Emission and distribution profiles of polycyclic aromatic hydrocarbons in solid residues of municipal and industrial waste incinerators, Northern Vietnam.

The concentrations and profiles of 18 polycyclic aromatic hydrocarbons (PAHs) in particulate matter (PM10), fly ash (FA), and bottom ash (BA) were examined in three incineration residues. Samples were collected from different municipal and industrial solid waste incinerators in Northern Vietnam. The average concentrations of total PAHs in PM10, fly ash, and bottom ash were 9.55 × 103 ng/Nm3, 215 × 103 ng/g, and 2.38 ng/g, respectively. Low-molecular-weight PAHs (2 to 3 rings) were predominant in most samples. The emission factor of total PAHs decreased in the order of FA > BA > PM10. A higher concentration of total PAHs was found in industrial facilities than that in municipal ones. The high carcinogenic proportion of PAHs together with significantly high annual emissions reflect the high pollution risk to the ecosystem by PAHs in the case of reuse of incineration ashes (e.g., brick production). Regarding the carcinogenic risk of PAH-bounded ashes or particles, calculations from this study imply the significant threat for workers who have been manipulated in the incineration facilities, directly exposed to fly and bottom ashes. Meanwhile, the risk from PAH-bound particulate was not considered a significant threat for both normal adults and children. Further study on PAHs contained in incinerator waste dumps should be conducted in Vietnam to assess the potential contamination risk of these incineration by-products.

Stromal Vascular Fraction and Mesenchymal Stem Cells from Human Adipose Tissue: A Comparison of Immune Modulation and Angiogenic Potential.

INTRODUCTION: In recent years, both stromal vascular fraction (SVF) from adipose tissue and mesenchymal stem cells (MSC) from adipose tissues were extensively used in both preclinical and clinical treatment for various diseases. Some studies reported differences in treatment efficacy between SVFs and MSCs in animals as well as in humans. Therefore, this study is aimed to evaluate the immune modulation and angiogenic potential of SVFs and MSCs from the same SVF samples to support an explanation when SVFs or MSCs should be used. METHODS: The adipose tissue samples from ten female donors with consent forms were collected. SVFs from these samples were isolated according to the published protocols. The existence of mesenchymal cells that positive with CD44, CD73, CD90, and CD105 and endothelial progenitor cells that positive with CD31 and CD34 was determined using flow cytometry. Three samples of SVFs with similar percentages of mesenchymal cell portion and endothelial progenitor cell portion were used to isolate MSCs. Obtained MSCs were confirmed as MSCs using the ISCT minimal criteria. To compare the immune modulation of SVF and MSCs, the mixed lymphocyte assay was used. The lymphocyte proliferation, as well as IFN-gamma and TNF-alpha concentrations, were determined. To compare the angiogenic potential, the angiogenesis in quail embryo assay was used. The angiogenesis efficacy was measured based on the vessel areas formed in the embryos after 7 days. RESULTS: The results showed that all SVF samples contained the portions of mesenchymal cells and endothelial progenitor cells. MSCs from SVFs meet all minimal criteria of MSCs that suggested by ISCT. MSCs from SVFs efficiently suppressed the immune cell proliferation compared to the SVFs, especially at ratios of 1:4 (1 MSCs: 4 immune cells). MSCs also inhibited the IFN-gamma and TNF-alpha production more efficiently than SVFs (p < 0.05). However, in quail embryo models, SVFs triggered the angiogenesis and neovessel formation better than MSCs with more significant vessel areas after 7 days (p < 0.05). CONCLUSION: This study suggested that SVFs and MSCs have different potentials for immune modulation and angiogenesis. SVFs help the angiogenesis better than MSCs, while MSCs displayed the more significant immune modulation. These results can guide the usage of SVFs or MSCs in disease treatment.

Targeting breast cancer stem cells by dendritic cell vaccination in humanized mice with breast tumor: preliminary results.

BACKGROUND: Breast cancer (BC) is one of the leading cancers in women. Recent progress has enabled BC to be cured with high efficiency. However, late detection or metastatic disease often renders the disease untreatable. Additionally, relapse is the main cause of death in BC patients. Breast cancer stem cells (BCSCs) are considered to cause the development of BC and are thought to be responsible for metastasis and relapse. This study aimed to target BCSCs using dendritic cells (DCs) to treat tumor-bearing humanized mice models. MATERIALS AND METHODS: NOD/SCID mice were used to produce the humanized mice by transplantation of human hematopoietic stem cells. Human BCSCs were injected into the mammary fat pad to produce BC humanized mice. Both hematopoietic stem cells and DCs were isolated from the human umbilical cord blood, and immature DCs were produced from cultured mononuclear cells. DCs were matured by BCSC-derived antigen incubation for 48 hours. Mature DCs were vaccinated to BC humanized mice with a dose of 10(6) cells/mice, and the survival percentage was monitored in both treated and untreated groups. RESULTS: The results showed that DC vaccination could target BCSCs and reduce the tumor size and prolong survival. CONCLUSION: These results suggested that targeting BCSCs with DCs is a promising therapy for BC.

Targeting specificity of dendritic cells on breast cancer stem cells: in vitro and in vivo evaluations.

Breast cancer is a leading cause of death in women, and almost all complications are due to chemotherapy resistance. Drug-resistant cells with stem cell phenotypes are thought to cause failure in breast cancer chemotherapy. Dendritic cell (DC) therapy is a potential approach to eradicate these cells. This study evaluates the specificity of DCs for breast cancer stem cells (BCSCs) in vitro and in vivo. BCSCs were enriched by a verapamil-resistant screening method, and reconfirmed by ALDH expression analysis and mammosphere assay. Mesenchymal stem cells (MSCs) were isolated from allogeneic murine bone marrow. DCs were induced from bone marrow-derived monocytes with 20 ng/mL GC-MSF and 20 ng/mL IL-4. Immature DCs were primed with BCSC- or MSC-derived antigens to make two kinds of mature DCs: BCSC-DCs and MSC-DCs, respectively. In vitro ability of BCSC-DCs and MSC-DCs with cytotoxic T lymphocytes (CTLs) to inhibit BCSCs was tested using the xCELLigence technique. In vivo, BCSC-DCs and MSC-DCs were transfused into the peripheral blood of BCSC tumor-bearing mice. The results show that in vitro BCSC-DCs significantly inhibited BCSC proliferation at a DC:CTL ratio of 1:40, while MSC-DCs nonsignificantly decreased BCSC proliferation. In vivo, tumor sizes decreased from 18.8% to 23% in groups treated with BCSC-DCs; in contrast, tumors increased 14% in the control group (RPMI 1640) and 47% in groups treated with MSC-DCs. The results showed that DC therapy could target and be specific to BCSCs. DCs primed with MSCs could trigger tumor growth. These results also indicate that DCs may be a promising therapy for treating drug-resistant cancer cells as well as cancer stem cells.

A simple in vitro method for evaluating dendritic cell-based vaccinations.

BACKGROUND: Dendritic cell (DC) therapy is a promising therapy for cancer-targeting treatments. Recently, DCs have been used for treatment of some cancers. We aimed to develop an in vitro assay to evaluate DC therapy in cancer treatment using a breast cancer model. METHODS: DCs were induced from murine bone marrow mononuclear cells in Roswell Park Memorial Institute (RPMI) 1640 medium supplemented with GM-CSF (20 ng/mL) and IL-4 (20 ng/mL). Immature DCs were primed with breast cancer stem cell (BCSC)-derived antigens. BCSCs were sorted from 4T1 cell lines based on aldehyde dehydrogenase expression. A mixture of DCs and cytotoxic T lymphocytes (CTLs) were used to evaluate the inhibitory effect of antigen-primed DCs on BCSCs. BCSC proliferation and doubling time were recorded based on impedance-based cell analysis using the xCELLigence system. The specification of inhibitory effects of DCs and CTLs was also evaluated using the same system. RESULTS: The results showed that impedance-based analysis of BCSCs reflected cytotoxicity and inhibitory effects of DCs and CTLs at 72 hours. Differences in ratios of DC:CTL changed the cytotoxicity of DCs and CTLs. CONCLUSION: This study successfully used impedance-based cell analysis as a new in vitro assay to evaluate DC efficacy in cancer immunotherapy. We hope this technique will contribute to the development and improvement of immunotherapies in the near future.

Suppression of human breast tumors in NOD/SCID mice by CD44 shRNA gene therapy combined with doxorubicin treatment.

BACKGROUND: Breast cancer stem cells with a CD44(+)CD24(-) phenotype are the origin of breast tumors. Strong CD44 expression in this population indicates its important role in maintaining the stem cell phenotype. Previous studies show that CD44 down-regulation causes CD44(+)CD24(-) breast cancer stem cells to differentiate into non-stem cells that are sensitive to antitumor drugs and lose many characteristics of the original cells. In this study, we determined tumor suppression in non-obese severe combined immunodeficiency mice using CD44 shRNA therapy combined with doxorubicin treatment. METHODS: Tumor-bearing non-obese severe combined immunodeficiency mice were established by injection of CD44(+)CD24(-) cells. To track CD44(+)CD24(-) cells, green fluorescence protein was stably transduced using a lentiviral vector prior to injection into mice. The amount of CD44 shRNA lentiviral vector used for transduction was based on CD44 down-regulation by in vitro CD44 shRNA transduction. Mice were treated with direct injection of CD44 shRNA lentiviral vector into tumors followed by doxorubicin administration after 48 hours. The effect was evaluated by changes in the size and weight of tumors compared with that of the control. RESULTS: The combination of CD44 down-regulation and doxorubicin strongly suppressed tumor growth with significant differences in tumor sizes and weights compared with that of CD44 down-regulation or doxorubicin treatment alone. In the combination of CD44 down-regulation and doxorubicin group, the tumor weight was significantly decreased by 4.38-fold compared with that of the control group. CONCLUSION: These results support a new strategy for breast cancer treatment by combining gene therapy with chemotherapy.