Objective To develop a method for determination of mercury in blood by atomic fluorescence spectrometry. Methods Using a thiourea extraction method, the mercury in blood is determined by atomic fluorescence spectrometry. Results The linearity of calibration curve of mercury was in the concentration of 0.000-10.00 ?g/L. The detection limit was 0.06 ?g/L. The recovery rates were 95.5%-100.3%.The RSDs were 4.1%-4.5%. Conclusion The method has the advantages of simple operation, high sensitivity, good repeatability and is applicable to the determination of mercury in blood.

Objective To explore the effect and molecular mechanism of N-myc downstream regulated gene 1 (NDRG1) on transforming growth factor-beta (TGF-β)-induced epithelial-mesenchymal transition (EMT) in human lung cancer cells.Methods Lung cancer A549 cells were transfected with NDRG1 overexpressed vector,and then treated with 5 μg/L TGF-β1.The abilities of invasion were detected by Transwell assay.The expressions of NDRG1 mRNA and protein were analyzed by teal-time reverse transcription polymerase chain reaction (RT-PCR) were examined with Western blot.The expressions of EMT-associated markers E-cadherin and Vimentin,and EMT-associated signaling molecules Snail,AKT and Smad were detected with Western blot.Results We found that TGF-β1 treatment could induce morphological alteration of A549 cells from epithelial morphology to mesenchymal morphology.TGF-β1 significantly increased the migration of A549 cells,and increased the expression of mesenchymal maker vimentin and decreased epithelial marker E-cadherin.More importantly,overexpression of NDRG1 significandy reversed the effects of TGF-β1 on A549 cells.Moreover,NDRG1 significandy decreased the levels of phospho-AKT,and suppressed the expression of EMT-related transcription factor Snail.Conclusions NDRG1 could reverse the effects of TGF-β1 on EMT in A549 cells,by which mechanism is related to reduction of the expressions of phospho-AKT and Snail.

Objective To investigate the correlation between carotid artery intima media thickness (IMT) and cerebrovascular hemodynamic analysis (CVA) and the diagnostic value in ischemic stroke.Methods Using colour Doppler IMT,IMT/D ratio and CVA were performed in 120 patients with hyperacute and acute ischemic stroke as compared with the health controls.Results IMT and IMT/D ratio were higher in patients with ischemic stroke than the health aduts. Vmean and Qmean in ischemic stroke hyperacute group were lower, and R,DR were higher obvious in hyperacute group than that of acute group. IMT and IMT/D ratio were negatively correlation with Vmean and Qmean and positively correlation with R and Zc.Conclusion The measurement of carotid artery IMT and CVA have clinical significance in early diagnosis of ischemic stroke.

Human proximal tubule epithelial cell line,HK-2 cells,were cultured with various concentrations of insulin for 48 h.Human urate transporter (hUAT) mRNA was detected by realtime quantitative PCR.hUAT mRNA levels were down-regulated by insulin (5,25,125,500 μIU/ml)in a dose-dependent manner (relative expression median were 0.95,0.40,0.24,and 0.23).In vitro,the expression of hUAT mRNA in HK-2 cells is associated with the concentration of insulin.

Gallbladder cancer (GBC) is the most common malignancy of the biliary tract.Most patients are diagnosed at the advanced stage,missing the optimal chance for curative surgery,thus leading to the fact that GBC is usually associated with poor prognosis.It is very crucial to strengthen the basic research on GBC,which may further improve the diagnosis and treatment.The research updates on the related genes in the initiation and progression,molecular mechanism of lymphatic metastasis,and tumor microenvironment of GBC in recent years were reviewed in this paper.

Objective To study the changes of insulin-like growth factor-1(IGF-1) in serum of patients with obstructive jaundice.Methods The clinical data of 20 patients with obstructive jaundice were collected and the measurement of serum TNF-?,ALT, ALP, endotoxin and IGF-1 were performed. Results The serum IGF-1 in obstructive jaundice was significantly lower than that in gallbladder stone(P

Objective To explore the role of forkhead box protein O3a (FOXO3a) in inhibiting the proliferation and metastasis of breast cancer cells by downregulation of vascular endothelial growth factorA (VEGF-A).Methods Cell proliferation bioassay and plate clone formation assay were used to compare the changes of proliferation after siRNA interference.Wound healing and Transwell were used to compare the changes of invasion metastasis after interference.Meanwhile,the changes of VEGF-A expression in the cells before and after interference were compared by real time polymerase chain reaction (RT-PCR) and Western blot.Furthermore,the expressions of mRNA FOXO3a and VEGF-A were detected in 20 cases of breast cancer patients in breast cancer tissues and adjacent normal breast tissues.Results The MCF-7 and MDA-MB-231 cells were increased in cell proliferation and invasion after interference.Further studies found that mRNA and protein expression of VEGF-A were up-regulated in MCF-7 and MDA-MB-231cells after interference.In vivo the expression of FOXO3a was lower in 15 cases of cancer compared to normal tissues,and the expression of VEGF-A was high in 15 cases of cancer (75％).FOXO3a and VEGF-A expression was highly negatively correlated.Conclusions This study showed that FOXO3a could inhibit the proliferation and invasion of breast cancer cells,which might be regulated by VEGF-A.It provides an important theoretical evidence for targeted inhibition of breast cancer metastasis.

Objective To analyse the significance and relation between soluble P-selectin (sP-selectin),D-dimer (D-d) and endotoxin (ET) in the patient with obstructive jaundice (OJ). Methods Blood plasma sP-selectin and D-d in OJ group,acute cholecystitis group and healthy group were detected by ELISA and ET was detected by the colorimetric method, Results In healthy group,the concentration of blood plasma sP-selectin was ( 93.43 ? 17.65 ) ng/ml,ET(0.0030?0.0004)EU/ml,and D-d(0.39?0.21)mg/L; in acute cholecystitis group,sP-selectin was (233.32?82.12) ng/ml, ET(0.4012?0.1506) EU/ml,and D-d(0.76?0.27)mg/L; in OJ group,sP-selectin was (351.90?93.83) ng/ml ,ET (0.3814?0.1430)EU/ml,and D-d(2.14?0.37)mg/L.The sP-selectin, D-d and ET in the acute cholecystitis group and the OJ group were higher than those in healthy group (P 0.05). sP-selectin and D-d in the OJ group were significantly higher than that in the acute cholecystitis group (P

[Summary] Type 2 diabetic rat model accompanied by insulin resistance was established by high fat/high glucose diet and streptozotocin.Following metformin treatment for 4 weeks,realtime PCR and Western blot were used to detect the expressions of SIRT3 mRNA and protein in skeletal muscle tissue,respectively.The results showed that insulin sensitivity,superoxide dismutase (SOD),and glutathione (GSH) levels were significantly reduced in diabetic group compared with the control group (P＜0.05),while methane dicarboxylic aldehyde (MDA) level was increased (P＜0.05),along with the decreased expressions of SIRT3 mRNA and protein in skeletal muscles (P＜0.01).After metformin treatment,the insulin sensitivity,SOD,GSH,and SIRT3 mRNA and protein levels were significantly increased (P＜ 0.05 or P＜ 0.01),while MDA level was decreased (P ＜ 0.05),suggesting that metformin may ameliorate insulin resistance via upregulating SIRT3 expression in skeletal muscles of diabetic rats.

Objective To investigate the effect of parecoxib pretreatment on the expression of aquaporin-4 (AQP4) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods One hundred and twenty-eight adult male Sprague-Dawley rats,aged 6-8 weeks,weighing 230-280 g,were randomly divided into 4 groups (n =32 each):sham operation group (S group),I/R group,parecoxib 5 mg/kg group (group P5) and parecoxib 10 mg/kg group (group P10).The rats were anesthetized with 10％ chloral hydrate 3.5 ml/kg.Focal cerebral I/R was induced by 2 h middle cerebral artery occlusion followed by reperfusion.Parecoxib 5 and 10 mg/kg were injected via the right internal jugular vein at 30 min before middle cerebral artery occlusion in groups P5 and P10,respectively.The equal volume of normal saline was injected instead of parecoxib in groups S and I/R.Neurological deficit score (NDS) was assessed at 2 and 24 h of reperfusion.The rats were then sacrificed and brains were removed for determination of infract volume (by TTC staining).Brain water content was measured by wet/dry brain weight ratio.Their brains were cut into sections which were stained with haematoxylin and eosin and examined under microscope.The expression of AQP4 in brain tissues was measured.Results Compared with S group,NDS and brain water content were significandy increased,the infarct volume was enlarged,and the expression of AQP4 in brain tissues was up-regulated in I/R group (P ＜ 0.05 or 0.01).NDS and brain water content were significantly lower,the infarct volume was smaller,and the expression of AQP4 in brain tissues was lower in groups P5 and P10 than in I/R group (P ＜ 0.05 or 0.01).Microscopic examination showed that brain injury was significantly attenuated in groups P5 and P10 as compared with I/R group.Conclusion The mechanism by which parecoxib pretreatment alleviates the focal cerebral I/R injury in rats is related to down-regulation of the expression of AQP4.