Application of Rectal Prolapse Constipation Balloon in Single Auxiliary Defecation / 中国医疗器械杂志

OBJECTIVE@#To explore the application value of rectal prolapse constipation balloon in single auxiliary defecation.@*METHODS@#Forty-one patients with moderate or severe rectocele were treated with a rectocele constipation balloon through the vagina. The defecography and VAS scores were compared before and after implantation.@*RESULTS@#There was a significant difference between the anorectal angle, rectocele, and VAS scores before and after intervention in defecography (<0.01).@*CONCLUSIONS@#A single assisted defecation of the rectocelicular constipation balloon is feasible.

Comparison of Two Kinds of Rat Model for Slow Transit Constipation and Expression of Aquaporins in Them / 中国康复理论与实践

Objective To compare the rat model of slow transit constipation (STC) established with gavage or feeding compound di-phenoxylate. Methods Forty Sprague-Dawley rats were randomly divided into gavage control group (A), gavage group (B), feeding control group (C) and feeding group (D) equally. Group B was given compound diphenoxylate suspension by gavage for 14 days while group A ac-cepted isodose normal saline. Group D were given feed containing compound diphenoxylate for 120 days while group C accepted normal feed. Carbon ink was poured into stomachs to observe the propelling rate after modeling, and the content of aquaporin 3 and aquaporin 4 were detected with immunohistochemistry. Results There were two rats died in group A and group B, respectively. The carbon ink propel-ling rate was lower in group D than in group B (P<0.05). Both aquaporin 3 and aquaporin 4 were more in group D than in group B (P<0.05). Conclusion STC rat model can be established by eating diphenoxylate feed for 120 days, which is safer and more stable than that of gavage for 14 days. Aquaporins in colons may play a role in onset and development of STC.

Effects of troglitazone on the proliferation and differentiation of HepG2 cells / 中华消化外科杂志

Objective To examine the effects of a peroxisome proliferator-activated receptor γ ligand troglitazone on the proliferation and differentiation of HepG2 cells. Methods After the pretreatment of HepG2 cells with troglitazone, MTT and flow cytometry were used to analyze the proliferation and cell cycle of HepG2 cells, respectively. Immunocytochemistry, bromocresol green dye-binding method and chemiluminessence immunosorbent assay was used to determine E-cadherin, albumin and AFP, respectively. The expression of cyclin D1 and c-myc protein were detected by Western blot. Results Troglitazone inhibited the proliferation of HepG2 cells in a concentration-dependent manner and arrested HepG2 ceils at the G0>/G1> phase. After pretreated with troglitazone, HepG2 cells showed E-cadherin expression, a decreased expression of cyclin D1 and c-myc protein, a reduction of AFP level and a dramatic increase of albumin level. Conclusions Troglitazone inhibits proliferation and induces differentiation of HepG2 cells, the mechanism of which might be attributable to the down-regulation of cyclin D1 and c-myc expression.

Hypoxia augments the killing effect of herpes simplex virus thymidine kinase gene expression actuated by the promoter of the vascular endothelial growth factor gene on human hepatocellular tumor cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the killing effect of herpes simplex virus thymidine kinase gene expression actuated by the promoter of the vascular endothelial growth factor gene on human hepatocellular tumor cells under hypoxic condition.</p><p><b>METHODS</b>Recombinant adenoviral vectors, AdVEGF-tk and AdVEGF-GFP, were constructed with HSV-tk or GFP under the control of VEGF promoter through AdEasy system. Then GFP expression in hepatoma cell line HepG2 and normal liver cell line L02 transfected with AdVEGF-GFP were observed under fluorescence microscope, and the sensitivity to GCV of the AdVEGF-tk-transfected cells under normoxia or hypoxia condition were monitored by MTT method.</p><p><b>RESULTS</b>GFP expression actuated by VEGF promoter was detected in sporadic L02 cells, but in almost all HepG2 cells after transfected with AdVEGF-GFP. With GCV at 10 micro g/ml and MOI at 100, L02 cells were insensitive to GCV under oxic condition, but more than 70% L02 cells were killed under hypoxic condition. Moreover, HepG2 cells infected with AdVEGF-tk showed the increased GCV sensitivity under hypoxia (over 80% killed) as compared with normoxia (over 60% killed) conditions.</p><p><b>CONCLUSION</b>Hypoxia enhances the GCV sensitivity of human hepatocellular tumor cells infected with recombinant AdVEGF-tk under the control of VEGF promoter.</p>

Correlation between midkine protein overexpression and intrahepatic metastasis in hepatocellular carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the correlation between midkine (MK) protein expression with local infiltration and metastasis in human hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>Immunohistochemical and Western Blot analysis for MK were performed on samples of tumor tissue and the paratumor tissue from HCC and benign liver tumors.</p><p><b>RESULTS</b>The overexpression of MK protein determined by immunohistochemical analysis was similar to that by Western Blot analysis. No specific positivity was detected in either benign liver tumor tissue or normal liver tissue, but most of HCC tissue showed a positive reaction to MK immunostain. No correlation between MK expression and other clinicopathological features in MK negative or positive HCC cases was found. Yet, the overexpression rate of MK protein in HCC with intra-hepatic metastasis was significantly higher than that in HCC without intra-hepatic metastasis.</p><p><b>CONCLUSION</b>In human hepatocellular carcinoma, MK overexpressed at protein level may very well be closely related to local infiltration and metastasis.</p>

Therapeutic efficacy of adenovirus-mediated gene transfer of thymidine kinase coded with vascular endothelial growth factor promoter on murine experimental hepatocellular carcinoma / 中国普通外科杂志

0.05). The mean growth values in AdCMV-tk/GCV- and AdVEGF-tk/GCV-treated tumors were significantly lower than those in untreated tumors and AdVEGF-tk/saline-untreated tumors( P