Objective To discuss the treatment and nursing effect for prevention of cystospasm in patients after prostatic surgery with irrigation of resinieratoxin (RTX) into urinary bladder. Methods Twenty patients were divided into the control group and observation group with 10 cases in each group according to the date of hospitalization.Four milliliters of RTX and 100 ml of normal saline were irrigated into the bladder 3 days before operation in the observation group.Only 104 ml normal saline was irrigated into the bladder in the control group.The frequency,intension and duration of cystospasm and clearing time of bladder flushing fluid were observed.The international prostatic symptom score (IPSS) and score of life quality were evaluated at the first,second and 4th week after removing of urinary catheter and bladder stoma. Results The outcome in the observation group and the control group were as followed: the incidence rate of cystospasm was 20% and 80%,the clearing time of bladder flushing fluid was (2.8±1.7)d and (5.2±1.0)d,the indwelling time of bladder stoma was (4.0±1.6)d and (5.8±1.1)d,the indwelling time of urinary catheter was (9.3±1.3)d and (11.8±1.1)d,the VAS score was (2.3±1.3)d and (4.6±1.1)d, the IPSS score at the first,second and 4th week were (11.1±3.3)and (16.0±3.0), (9.5±1.4) and (12.7±13.2), (8.4±1.6) and (11.3±2.7),the score of life quality at the 4th week was (1.6±0.5) and (2.8±0.9), respectively. All the above results had statistical difference between the observation group and the control group (P<0.05). Conclusion Standard bladder irrigation,rigorous monitoring of patients condition and maintenance of smooth flush of bladder were the important nursing basis to ensure the exertion of best effect of RTX irrigation.

Aim To investigate the apoptotic mechanism and polyamine transporter recognition of 3-nitro-naphthalimide norspermine conjugate (NNINspm),a novel naphthalimide-polyamine conjugate, in HepG2 cells.Methods The cytotoxicity of NNINspm was assessed by MTT assay.Cell cycle distribution and apoptosis were measured by flow cytometry.The protein expression of cytochrome C,14-3-3,Bad,Bcl-xL,mTOR,p70S6K,Cdk4,p27~(kip1),Akt,Caspase-3,Caspase-9 was evaluated by Western blot.The translocation of Akt was detected by high content screening (HCS) analysis.Results NNINspm induced HepG2 cells apoptosis via Akt dephosphorylation and then triggered a series of signal events, such as Bad dephosphorylation, dissociation of 14-3-3 and Bad, and then binding to Bcl-xL,which finally resulted in mitochondrial disruption,cytochrome c release and caspase cascade activation.Furthermore,the NNINspm-mediated cell cycle arrest was due to mTOR and p70S6K dephosphorylation,Cdk4 down-regulation and p27~(kip1) up-regulation.Conclusion NNINspm induces HepG2 cell apoptosis via PI_3K/Akt signal pathway.

In the present study, the apoptotic mechanism and polyamine transporter recognition of WJH-6, a novel polyamine conjugate, were investigated in K562 and HL-60 cells. The cytotoxicity of WJH-6 was assessed by MTT assay; cell cycle distribution and apoptosis were measured by flow cytometry; the protein expression of Caspase-3, Caspase-8, Caspase-9, Bid and mitochondrial membrane potential (MMP) were evaluated by high content screening (HCS) analysis; the protein expression of cytochrome c was measured by Western blotting. The results showed that WJH-6 could be recognized and transported by polyamine transporter (PAT). Furthermore, WJH-6 was able to inhibit K562 and HL-60 cells proliferation and induce apoptosis. This apoptotic effect was relative to MMP loss, cytochrome c release from mitochondria to cytoplasm and the activation of Caspase-8, Caspase-9, Caspase-3 and Bid. These results suggested that WJH-6-induced K562 and HL-60 cells apoptosis was related with mitochondrial damage.

Objective To investigate the influence of tethered cord syndrome (TCS) on the up-per urinary tract and its etiology. Methods Forty patients with TCS diagnosed by spinal MRI were enrolled in this study. There were 21 males and 19 females with mean age of 23 years old. The course of disease ranged from 1 to 40 years. Urinalysis, mid-stream urine culture, serum creatinine(SCr), urinary system ultrasound, IVU, eystography and urodynamic study were carried out on all patients. Results Urinary tract infection was found in 17 patients and increased level of SCr was found in 6 pa-tients (251.64±98.5μmol/L). Of the 29 patients who underwent urinary system ultrasound examina-tion, 12 cases had hydronephroais and dilated upper ureter. Of the 30 patients who underwent IVU, 10(33.3%) had ureterectasia and hydronephrosis, 22 cases had bladder turriform or Christmas tree like deformity with diverticulum and trabeculum. Of the 22 patients accepted cystography, 17 cases had vesieoureteral reflux on 27 sides. Post-void residual (PVR) was evaluated in 35 patients and found increased in 31 cases. Cystometry had been done in 33 patients. The mean value of maximal detrusor pressure (Pdetmax) during filling phase was 41.2±20.9 cm H2O. The detrusor compliance was 22.35±18.8 ml/cm H2O. During voiding phase, detrusor-sphincter dyssynergia(DSD)was observed in 16 patients, detrusor areflexia was observed in 16 patients and detrusor underactivity was observed in 13 patients. Resting urethral pressure profilemetry was measured in 16 patients. Maximal urethral closure pressure (MUCP) was 76.1±33.1 cm H2O. The upper urinary tract deterioration was de-fined as increased SCr, hydronephrosis or vesicoureteral reflux. There were 20 patients diagnosed as upper urinary tract deterioration. The compliance of the upper urinary tract deteriorating group and the no-deteriorating group was 9.4±7.8 vs 19.3±15.8 ml/cm H2O, Pdetmax was 43.1±21.2 vs 24.0±11.9 cm H2O, PVR 189.0±138.0 vs 47.8±36.8 ml, MUCP 86.2±32.4 vs 46.8 5±20.8 cm H2O, incidence of damaged detrusor 100.0% vs 69.2% and DSD 65.0% vs 23.1%, respectively. There were significant differences between the 2 groups(P<0.05). And when comparing the VUR group with no VUR group, the incidence of urinary tract infection was 94.1%(16/17) vs 20.0%(1/ 5) (P=0.003). And when comparing urinary tract infection group with no infection group, the inci-dence of upper urinary tract deterioration was 88.2% (15/17) vs 21.7%(5/23)(P=0.000). Condn-sion Low compliance bladder, high Pdetmax during filling phase, increased PVR, high MUCP, damage of detrusor contractive function and DSD are the risk factors for upper urinary tract deteriora-tion in the TCS patients.

0.1 ?mol?L-1), inducing differentiation through enhancement of melanogenesis and increase of the activity of tyrosinase at lower doses(

This study is to examine the effects of NNIspm-mediated cellular senescence of HepG2 cells and elucidate its potential molecular mechanism. Cellular senescence was detected with senescence-associated beta-galactosidase staining. Cell cycle distribution, intracellular fluorescence intensity and accumulation of intracellular reactive oxygen species (ROS) were detected by high content screening (HCS). Protein expression was detected by Western blotting. Polyamines content was analyzed by high performance liquid chromatography (HPLC). The results demonstrated that NNIspm significantly induced HepG2 cells senescence. This effect was due to the decrease of intracellular polyamines, the arrest at G0/G1 phase and an increase of ROS level. The molecular senescence marker p21 increased significantly after NNIspm treatment. In contrast, the protein expressions of Cyclin E and CDK2 were obvious down-regulation. The results indicated that cellular senescence induced by NNIspm was one of its antitumor mechanisms.

Objective To explore the effect of vitamin D receptor (VDR) in intestinal tumor development and the relationship between VDR and β-catenin signaling pathway. Methods The interaction of vitamin D receptor and β-catenin were detected by co-immunoprecipitation assay after human colonic carcinoma cells SW480 were treated with vitamin D in vitro for 4 hours. The expression of E-cadherin protein was detected by Western blot after treated for 24 hours. To compare APCmin/+VDR-/- and APCmin/+ mice in vivo, the expression of VDR,β-catenin and BrdU proteins in intestinal tumor were determined by immunohistochemistry. The expression of β-catenin protein in tumor and adjacency intestinal was further determined by Western blot. Results After SW480 cells were treated with vitamin D, vitamin D receptor and β-catenin protein showed binding, the expression of E-cadherin protein further increased (Gray value the control group 145.57±4.21,Gray value of the experimental group 109.35±3.56,t＝32.63,P＜0.05). Immunostaining and Western blot detection（Gray value 166.47±2.36） showed a marked increase of β-catenin level(Gray value 140.51±2.57) in APCmin/+VDR-/- tumor compared to APCmin/+ tumor(145.41±3.62,182.35±3.24,t＝2.65,4.36,P＜0.05). Conclusions The role of vitamin D suppressing intestinal tumor may be achieved through VDR affectingβ-catenin signaling pathway.

ObjectiveTo explore the relationship among 25-hydroxyvitamin D,serum calcium,calcium-sensing receptor,and breast cancer. Methods The expressions of calcium-sensing receptor (CaSR) in primary breast cancer,breast benign tumors,and normal breast tissue beside tumors were determined by immunohistochemistry S-P method as well as the concentration of serum 25 (OH) D and serum calcium in breast cancer and breast benign tumors by Enzyme-linked immunosorbent assay (ELISA),Tribromoarsenazo Ⅲ method.ResultsSerum 25 (OH) D level of breast cancer was significantly lower than the breast benign tumors [ (34.13 ± 14.14) nmol/L vs (50.29 ± 25.65 ) nmol/L,t =2.870,P =0.001 ].Serum level of 25 ( OH ) D in lymph node metastasis positive patient was lower than that in negative group [ (30.8 ± 9.71 ) nmol/L vs (43.7 ± 23.59) nmol/L,t =2.467,P =0.021 ].The positive expression of CaSR in breast cancer(88.9％ )was higher than breast benign tumors(60％,x2 =6.717,P ＜ 0.01 ) and normal breast tissue beside tumors (60％,x2 =5.628,P ＜ 0.05 ).ConclusionsConcentration of serum 25 (OH)D and expression of calcium-sensing receptor in the tissues may be associated with occurrence,development and prognosis of breast cancer.

Objective To investigate the expression and clinical significance of CXCR3/CXCL10in human cancer.Methods CXCR3 and CXCL10 were detected in 60 paraffinic tissues of patients with primary breast cancer,20 of mammary fibroma and 20 of mastopathy by immunohistochemistry S-P method and two stage method.Results The expression of CXCR3 (40/60,66.7％ ) and CXCL10 (45/60,75％)in breast cancer was higher than that in mastopathy [CXCR3(8/20,40％ )x2 =4.44,P =0.035 ;CXCL10( 10/20,50％ )x2 =4.36,P =0.037)].The expression of CXCR3 was related to status of axillary lymph node metastasis,clinical stage and the expression of HER-2 (x2 =4.15,P =0.042; x2 =7.74,P =0.021 ;x2 =4.27,P =0.039).The expression of CXCR3 had positive relationship to the number axillary lymph node metastasis( rs =0.375,P =0.003 ),clinical stage ( rs =0.451,P =0.000).Conclusions CXCR3 may be related to the progression and metastasis of breast cancer,and it may be used as a marker of breast cancer prognosis.

The objective of this study is to examine the effects of ANISpm, a novel polyamine naphthalimide conjugate, with acetylsalicylic acid against hepatocellular carcinoma in vivo and in vitro and elucidate its potential molecular mechanism. The proliferation inhibition was detected by MTT assay. Cell apoptosis, intracellular fluorescence intensity and mitochondrial membrane potential (MMP) were detected by high content screening (HCS) analysis. Polyamines content was analyzed by reverse-phase high performance liquid chromatography Protein expression levels were quantified by Western blotting assay. The combination treatment strongly inhibited cell proliferation, induced cell apoptosis in HepG2 cells and H22 hepatoma cells, which was mediated by enhanced ANISpm uptake via up-regulation of spermidine/spermine N1-acetyltransferase (SSAT) and depression of intracellular polyamine. Furthermore, this synergistic apoptosis was involved in mitochondria and death-receptor signal pathway. All these findings demonstrated that the combination treatment with acetylsalicylic acid and ANISpm resulted in synergistic antitumor effects on hepatoma cells. Thus, combination therapy with these agents may be useful as a potential template for the development of better chemotherapeutic strategy against hepatoma.