Objective To understand the expression change of SFRP2 in human cervical cancer tissue and to investigate the effect of SFRP2 on cervical cancer cell proliferation.Methods The expression of SFRP2 in cervical cancer tissue was detected by using Western blot and qRT-PCR;the SFRP overexpressed human cervical cancer line was constructed by using lentivirus,the effect of SFRP2 on the proliferation of human cervical cancer cell line was analyzed by CCK-8 and plate cloning.The effect of SFRP2 on the expression of WNT pathway related proteins and genes in human cervical cancer cell was detected by Western Bolt and qRTPCR.Results Compared with paracancerous tissue,SFRP2 was lowly expressed in human cervical cancer tissue;overexpressed SFRP2 cervical cancer cell proliferation was inhibited;SFRP2 inhibiting cellular proliferation was occurred via WNT signal pathway.Conclusion The role of SFRP2 as a candidate gene for cervical cancer remains to be deeply studied.

Objective To observe the expression and localization of D J-1 in renal fibrosis, and to investigate the expressions of E-cadherin, vimentin and the level of β-catenin tyrosine phosphorylation in human tubular epithelial cells. Methods In vitro, the human tubular epithehal cells (HKC cell line) were cultured with 10 μg/L TGF-β1 for 72 h. The protein expressions of E-cadherin, vimentin and DJ-1 were measured by Western blot. RT-PCR was used to detect the expression of D J-1 mRNA. The intracellular distribution of DJ-1 was observed by confocal microscope. In vivo, Masson stain was used to evaluate the level of renal fibrosis. The expression and disposition of DJ-1 in renal tissue were detected by immunohistochemistry. HKC cells were transfected with pEGFP-N1-DJ-1 via lipofectamine 2000. The efficiency of transfection was detected by fluorescence microscope. The expressions of DJ-1, E-cadherin, vimentin and β-catenin tyrosine phosphorylation level in the transfected cells were detected by Western blot. Results The expressions of DJ-1 protein and DJ-1 mRNA were up-regulated in renal tubular EMT cells. Most of DJ-1 protein localized in cytoplasm, and some was in nucleus. After stimulation by TGF-β1, the expressions of DJ-1 protein both in cytoplasm and nucleus was greatly increased, especially in nucleus. In vivo, renal tissue expressed DJ-1 in tubular epithelia, but little expression in glomeruli. In renal tissue from 5/6-nephrectomized rots, DJ-1 expression was greatly increased. In the DJ-1 transfectants, the expressions of DJ-1, vimentin and β-catenin tyrosine phosphorylation level were up-regulated, but E-cadherin expression was suppressed. Conclusion The increased expression of DJ-1 may promote renal fibrosis.

AIM To study the protective and antiperoxidative effects of baicalin on myocardial ischemia. METHODS The rat anterior decenging branch of left coronary artery was occluded for 40 min and reperfusion for 120 min. Hemodynamics (LVP, LV d p /d t ) and electrocardiogram (ECG, lead Ⅱ) monitored continuously with polygraph,then the myocardium were taken to assay lactate dehydrogenase(LDH), malondialdehyde (MDA) contents and superoxide dismatase (SOD). RESULTS Baicalin 10 or 40 mg?kg -1 iv depressed changes in LDH, MDA and SOD in myocardium after ischemia for 40 min and reperfusion for 120 min in rats. Baicalin 10 and 40 mg?kg -1 iv markedly improved the ?d p /d t max (kPa?s -1 ), LVSP in rat after ischemia for 40 min and reperfusion. CONCLUSION Baicalin possesses a protective effect against myocardial ischemia via attenuating lipid peroxidation.

A novel electrogenerated chemiluminescence (ECL) sensor for the determination of metoclopramide was developed by employing ruthenium complex as an ECL signal producer and an ordered mesoporous carbon (OMC) material as modified material. The ECL sensor was fabricated by adsorption ruthenium complex into a mixture of OMC and Nafion, which showed good electrochemical and ECL behaviors. It was found that the ECL intensity of the sensor fabricated was greatly enhanced in the presence of metoclopramide. Based on this finding, a highly sensitive and reproducible ECL method was developed for the determination of metoclopramide. The result showed that the ECL intensity was linear with the concentration of metoclopramide in the range from 1.0×10-10 to 5.0×10-7M and the detection limit was 3×10-11M. The ECL sensor exhibited a long-term stability and a fine reproducibility with relative standard deviation of 1.0 % for 1.0×10-10M metoclopramide in 18 continuous determinations. The developed method has been applied to the determination of metoclopramide in tablet samples with satisfactory results.

Purpose To investigate the diagnostic utility of the immunohistochemical markers SALL4, D2-40 and Glypican-3 in prima-ry testicular germ cell tumors (TGCTs). Methods The expression of SALL4, D2-40 and Glypican-3 protein was detected by EnVi-sion immunohistochemical method in 56 cases of primary testicular germ cell tumors, including 5 intratubular germ cell neoplasms ( IT-GCNs) , 10 seminomas, 14 embryonal carcinomas ( ECs) , 14 yolk sac tumors ( YSTs) , 1 choriocarcinoma, 5 immature teratomas and 12 mature teratomas. 10 normal testicular tissues and 5 lymphomas were selected as control. Results All of ITGCNs, seminomas, YSTs and ECs were diffusely strongly positive for SALL4. Focal SALL4 staining was seen in choriocarcinoma, 3 of 5 immature terato-mas and 3 of 12 mature teratomas. All of ITGCNs, seminomas showed diffusely strong D2-40 staining. ECs (4/14) were focally posi-tive for D2-40, while choriocarcinoma, YSTs and teratomas were negative for D2-40. Glypican-3 was diffusely positive in YSTs (13/14), and focally weakly positive in ECs (2/14), respectively. ITGCNs, seminomas, choriocarcinoma and teratoma were negative for Glypican-3. In contrast, 10 normal testicular tissues and 5 lymphomas showed no SALL4, D2-40 and Glypican-3 staining. Conclu-sions SALL4 is a useful diagnostic marker with high sensitivity and specificity for TGCTs. Combination of SALL4, D2-40 and Glypi-can-3 is helpful to the diagnosis and differential diagnosis for TGCTs.

Objective To investigate the inhibitory effects of overexpression of PTEN on renal epithelial-mesenchymal trans-differentiation induced by TGF-β1,and the signaling transduction mechanism.Methods HKC cells were transfected with GFP-PTEN via lipofectAMINE2000.The efficiency of transfection was detected by fluorescence microscope.The expression of PTEN protein and mRNA in the translected cells was detected by Western blot and RT-PCR respectively.The experiment was divided into four groups:normal group,TGF-β1 stimulation group,GFP-PTEN+TGF-β1 group and empty vector+TGF-β1 group.The expression of E-cadherin,a-SMA,Akt and p-Akt was detected by Western blot.Results Most ceils transfected with GFP-PTEN expressed GFP.The expression of PTEN protein and mRNA was strongly increased when HKC cells were transfected with GFP-PTEN(all P<0.05).In both TGF-β1 stimulation group and empty vector+TGF-β1 group,the expression level of E-cadherin was lower(all P<0.05),while that of p-Akt and a-SMA was higher than in normal group(both P<0.05).The expression level of p-Akt and a-SMA in GFP-PTEN+TGF-β1 group was Iower(both P<0.05),while that of E-cadherin was higher than in TGF-β1 stimulation group and empty vector+TGF-β1 group(both P<0.05).The expression of Akt was similar in the four groups.Conclusion Overexpression of PTEN can inhibit renal epithelial-mesenehymal trans-differentiation induced by TGF-β1 through suppressing the activation of PI3K/Akt signal pathway.

Objective To investigate the effectiveness of disodium Aidi injection for cancer-related fatigue in nasopharyngeal carcinoma patients of Ⅲ-Ⅳ B stage undergoing radiotherapy and chemotherapy.Methods Eighty nasopharyngeal carcinoma patients of Ⅲ-Ⅳ B stage with fatigue symptoms from December 2011 to May 2012 in our hospital were divided into two groups.All patients received treatment of sequential 3 cycles with platinum-based chemotherapy after concurrent chemoradiation.One group of 40 patients also received intravenous infusion of disodium Aidi injection (experimental group),the other group of 40 patients only received conventional therapy (control group).Brief fatigue inventory (BFI) questionnaires data were collected at baseline,the eighth week and the twentieth week after treatment.The changes of fatigue severity and the occurrence of Ⅲ-Ⅳ degree adverse reactions in the two groups were compared.Results At the eighth week,the improvement in fatigue severity was not significantly different between two groups (x2 =1.758,P =0.32).However,significant improvement in cancer-related fatigue of experimental group was found than that of control group at the twentieth week(x2 =8.12,P =0.005).The Ⅲ-Ⅳ degree adverse reactions of experimental group were significantly lower than that of control group.Conclusion Disodium Aidi injection combined with radiotherapy and chemotherapy can improve the cancer-related fatigue of nasopharyngeal carcinoma patients of Ⅲ-ⅣB stage and it can also reduce the incidence rate of Ⅲ-Ⅳ degree adverse reactions.

Objective To study the changes of hearing function and cochlear morphology on diffuse brain in-jury model in rat .Methods One hundred and fifty SD rats with normal hearing were randomly divided into five groups ,each group consisted of 30 SD rats ,including a control group and four experimental groups which endured diffuse brain injury(DBI) from one to four weeks .Diffuse brain injury model of rats were established ,then ABR , 40 Hz AERP and ASSR examination ,light microscopy ,electron microscopy were used to evaluate the change of hearing function and morphology .Results The difference of ABR ,40 Hz AERP and ASSR thresholds between the experimental and the normal control group were significant (P<0 .05) .The thresholds of ABR ,40HzAERP and AS-SR were increased in the first week of DBI ,then the threshold continuously increased in the second and third week , at last the threshold decreased in the fourth week .The results under scaning electron microscope demonstrated that the ciliums of the majority of outer hair cells lodged in the first week of DBI .The results under transmission electron microscope showed that in the first week of DBI ,there were edema and denuration of mitochondrial ,mitochondrial cristaes were obscured or disappeared .The changes were deteriorate in the second and third week ,whereas the changes were mitigatal in the fourth week .Conclusion Cochlear morphology and hearing damage were observed in diffuse brain injury model of rats .

Objective To explore the effects of Zinc Protoporphyrin and Heme on the expression of HO-1 in cochlear and the change of auditory brainstem response on diffuse traumatic brain injury model of rats.Methods Diffuse traumatic brain injury model of rats were established and randomly divided into thirteen groups.Then auditory brainstem response examination,light microscope,immunohistochemistry technique were used to evaluate the change of auditory brainstem response and the expression of HO-1 in cochlear.Results The differences of auditory brainstem response threshold and latency of wave between the experimental and the normal control group were obvious(P＜0.05).The expression of HO-1 in the control group was normal,whereas there were obvious changes of inner ear HO-1 expression in the traumatic groups.The grey value of HO-1 expression in trauma group,Znpp group and heme group was significantly associated with auditory function change(P＜0.05).Conclusion There were influence of Zinc Protoporphyrin and Hemeon the inner ear HO-1 expression and the change of auditory brainstem response with diffuse traumatic brain injury model of rats.The protective effect of heme on auditory function may be associated with the increased expression of HO-1.

Recently, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is suggested as a new agent in the fighting against fibrogenesis. In tumor, DJ-1 is identified as a negative regulator of PTEN. But the expression of DJ-1 and the regulation of PTEN in fibrosis are unclear. Renal fibrosis was induced in 5/6 subtotal nephrectomy rat model. Human proximal tubular epithelial cells (HKC) were treated with transforming growth factor-beta 1 (TGF-β1), or transfected with DJ-1 or PTEN. Confocal microscope was used to investigate the localization of DJ-1 and PTEN. The selective phosphoinositide-3 kinase (PI3K) inhibitor, LY294002, was administered to inhibit PI3K pathway. The DJ-1 and PTEN expression, markers of epithelial-mesenchymal transition (EMT) and Akt phosphorylation were measured by RT-PCR, Western blotting or immunocytochemistry. In vitro, after HKC cells were stimulated with 10 ng/mL TGF-β1 for 72 h, the expression of DJ-1 was increased, and that of PTEN was decreased. In vivo, the same results were identified in 5/6-nephrectomized rats. In normal HKC cells, most of DJ-1 protein localized in cytoplasm, and little in nucleus. TGF-β1 upregulated DJ-1 expression in both cytoplasma and nuclei. In contrary, TGF-β1 emptied cytoplasmic PTEN protein into nucleus. Overexpression of DJ-1 decreased the expression of PTEN, promoted the activation of Akt and the expression of vimentin, and also led to the loss of cytoplasmic PTEN. Contrarily, overexpression of PTEN protected HKC cells from TGF-β1-induced EMT. In conclusion, DJ-1 is upregulated in renal fibrosis and DJ-1 mediates EMT by suppressing cytoplasmic PTEN expression and Akt activation.