Chronic hypoxia-induced slug promotes invasive behavior of prostate cancer cells by activating expression of ephrin-B1.

Advanced solid tumors are exposed to hypoxic conditions over longer periods of time as they grow. Tumor hypoxia is a major factor that induces malignant progression, but most previous studies on tumor hypoxia were performed under short-term hypoxia for up to 72 hours and few studies have focused on tumor response to chronic hypoxic conditions. Here we show a molecular mechanism by which chronic hypoxia promotes invasive behavior in prostate cancer cells. We found that an epithelial-mesenchymal transition (EMT)-driving transcription factor, slug, is specifically upregulated under chronic hypoxia and promotes tumor cell migration and invasion. Unexpectedly, processes associated with EMT, such as loss of E-cadherin, are not observed under chronic hypoxia. Instead, expression of ephrin-B1, a ligand of Eph-related receptor tyrosine kinases, is markedly induced by slug through E-box motifs and promotes cell migration and invasion. Furthermore, slug and ephrin-B1 are highly coexpressed in chronic hypoxic cells of human prostate adenocarcinoma tissues after androgen deprivation, which is known to cause tumor hypoxia. Taken together, these results indicate that chronic hypoxia-induced slug promotes invasive behavior of prostate cancer cells by activating the expression of ephrin-B1. In addition, ephrin-B1 may be a novel therapeutic target in combination with androgen deprivation therapy for aggressive prostate cancer.

Laparoendoscopic single-site nephrectomy for hemodialysis patients with dialysis-related renal tumors.

PURPOSE: The purpose of this study is to assess the efficacy of laparoendoscopic single-site (LESS) nephrectomy in hemodialysis patients, we compared outcomes between LESS nephrectomy and conventional laparoendoscopic nephrectomy in hemodialysis patients with dialysis-related renal tumors. MATERIAL AND METHODS: A total of 16 hemodialysis patients who underwent LESS nephrectomy (LESS-N; n = 8) or conventional laparoendoscopic nephrectomy (C-N; n = 8) between November 2003 and July 2012 were retrospectively evaluated. Outcomes were compared between the two groups. RESULTS: Patient and tumor characteristics were similar between the LESS-N and C-N groups. The mean operative duration was longer in the LESS-N than in the C-N group (231.0 ± 26.7 min versus 188.6 ± 36.4 min; p = .025). The mean estimated blood loss was lower in the LESS-N compared with the C-N group (26.4 ± 14.4 ml versus 65.6 ± 45.2 ml; p = .047). Postoperative complications were observed in three cases, comprising one case of retroperitoneal hematoma in the LESS-N group and one case each of peritoneal hematoma and retroperitoneal abscess in the C-N group. Surgical scarring was minimal in the LESS-N group. CONCLUSIONS: Although there is a little extension of the operating time, LESS nephrectomy in hemodialysis patients is a feasible procedure compared with the conventional method.

Kidney-specific knockout of Sav1 in the mouse promotes hyperproliferation of renal tubular epithelium through suppression of the Hippo pathway.

We have previously reported that Salvador homologue 1 (SAV1), a component of the Hippo pathway, is significantly down-regulated in high-grade clear cell renal cell carcinoma (ccRCC) due to 14q copy number loss, and that this down-regulation contributes to the proliferation and survival of renal tubular epithelial cells through activation of Yes-associated protein 1 (YAP1), a downstream target of the Hippo pathway. However, the impact of SAV1 loss on the proliferation and survival of kidney cells in vivo remained to be determined. To address this issue, we generated kidney-specific Sav1-knockout (Cdh16-Cre;Sav1(fl/fl) ) mice. Sav1 deficiency enhanced the proliferation of renal tubular epithelial cells in Cdh16-Cre;Sav1(fl/fl) mice, accompanied by nuclear localization of Yap1, suggesting suppression of the Hippo pathway. Sav1 deficiency in renal tubules also caused structural and cellular abnormalities of the epithelial cells, including significant enlargement of their nuclei. Furthermore, Cdh16-Cre;Sav1(fl/fl) mice developed both glomerular and tubular cysts. Although lining cells of the glomerular cysts showed no atypia, those of the tubular cysts showed variations in cell size and nuclear shape, which became more severe as the mice aged. In aged Cdh16-Cre;Sav1(fl/fl) mice, we observed focal disruption of proximal tubules and perivascular lymphocytic infiltration. In conclusion, Sav1 is required for the maintenance of growth, nuclear size and structure of renal tubules under physiological conditions, and its deficiency leads to the acquisition of enhanced proliferation of renal epithelial cells through suppression of Hippo signalling.

Downregulation of WDR20 due to loss of 14q is involved in the malignant transformation of clear cell renal cell carcinoma.

Previously, we reported that genomic loss of 14q occurs more frequently in high-grade than in low-grade clear cell renal cell carcinomas (ccRCCs), and has a significant impact on the levels of expression of genes located in this region, suggesting that such genes may be involved in the malignant transformation of ccRCCs. Here, we found that six of the genes located in the minimal common region of 14q loss were significantly downregulated in high-grade ccRCCs due to copy number loss. Using a dataset from The Cancer Genome Atlas Research Network, we found that downregulation of one of these six genes, WDR20, was significantly associated with poorer outcome in patients with ccRCC, suggesting that WDR20 downregulation may be involved in the malignant transformation of ccRCCs. In functional assays, exogenous WDR20 significantly inhibited the growth of RCC cell lines and induced apoptosis. Interestingly, the phosphorylation levels of ERK and protein kinase B/AKT, which reportedly contribute to the malignant phenotype of RCC cells, were clearly reduced by exogenous expression of WDR20. Thus, our data suggest that downregulation of WDR20 due to 14q loss may be involved in the malignant transformation of ccRCCs, in part through activation of the ERK and protein kinase B/AKT pathways.

Differential effects of water-based exercise on the cognitive function in independent elderly adults.

BACKGROUND: Physical exercise has been reported to be the most effective method to improve cognitive function and brain health, but there is as yet no research on the effect of water-based exercise. AIMS: The aim of the present study was to compare the effects of water-based exercise with and without cognitive stimuli on cognitive and physical functions. METHODS: The design is a single-blind randomized controlled study. Twenty-one participants were randomly assigned to a normal water-based exercise (Nor-WE) group or a cognitive water-based exercise (Cog-WE) group. The exercise sessions were divided into two exercise series: a 10-min series of land-based warm-up, consisting of flexibility exercises, and a 50-min series of exercises in water. The Nor-WE consisted of 10 min of walking, 30 min of strength and stepping exercise, including stride over, and 10 min of stretching and relaxation in water. The Cog-WE consisted of 10 min of walking, 30 min of water-cognitive exercises, and 10 min of stretching and relaxation in water. Cognitive function, physical function, and ADL were measured before the exercise intervention (pre-intervention) and 10 weeks after the intervention (post-intervention). RESULTS: Participation in the Cog-WE performed significantly better on the pegboard test and the choice stepping reaction test and showed a significantly improved attention, memory, and learning, and in the general cognitive function (measured as the total score in the 5-Cog test). Participation in the Nor-WE dramatically improved walking ability and lower limb muscle strength. CONCLUSION: Our results reveal that the benefits elderly adults may obtain from water-based exercise depend on the characteristics of each specific exercise program. These findings highlight the importance of prescription for personalized water-based exercises to elderly adults to improve cognitive function.

[Elucidating the molecular mechanism of prostate cancer progression under chronic hypoxia and development of the novel therapeutic approach].

Cancer cells encounter a hypoxic microenvironment during tumor growth and progression. In addition, androgen-deprivation therapy against prostate cancer can develop secondary to a hypoxic condition caused by drastic blood supply reduction because androgen drives angiogenic inducers including vascular endothelial growth factor (VEGF) and inhibits angiogenesis inhibitor prostatic pigment epithelium-derived factor (PEDF). Extreme hypoxic conditions are not suitable for cancer survival, however, cancer cells soon adapt to a hypoxic environment and survive. We established a prostate cancer cell line cultured under chronic hypoxia and analyzed a castration-resistant phenotype. Here, the Vav3 was identified as a key oncogenic molecule associated with castration-resistance under chronic hypoxia. We analyzed the functions of Vav3 and Vav3-mediated signaling to establish a novel therapeutic target for castration-resistant prostate cancer.

Targeting the Vav3 oncogene enhances docetaxel-induced apoptosis through the inhibition of androgen receptor phosphorylation in LNCaP prostate cancer cells under chronic hypoxia.

BACKGROUND: The Vav family of Rho/Rac guanosine nucleotide exchange factors comprises three members in mammalian cells. Vav3 enhances androgen receptor (AR) activity during progression to androgen independence in prostate cancer. We examined Vav3 small interfering RNA (siRNA) effects on cell proliferation and apoptosis in docetaxel-treated LNCaP cells under chronic hypoxia (LNCaPH). METHODS: We examined individual and combined effects of Vav3 siRNA (si-Vav3) and docetaxel on cell growth and apoptosis under chronic hypoxia by cell proliferation, flow cytometric, DNA fragmentation, and immunoblot analyses. To clarify the molecular basis of si-Vav3- and docetaxel-induced apoptosis, we analyzed alterations in phosphatidylinositol 3-kinase (PI3K)/Akt, extracellular signal-regulate kinase (ERK), c-jun N-terminal kinase (JNK), and AR pathways using kinase inhibitors in LNCaPH cells. The effects of si-Vav3/atelocollagen complex alone or in combination with docetaxel were assessed on xenografts in nude mice by tumor growth delay. RESULTS: Vav3 overexpression was observed in LNCaPH compared with the expression under normoxia. Interrupting Vav3 signaling using siRNA enhanced docetaxel-induced cell growth suppression compared with that induced by docetaxel alone by inhibition of Akt and ERK phosphorylation, resulting in AR phosphorylation inhibition. In addition to increased B-cell lymphoma 2 (Bcl-2) phosphorylation through JNK signaling in response to docetaxel, si-Vav3 enhanced docetaxel-induced apoptosis, as characterized by the accumulation of sub-G1 phase cells and DNA fragmentation, through Bcl-xL/Bcl-2-associated death promoter (Bad) dephosphorylation, resulting in increased caspase-9, caspase-3, and cleaved poly(ADP-ribose) polymerase activation. Xenograft tumor growth was slightly inhibited by si-Vav3/atelocollagen complex injection and combined use of si-Vav3/atelocollagen complex and docetaxel produced a greater effect than docetaxel alone. CONCLUSIONS: Interrupting Vav3 signaling enhances docetaxel-induced apoptosis in LNCaP cells under chronic hypoxia by inhibiting the PI3K/Akt, ERK, and AR signaling pathways. Therapy targeting Vav3 in combination with docetaxel may have practical implications for managing castration-resistant prostate cancer.

Myostatin inhibits proliferation of human urethral rhabdosphincter satellite cells.

OBJECTIVES: Myostatin, a member of the transforming growth factor-ß superfamily, is a negative regulator of myogenesis in skeletal muscle. We examined the effect of myostatin and myostatin inhibition by an antagonistic agent, follistatin, on growth of human urethral rhabdosphincter satellite cells (muscle stem cells) to develop a new strategy for treatment of stress urinary incontinence. METHODS: Rhabdosphincter satellite cells were cultured and selected by magnetic affinity cell sorting using an anti-neural cell adhesion molecule antibody. The cells were transfected with simian virus-40 antigen to extend their lifespan. A cell proliferation assay, a cell cycle analysis and an investigation of signal transduction were carried out. The autocrine action of endogenous myostatin by western blotting, real-time reverse transcription polymerase chain reaction and immunoneutralization using an anti-myostatin antibody was also evaluated. RESULTS: Selectively cultured cells expressed markers of striated muscles and successfully differentiated into myotubes. Myostatin inhibited proliferation of these cells through Smad2 phosphorylation and cell cycle arrest. Inhibitory effects of myostatin were reversed by addition of follistatin. However, rhabdosphincter satellite cells did not appear to use autocrine secretion of myostatin to regulate their proliferation. CONCLUSIONS: Inhibition of myostatin function might be a useful pathway in the development of novel strategies for stimulating rhabdosphincter cells regeneration to treat stress urinary incontinence.

[Study of laparoendoscopic single-site surgery (LESS) for urachal remnants in our department].

OBJECTIVE: We examined laparoendoscopic single-site surgery (LESS) for urachal remnants and evaluated its usefulness and efficacy. PATIENTS AND METHODS: From August 2011 to July 2012, we underwent this surgery for 5 patients (3 males, 2 females). The mean age was 30.8 (25-36) years old. A 2 cm incision was made around the umbilicus and Access Platform was placed. The entire urachal tissues were excised, and this 2 cm incison was reshaped as the umbilicus. RESULTS: The median operative time was 220 (156-460) minutes, and the median operative blood loss was 10 (10-70) ml. They had no operative complications, and were discharged 6 (5-14) days after surgery. CONCLUSIONS: Our surgical procedures have very excellent cosmesis and advantages in particular for young because we reshape as the umbilicus the surgical wound. We think that this surgery can be performed safe and effectively for surgeons trained in the conventional laparoscopic procedures.

Genomic profiling of renal cell carcinoma in patients with end-stage renal disease.

The purpose of the present study was to determine the genomic profile of renal cell carcinoma (RCC) in end-stage renal disease (ESRD) by analyzing genomic copy number aberrations. Seventy-nine tumor samples from 63 patients with RCC-ESRD were analyzed by array comparative genomic hybridization using the Agilent Whole Human Genome 4 × 44K Oligo Micro Array (Agilent Technologies Inc., Palo Alto, CA, USA). Unsupervised hierarchical clustering analysis revealed that the 63 cases could be divided into two groups, Clusters A and B. Cluster A was comprised mainly of clear cell RCC (CCRCC), whereas Cluster B was comprised mainly of papillary RCC (PRCC), acquired cystic disease (ACD)-associated RCC, and clear cell papillary RCC. Analysis of the averaged frequencies revealed that the genomic profiles of Clusters A and B resembled those of sporadic CCRCC and sporadic PRCC, respectively. Although it has been proposed on the basis of histopathology that ACD-associated RCC, clear cell papillary RCC and PRCC-ESRD are distinct subtypes, the present data reveal that the genomic profiles of these types, categorized as Cluster B, resemble one another. Furthermore, the genomic profiles of PRCC, ACD-associated RCC and clear cell papillary RCC admixed in one tissue tended to resemble one another. On the basis of genomic profiling of RCC-ESRD, we conclude that the molecular pathogenesis of CCRCC-ESRD resembles that of sporadic CCRCC. Although various histologic subtypes of non-clear cell RCC-ESRD have been proposed, their genomic profiles resemble those of sporadic PRCC, suggesting that the molecular pathogenesis of non-CCRCC-ESRD may be related to that of sporadic PRCC.

Downregulation of SAV1 plays a role in pathogenesis of high-grade clear cell renal cell carcinoma.

BACKGROUND: Clinical outcome of patients with high-grade ccRCC (clear cell renal cell carcinoma) remains still poor despite recent advances in treatment strategies. Molecular mechanism of pathogenesis in developing high-grade ccRCC must be clarified. In the present study, we found that SAV1 was significantly downregulated with copy number loss in high-grade ccRCCs. Therefore, we investigated the SAV1 function on cell proliferation and apoptosis in vitro. Furthermore, we attempted to clarify the downstream signaling which is regulated by SAV1. METHODS: We performed array CGH and gene expression analysis of 8 RCC cell lines (786-O, 769-P, KMRC-1, KMRC-2, KMRC-3, KMRC-20, TUHR4TKB, and Caki-2), and expression level of mRNA was confirmed by quantitative RT-PCR (qRT-PCR) analysis. We next re-expressed SAV1 in 786-O cells, and analyzed its colony-forming activity. Then, we transfected siRNAs of SAV1 into the kidney epithelial cell line HK2 and renal proximal tubule epithelial cells (RPTECs), and analyzed their proliferation and apoptosis. Furthermore, the activity of YAP1, which is a downstream molecule of SAV1, was evaluated by western blot analysis, reporter assay and immunohistochemical analysis. RESULTS: We found that SAV1, a component of the Hippo pathway, is frequently downregulated in high-grade ccRCC. SAV1 is located on chromosome 14q22.1, where copy number loss had been observed in 7 of 12 high-grade ccRCCs in our previous study, suggesting that gene copy number loss is responsible for the downregulation of SAV1. Colony-forming activity by 786-O cells, which show homozygous loss of SAV1, was significantly reduced when SAV1 was re-introduced exogenously. Knockdown of SAV1 promoted proliferation of HK2 and RPTEC. Although the phosphorylation level of YAP1 was low in 786-O cells, it was elevated in SAV1-transduced 786-O cells. Furthermore, the transcriptional activity of the YAP1 and TEAD3 complex was inhibited in SAV1-transduced 786-O cells. Immunohistochemistry frequently demonstrated nuclear localization of YAP1 in ccRCC cases with SAV1 downregulation, and it was preferentially detected in high-grade ccRCC. CONCLUSIONS: Taken together, downregulation of SAV1 and the consequent YAP1 activation are involved in the pathogenesis of high-grade ccRCC. It is an attractive hypothesis that Hippo signaling could be candidates for new therapeutic target.

Gender differences in the ST segment: effect of androgen-deprivation therapy and possible role of testosterone.

BACKGROUND: ST-segment elevation in a structurally normal heart is observed in Brugada- and early repolarization syndrome. The incidence of both syndromes is much higher in males than females. Clinical and basic studies suggest that testosterone plays an important role in ventricular repolarization. METHODS AND RESULTS: Standard surface 12-lead electrocardiograms recorded in 640 healthy subjects were studied (310 males, 330 females ranging in age from 5 to 89 years) (Study 1). The 3 ST levels (ST-J, -M, and -E) were measured in leads V(2) and V(5), which are representative of the right and left ventricles, respectively. The effect of androgen-deprivation therapy on the ST segment was also evaluated in 21 prostate cancer patients (Study 2). In both leads, the 3 ST levels were significantly higher in adult males than females (P<0.0001) due to a marked increase after puberty in males. As their age increased, males manifested a gradual reduction in the ST level in both leads; in females, there was a reduction in lead V(5) only. In both sexes, all 3 ST levels were significantly higher in lead V(2) than V(5) (P<0.0001). Androgen-deprivation therapy significantly decreased all 3 ST segments in both leads. CONCLUSIONS: Significant age- and gender differences in the ST segment in healthy adults were found, suggesting that testosterone modulates the early phase of ventricular repolarization.

Beta2-microglobulin signaling blockade inhibited androgen receptor axis and caused apoptosis in human prostate cancer cells.

PURPOSE: beta2-Microglobulin (beta2M) has been shown to promote osteomimicry and the proliferation of human prostate cancer cells. The objective of this study is to determine the mechanism by which targeting beta2M using anti-beta2M antibody inhibited growth and induced apoptosis in prostate cancer cells. EXPERIMENTAL DESIGN: Polyclonal and monoclonal beta2M antibodies were used to interrupt beta2M signaling in human prostate cancer cell lines and the growth of prostate tumors in mice. The effects of the beta2M antibody on a survival factor, androgen receptor (AR), and its target gene, prostate-specific antigen (PSA) expression, were investigated in cultured cells and in tumor xenografts. RESULTS: The beta2M antibody inhibited growth and promoted apoptosis in both AR-positive and PSA-positive, and AR-negative and PSA-negative, prostate cancer cells via the down-regulation of the AR in AR-positive prostate cancer cells and directly caused apoptosis in AR-negative prostate cancer cells in vitro and in tumor xenografts. The beta2M antibody had no effect on AR expression or the growth of normal prostate cells. CONCLUSIONS: beta2M downstream signaling regulates AR and PSA expression directly in AR-positive prostate cancer cells. In both AR-positive and AR-negative prostate cancer cells, interrupting beta2M signaling with the beta2M antibody inhibited cancer cell growth and induced its apoptosis. The beta2M antibody is a novel and promising therapeutic agent for the treatment of human prostate cancers.

Relationships between swim performance, maximal oxygen uptake and peak power output when wearing a wetsuit.

This study was intended to investigate the effect of wearing a wetsuit (WS) on physical performance capacity, which are maximal oxygen uptake (V O(2)max) and maximal mechanical power output (POmax), and to demonstrate whether wearing a WS affected the relationship between maximal 400m swim performance (V400) and V O(2)max, and between sprint swim performance (Vsprint) and V O(2)max. Twelve triathletes participated in this study. V O(2)max was determined during the continuous progressive swimming test. The mean velocity over maximal 400m swim was defined as V400. Active drag (AD), Vsprint and POmax were measured by a specific method called "perturbation method". Compared with wearing a swimsuit (SS), V400 was improved without enhancing V O(2)max and Vsprint was also improved without enhancing POmax and AD by wearing a WS. Significant correlations were found between V400 and V O(2)max and between Vsprint and POmax in the both suit conditions, but a higher correlation was found in the WS condition than in the SS condition. These results suggested that improved swim performance from wearing a WS was attributable only to improvement in technical factors, such as propulsion efficiency. In conclusion, during swimming with a WS, performance gain was not associated with physiological factors but with propulsion efficiency related to a gain in buoyancy and to drag reduction. However, when wearing a WS, V400 and Vsprint more reflected the values of V O(2)max and POmax, respectively.

Comparison two-year effects of once-weekly and twice-weekly water exercise on health-related quality of life of community-dwelling frail elderly people at a day-service facility.

PURPOSE: The purpose of this study was to compare two-year effects of once-weekly and twice-weekly water exercise programmes at a day-service facility on the health-related quality of life (HRQL) of frail elderly people. METHOD: This single blind, prospective, longitudinal randomized pilot study separated 22 community-dwelling frail elderly people into once-weekly (once group: n = 10) and twice-weekly (twice group: n = 12) groups: the two-year exercise interventions were once- or twice-weekly 1-h sessions. Water exercise sessions comprised warming-up on land, activities of daily living (ADL) exercise, stretching, strength, and relaxation in water. The HRQL was evaluated using the Medical Outcomes Survey Short Form-36 questionnaire (SF-36); ADL dependence was assessed using the Functional Independence Measure (FIM). RESULT: Both groups showed significant increases over pre-intervention (pre) scores at 6 months and 12 months on Physical Component Summary and Mental Component Summary. In the once group, both were lower at 24 months than at 6 months and 12 months. The FIM scores were significantly different from pre at 6 months and 12 months in both once and twice groups, and between pre and 24 month in the twice group. CONCLUSION: Better than once-weekly exercise, twice-weekly water exercise controlled deterioration of HRQL, ADL, and knee extensor muscle strength (KEX) with ageing.

Epithelial to mesenchymal transition (EMT) in human prostate cancer: lessons learned from ARCaP model.

Androgen refractory cancer of the prostate (ARCaP) cells contain androgen receptor (AR) and synthesize and secrete prostate specific antigen (PSA). We isolated epithelia-like ARCaP(E) from parental ARCaP cells and induced them to undergo epithelial-mesenchymal transition (EMT) by exposing these cells to soluble factors including TGFbeta1 plus EGF, IGF-1, beta2-microglobulin (beta2-m), or a bone microenvironment. The molecular and behavioral characteristics of the resultant ARCaP(M) were characterized extensively in comparison to the parental ARCaP(E) cells. In addition to expressing mesenchymal biomarkers, ARCaP(M) gained 100% incidence of bone metastasis. ARCaP(M) cells express receptor activator of NF-kappaB ligand (RANKL), which was shown to increase tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts in culture, and when metastatic to bone in vivo. We provide evidence that RANKL expression was promoted by increased cell signaling mediated by the activation of Stat3-Snail-LIV-1. RANKL expressed by ARCaP(M) cells is functional both in vitro and in vivo. The lesson we learned from the ARCaP model of EMT is that activation of a specific cell signaling pathway by soluble factors can lead to increased bone turnover, mediated by enhanced RANKL expression by tumor cells, which is implicated in the high incidence of prostate cancer bone colonization. The ARCaP EMT model is highly attractive for developing new therapeutic agents to treat prostate cancer bone metastasis.

Lower extremity muscle activity during deep-water running on self-determined pace.

Although deep-water running (DWR) is often used to obtain the benefits of aerobic fitness and to reduce vertical component stress, its attendant muscle stress remains unclear. The present study investigated lower extremity muscle activity and during DWR compared to that during land walking (LW) and water walking (WW). Surface electromyography was used to evaluate muscle activity in nine healthy adults during each exercise at self-determined slow, moderate, and fast paces. The duration of swing phase, ankle, knee and hip joint angle, and each joint range of motion (ROM) also investigated. Results show that the percentages of maximal voluntary contraction (%MVC) of the soleus and medial gastrocnemius were lower during DWR than during LW or WW in the backward swing phase. The %MVC of the rectus femoris was higher during WW and DWR than during LW; that of the vastus lateralis was lower during WW and DWR than during LW in the forward swing phase. In the biceps femoris, the %MVC was higher during DWR than during LW or WW in the forward and backward swing phase. Every pace showed a similar trend. These results suggest that DWR can stimulate the hip joint flexor or extensor muscles.

Retroperitoneoscopic treatment of ovarian vein syndrome.

In this paper, we describe a case of ovarian vein syndrome (OVS) successfully treated with retroperitoneoscopic techniques. A 41-year-old woman complained with right flank pain, especially with a recumbent position. OVS was diagnosed and ureterolysis and ovarian vein resection were successfully performed, using retroperitoneoscopic techniques. The patient has been completely pain free for 36 months of follow-up. To our knowledge, no previous reports have described the retroperitoneoscopic treatment of OVS. With the minimally invasive approach, postoperative recovery and patient quality of life were markedly improved.