RESUMO
<p><b>OBJECTIVE</b>To establish a prediction model of fetal meconium-stained amniotic fluid in re-pregnant women with intrahepatic cholestasis of pregnancy (ICP).</p><p><b>METHODS</b>Clinical data of 180 re-pregnant women with ICP delivering in Women's Hospital, Zhejiang University School of Medicine between January 2009 to August 2014 were collected. An artificial neural network model (ANN) for risk evaluation of fetal meconium-stained fluid was established and assessed.</p><p><b>RESULTS</b>The sensitivity, specificity and accuracy of ANN for predicting fetal meconium-stained fluid were 68.0%, 85.0% and 80.3%, respectively. The risk factors with effect weight >10% were pregnancy complications, serum cholyglycine level,maternal age.</p><p><b>CONCLUSION</b>The established ANN model can be used for predicting fetal meconium-stained amniotic fluid in re-pregnant women with ICP.</p>
Assuntos
Feminino , Humanos , Recém-Nascido , Gravidez , Líquido Amniótico , Química , Colestase Intra-Hepática , Patologia , Feto , Mecônio , Química , Redes Neurais de Computação , Complicações na Gravidez , Patologia , Sensibilidade e EspecificidadeRESUMO
<p><b>OBJECTIVE</b>To investigate the effects of fluoride on Fas expression, caspase-3 and caspase-8 activity and apoptosis in rat incisor cells.</p><p><b>METHODS</b>Forty male SD rats were divided into 4 groups randomly and provided with distilled water containing NaF at the doses of 0, 10, 50 and 100 mg/L respectively. Each group had 10 animals. Five animals were sacrificed at 60 and 90 days respectively. Fas expression was measured with immunohistochemistry, and colorimetric assay was used to examine caspase-3 and caspase-8 activity with enzyme-labelled meter. The apoptosis was detected by flow cytometry in mandibular incisor cells.</p><p><b>RESULTS</b>NaF at the doses of 10, 50 and 100 mg/L for 60 d and 90 d caused Fas overexpression, promoted activity of caspase-3 and caspase-8, increased apoptosis rate in mandibular incisor cells. At 60 days, the value of Fas expression was 0.1819 ± 0.0025 for control, 0.2120 ± 0.0084 for 10 mg/L NaF group, 0.2283 ± 0.0183 for 50 mg/L NaF group, 0.2818 ± 0.0233 for 100 mg/L NaF group. At 90 days, the value of Fas expression was 0.2077 ± 0.0289 for control, 0.2216 ± 0.0105 for 10 mg/L NaF group, 0.2377 ± 0.0059 for 50 mg/L NaF group, 0.2775 ± 0.0088 for 100 mg/L NaF group. Statistics analysis yielded close relationship between the dose of NaF in water and the Fas expression, and also between the dose of NaF in water and caspase-3 activities, and the relative coefficient was 0.9728 (60 d, P < 0.01) and 0.9889 (90 d, P < 0.01) for Fas expression, 0.9533 (60 d, P < 0.01) and 0.9849 (90 d, P < 0.01) for caspase-3 activity respectively. Apoptosis rate and caspase-8 activity also had close relationship with the NaF doses, and the relative coefficient was 0.9733 (90 d, P < 0.01) for apoptosis, 0.9928 (90 d, P < 0.01) for caspase-8. At the doses of 10, 50 and 100 mg/L NaF for 60 d and 90 d, obvious relationship was found between Fas expression and caspase-3 activity, and the relative coefficient was 0.9619 (60 d, P < 0.01) and 0.9912 (90 d, P < 0.01). Obvious relationship between Fas expression and apoptosis, between Fas expression and caspase-8 activity was found in groups for 90 d, and the relative coefficient was 0.9841 (P < 0.01) for apoptosis, 0.9767 (P < 0.01) for caspase-8.</p><p><b>CONCLUSIONS</b>Fluoride could induce Fas overexpression and mediate caspase activation and apoptosis at the doses of 10, 50 and 100 mg/L for 60 d and 90 d in rat mandibular incisor cells.</p>
Assuntos
Animais , Masculino , Ratos , Apoptose , Cariostáticos , Farmacologia , Caspase 3 , Metabolismo , Caspase 8 , Metabolismo , Relação Dose-Resposta a Droga , Incisivo , Biologia Celular , Metabolismo , Distribuição Aleatória , Ratos Sprague-Dawley , Transdução de Sinais , Fluoreto de Sódio , Farmacologia , Receptor fas , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To investigate the effects of sodium selenite on telomerase activity, apoptosis and expression of TERT, c-myc and p53 in rat hepatocytes.</p><p><b>METHODS</b>Selenium at doses of 2.5, 5.0, and 10 micromol/kg was given to SD rats by gavage. In rat hepatocytes, telomerase activity was measured by the telomeric repeat amplification protocol (TRAP), apoptosis was detected by flow cytometry, and expressions of telomerase reverse transcriptase (TERT), c-myc and p53 were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). c-Myc and P53 proteins were detected by immunochemistry.</p><p><b>RESULTS</b>Selenium at doses of 2.5, 5.0, and 10 micromol/kg significantly increased hepatocellular telomerase activity and induced apoptosis in a dose-dependent manner. Although selenium at doses of 2.5, 5.0, and 10 micromol/kg displayed no obvious enhancing effect on the TERT mRNA expression in rat hepatocytes (P > 0.05), it significantly increased the c-myc mRNA and p53 mRNA expression at the dose of 10 micromol/kg (P < 0.05). Selenium at doses of 5.0 and 10 micromol/kg obviously increased the content of P53 protein in rat hepatocytes, but only at the dose of 10 micromol/kg, it significantly promoted the value of c-Myc protein in them.</p><p><b>CONCLUSION</b>Selenium can slightly increase telomerase activity and TERT expression, and significantly induce apoptosis and over-expression of c-myc and p53 at relatively high doses. The beneficial effects of selenium on senescence and aging may be mediated by telomerase activation and expression of TERT, c-myc, and p53 in rat hepatocytes.</p>
Assuntos
Animais , Masculino , Ratos , Apoptose , Regulação da Expressão Gênica , Hepatócitos , Biologia Celular , Proteínas Proto-Oncogênicas c-myc , Genética , Metabolismo , RNA Mensageiro , Genética , Metabolismo , Ratos Sprague-Dawley , Selênio , Farmacologia , Telomerase , Genética , Metabolismo , Proteína Supressora de Tumor p53 , Genética , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To investigate the effects of sodium selenite on telomerase activity and expression of hTERT mRNA in cadmium-transformed 16HBE cells.</p><p><b>METHODS</b>Telomerase activity and expression of genes were measured after cultured cadmium-transformed 16HBE cells were exposed to sodium selenite at different doses (0.625, 1.25, 2.50, 5.00 micromol/L) for 24 hours.</p><p><b>RESULTS</b>Selenium decreased telomerase activity in cadmium-transformed 16HBE cells. There existed an obvious dose-effect relationship between the selenium concentration and these changes. The expression of hTERT and c-myc mRNA also decreased but the expression of mad1 mRNA increased after exposure to selenium for 24 hours. No difference was found in expression of hTRF1 and hTRF2 mRNA after incubated with sodium selenite for 24 hours, compared with control group.</p><p><b>CONCLUSION</b>Selenium inhibits telomerase activity by decreasing hTERT and c-myc mRNA expression and increasing mad1 mRNA expression in cadmium-transformed 16HBE cells and selenium concentration is significantly correlated with these changes.</p>
Assuntos
Humanos , Sequência de Bases , Cádmio , Farmacologia , Linhagem Celular Transformada , Primers do DNA , RNA Mensageiro , Genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Selenito de Sódio , Farmacologia , Telomerase , GenéticaRESUMO
<p><b>OBJECTIVE</b>To study the effects of cadmium on hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.</p><p><b>METHODS</b>Cadmium chloride at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by single cell gel electrophoresis (or comet assay), while expression of proto-oncogenes c-myc, c-fos, and c-jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc, c-Fos, and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry.</p><p><b>RESULTS</b>At the doses of 5, 10, and 20 micromol/kg, cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%, 88.40%, and 93.80%, respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the dose of cadmium chloride (r = 0.9172, P < 0.01). Cadmium chloride at the doses of 5, 10, and 20 micromol/kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun. The positive brown-yellow signal for c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rat livers. Apoptotic rates (%) of cadmium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (17.24 +/- 2.98), (20.58 +/- 1.35), and (24.06 +/- 1.77) respectively, being significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride (r = 0.8619, P < 0.05).</p><p><b>CONCLUSION</b>Cadmium at 5-20 micromol/kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.</p>