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Query: UMLS:C0016632 (Fox)
1,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Samples of sediment and biota were collected from sites in the lower Fox River and southern Green Bay to determine existing or potential impacts of sediment-associated contaminants on different ecosystem components of this Great Lakes area of concern. Evaluation of benthos revealed a relatively depauperate community, particularly at the lower Fox River sites. Sediment pore water and bulk sediments from several lower Fox River sites were toxic to a number of test species including Pimephales promelas, Ceriodaphnia dubia, Hexagenia limbata, Selenastrum capricornutum, and Photobacterium phosphorum. An important component of the observed toxicity appeared to be due to ammonia. Evaluation of three bullhead (Ictalurus) species from the lower Fox River revealed an absence of preneoplastic or neoplastic liver lesions, and the Salmonella typhimurium bioassay indicated relatively little mutagenicity in sediment extracts. Apparent adverse reproductive effects were noted in two species of birds nesting along the lower Fox River and on a confined disposal facility for sediments near the mouth of the river, and there were measurable concentrations of potentially toxic 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), and planar polychlorinated biphenyls (PCBs) both in the birds and in sediments from several of the study sites. Based on toxic equivalency factors and the results of an in vitro bioassay with H4IIE rat hepatoma cells, it appeared that the majority of potential toxicity of the PCB/PCDF/PCDD mixture in biota from the lower Fox River/Green Bay system was due to the planar PCBs. The results of these studies are discussed in terms of an integrated assessment focused on providing data for remedial action planning.
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PMID:Integrated assessment of contaminated sediments in the lower Fox River and Green Bay, Wisconsin. 137 48

The endoplasmatic glucose-6-phosphate transporter is involved in the control of hepatic glucose production and blood glucose homeostasis. In this study, the expression of a luciferase reporter gene under the control of the glucose-6-phosphate transporter gene promoter was examined in transiently transfected hepatoma cells. The promoter activity was stimulated approximately 2.5-fold by dexamethasone. Mutational analyses demonstrated that the regions nucleotide (nt) -215/-209 and nt -197/-183 relative to the translation start site were critical for this regulation. In gel electrophoretic mobility shift assays the transcription factor Fox O1, also called forkhead in rhabdomyosarcoma (FKHR), overexpressed in 293 cells, bound to a probe with the sequence nt -215/-209. The overexpression of Fox O1 stimulated the induction of glucose-6-phosphate transporter promoter activity by dexamethasone via nt -215/-209 in hepatoma cells. Recombinant glucocorticoid receptor DNA binding domain protein bound to a probe with the sequence of nt -197/-183 in gel electrophoretic mobility shift assays and an oligonucleotide with this sequence transferred glucocorticoid responsiveness to a heterologous promoter. The data indicate that the glucose-6-phosphate transporter promoter contains a glucocorticoid response unit consisting of binding sites for Fox O1 and the glucocorticoid receptor.
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PMID:Characterization of cis-elements mediating the stimulation of glucose-6-phosphate transporter promoter activity by glucocorticoids. 1459 89

Forkhead box M1 (FOXM1), a member of the Fox transcription factors family, was closely related with cell cycle. FOXM1 played an important role in MST and prompted a poor prognosis for MST patients. However, there were also some studies revealing no significant association between the FOXM1 expression and prognosis of patients. Therefore, we conducted meta-analysis to investigate whether the expression of FOXM1 was associated with MST prognosis. We collected 36 relevant studies through PubMed database and obtained research data of 4946 patients. Stata 12.0 was used to express the results as hazard ratio (HR) for time-to-event outcomes with 95% confidence intervals (95% CI). It was shown that overexpression of FOXM1 was relevant to worse survival of MST patients (HR = 1.99, 95% CI = 1.79-2.21, P < 0.001; I(2) = 26.4%, P h = 0.076). Subgroup analysis suggested that overexpression of FOXM1 in breast cancer (BC), gastric cancer (GC), hepatocellular carcinoma (HCC), pancreatic ductal adenocarcinoma (PDA), and non-small-cell lung cancer (NSCLC) all predicted a worse survival (P < 0.05), in addition to ovarian cancer (OC) (P = 0.084). In conclusion, our research indicated that overexpression of FOXM1 was to the disadvantage of the prognosis for majority of MST and therefore can be used as an evaluation index of prognosis.
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PMID:Prognostic Value of FOXM1 in Patients with Malignant Solid Tumor: A Meta-Analysis and System Review. 2645 Oct 68