A cross-sectional survey was conducted to determine seroprevalence and correlates of coinfections of hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Bar virus (EBV), herpes simplex virus including type 1 (HSV-1) and type 2 (HSV-2) among human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) patients in China. A total of 1,110 HIV/AIDS patients from Shanxi (Central area, n = 287), Zhejiang (Eastern area, n = 163), Yunnan (Southwestern area, n = 300) and Xinjiang (Northwestern area, n = 360) provinces were analyzed. The overall seroprevalence was 6.3% for HBsAg, 59.0% for anti-HCV IgG, 96.6% for anti-EBV IgG, 91.5% for anti-HSV-1 IgG, and 34.1% for anti-HSV-2 IgG. Eleven (1.0%) HIV/AIDS patients were coinfected with all five viruses, 177 (15.9%) with four viruses, 611 (55.0%) with three viruses, 288 (25.9%) with two viruses, 23 (2.1%) with single virus, and 1 (0.1%) with none of the five viruses. Multiple logistic regression analyses indicated that neither HBV, nor EBV and HSV-1 coinfection was associated with sociodemographic characteristics and HIV transmission mode, but HCV coinfection was associated with geographic region, age, gender, ethnicity, marital status, and HIV transmission mode, whereas HSV-2 coinfection was associated with geographic region, ethnicity and HIV transmission mode. This study suggests that HIV/AIDS patients with different regional and sociodemographic backgrounds and HIV transmission mode in China have different profiles of viral coinfections and should be subject to differential considerations in related health care programs.

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Stromal-epithelial interactions play a critical role in promoting tumorigenesis and invasion. To obtain detailed information on cancer cell behaviors on the stroma and kinetics of cell migration, which cannot be observed by conventionally-used Boyden chamber assays, this study was aimed at analyzing the cell invasion process in vitro using time-lapse microscopic observation. Serum-free conditions and reconstituted type I collagen gels which provided a basal membrane-stroma-like microenvironment were used to first establish a basal condition. Time-lapse microscopic observation for 30 h of cell invasion into the collagen gel revealed kinetic parameters and individualistic behavior of cancer cells. Of breast cancer MDA-MB-231 or MCF-7 cells and colon cancer LS180 or HT29 cells examined, MDA-MB-231 cells most rapidly disappeared from the collagen gel surface under basal conditions. Estrogen-dependent MCF-7 cells disappeared at a rate approximately two times slower than that of MDA-MB-231 cells under serum- and phenol red-free conditions. By the addition of 10 nM β-estradiol to the basal medium, MCF-7 cell invasion was facilitated to a rate similar to that of MDA-MB-231 cells. Microscopic analyses of collagen gel-sections demonstrated that most of the MDA-MB-231 and MCF-7 cells remained within 60 μm from the gel top under basal conditions, which is consistent with the observation obtained using Boyden chambers that no cells could cross the collagen I gel barrier unless 1% fetal calf serum was added to basal conditions. In summary, this study demonstrated future applicability of this method to understand the initial phase of cancer cell invasion processes.

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Histone deacetylase (HDAC) 8 is a zinc ion dependent enzyme involved in removing the acetyl group from the core histones and other proteins which belong to Class I HDACs. It was reported that nitric oxide (NO) is a key regulator of HDAC function and S-nitrosylation of HDAC2 induces chromatin remodelling in neurons. This work reports the successful recombinant expression of human HDAC8 in Escherichia coli with two plasmids and the purification and S-nitrosylation in vitro. It was found that HDAC8 can be S-nitrosylated by the NO donor S-nitrosoglutathione (GSNO) in vitro, and the activity of HDAC8 was significantly inhibited when incubated with GSNO and S-nitrosocysteine in a time- and dosage-dependent manner, but sodium nitroprusside (SNP), and dithiothreitol cannot reverse this inhibition. These observations support and extend the concept that NO may regulate HDAC8 function by S-nitrosylation.

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Ultraviolet A (UVA, 320-400 nm) radiation is an oxidizing agent that causes significant damage to cellular components and that leads to photoaging and cancer. It strongly induces NF-E2-related factor 2 (Nrf2) expressions in cultured FEK4 human skin fibroblasts but weakly induces it in transformed HaCaT skin keratinocytes. Nrf2 silencing increases cell damage at a moderate dose of UVA irradiation (250 kJ•m⁻²) in FEK4 fibroblasts, but whether a decrease in Nrf2 sensitizes HaCaT keratinocytes to a moderate to high dose (250-500 kJ•m⁻²) of UVA irradiation (i.e., 400 kJ•m⁻², peak emission 365 nm) is currently unknown. A moderate to high dose of UVA irradiation only slightly increased Nrf2 expression in HaCaT skin keratinocytes. Knockdown of Nrf2 by specific silencing of Nrf2 (siNrf2) strongly increased cell damage as gauged by membrane damage (LDH) and cell viability (MTT assay) following this dose of UVA irradiation. These results suggest that decreased Nrf2 significantly increased UVA irradiation-induced cell damage in skin keratinocytes. Nrf2 may play a role in protecting human skin keratinocytes from UVA radiation-induced damage.

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Oxidative stress takes place due to an imbalance between the production of reactive oxygen species (ROS) and the protection provided by cellular antioxidants. High levels of ROS are caused by tumor cells during tumor progression and may affect the functions of other important organs. The present study sought to investigate whether non-primary brain tumors affect reduced glutathione (GSH) levels and the activity of related enzymes in the brain. GSH contents, the activity of glutathione peroxidase (GPx), glutathione-s-transferase (GST), glutathione reductase (GR) as well as glutamate cysteine ligase (GCL) were determined in the brains of normal and tumor-bearing mice treated with the chemotherapy drug 5-Fluorouracil (5-Fu) or not. The results in S180 and H22 tumor-bearing mice showed that GSH levels and the activity of GPx, GST, and GCL all decreased while GR activity markedly increased in the brains of tumor-bearing mice compared to those of normal mice. Further investigation found that 5-Fu, a typical chemotherapy drug, significantly inhibited tumor growth but did not improve the loss of redox homeostasis in the brain caused by non-primary brain tumors. Overall, these results suggest that non-primary brain tumors can induce an ROS burden in the brain that cannot be reversed by the chemotherapy drug 5-Fu.

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Concern about environmental lead exposure as a significant public health threat has increased as evidence has accumulated regarding adverse health effects at successively lower levels. Aplastic anemia is a hematological disorder of unknown etiology with a high lethality rate. Lead is a known toxicant for the hematopoietic system. Oxidative stress appears to be the possible mode of lead toxicity. We evaluated the effects of blood lead level on oxidative stress parameters in children suffering from aplastic anemia disease. Seventeen children with aplastic anemia disease (15 male and 2 female, age 3-12 y) were recruited in the study group. Fifty one healthy children (45 male and 6 female, age 3-12 y) having normal blood profiles and not suffering from any chronic disease(s) were used as controls. Blood lead level and oxidative stress parameters were determined. Mean blood lead level was significantly higher while δ-aminolevulinic acid dehydratase (δ-ALAD) activity, a biomarker for lead exposure was significantly lower in the study group as compared to the control group (p < 0.05 for each). Thiobarbituric acid reactive species (TBARS), a marker of lipid peroxidation, was significantly higher while the antioxidant glutathione (GSH) level was significantly lower in the study group as compared to the control group (p < 0.05 for each). Activity of the antioxidant enzyme catalase (CAT) was significantly higher in the study group than in the control group (p < 0.05). There was a significant negative correlation of blood lead levels with δ-ALAD (r = −0.45; p < 0.05) and GSH (r = −0.32; p < 0.05), and a positive correlation with TBARS (r = 0.41; p < 0.05) and CAT (r = 0.37; p < 0.05). Although a causal pathway cannot be determined from this study, our results indicated that lead induces oxidative stress in children suffering from aplastic anemia. Lead-induced oxidative stress as an underlying mechanism for aplastic anemia warrants further research.

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Dengue is an acute febrile illness resulting from infection by a flavivirus transmitted by the Aedes mosquito. It is characterized by bleeding manifestations and a plasma leak syndrome. Hepatic involvement in the form of elevation in transaminases is common. However, acute hepatic failure is uncommon. It is not known how the presence of an underlying chronic hepatitis or liver disease affects the likelihood of severity of hepatitis from dengue. The present report is of a 33-year-old man, a carrier of hepatitis B virus, who presented with fever, altered sensorium, thrombocytopenia, and coagulopathy. He was diagnosed to have developed acute hepatic failure due to dengue. The patient improved with supportive measures.

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