Tumor-suppressive microRNA-497 targets IKKß to regulate NF-κB signaling pathway in human prostate cancer cells.

BACKGROUND: Prostate cancer (PCa) is one of the most prevalent malignant tumors, PCa-related death is mainly due to the high probability of metastasis. MicroRNAs (miRNAs) play an important role in cancer initiation, progression and metastasis by regulating their target genes. METHODS: real-time PCR was used to detected the expression of microRNA-497. The molecular biological function was investigated by using cell proliferation assays, cell cycle assay, and migration and invasion assay. We used several Algorithms and confirmed that IKKß is directly regulated by miR-497. RESULTS: Here, we found miR-497 is downregulated in human prostate cancer (PCa) and inhibites the proliferation activity, migration and invasion of PC3-AR cells. Subsequently, IKKß is confi rmed as a target of miR-497. Furthermore, knockdown of IKKß expression resulted in decreased proliferation activity, migration and invasion. Finally, similar results was found after treatment with a novel IKK-ß inhibitor (IMD-0354) in PC3-AR cells. CDK8, MMP-9, and PSA were involved in all these process. CONCLUSION: Taken together, our results show evidence that miR-497 may function as a tumor suppressor genes by regulating IKK-ß in PCa, and may provide a strategy for blocking PCa metastasis.

Time-dependent bladder tissue regeneration using bilayer bladder acellular matrix graft-silk fibroin scaffolds in a rat bladder augmentation model.

With advances in tissue engineering, various synthetic and natural biomaterials have been widely used in tissue regeneration of the urinary bladder in rat models. However, reconstructive procedures remain insufficient due to the lack of appropriate scaffolding, which should provide a waterproof barrier function and support the needs of various cell types. To address these problems, we have developed a bilayer scaffold comprising a porous network (silk fibroin [SF]) and an underlying natural acellular matrix (bladder acellular matrix graft [BAMG]) and evaluated its feasibility and potential for bladder regeneration in a rat bladder augmentation model. Histological (hematoxylin and eosin and Masson's trichrome staining) and immunohistochemical analyses demonstrated that the bilayer BAMG-SF scaffold promoted smooth muscle, blood vessel, and nerve regeneration in a time-dependent manner. At 12weeks after implantation, bladders reconstructed with the BAMG-SF matrix displayed superior structural and functional properties without significant local tissue responses or systemic toxicity. These results demonstrated that the bilayer BAMG-SF scaffold may be a promising scaffold with good biocompatibility for bladder regeneration in the rat bladder augmentation model.

Microvesicles derived from human umbilical cord mesenchymal stem cells facilitate tubular epithelial cell dedifferentiation and growth via hepatocyte growth factor induction.

During acute kidney injury (AKI), tubular cell dedifferentiation initiates cell regeneration; hepatocyte growth factor (HGF) is involved in modulating cell dedifferentiation. Mesenchymal stem cell (MSC)-derived microvesicles (MVs) deliver RNA into injured tubular cells and alter their gene expression, thus regenerating these cells. We boldly speculated that MVs might induce HGF synthesis via RNA transfer, thereby facilitating tubular cell dedifferentiation and regeneration. In a rat model of unilateral AKI, the administration of MVs promoted kidney recovery. One of the mechanisms of action is the acceleration of tubular cell dedifferentiation and growth. Both in vivo and in vitro, rat HGF expression in damaged rat tubular cells was greatly enhanced by MV treatment. In addition, human HGF mRNA present in MVs was delivered into rat tubular cells and translated into the HGF protein as another mechanism of HGF induction. RNase treatment abrogated all MV effects. In the in vitro experimental setting, the conditioned medium of MV-treated injured tubular cells, which contains a higher concentration of HGF, strongly stimulated cell dedifferentiation and growth, as well as Erk1/2 signaling activation. Intriguingly, these effects were completely abrogated by either c-Met inhibitor or MEK inhibitor, suggesting that HGF induction is a crucial contributor to the acceleration of cell dedifferentiation and growth. All these findings indicate that MV-induced HGF synthesis in damaged tubular cells via RNA transfer facilitates cell dedifferentiation and growth, which are important regenerative mechanisms.

The regulation of inflammatory mediators in acute kidney injury via exogenous mesenchymal stem cells.

Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is believed to play a major role in the pathophysiology of AKI. Exogenous mesenchymal stem cells (MSCs) are now under extensive investigation as a potential therapy for AKI. Various preclinical studies indicated the beneficial effects of MSCs in alleviating renal injury and accelerating tissue repair. However the mechanisms responsible for these effects are incompletely understood. In the recent years, anti-inflammatory/immunoregulatory properties of MSCs have become one of the important issues in the treatment of AKI. This review will summarize the current literature on the regulation of inflammatory mediators via exogenous MSCs contributing to the recovery from AKI.

Microvesicles derived from human umbilical cord Wharton's jelly mesenchymal stem cells attenuate bladder tumor cell growth in vitro and in vivo.

Several studies suggest that mesenchymal stem cells (MSCs) possess antitumor properties; however, the exact mechanisms remain unclear. Recently, microvesicles (MVs) are considered as a novel avenue intercellular communication, which may be a mediator in MSCs-related antitumor effect. In the present study, we evaluated whether MVs derived from human umbilical cord Wharton's jelly mesenchymal stem cells (hWJMSCs) may inhibit bladder tumor T24 cells growth using cell culture and the BALB/c nu/nu mice xenograft model. CCK-8 assay and Ki-67 immunostaining were performed to estimate cell proliferation in vitro and in vivo. Flow cytometry and TUNEL assay were used to assess cell cycle and apoptosis. To study the conceivable mechanism by which hWJMSC-MVs attenuate bladder tumor T24 cells, we estimated the expression of Akt/p-Akt, p-p53, p21 and cleaved Caspase 3 by Western blot technique after exposing T24 cells to hWJMSC-MVs for 24, 48 and 72h. Our data indicated that hWJMSC-MVs can inhibit T24 cells proliferative viability via cell cycle arrest and induce apoptosis in T24 cells in vitro and in vivo. This study showed that hWJMSC-MVs down-regulated phosphorylation of Akt protein kinase and up-regulated cleaved Caspase 3 during the process of anti-proliferation and pro-apoptosis in T24 cells. These results demonstrate that hWJMSC-MVs play a vital role in hWJMSC-induced antitumor effect and may be a novel tool for cancer therapy as a new mechanism of cell-to-cell communication.

Research on the steroidogenesis of proliferated Leydig cells in vitro.

Several treatments for patients with primary hypogonadism are available, but these are associated with major complications. In this study, we explored the possibility of testosterone secretion by proliferated Leydig cells embedded in Matrigel with the aim of developing a source of endogenous testosterone supplement for recipients while reducing the need for donor material. Leydig cells were isolated and proliferated in vitro. The expression of 3ß-hydroxysteroid dehydrogenase, cholesterol side-chain cleaving enzyme (CYP11A1), and 17α-hydroxylase/17,20-lyase (CYP17A1) was analyzed to confirm the purity and steroidogenesis capability of Leydig cells. The proliferated cells were then embedded in three-dimensional Matrigel, and following culture the supernatant medium was collected for measurement of testosterone concentration by radioimmunoassay. The biological behavior of the Leydig cells in the Matrigel was carefully observed under the microscope. Approximately 6.0 × 10(5) Leydig cells were obtained from one testis after primary culture in vitro. Aliquots of 1.0 × 10(5) Leydig cells were mixed with Matrigel, with the amount of cells in one pellet being equal to that in an adult testis. Leydig cells gradually formed aggregates when maintained in Matrigel. A rapid and constant linear increase in testosterone levels was detected in the supernatant medium. Our results demonstrate that Matrigel is a perfect support matrix for Leydig cells. Proliferated Leydig cells embedded in Matrigel have a great steroidogenesis reserve. In our study, they contributed to continuous steroidogenesis, which implies that the pellet may provide the physiological demand for endogenous androgen once engrafted in vivo. This system may ultimately provide a novel alternative treatment for people who are in need of androgen replacement.

The alleviation of acute and chronic kidney injury by human Wharton's jelly-derived mesenchymal stromal cells triggered by ischemia-reperfusion injury via an endocrine mechanism.

BACKGROUND AIMS: The effects of human Wharton's jelly-derived mesenchymal stromal cells (WJ-MSC) on acute and chronic kidney injury induced by ischemia-reperfusion injury (IRI) were assessed. METHODS: WJ-MSC were injected intravenously immediately after solitary kidney ischemia for 45 min. Cells were labeled with 5-bromo-2'deoxy-uridine (BrdU) for tracing in vivo. At 48 h post-IRI, serum creatinine and blood urea nitrogen (BUN) were measured. Tubular cell proliferation and apoptosis as well as activation of the Akt signal were identified by immunostaining. Real-time polymerase chain reaction (PCR) was employed to determine gene expression of inflammation-related cytokines and hepatocyte growth factor (HGF). Levels of human HGF were assayed by enzyme-linked immunosorbant assay (ELISA). Twenty-two weeks later, renal fibrosis was assessed by Masson's tri-chrome staining, collagen content and α-smooth muscle actin (α-SMA) staining. RESULTS: There was no sign of labeled cells residing in the damaged kidney. Acute renal dysfunction elicited by IRI was considerably improved by WJ-MSC, in parallel with a stronger proliferative response and less apoptotic events. Additionally, phosphoAkt staining in injured tubular cells was substantially intensified. Cell treatment also caused a remarkable up-regulation of kidney interleukin (IL)-10, heme oxygenase (HO)-1 and HGF expression. Human HGF was detected in cell supernatants and the serum of cell-infused rats. Moreover, IRI-initiated fibrosis was abrogated by cell therapy, coincident with function amelioration. CONCLUSIONS: WJ-MSC alleviate acute kidney injury, thereby rescuing the ensuing fibrotic lesions in an endocrine manner. The Akt signal in impaired tubular cells is reinforced by WJ-MSC, facilitating cell resistance to apoptosis and cell proliferation. HGF, either delivered or induced by WJ-MSC, is an important contributor.

Tubularized urethral replacement using tissue-engineered peritoneum-like tissue in a rabbit model.

INTRODUCTION: This study aims to investigate whether mesothelial cells could function as seed cells to construct tissue-engineered peritoneum-like tissue for urethral reconstruction in a rabbit model. MATERIALS AND METHODS: Bladder acellular matrices were prepared and trimmed to 1.5 × 1 cm. Nine male rabbits underwent omentum biopsy and autologous mesothelial cells were isolated. After in vitro expansion, the cells were seeded onto the matrices and incubated for 7 days. In 18 rabbits, a pendulous urethral segment 1.5 cm long was totally excised and urethroplasty was performed with tubularized matrices seeded with cells in 9 animals and without cells in 9 as controls. Urethrography was performed at 1, 2 and 6 months postoperatively. Meanwhile, the neourethras were harvested and analyzed grossly and histologically. RESULTS: Histological analysis of the cell-seeded grafts revealed a loose collagen matrix covered with a single layer of mesothelim. Serial urethrography indicated a wide urethral caliber without stricture formation in animals implanted with cell-seeded matrices, while all animals of the control group developed stricture. Histological analysis of the implanted cell-seeded matrices demonstrated a normal urethral architecture by 1 month, composed of multilayers of urothelium surrounded by smooth muscle bundles, which became increasingly organized with time. By 6 months, the neourethra could be hardly distinguished from native urethra both grossly and histologically. CONCLUSIONS: Autologous mesothelial cells could be successfully used as seed cells for tubularized urethral reconstruction in male rabbits.

Ureteral reconstruction using autologous tubular grafts for the management of ureteral strictures and defects: an experimental study.

OBJECTIVE: To investigate whether the peritoneal cavity could function as a bioreactor to produce autologous tubular grafts for ureteral reconstruction in beagles. MATERIALS AND METHODS: 8-Fr Silastic tubes were implanted into the peritoneal cavities of 6 female beagles. At 3 weeks, the tubes were harvested and the tubular tissue covering the tubes was gently everted. A segment 3 cm in length of the right mid-ureter, involving two thirds of its diameter, was removed parallel to the ureteral axis, leaving a third of the ureteral wall. A 5-Fr double-J stent was inserted into the ureter through the created defect, and two thirds of the graft were anastomosed to both edges of the ureteral defect. One third of the graft was overlapped with the retained normal ureter and anastomosed to the external surface of the lumens. Thus, the graft was partly encapsulated by the remainder of ureteral wall. The stent was maintained for 6 weeks and removed. Excretory urography was performed at 8 (n = 3) and 12 weeks (n = 3), postoperatively. Meanwhile, the neoureter was harvested and analyzed. The left ureter served as the control and a simple intubated ureterotomy was performed. RESULTS: Histological analysis of the tubular tissue demonstrated transversely arranged myofibroblasts and an outer layer of mesothelium. The tissue was easily everted and transplanted as a ureteral graft. Eight weeks postoperatively, the neoureter demonstrated normal ureteral architecture, composed of multilayers of urothelium surrounded by smooth muscle bundles, which became increasingly organized with time. Excretory urography indicated no stenosis or hydronephrosis. CONCLUSIONS: These results show that autologous tubular tissue grown within the recipients' peritoneal cavity can be used for ureteral reconstruction in the beagle model.

Laparoscopic radical excision of urachal remnants with recurrent infection in infants.

PURPOSE: To evaluate the usefulness of laparoscopic surgery in the management of urachal remnants with recurrent infection in infants. PATIENTS AND METHODS: Eight infants (mean age 9.6 months, range 2-16 months) underwent laparoscopic excision of urachal remnants with recurrent infection between June 2006 and December 2008. During the same period, 10 infants (mean age 13.2, range 4-17 months) underwent open surgery for the same condition. The laparoscopic surgery was performed transperitoneally by using three ports. The urachal remnant was dissected from the umbilicus to the bladder dome and then removed completely. RESULTS: Immediate complications did not develop in any patient. Blood loss, hospital stay, and operative time with laparoscopic surgery were less than those with open surgery. Recurrence did not develop in any patient who underwent laparoscopic surgery, while it did develop in one patient who underwent open surgery. CONCLUSION: The laparoscopic approach appears to be a safe and effective alternative to open surgery in the management of urachal remnants with recurrent infection in infants.

Peritoneal cavity as bioreactor to grow autologous tubular urethral grafts in a rabbit model.

PURPOSE: To investigate whether peritoneal cavity could function as bioreactor to produce autologous tubular grafts for urethral reconstruction in male rabbits. METHODS: 8Fr silastic tubes were implanted into peritoneal cavities of nine male rabbits. By 2 weeks, tubes were harvested and the tubular tissue covering the tubes was everted. A pendulous urethral segment of 1.5 cm long was totally excised and urethroplasty was performed with the everted tubular tissue in an end-to-end fashion. Another nine male rabbits underwent the same urethral resection and re-anastomosis as controls. Urethrography was performed at 1, 2 and 6 months postoperatively. Meanwhile, the neo-urethra were harvested and analyzed grossly and histologically. RESULTS: Histological analysis of the tubular tissue demonstrated transversely arranged myofibroblasts embedded in homogeneous collagen bundles and an outer layer of mesothelium. The tissue was easily everted and successfully transplanted as a urethral graft. Serial urethrography indicated no stricture or diverticula formation. While all animals of the control group developed stricture. Histological analysis of the neo-urethra demonstrated normal urethral architecture by 1 month, composed of multi-layers of urothelium surrounded by smooth muscle bundles, which became increasingly organized with time. By 6 months, the neo-urethra could be hardly distinguished from native urethra both grossly and histologically. CONCLUSIONS: These results show that the autologous tissue grown within the recipients' peritoneal cavity can be used successfully for tubularized urethral reconstruction in male rabbits.

Molecular and toxicologic research in newborn hypospadiac male rats following in utero exposure to di-n-butyl phthalate (DBP).

The objective of this study was to first evaluate the developmental abnormalities and carry out the molecular analysis of external genitalia in newborn hypospadiac male rats induced by maternal exposure to di-n-butyl phthalate (DBP). Timed-pregnant rats were given DBP by gastric intubation at dose of 750 mg/kg body weight (bw)/day from gestation day (GD) 14 to GD18 to establish a hypospadiac rat model. The incidence of hypospadias was 46.67% in male offsprings. On postnatal day (PND) 7, at the newborn stage, decreased body weight and anogenital distance (AGD)/body weight ratio were observed in newborn hypospadiac male rats. The general image and transverse serial histological analysis of genitalia of newborn hypospadiac male rats confirmed the malformation. Autopsy analysis revealed development of reproductive organs (testes, genital tubercle (GT)), hollow organs (stomach, bladder), and solid organs (brain, heart, liver, spleen, lung, kidney, pancreas) in newborn hypospadiac male rats affected by DBP. Moreover, significantly decreased gene expression of important signaling molecules necessary for GT formation including sonic hedgehog signaling molecules (Shh and Ptched 1), bone morphogenetic proteins signaling molecules (Bmp4 and Bmp7), fibroblast growth factor signaling molecules (Fgf8, Fgf10 and Fgfr2), and the transforming growth factor-beta superfamily signaling molecules (TGF-beta1 and TGF-beta receptor III) were observed, for the first time, in the GT of newborn hypospadias induced by DBP. These results showed that the reproductive system and development conditions of newborn hypospadiac rats were damaged by DBP. These disturbed signaling pathways which orchestrating genital development might play an important role in the toxic process of DBP induced hypospadias.

Effects of acrylamide on the nervous tissue antioxidant system and sciatic nerve electrophysiology in the rat.

To investigate the time-dependent effects of acrylamide (ACR) on the antioxidative status in rat nerve tissues, adult male Wistar rats were given ACR (40 mg/kg, i.p., 3 times/week) for 2, 4, 6 and 10 weeks, respectively. The time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; superoxide dismutase, SOD and anti-reactive oxygen species, anti-ROS) in nerve tissues were investigated. The electrophysiology indices (nerve conduction velocity, NCV; compound action potential duration, CAPD; compound action potential amplitude, CAPA; compound action potential latency, CAPL) in the sciatic nerve were determined using BL-420E Biologic Function Determining System. The results showed that MDA levels increased significantly (P < 0.05) in nerve tissues, while GSH levels markedly decreased (P < 0.05) in a time-dependent manner. SOD activity (in the spinal cord and sciatic nerve) and GR activity (in the sciatic nerve) increased significantly after 4 weeks ACR treatment (P < 0.01), but then decreased (P < 0.05). The anti-ROS activity in the sciatic nerve was markedly decreased at the end of week 6 and 10 (P < 0.01). The above indices changed most in the sciatic nerve. The levels of GSH, MDA and anti-ROS in rat sciatic nerve were in high correlation (P < 0.05, |r| > 0.80) with the electrophysiology indices according to the exposure time. Thus, ACR-induced neurotoxicity may be associated with the enhancement of lipid peroxidation and reduction of the antioxidative capacity. Depletion of neural GSH level might be one of the primary events in ACR-induced neuropathy.

[In vivo and in vitro determination of changes of electrophysiology in rats with allyl chloride poisoning].

OBJECTIVE: To compare the results of in vivo and in vitro in determination of the changes of allyl chloride (AC)-induced electrophysiology in rats sciatic nerve. METHODS: Ninety male Wistar rats weighted 180 approximately 220 g were divided randomly into two groups, i.e. experimental group (n=40) and control group (n=50). The rats in experimental group were treated with AC dissolved in corn oil (200 mg/kg ip 3 days/week) by gavage for 12 weeks. Electrophysiological indexes of each group were determined on 3, 6, 9 and 12 weeks of AC intoxication. The indexes included measurements of sciatic nerve conduct velocity (NCV), compound action potential amplitude (CAPA), potential latency (PL), time course (TC), threshold potential (TP) and max stimulate potential (MSP). RESULTS: Compared to the corresponding time-matched control rats, on 6, 9 and 12 weeks of AC intoxication, NCV were decreased by 23.6%, 40.4% and 48.6% (P<0.05, P<0.01) in vivo, while in vitro it was decreased by 15.4% (P<0.05) on 12 week, CAPA were reduced by 31.7% in vivo, while in vitro it was reduced by 31.7%, 38.9% and 58.9% (P<0.05, P<0.01), respectively, PL were prolonged 22.6% and 40.7% (P<0.01) on 9, 12 weeks in vivo, while in vitro it was prolonged 8.0% (P<0.05), TC were increased 22.5%, 34.6% and 47.5% (P<0.01) in vivo, while in vitro it was increased 11.6%, 20.0% (P>0.05) and 19.5% (P<0.01), respectively, TP were elevated 12.1% (P>0.05), 32.3% and 40.0% (P<0.05) in vivo, while in vitro it was elevated 16.4% (P>0.05), 29.2% and 35.6% (P<0.05), respectively, MSP were increased 40.5% (P>0.05), 69.0% and 86.5% (P<0.01) in vivo, while in vitro it was increased 29.7% (P>0.05), 52.0% and 61.9% (P<0.01), respectively. CONCLUSION: The two methods of in vivo and in vitro showed that AC could significantly affect the electrophysiology of sciatic nerve, and the time-dependent changes occurred. The NCV is the most sensitive indicator in vivo to the early diagnosis of AC intoxication, while CAPA is the most sensitive indicator in vitro.

Time-dependent changes of lipid peroxidation and antioxidative status in nerve tissues of hens treated with tri-ortho-cresyl phosphate (TOCP).

Tri-ortho-cresyl phosphate (TOCP) could induce a delayed neurodegenerative condition known as organophosphorus easter-induced delayed neurotoxicity (OPIDN) in human beings and sensitive animals. However, the mechanisms of OPIDN remain unknown. This study investigated the time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; superoxide dismutase, SOD and anti-reactive oxygen species, anti-ROS) in nerve tissues for elucidating the mechanism of OPIDN induced by TOCP. Adult hens were treated with TOCP by gavage at a single dosage of 750 mg/kg. TOCP was dissolved in corn oil and administered at 0.65 ml/kg. The control hens received an equivalent volume of corn oil by gavage. Hens were sacrificed after 0, 5, 10, 15 and 21 days of treatment and the cerebrum, spinal cord, sciatic nerve were dissected, homogenized and used for the determination of lipid peroxidation and antioxidative status. The results showed that treatment with TOCP increased lipid peroxidation and reduced the antioxidative status in cerebrum, spinal cord and sciatic nerve. The levels of MDA increased by 33% (P<0.01) in cerebrum on 5th day after TOCP treatment and at clinical sign score of 1-2, and increased respectively by 32% and 15% (P<0.01) in spinal cord and sciatic nerve on 10th day after TOCP treatment and at clinical sign score of 3-4. Further changes of MDA were also observed after 15 and 21 days post-dosing and at clinical sign score of 5-6 and 7-8. There is a decrease in the activities of SOD, GSH-Px, GR, anti-ROS, and GSH content in cerebrum, spinal cord and sciatic nerve of hens after 5, 10, 15 and 21 days post-dosing and at clinical sign score of 1-2, 3-4, 5-6 and 7-8. Thus, OPIDN induced by TOCP was associated with elevation of lipid peroxidation and reduction of antioxidative status, and the time-dependent changes of these indexes in hens nerve tissues occurred. Sciatic nerve was the main target tissue and MDA was most sensitive among all indexes. The time-dependent and tissue specific changes of lipid peroxidation and antioxidative status in cerebrum, spinal cord and sciatic nerve suggest that ROS and concomitant lipid peroxidation, at least in part, are involved in the toxic effects of TOCP on nerve tissues and that oxidative stress may play a role in the occurrence and development of OPIDN induced by TOCP.

[Time dependent changes in antioxidation of rat serums and sciatic nerves caused by toxicology].

OBJECTIVE: To study the time dependent antioxidation changes of serum and sciatic nerve in rats intoxicated with acrylamide. METHODS: Male Wistar rats weighing 180 to 220 g were given acrylamide dissolved in physiological saline (40 mg/kg ip 3 days/week). The control groups received normal saline. The gait was observed and antioxidant indexes of rat serum and sciatic nerve were determined on 0, second, fourth, sixth, 10th week. RESULTS: With the extension of the intoxication period, compared with the control, the contents of glutathione in serum and sciatic nerve gradually decreased (P < 0.05; after 6 and 10 weeks to 92% and 77%; after 2, 4, 6 and 10 weeks to 92%, 82%, 67% and 66%); the levels of malondialdehyde gradually increased (P < 0.05; after 4, 6 and 10 weeks to 113%, 118% and 120%; after 4, 6 and 10 weeks to 153%, 167%, 174%); the abilities of the resistance to reactive oxygen species gradually decreased (P < 0.05; after 10 weeks to 82%; after 6 and 10 weeks to 76% and 71%); the activities of glutathione peroxidase gradually increased (P < 0.05; after 2, 4, 6 and 10 weeks to 122%, 130%, 160% and 124%; after 4, 6 and 10 weeks to 134%, 152% 164%); the activities of glutathione reductase increased at early stage (P < 0.01; after 4 and 6 weeks to 300% and 217%; after 4 weeks to 142%) and decreased later (P < 0.01; 6 and 10 weeks to 59% and 33% in sciatic nerve); the activities of superoxide dismutase increased primitively (P < 0.05; after 2 weeks to 110%; after 4 weeks to 124%) and decreased later (P < 0.05; after 10 weeks to 85% in serum). The changes of antioxidant indexes in serum and sciatic nerve according to gait score were similar. The level of MDA in serum was in high correlation (P < 0.01) with that in sciatic nerve. The regression coefficients were 0.99 and 0.96 according to the administration time and gait score respectively. CONCLUSION: The changes of the antioxidant indexes in serum and sciatic nerve of rat treated with acrylamide are time dependent. The changes in serum and sciatic nerve are similar but those in sciatic nerve are more remarkable.

[Clinical significance of prostatic-specific antigen levels in patients with benign prostatic hyperplasia complicated by low urinary tract syndrome].

OBJECTIVE: To evaluate the clinical significance of prostatic-specific antigen (PSA) levels in patients with benign prostatic hyperplasia (BPH) complicated by low urinary tract syndrome( LUTS). METHODS: The levels of tPSA, fPSA and fPSA/tPSA ratio were detected and compared in 520 cases of BPH with LUTS and 196 cases without LUTS. RESULTS: The mean levels of tPSA in the cases of BPH with LUTS and without LUTS were (5.13 +/- 2.49) microg/L and (1.73 +/- 1.26) microg/L respectively (P<0.01). The mean levels fPSA were (1.57 +/- 0.80) microg/L and (0.54 +/- 0.38) microg/L respectively (P < 0.01). The mean ratios of fPSA/tPSA were (0.31 +/- 0.09) and (0.30 +/- 0.11) respectively ( P > 0.05). CONCLUSION: The levels of tPSA, fPSA are significantly higher in the cases of BPH with LUTS than those in the cases without LUTS, but the ratio of fPSA/tPSA is stable in BPH.

Allyl chloride-induced time dependent changes of lipid peroxidation in rat nerve tissue.

To accurately know the time-dependent changes of the lipid peroxidation and antioxidative status for elucidating the mechanism of neuropathy induced by allyl chloride (AC), the malondialdehyde (MDA), anti-reactive oxygen species (anti-ROS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) were investigated in cerebrum, spinal cord and sciatic nerve of rats after 0, 3, 6, 9, 12 weeks of AC administration. AC was administrated to Wistar rats by gavage at a single dosage of 200 mg/kg/per dose (three times per week). Rats were sacrificed after 0, 3, 6, 9, 12 weeks of treatment, and cerebrum, spinal cord, sciatic nerves were dissected, homogenized and used for the determination of lipid peroxidation and antioxidative status. The results showed that MDA in cerebrum (112.4%) and sciatic nerve (113.1%) significantly increased (P<0.05) on third week of AC treatment and at gait score of 2, and further changes of MDA were observed after 6, 9, 12 weeks and at gait score of 3, 4. While a decrease (P<0.05) in the activities of GSH, CAT, GPx and SOD after 6, 9, 12 weeks intoxication and at gait score of 2, 3, 4 were observed in cerebrum, spinal cord and sciatic nerve. Anti-ROS activities also decreased in all three nerve tissues after 3, 6, 9, 12 weeks intoxication and at gait score of 2, 3, 4. Thus, AC intoxication was associated with elevation of lipid peroxidation and reduction of antioxidative status, and the time-dependent changes of these indexes in Wistar rats nerve tissues occurred. Sciatic nerve was the main target tissue and MDA was most sensitive among all indexes. The changes of lipid peroxidation and antioxidative status might be related to the degradation of nerve fiber and served as one of mechanisms of toxic neuropathy induced by AC.

[Experience in treating advanced prostate cancer with bladder outlet obstruction].

BACKGROUND & OBJECTIVE: The incidence and discovery rate of prostate cancer is increased in recent years; with advanced age and multiple organs dysfunction, the advanced prostate cancer patients have poor quality of life. This study was to explore suitable treatment for these patients. METHODS: A total of 80 advanced prostate cancer patients with bladder outlet obstruction were treated by transurethral electrovaporization of the prostate (TVP), plus castration and antiandrogen therapy. Preoperative individualized preparation was performed for each patient. International prostatic symptom score (IPSS), maximum flow rate of urine (Q(max)), prostatic-special antigen (PSA), and ultrasonography were measured before and 3 months after operation. RESULTS: TVP were successful in all cases. Postoperative IPSS was significantly lower than preoperative IPSS in patients with or without urine retention (13+/-3 vs. 31+/-2, 11+/-3 vs. 31+/-2, P<0.01); postoperative Q(max) was significantly higher than preoperative Q(max) in patients with or without urine retention [(19.0+/-3.3) ml/s vs. 0, (19.4+/-2.7) ml/s vs. (8.9+/-3.4) ml/s, P<0.01]. Postoperative PSA was significantly lower than preoperative PSA [(80.4+/-133.4) mg/L vs. (0.1+/-0.4) mg/L, P<0.05]. The volume of prostate was obviously reduced. CONCLUSION: TVP plus castration and endocrine therapy is a safe and effective treatment for advanced prostate cancer patients with bladder outlet obstruction.

[Comparison of endoscopic irsection and vaporization for superficial bladder cancer].

OBJECTIVE: To evaluate the method and clinical value of endoscopic surgery by comparing endoscopic resection and vaporization for superficial bladder tumor. METHODS: 396 patients with superficial bladder papillary transitional cell carcinoma were treated by endoscopic therapy. 180 patients (Group A) were treated by transurethral resection of bladder tumor (TURBT) and 216 (Group B) by transurethral vaporization of bladder tumor (TVBT). Periodic postoperative intra-vascular instillation of chemotherapy was given to both groups. Operating time, amount of bleeding during operation, complications and recurrence rate were compared. RESULTS: In group B, the amount of bleeding and complications during operation were lower than those in group A, but TVBT rated better by clearer view and simplicity in maneuver. The operating time, recurrence rate in group B were similar to those in group A. CONCLUSION: Transurethral vaporization of bladder cancer, with simplicity in maneuver, less bleeding and fewer complications, rates better in effectiveness and clinical value than resection.