Effects of PCBs and PBDEs on thyroid hormone, lymphocyte proliferation, hematology and kidney injury markers in residents of an e-waste dismantling area in Zhejiang, China.

Polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are two typical categories of contaminants released from e-waste dismantling environments. In China, the body burdens of PCBs and PBDEs are associated with abnormal thyroid hormones in populations from e-waste dismantling sites, but the results are limited and contradictory. In this study, we measured the serum levels of PCBs and PBDEs and the thyroid hormone free triiodothyronine (FT3), free thyroxine (FT4) and thyroid-stimulating hormone (TSH) in 40 residents in an e-waste dismantling area and in 15 residents in a control area.

Assessment of dietary intake of polychlorinated dibenzo-p-dioxins and dibenzofurans and dioxin-like polychlorinated biphenyls from the Chinese Total Diet Study in 2011.

The concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) as well as dioxin-like polychlorinated biphenyls (dl-PCBs) were measured in food samples from the fifth Chinese Total Diet Study (TDS) performed in 2011. A total of 152 composite samples from various food groups were analyzed by high resolution gas chromatography-high resolution mass spectrometer (HRGC-HRMS). The dietary intakes of PCDD/Fs and dl-PCBs were subsequently estimated for the adult from various regions in China.

Cyclophilin A/Cluster of Differentiation 147 Interactions Participate in Early Brain Injury After Subarachnoid Hemorrhage in Rats.

Objectives: Cyclophilin A has been found to be involved in many inflammatory diseases via its receptor, cluster of differentiation 147 (CD147). This study was designed to estimate the potential role of cyclophilin A/CD147 in subarachnoid hemorrhage-induced early brain injury.

Design: Controlled in vivo laboratory study.

High density lipoprotein promotes proliferation of adipose-derived stem cells via S1P1 receptor and Akt, ERK1/2 signal pathways.

Introduction: Adipose-derived stem cells (ADSC) are non-hematopoietic mesenchymal stem cells that have shown great promise in their ability to differentiate into multiple cell lineages. Their ubiquitous nature and the ease of harvesting have attracted the attention of many researchers, and they pose as an ideal candidate for applications in regenerative medicine. Several reports have demonstrated that transplanting ADSC can promote repair of injured tissue and angiogenesis in animal models.

Levels of polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) and dioxin-like polychlorinated biphenyls (DL-PCBs) in breast milk in Shanghai, China: A temporal upward trend.

Human milk samples were collected from 150 mothers in 2011 and 2012 in Shanghai, China and analyzed for 17 polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) and 12 dioxin-like polychlorinated biphenyls (DL-PCBs). The up-bound Toxic Equivalent Quantity (TEQ) ranged from 0.27 to 16.

Biological characteristics of a new human glioma cell line transformed into A2B5(+) stem cells.

Objective: The new glioma cell line SHG-139 was established and its phenotype, tumorigenicity, pathological characteristics, derived stem cells SHG139S were studied.

Methods: Immunohistochemistry was used to assess expressions in the patient and mouse tumor tissues, SHG-139 and SHG-139S. Primary SHG-139 culture was performed, cell proliferation, cell cycle and genetic characteristics were assessed.

Oral administration of aflatoxin G₁ induces chronic alveolar inflammation associated with lung tumorigenesis.

Our previous studies showed oral gavage of aflatoxin G₁ (AFG₁) induced lung adenocarcinoma in NIH mice. We recently found that a single intratracheal administration of AFG₁ caused chronic inflammatory changes in rat alveolar septum. Here, we examine whether oral gavage of AFG₁ induces chronic lung inflammation and how it contributes to carcinogenesis.

Pim-1 kinase is a target of miR-486-5p and eukaryotic translation initiation factor 4E, and plays a critical role in lung cancer.

Background: Pim-1 kinase is a proto-oncogene and its dysregulation contributes to tumorigenesis and progression of a variety of malignancies. Pim-1 was suggested as a therapeutic target of cancers. The functional relevance of Pim-1 and the mechanism underlying its dysregulation in lung tumorigenesis remained unclear.

Enhanced phenotypic alterations of alveolar type II cells in response to Aflatoxin G1 -induced lung inflammation.

Recently, we discovered that Aflatoxin G1 (AFG1 ) induces chronic lung inflammatory responses, which may contribute to lung tumorigenesis in Balb/C mice. The cancer cells originate from alveolar type II cells (AT-II cells). The activated AT-II cells express high levels of MHC-II and COX-2, may exhibit altered phenotypes, and likely inhibit antitumor immunity by triggering regulatory T cells (Tregs).

Sterigmatocystin induces G1 arrest in primary human esophageal epithelial cells but induces G2 arrest in immortalized cells: key mechanistic differences in these two models.

Sterigmatocystin (ST), a mycotoxin commonly found in food and feed commodities, has been classified as a "possible human carcinogen." Our previous studies suggested that ST exposure might be a risk factor for esophageal cancer and that ST may induce DNA damage and G2 phase arrest in immortalized human esophageal epithelial cells (Het-1A). To further confirm and explore the cellular responses of ST in human esophageal epithelia, we comparatively evaluated DNA damage, cell cycle distribution and the relative mechanisms in primary cultured human esophageal epithelial cells (EPC), which represent a more representative model of the in vivo state, and Het-1A cells.

Mutations of rat surfactant protein A have distinct effects on its glycosylation, secretion, aggregation and degradation.

Aims: Surfactant protein A (SP-A) plays critical roles in the innate immune system and surfactant homeostasis of the lung. Mutations in SP-A2 of the carbohydrate recognition domain (CRD) impair its glycosylation and are associated with pulmonary fibrosis in humans. We aim to examine how mutations in SP-A that impair its glycosylation affect its biological properties and lead to disease.

Association of PCB, PBDE and PCDD/F body burdens with hormone levels for children in an e-waste dismantling area of Zhejiang Province, China.

Increased electronic waste (e-waste) has raised public concerns regarding exposure to numerous toxic contaminants, particularly polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs). In China, the body burdens of PCBs, PBDEs and PCDD/Fs are associated with thyroid hormones in populations from e-waste dismantling sites; however, it is unclear whether this association occurs in children. In this study, we determined the serum levels of PCBs, PBDEs and PCDD/Fs and the endocrine hormones including free triiodothyronine (FT3), total triiodothyronine (TT3), free thyroxine (FT4), total thyroxine (TT4), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), cortisol and growth hormone (GH) in 21 children from an e-waste dismantling area and 24 children from a control area.

Downregulation of Rad51 participates in OTA-induced DNA double-strand breaks in GES-1 cells in vitro.

Ochratoxin A (OTA), a mycotoxin produced by ubiquitous Aspergilli, is carcinogenic, teratogenic, and nephrotoxic in both humans and animals. Our previous study found that OTA induced DNA double-strand breaks (DSBs) and resulted in G2 phase arrest in human gastric epithelium immortalized (GES-1) cells. DSBs can cause genomic instability, mutations, and neoplastic transformations, and improper repair of DSBs may lead to the development of cancer.

Impairment of cell cycle progression by sterigmatocystin in human pulmonary cells in vitro.

Sterigmatocystin (ST) is a carcinogenic mycotoxin that is commonly found in human food, animal feed and in the indoor environment. Although the correlation between ST exposure and lung cancer has been widely reported in many studies, the cytotoxicity of ST on human pulmonary cells is not yet fully understood. In the current study, we found that ST could induce DNA double-strand breaks in a human immortalized bronchial epithelial cell line (BEAS-2B cells) and a human lung cancer cell line (A549 cells).

Aflatoxin G1-induced oxidative stress causes DNA damage and triggers apoptosis through MAPK signaling pathway in A549 cells.

Our previous studies showed that Aflatoxin G1 (AFG1) could induce lung adenocarcinoma, and that the cancer cells originated from alveolar type II cells (AT-II cells). Recently, we found AFG1 induced structural impairment in rat AT-II cells, which may account for an early event in lung tumorigenesis. However, the mechanism of AFG1-induced AT-II cell damage remains unclear.

Serum pepsinogens and Helicobacter pylori are not associated with esophageal squamous cell carcinoma in a high-risk area in China.

Aims And Background: The role of serum pepsinogen level and Helicobacter pylori infection in esophageal carcinoma remains controversial. It may be a risk or protective factor, or without association with esophageal carcinoma. We prospectively examined associations between serum pepsinogen status, H pylori infection and the risk of esophageal squamous cell carcinoma in the Chinese population.

Comparison of anticancer activity between lactoferrin nanoliposome and lactoferrin in Caco-2 cells in vitro.

The anticancer activities of Lactoferrin (Lf) and Lf nanoliposomes in Caco-2 cells were observed in this study, and mitochondrial function (MTT assay), count kit-8(CCK-8), detection of intracellular reactive oxygen species (ROS) and apoptosis induction (AO/EB staining) assays were used to evaluate the anticancer activity. MTT results demonstrated that Lf nanoliposomes and Lf reduced the mitochondrial activity of cells in a manner of dose and time effect, and the viabilities of Caco-2 cell were significantly decreased in vitro following exposure to Lf nanoliposomes at the concentrations of 5 and 10 mg/mL. LDH leakage and ROS significantly increased in cells exposed to Lf nanoliposomes (≥5 mg/mL), while Lf induced ROS only at higher doses (10mg/mL).

Polybrominated diphenyl ethers (PBDEs) and indicator polychlorinated biphenyls (PCBs) in foods from China: levels, dietary intake, and risk assessment.

A national survey of polybrominated diphenyl ethers (PBDEs) and indicator polychlorinated biphenyls (PCBs) congeners in various foodstuffs from the Chinese total diet study (TDS) performed in 2007 was conducted for the first time. Meats and aquatic foods had the highest average sum PBDEs (192.5 and 190.

Sterigmatocystin-induced DNA damage triggers G2 arrest via an ATM/p53-related pathway in human gastric epithelium GES-1 cells in vitro.

Sterigmatocystin (ST), which is commonly detected in food and feed commodities, is a mutagenic and carcinogenic mycotoxin that has been recognized as a possible human carcinogen. Our previous study showed that ST can induce G2 phase arrest in GES-1 cells in vitro and that the MAPK and PI3K signaling pathways are involved in the ST-induced G2 arrest. It is now widely accepted that DNA damage plays a critical role in the regulation of cell cycle arrest and apoptosis.

[Exposure level and characteristics of dioxins in children living near the waste incineration power plant].

Objective: To study the internal and external dioxins exposure level of children living near the waste incineration power plant.

Methods: Peripheral blood of children (90 in S, 60 in L), soils, crucians, chicken eggs were sampled in town S (1 km away from a big waste incineration power plant), as well as in town L (200 km away from S), which is the control. The contents, distribution characteristics and toxic equivalent (TEQ) of dioxins in samples were evaluated by ultra-trace detection methods.

Oxidative DNA damage is involved in ochratoxin A-induced G2 arrest through ataxia telangiectasia-mutated (ATM) pathways in human gastric epithelium GES-1 cells in vitro.

Ochratoxin A (OTA), one of the most abundant mycotoxin food contaminants, is classified as "possibly carcinogenic to humans." Our previous study showed that OTA could induce a G2 arrest in immortalized human gastric epithelium cells (GES-1). To explore the putative roles of oxidative DNA damage and the ataxia telangiectasia-mutated (ATM) pathways on the OTA-induced G2 arrest, the current study systematically evaluated the roles of reactive oxygen species (ROS) production, DNA damage, and ATM-dependent pathway activation on the OTA-induced G2 phase arrest in GES-1 cells.

Determination of dioxin-like polychlorinated biphenyls in 1 mL whole blood using programmable temperature vaporization large volume injection coupled to gas chromatogram and high-resolution mass spectrometry.

A sensitive method based on programmable temperature vaporization large volume injection coupled to gas chromatogram and high-resolution mass spectrometry (PTV-GC-HRMS) has been developed for the determination of ultra trace levels of dioxin-like polychlorinated biphenyls (DL PCBs) in small amounts of human blood. Blood samples (1mL) were first extracted by column extraction and then purified with column chromatorgraphies. Final extracts (20μL) were introduced to the PTV injector under the solvent vent mode and detected by GC-HRMS (SIM mode).

Role of hMLH1 in sterigmatocystin-induced G₂ phase arrest in human esophageal epithelial Het-1A cells in vitro.

Sterigmatocystin (ST), a common environmental contaminant found across the world, is generally recognized as a potential carcinogen, mutagen and teratogen. Our previous epidemiological studies suggested that ST exposure might be a risk factor for esophageal cancer. However, the direct effects of ST on human esophageal epithelial cells are currently unknown.

Simultaneous determination of 3-monochloropropane-1,2-diol and acrylamide in food by gas chromatography-triple quadrupole mass spectrometry with coupled column separation.

Both 3-monochloropropane-1,2-diol (3-MCPD) and acrylamide are contaminants found in heat-processed foods and their related products. A quantitative method was developed for the simultaneous determination of both contaminants in food by gas chromatography-triple quadrupole mass spectrometry (GC-MS/MS). The analytes were purified and extracted by the matrix solid-phase dispersion extraction (MSPDE) technique with Extrelut NT.

Burn injury triggered dysfunction in dendritic cell response to TLR9 activation and resulted in skewed T cell functions.

Severe trauma such as burn injury is often associated with a systemic inflammatory syndrome characterized by a hyperactive innate immune response and suppressed adaptive immune function. Dendritic cells (DCs), which sense pathogens via their Toll-like receptors (TLRs), play a pivotal role in protecting the host against infections. The effect of burn injury on TLR-mediated DC function is a debated topic and the mechanism controlling the purported immunosuppressive response remains to be elucidated.