Objective To assess the efficacy of radical transurethral electrovaporization for invasive bladder cancer. Methods Thirty-six patients with invasive bladder cancer from february 2008 to February 2010 were treated by transurethral electrovaporization resection of bladder tumor (TURBT). The operation procedure was based upon the principle of radical transurethral resection for bladder tumor. The tumor was resected to fatty layer outside the bladder wall. After operation Bacillus Calmette-Guerin (BCG) irrigation of bladder was given,all patients were followed up for 3 to 24 months. Results The recurrence occurred in 12 cases in 2 years,with a recurrence rate of 33. 3% (12/36). These recurrence cases were treated with TURBT again. Six cases dead in 2 years,with a mortality of 16. 7% (6/36). Conclusion TURBT is suitable for those who are older or weak,and not medically fit for radical cystectomy or those who refuse the open surgery,which can prolong the survival time and improve the quality of life.

Renal cell carcinoma (RCC) is one of the most lethal malignancies of the urinary system, however, its pathogenic mechanism is not clear.Stanniocalcin (STC) is a type of glycoprotein hormone with multiple biological functions.Recently, the role of STC in the pathogenesis of cancer is of intriguing interest, and many researches have been performed to clarify underlying mechanism. We emphasized the role of STC in the underlying mechanism of RCC progression, from the aspects of STC inducing hypoxia adaptation of tumor cells, promoting tumor angiogenesis, also promoting cell proliferation, apoptosis, invasion and metastasis, and inhibiting the immune response.Conclusively, STC could be used as both a promising biomarker for RCC diagnosis and a theraputic target of renal cell carcinoma.

Objective:To assess the impacts of feeding type and non-nutritive sucking activity on occlusion in deciduous dentition in WeiFang city.Methods:The occlusion of 958 children aged 3 -5 years old in WeiFang city and their feeding types as well as the non-nutritive sucking habit during the first 1 2 months after birth were investigated by questionaire study.Data were statistically ana-lysed.Results:The prevalence of malocclusion in non-nutritive sucking habit group and non-habit group was 42% and 22% respec-tively(P =0.000 2).The type of feeding did not have effect on occlusion and openbite.The prevalence of openbite in the children with sucking habit and in those without habit was 17% and 4% respectively(P <0.000 1 ).The prevalence of posterior crossbite in the chil-dren with bottlefeeding and those with breastfeeding was 1 1 % and 4% respectively(P =0.000 2).The prevalence of posterior crossbite in the children with sucking habit and those without habit was 9% and 4% respectively(P =0.036 7).Conclusion:Non-nutritive sucking habit rather than feeding type in the first 1 2 months after birth is the main risk factor of malocclusion,breastfeeding is the pro-tective factor to occlusion.

Objective To investigate the effect of adipose derived stem cells (ADSCs) on hepatic stellate cells (HSCs) in vitro and on liver fibrosis in vivo.Methods ADSCs and HSCs were isolated from adipose tissue and liver respectively in SD rats.The coculture system was set up by transwell insert.The 5th passage HSCs were cultured on the 6-well plastic plate,and ADSCs or BRLs seeded on the transwell insert.The proliferation of HSCs was tested by CCK-8 test kit.Smoothmuscle α-actin (α-SMA) expression of HSCs were tested by Western blot.Rat models of liver fibrosis was established.Rats in ADSCs treatment group were infused with ADSCs and those in control group were infused with Buffalo rat liver cells (BRLs).Liver sections were studied by immunocytochemistry.Liver hydroxyproline (Hyp) content,serum laminin (LN)and hyaluronic acid (HA) were tested,the cytokines in the culture medium were assayed.Results HSCs and ADSCs were isolated successfully.After coculture for 72 h,compared with the control group,the proliferation and activation of HSCs was inhibited by ADSCs( absorbance of each group were 2.172 ±0.107,1.424 ± 0.013,1.209 ± 0.117,F =90.605,P ＜ 0.05 ; Gray-scale values of each group were 1.4 ± 0.2,152 ± 14,258 ± 18,F =283.348,P ＜ 0.05 ),ADSCs infusion inhibits liver fibrosis in model rats ( F =77.234,65.164,58.309,all P ＜ 0.05 ).More hepatocyte growth factor(HGF) and less transforming growth factor-β1 (TGF-β1) (F=1.767,P＜0.05)and nerve growth factor (NGF) (F=2.301,P＜0.05) were secreted by ADSCs than by BRLs.Conclusions ADSCs inhibit the proliferation and activation of hepatic stellate cells.Treatment with ADSCs decreases collagen deposition in the liver and inhibits liver fibrosis.

Objective To explore the role of CD4+ CDhigh25 regulatory T cells in the pathogenesis of chronic abacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS).Methods The percentage of CD4+ CD+25 and CD4+ CDhigh25 regulatory T cells was detected by flow cytometry from 45 CAP/CPPS pa-tients and 18 normal controls.The levels of interleukin-6(IL-6),IL-10,tumor necrosis factor-α(TNF-α) and transforming growth factor-β1 (TGF-β1) in serum and seminal plasma were measured by ELISA in the same cohort.Results There was no significant difference in the percentage of peripheral blood CD4+CD+25 and CD4+Cdhigh+ cells between CAP/CPPS patients and normal control (P>0.05).The ser-CD4+CD+25 and CD4+Cdhigh+ cells between CAP/CPPS patients and normal control (P>0.05>.The ser-um levels of TGF-β1 in patients with CAP/CPPS were markedly lower than those in controls (P<0.05),serum TNF-α and seminal plasma IL-6,TGF-β1 and TNF-α in CAP/CPPS patients were markedly higher than those in controls (P<0.05).There was a positive correlation between the IL-6 and the NIH-CPSI.There was also a positive correlation between the IL-10 and the pain index.In ad-dition,the percentage of peripheral blood CD+4CDhigh25 cells was positively correlated with serum TGF-β1.But the percentage of CD+4CDhigh25 cells had no correlation with ages,duration of CAP/CPPS pa-tients,NIH-CPSI and the other cytokines.Conclusions The defective function of peripheral blood CD+4CD+25 regulatory T cells may be related with the pathogenesis of CAP/CPPS.The cytokines may also play an important role in the process of pathogenesis of CAP/CPPS.

Objective Cystic nephroma ( CN ) is an unusual benign neoplasm with high misdiagnosis rate , and at present there is no general method on its treatment .This study aimed to analyze the diagnosis and treatment of CN based on clinical data of CN patients. Methods We retrospectively analyzed the clinical data on 25 patients (including 2 cases of male pediatric patients , aged 14 and 16 years old, and the remaining 23 cases were adults, 11 males and 12 females, aged 14-69[45.1 ±19.6]years) treated in our department of the First Hospital of Shijiazhuang from January 2003 to July 2015 .All patients underwent ultrasound , CT and MRI examination , as well as surgical resection . Results Among these 25 CN patients , there were 15 cases of partial nephrectomy , 5 ca-ses of nephrectomy , 2 cases of retroperitoneal laparoscopic cyst unroofing , 1 case of laparoscopic enucleation of the tumors with nephron-sparing surgery , 1 case of laparoscopic radical nephroureterectomy , and 1 case of retroperitoneal laparoscopic radical nephrectomy .All the patients were successfully followed up for 6 months to 132 months, 1 patient recurred 6 months after retroperitoneal laparoscopic cyst unroo-fing and underwent open partial nephrectomy .No recurrence and me-tastasis were found in the remaining patients . Conclusion Imaging examination is an important measurement for CN , and intraoperative frozen pathology contributes to pathological diagnosis .Since most CN cases are benign , CN patients with no symptom or small cysts can take follow up survey .The principle of the operation is complete resection of the tumor , and nephron-sparing surgery is the first choice . In addition , regular follow-up is necessary in case of recurrence and malignant potential .

Desmoid-type fibromatosis is a rare benign tumor with invasive growth, which can occur in all parts of the body, mostly in the abdominal wall, and also in the abdomen and skeletal muscle. This paper reports a case of right ureteral stenosis caused by pelvic desmoid-type fibromatosis. Pelvic tumor resection, ileocecal resection and ureterovesical replantation were performed. The patients were followed up for 18 months without local recurrence and distant metastasis.

Summary: The expression of calcium epithelium TRPV5, alcium binding protein Calbindin-D28k and Na+/Ca2+ exchanger NCX1 was detected in renal distal convoluted tubule, and their effects on urine calcium reabsorption and the possible pathogenic mechanism in idiopathic hypercalciuria (IH) were investigated. Genetic hypercalciuric stone-forming (GHS) rats were chosen as animal models to study urine calcium reabsorption and IH. The cognate female and male rats that had maximal urine calcium were matched to breed next generation. Twelve GHS rats and 12 normal control (NC) SD rats were selected. Western blot and real time quantitative PCR were used to detect the protein and gene expression of TRPV5, Calbindin-D28k and NCX1 respectively. The expression levels of TRPV5 protein and mRNA in GHS rats were significantly lower than in NC rats (P<0.05). Western blot revealed that the expression levels of Caibindin-D28k in GHS rats and NC rats were 0.49±0.02 and 0.20±0.01 respectively, with the difference being significant between them (P<0.05). By using real time quantitative PCR, it was found that there was no significant difference in Calbindin-28k mRNA expression levels between GHS rats and NC rats (P0.05). There was no significant difference in the NCX1 expression between GHS rats and NC rats (P0.05). It was suggested that TRPV5 and Caibindin-D28k might play an important role in urine calcium reabsorption and IH, but they differently contributed to the pathogenesis: The down-regulation of TRPV5 decreases urine calcium reabsorption, directly leading to loss of the urine calcium and resulting in hypercalciuria, and the increased Calbindin-D28k expression could relieve, neutralize and decrease intracellular Ca2+ concentration to maintain calcium balance. NCX1 is not the key protein in urine calcium reabsorption.