWRK) equation and the obtained contact angles of solvent on quartz sand, oil sand, and mineral powder, the surface free energy of quartz sand with different particle sizes is calculated as 76.09, 76.65, and 76.42 mN/m, respectively, which are close to the literature results. In addition, the surface free energy of oil sand with different particle sizes was 23.22, 23.45, and 23.63 mN/m, and the results indicated that the polarity of oil sand was low. Meanwhile, the surface free energies of kaolinite, illite, feldspar, and montmorillonite were 61.59, 32.85, 35.87, and 25.91 mN/m, respectively. By the improved Washburn method in this paper, the wettability of different solvents on the surface of reservoir rocks was investigated, and the surface free energy of specific solid particles was calculated, which is important for studying the extraction of crude oil from subsurface reservoir rocks.

Synergism between cryoablation and GM-CSF: enhanced immune function of splenic dendritic cells in mice with glioma.

Glioma is the most common malignant primary brain tumor, and it has a poor prognosis. Studies have shown that cryoablation can activate antitumor immunoeffects by promoting the augmentation of dendritic cells (DCs). Granulocyte macrophage colony-stimulating factor (GM-CSF) has been shown to be useful for immunotherapy against glioma because it can stimulate DCs to present tumor antigen. Previous studies have shown that cryoablation and GM-CSF can exert antitumor effects. To test the hypothesis that combined therapy with cryoablation and GM-CSF for glioma could synergistically improve specific antiglioma immunity in mice, we tested the validity of this assumption in a murine subcutaneous GL261 glioma model. C57BL/6 mice with subcutaneous GL261 glioma were created and divided into four groups: no treatment, GM-CSF injection, cryoablation treatment, and GM-CSF and cryoablation combined treatment (n=20 in each group). Serial immune indicators were detected at sequential time points during treatment. Compared with the other groups, in the combined treatment group, DCs were more activated and their numbers were markedly upregulated, the secretion of interferon-γ from Th1 cells of mice spleen was increased, and the cytolytic activity of CD8 CTLs exerted a more significant cytotoxic effect on GL261 glioma cells (P<0.05 for all). Furthermore, these changes peaked on the 7th day after treatment, and then gradually reduced, until the 21st day; these changes were higher than those at pretreatment (P<0.05). It is concluded that combined therapy with argon-helium cryoablation and GM-CSF could synergistically enhance the activation of DCs and induce a robust tumor-specific immunologic response in glioma-bearing mice.

Immune responsive gene 1, a novel oncogene, increases the growth and tumorigenicity of glioma.

Immune responsive gene 1 (IRG1) is highly expressed in mammalian macrophages during inflammation. However, the role of IRG1 in tumorigenesis remains unclear. In the present study, we aimed to clarify the epigenetic regulation and biological functions of IRG1 in glioma. We found that the expression level of IRG1 influenced the WHO stage in 140 glioma patients. Overexpression of IRG1 increased the growth, invasion, and tumorigenesis in U251 and SHG-44 glioma cells both in vitro and in vivo. Suppression of IRG1 expression by si-IRG1 decreased the levels of cell cycle regulatory proteins, namely, E2F1, p21, CDK4, CDK6 and cyclin D1. Knockdown of IRG1 expression by RNA interference increased E-cadherin expression and decreased the amounts of snail and vimentin. Furthermore, the suppression of IRG1 expression inhibited the expression of NF-κB and STAT3, suggesting a role of IRG1 in regulating the genes associated with these factors and thereby contributing to a decrease in glioma cell proliferation, migration and invasion. Collectively, our findings revealed that IRG1 is a candidate oncogene that is amplified in glioma and is involved in novel mechanisms that influence glioma pathogenesis.

MSCs inhibit bone marrow-derived DC maturation and function through the release of TSG-6.

Dendritic cells (DCs) are potent antigen-presenting cells (APCs) that are characterized by the ability to take up and process antigens and prime T cell responses. Mesenchymal stem cells (MSCs) are multipotent cells that have been shown to have immunomodulatory abilities, including inhibition of DC maturation and function in vivo and in vitro; however, the underlying mechanism is far from clear. In this study we found that MSCs can inhibit the maturation and function of bone marrow-derived DCs by releasing TSG-6. In the presence of MSCs, lower expression of mature DC surface phenotype (CD80, CD86, MHC-II, and CD11c) was observed. In addition, typical DC functions, such as the production of IL-12 and the ability to prime T cells, were decreased when co-cultured with MSCs. In contrast, knockdown of TSG-6 reduced the inhibitory effect of MSCs on DC. Moreover, we found that TSG-6 can suppress the activation of MAPKs, and NF-κB signaling pathways within DCs during Lipopolysaccharides (LPS) stimulation. In conclusion, we suggest that TSG-6 plays an important role in MSCs-mediated immunosuppressive effect on DC.

In-situ administration of dendritic cells following argon-helium cryosurgery enhances specific antiglioma immunity in mice.

Dendritic cells (DCs) are highly specialized antigen-presenting cells that play a key role in the activation of naive T cells. With an aim to explore whether in-situ administration of DCs following argon-helium cryosurgery could enhance specific antiglioma immunity in mice, we evaluated the validity of this approach in a murine subcutaneous GL261 glioma model. C57BL/6 mice models bearing subcutaneous GL261 glioma were established and then divided into four groups, namely, no-treatment group (n=14), DC group (n=14), cryosurgery group (n=15), and cryosurgery+DC group (n=15). Compared with the other groups, cryosurgery combined with DCs injection reduced tumor sizes and significantly prolonged survival. In addition, the combined treatment resulted in significantly increasing percentages of CD3, CD3CD4 cells, the ratio of CD3CD4/CD3CD8, and the level of serum interleukin-12 10 days after treatments. Furthermore, in the combined treatment group, Th1 cells were significantly higher than those in the other groups, and the splenic cytotoxic T lymphocyte of mice showed significantly increasing specific cytotoxicity against GL261 cells. These results indicated that in addition to the destruction of tumor, cryosurgery combined with DCs injection enhanced systemic antitumor immunity, suggesting the potential usefulness of the combined treatment in the clinical management of gliomas.

Extracts from glioma tissues following cryoablation have proapoptosis, antiproliferation, and anti-invasion effects on glioma cells.

OBJECTIVE: This study is to investigate the in vivo apoptotic processes in glioma tissues following cryoablation and the effects of glioma tissue extracts on GL261 glioma cells in vitro. METHODS: TUNEL and flow cytometry analysis were performed to detect the apoptotic processes in the glioma tissues following cryoablation and in the GL261 cells treated with cryoablated tumor extracts. The scratch assay, the transwell assay, and Western blot analysis were carried out to evaluate the effects of cryoablated tumor extracts on the migration, invasion, and proliferation of tumor cells. RESULTS: Our in vivo results indicated that the rapid-onset apoptosis was induced via the intrinsic pathway and the delayed apoptosis was triggered through the extrinsic pathway. The in vitro results showed that extracts from glioma tissues following cryoablation induced apoptosis via extrinsic pathways in GL261 glioma cells. Furthermore, cryoablated tumor extracts significantly inhibited the migration and proliferation of these cells, which would be related to the inhibition of ERK1/2 pathway and the activation of P38 pathway. CONCLUSION: Glioma cells surviving in cryoablation undergo intrinsic or extrinsic apoptosis. Augmenting the induction of apoptosis or enhancing the cryosensitization of tumor cells by coupling cryoablation with specific chemotherapy effectively increases the efficiency of this therapeutic treatment.

Antitumor efficacy of argon-helium cryoablation-generated dendritic cell vaccine in glioma.

Dendritic cells (DCs) are potent antigen-presenting cells that play a critical role in priming tumor immune responses. We investigated the mechanisms of antitumor efficacy of DCs pulsed with argon-helium-cryotreated glioma cells. There was significant upregulation of maturation markers (CD80, CD86, MHC-I, and MHC-II) in argon-helium freeze-thawed lysate-pulsed DCs. The concentration of interleukin-6 (IL-6), IL-1ß, tumor necrosis factor-α, and IL-12 secreted by lysate-pulsed DCs was increased. The concentration of interferon-γ secreted by T cells stimulated by lysate-pulsed DCs was increased. The cytotoxicity assay showed that T cells stimulated by lysate-pulsed DCs could kill glioma cells significantly more effectively. Our results suggest that argon-helium freeze-thawed lysate-pulsed DCs in vitro can promote DC maturation and enhance DC antigen-presenting function, and induce cytotoxic T lymphocytes to kill tumor cells. Therefore, the combination of argon-helium cryoablation and DC vaccine may represent a novel treatment method for glioma.

ADAM17 promotes U87 glioblastoma stem cell migration and invasion.

Glioblastoma stem cells (GSCs) are thought to contribute to the diffuse invasiveness of malignant gliomas. Emerging evidence supports a role for a disintegrin and metalloproteinase 17 (ADAM17) in proteolytic ectodomain shedding of several EGFR-binding ligands, which subsequently activate PI3K/AKT and MEK/ERK pathways through EGFR phosphorylation thus mediating glioma invasiveness. However, it is not clear if ADAM17 also plays important roles in promoting GSC invasion. In this study, we isolated CD133+ GSCs from the human glioblastoma cell line U87 using fluorescence-activated cell sorting and demonstrated their increased invasive potential compared with matched non-stem tumor cells. Furthermore, we showed that CD133+ GSCs expressed higher levels of ADAM17. Immunofluorescence staining revealed that high expression levels of ADAM17 at the invasive front were correlated with the presence of CD133+ GSCs in human glioblastoma specimens. Stimulation with the ADAM17 agonist chemokine phorbol myristate acetate increased migration and invasion of GSCs, which was counteracted by ADAM17 knockdown. In addition, ADAM17 also induced CD133+ GSC invasion via activation of the EGFR/PI3K/AKT signaling pathway. These findings suggest that ADAM17 is involved in U87 GSC invasive process and may provide a potential therapeutic target for glioma treatment.