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1.
Sci Total Environ ; 408(3): 518-23, 2010 Jan 01.
Article in English | MEDLINE | ID: mdl-19903566

ABSTRACT

Meconium is a matrix that can be obtained easily and noninvasively and is useful for detecting antenatal fetal exposure to environmental toxins. Taiwan is an island with high fish consumption, and many pregnant women would like to enjoy the benefits of fish without jeopardizing their health or that of their child. The aim of this study is to assess the mercury concentration in meconium in relation to the health risk of mercury exposure. A total of 198 mother-infant pairs residing in the city of HsinChu were recruited for the study between January 2007 and June 2007. The average mean concentration of mercury in meconium was 79.2+/-7.3 ng g(-1) dry wt We use the Monte Carlo technique to assess the uncertainty in risk assessment and the impact of these uncertainties on the estimation of expected risk of mercury intake from fish in mothers. Based on the FAO/WHO's tolerable daily intake of methylmercury (0.23 microg kg(-1)d(-1)), we found that 17.3% and 14.0% of the daily mercury exposure estimated exceeded the reference dose for foreign-born and Taiwan-born mothers, respectively. We found that the mercury concentration in meconium was much higher than in other studies, except for one study done in Tagum in the Philippines where mercury is used in gold mining. This may be because Asia is the largest emitter of anthropogenic mercury, accounting for 53% of worldwide emissions. Sensitivity analysis suggests that mercury concentration in fish and the rate of ingesting fish may be the key parameters for governments offering risk management guidance to protect the health of mothers and unborn babies.


Subject(s)
Fishes , Food Contamination/analysis , Food Contamination/statistics & numerical data , Meconium/chemistry , Mercury/analysis , Methylmercury Compounds/analysis , Water Pollutants, Chemical/analysis , Adult , Animals , Female , Health Surveys , Humans , Infant , Infant, Newborn , Male , Mercury/toxicity , Methylmercury Compounds/toxicity , Middle Aged , Monte Carlo Method , Pregnancy , Risk Assessment , Socioeconomic Factors , Surveys and Questionnaires , Taiwan/epidemiology , Time Factors , Water Pollutants, Chemical/toxicity
2.
J Biomed Sci ; 16: 97, 2009 Oct 23.
Article in English | MEDLINE | ID: mdl-19852794

ABSTRACT

To investigate the mechanism how Transforming growth factor-beta(TGF-beta) represses Interleukin-1beta (IL-1beta)-induced Proteinase-Activated Receptor-2 (PAR-2) expression in human primary synovial cells (hPSCs). Human chondrocytes and hPSCs isolated from cartilages and synovium of Osteoarthritis (OA) patients were cultured with 10% fetal bovine serum media or serum free media before treatment with IL-1beta, TGF-beta1, or Connective tissue growth factor (CTGF). The expression of PAR-2 was detected using reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting. Collagen zymography was performed to assess the activity of Matrix metalloproteinases-13 (MMP-13). It was demonstrated that IL-1beta induces PAR-2 expression via p38 pathway in hPSCs. This induction can be repressed by TGF-beta and was observed to persist for at least 48 hrs, suggesting that TGF-beta inhibits PAR-2 expression through multiple pathways. First of all, TGF-beta was able to inhibit PAR-2 activity by inhibiting IL-1beta-induced p38 signal transduction and secondly the inhibition was also indirectly due to MMP-13 inactivation. Finally, TGF-beta was able to induce CTGF, and in turn CTGF represses PAR-2 expression by inhibiting IL-1beta-induced phospho-p38 level. TGF-beta could prevent OA from progression with the anabolic ability to induce CTGF production to maintain extracellular matrix (ECM) integrity and to down regulate PAR-2 expression, and the anti-catabolic ability to induce Tissue inhibitors of metalloproteinase-3 (TIMP-3) production to inhibit MMPs leading to avoid PAR-2 over-expression. Because IL-1beta-induced PAR-2 expressed in hPSCs might play a significantly important role in early phase of OA, PAR-2 repression by exogenous TGF-beta or other agents might be an ideal therapeutic target to prevent OA from progression.


Subject(s)
Gene Expression Regulation, Enzymologic , Interleukin-1beta/metabolism , Receptor, PAR-2/biosynthesis , Synovial Membrane/enzymology , Transforming Growth Factor beta/metabolism , Collagen/chemistry , Connective Tissue Growth Factor/metabolism , Culture Media, Serum-Free , Disease Progression , Extracellular Matrix/metabolism , Gene Expression Profiling , Humans , Osteoarthritis/drug therapy , Signal Transduction , p38 Mitogen-Activated Protein Kinases/metabolism
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