ObjectiveTo evaluate the influence of an extract ofGenista tinctoria L. herba (GT) or methylparaben (MP) on histopathological changes and2 biomarkers of oxidative stress in rats subchronicly exposed to bisphenol A (BPA).
MethodsAdult female Wistar rats were orally exposed for 90 d to BPA (50 mg/kg), BPA+GT (35 mg isoflavones/kg) or BPA+MP (250 mg/kg). Plasma and tissue samples weretaken from liver, kidney, thyroid, uterus, ovary, and mammary gland after 30, 60, and 90 d of exposure respectively. Lipid peroxidation andin vivo hydroxyl radical production were evaluated byhistological analysis along withmalondialdehyde and 2,3-dihydroxybenzoic aciddetection.
ResultsTheseverity of histopathological changes in liver and kidneyswas lower afterGT treatmentthan afterBPA or BPA+MPtreatment. A minimal thyroid receptor antagonist effect was only observedafter BPA+MPtreatment.Theabnormal folliculogenesis increased in a time-dependent manner,and the number of corpus luteum decreased.No significant histological alterationswere foundin the uterus.The mammary gland displayed specific estrogen stimulation changes at all periods. Both MP and GT revealed antioxidant properties reducing lipid peroxidation and BPA-inducedhydroxyl radical generation.
ConclusionGTL. extract ameliorates the toxic effects of BPA andisprovedto haveantioxidant potential and antitoxic effect. MP has antioxidant properties, but has either no effect or exacerbates the BPA-induced histopathological changes.

ObjectiveTo investigate the bioeffects of extremely low frequency (ELF) magnetic field (MF) (50 Hz, 400μT) and magnetic nanoparticles (MNPs) via cytotoxicity and apoptosis assays on PC12 cells.
MethodsMNPs modified by SiO2 (MNP-SiO2) were characterized by transmission electron microscopy (TEM), dynamic light scattering and hysteresis loop measurement.PC12 cells were administrated with MNP-SiO2 with or without MF exposure for 48 h. Cytotoxicity and apoptosis were evaluated with MTT assay and annexin V-FITC/PI staining, respectively. The morphology and uptake of MNP-SiO2 were determined by TEM. MF simulation was performed by Ansoft Maxwell based on the finite element method.
ResultsMNP-SiO2 were identified as~20nm (diameter) ferromagnetic particles. MNP-SiO2reduced cell viability in a dose-dependent manner. MF also reduced cell viability with increasing concentrations of MNP-SiO2. MNP-SiO2 alone did not cause apoptosis in PC12 cells; instead, the proportion of apoptotic cells increased significantly under MF exposure and increasing doses of MNP-SiO2. MNP-SiO2 could be ingested andthen cause a slight change in cellmorphology.
ConclusionCombined exposure of MF and MNP-SiO2 resulted in remarkable cytotoxicity and increased apoptosis in PC12 cells. The results suggested that MF exposure couldstrengthen the MF of MNPs, which may enhance the bioeffects of ELF MF.

ObjectiveTo study the relationship between dyslipidemia and outcome in patients with acute ischemic stroke.
MethodsData about 1 568 patients with acute ischemic stroke werecollected from 4 hospitals in Shandong Province from January 2006 to December 2008. National Institute of Health Stroke Scale (NIHSS) >10 at discharge or death was defined as the outcome. Effect of dyslipidemia on outcome in patients with acute ischemic stroke was analyzed by multivariate logistic regression analysis and propensity score-adjusted analysis, respectively.
ResultsThe serum levels of TC, LDL-C, and HDL-C were significantly associated with the outcome in patients with acute ischemic stroke. Multivariate logistic regression analysis and propensity score-adjusted analysis showed that the ORs and 95% CIs were 3.013 (1.259, 7.214)/2.655 (1.298, 5.43), 3.157(1.306, 7.631)/3.405(1.621, 7.154), and 0.482 (0.245, 0.946)/0.51 (0.282, 0.921), respectively, for patients with acute ischemic stroke. Hosmer-Lemeshow goodness-of-fit test showed no significant difference in observed and predicted risk in patients with acute ischemic stroke (chi-square=8.235, P=0.411).
ConclusionSerum levels of TC, LDL-C, and HDL-C are positively related with the outcome in patients with acute ischemic stroke.

ObjectiveToexplore the role of HIV-1 tat gene variations in AIDSdementia complex(ADC) pathogenesis.
MethodsHIV-1tat genes derived from peripheral spleen and central basal ganglia of anAIDSpatient with ADC and anAIDSpatientwithoutADC were cloned for sequence analysis. HIV-1 tat genesequence alignmentwasperformed by using CLUSTAL W andthephylogentic analysiswas conductedbyusing Neighbor-joining with MEGA4 software.All tat genes wereused to construct recombinant retroviral expressing vector MSCV-IRES-GFP/tat. The MSCV-IRES-GFP/tat was cotransfected into 293T cells with pCMV-VSV-G and pUMVC vectorsto assemble the recombinant retrovirus. After infection of gliomas U87 cells with equal amount of the recombinant retrovirus, TNF-α, and IL-1β concentrations inthe supernatant of U87 cells were determined with ELISA.
ResultsHIV-1tat genes derived from peripheral spleen and central basal ganglia ofthe AIDS patient with ADC andtheother onewithoutADCexhibited genetic variations.Tat variations and amino acid mutation sites existed mainly at Tat protein core functional area (38-47aa). All Tat proteinscould induce U87 cells to produce TNF-α and IL-1β, but thelevel of IL-1β production was different among Tatproteins derived fromtheADC patient’s spleen, basal ganglia, andthenon-ADC patient’s spleen.The level ofTat proteinsderived fromtheADC patient’s spleen,basal ganglia, andthenon-ADC patient’sspleen were obviously higher thanthat fromthe non-ADC patient’s basal ganglia.
ConclusionTat protein core functional area (38-47aa) mayserve as the key area of enhancing the secretion of IL-1β.This may be related with the neurotoxicity of HIV-1 Tat.
ObjectiveToexplore the role of HIV-1 tat gene variations in AIDSdementia complex(ADC) pathogenesis.
MethodsHIV-1tat genes derived from peripheral spleen and central basal ganglia of anAIDSpatient with ADC and anAIDSpatientwithoutADC were cloned for sequence analysis. HIV-1 tat genesequence alignmentwasperformed by using CLUSTAL W andthephylogentic analysiswas conductedbyusing Neighbor-joining with MEGA4 software.All tat genes wereused to construct recombinant retroviral expressing vector MSCV-IRES-GFP/tat. The MSCV-IRES-GFP/tat was cotransfected into 293T cells with pCMV-VSV-G and pUMVC vectorsto assemble the recombinant retrovirus. After infection of gliomas U87 cells with equal amount of the recombinant retrovirus, TNF-α, and IL-1β concentrations inthe supernatant of U87 cells were determined with ELISA.
ResultsHIV-1tat genes derived from peripheral spleen and central basal ganglia ofthe AIDS patient with ADC andtheother onewithoutADCexhibited genetic variations.Tat variations and amino acid mutation sites existed mainly at Tat protein core functional area (38-47aa). All Tat proteinscould induce U87 cells to produce TNF-α and IL-1β, but thelevel of IL-1β production was different among Tatproteins derived fromtheADC patient’s spleen, basal ganglia, andthenon-ADC patient’s spleen.The level ofTat proteinsderived fromtheADC patient’s spleen,basal ganglia, andthenon-ADC patient’sspleen were obviously higher thanthat fromthe non-ADC patient’s basal ganglia.
ConclusionTat protein core functional area (38-47aa) mayserve as the key area of enhancing the secretion of IL-1β.This may be related with the neurotoxicity of HIV-1 Tat.

ObjectiveTo explore the effects of exposure to aluminum(Al) on long-term potentiation(LTP) and AMPA receptor subunits in rats in vivo.
MethodsDifferent dosages of aluminum-maltolate complex[Al(mal)3] were given to rats via acute intracerebroventricular (i.c.v.)injection and subchronic intraperitoneal (i.p.) injection. Following Al exposure, the hippocampal LTP were recorded by field potentiation techniquein vivo and the expression of AMPAR subunit proteins (GluR1 and GluR2) in both total and membrane-enriched extracts from the CA1 area of rat hippocampus were detected by Western blot assay.
ResultsAcute Al treatment produced dose-dependent suppression of LTP in the rat hippocampus and dose-dependent decreases of GluR1and GluR2in membrane extracts; however, no similar changes were found in the total cell extracts, which suggests decreased trafficking of AMPA receptor subunits from intracellular pools to synaptic sites in the hippocampus. Thedose-dependent suppressive effects on LTP and the expression of AMPA receptor subunits both in the membrane and in total extracts were found after subchronic Al treatment, indicating a decrease in AMPA receptor subunit trafficking from intracellular poolsto synaptic sites and an additional reduction in the expression of the subunits.
ConclusionAl(mal)3obviously and dose-dependently suppressed LTP in the rat hippocampal CA1 region in vivo, and this suppression may be related to both trafficking and decreases in the expression of AMPA receptor subunit proteins. However, the mechanisms underlying these observations need further investigation.