We examine serum level of galectin-3 in patients with bladder cancer. We used serum samples of 67 patients with urological diseases and classified these patients into bladder cancer group (n=43) and control group (n=24). Galectin-3 concentration was measured by ELISA (Human Galectin-3 Assay Kit, IBL). And we selected the patient with high serum galectin-3 concentration (Urothelial Carcinoma, G3, pT3a pN0M0), we performed immunohistochemical staining with the VECTASTAIN ABC (Avidin Biotinylated enzyme Complex) system. Median value of serum galectin-3 concentration was 1068 pg/ml (range 551-2028) in the cancer group vs 584 pg/ml (range 259-1262) in controls. Serum galectin-3 concentration of the bladder cancer patients was statistically higher than that of controls (p<0.0005). There was no apparent correlation in serum galectin-3 concentration with the clinico-pathological features such as stage and grade. Higher expression of galectin-3 was observed in bladder cancer tissue than in normal bladder tissue. We suggest the measurement of serum galectin-3 is useful for diagnosis of bladder cancer.

Adiponectin, an adipocyte-derived hormone, has been proposed to show antiatherogenic properties through the inhibitory effects against various growth factors. Insulin-like growth factor-1 (IGF-1) is one of the potent mitogens, which has been considered to play important roles in both atherogenesis and plaque stabilization in accordance to the phase of atherosclerosis. The aim of this study is to elucidate the adiponectin effects on IGF-1-induced cell migration and its intracellular signaling pathways in vascular smooth muscle cells (VSMCs). In this study, we assessed cell migration and several kinase activities in cultured rat aortic smooth muscle cells (RASMCs). Adiponectin pretreatment suppressed IGF-1-induced cell migration and extracellular signal-regulated kinase (ERK)1/2 activation, which is one of the major mediators for IGF-1-induced cell migration. In RASMCs, adiponectin and 5-aminoimidazole-4-carboxamide riboside (AICAR), a 5¢-AMP-activated protein kinase (AMPK) activator, stimulated AMPK activation. AMPK activation by AICAR inhibited IGF-1-induced ERK1/2 activation and cell migration in RASMCs. On the other hand, phosphorylation of Akt and Bad, proapoptotic molecules of the Bcl-2 family, which were increased by IGF-1 stimulation, was not diminished by the pretreatment with adiponectin. It was shown that adiponectin inhibited IGF-1-induced VSMC migration through suppression of ERK1/2 activation, which might be implicated in AMPK activation. Furthermore, adiponectin selectively inhibited ERK1/2 pathway, not Akt-Bad pathway, stimulated by IGF-1. From these findings, it was implied that adiponectin suppressed IGF-1-induced VSMC migration and its signaling selectivity.

We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in N -nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1 g/l) or L-NAME ϩ nitrite (low dose: 0.1 mg/l, medium dose: 1 mg/l, high dose: 10 mg/l) for 8 wk. We evaluated blood NO levels as hemoglobin-NO adducts (ironnitrosyl-hemoglobin), using an electron paramagnetic resonance method. Chronic administration of L-NAME for 8 wk induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control 38.8 Ϯ 8.9 vs. L-NAME 6.0 Ϯ 3.1 arbitrary units). Coadministration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAMEinduced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histological changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude that dietary nitrite-derived NO generation may serve as a backup system when the nitric oxide synthase/L-arginine-dependent NO generation system is compromised.vegetables; N -nitro-L-arginine methyl ester; kidney NITRIC OXIDE (NO) is a gaseous signaling molecule and exerts a variety of biological actions under physiological and pathophysiological conditions, such as regulation of the cardiovascular, inflammation, immune, and neuronal systems. NO also has numerous important functions in the kidney, such as the regulation of renal hemodynamics and glomerular microcirculation, the regulation of salt balance, the blunting of tubuloglomerular feedback, and the modulation of renal sympathetic nerve activity (18,26). Chronic blockade of nitric oxide synthases (NOSs) with N -nitro-L-arginine methyl ester (L-NAME) in rats results in severe hypertension and progressive kidney damage (3, 11). On the other hand, NO production seems to be low in chronic kidney disease (CKD) patients, and NO deficiency may play a role in CKD progression (5, 32). Treatment strategies to maintain the circulating NO level in healthy young people may be useful in preventing or slowing the progression of renal diseases.It is believed that NO is synthesized from L-arginine, NADPH, tetrahydrobiopterin, and the molecular oxygen catalyzed by NOSs in endothelial and other cells. The biological activity of NO is terminated by oxidation into nitrite and nitrate. Therefore, nitrite and nitrate in the blood are recognized as waste forms of NO. However, this dogma is now being challe...

: No adequate serum predictive biomarker currently exists, which can identify the activity of renal cell carcinoma (RCC). We investigate the association of serum hepatocyte growth factor (HGF) and serum vascular endothelial growth factor (VEGF) levels with clinicopathologic parameters in untreated clear cell RCC patients. We measured serum levels of HGF and VEGF in 45 patients with untreated clear cell RCC and 45 healthy controls using an enzyme-linked immunosorbent assay (ELISA). Patients with clear cell RCC had significantly higher serum HGF and VEGF concentrations than healthy subjects : median, 1070.7 versus 728.3 pg/ml (p 0.0001) for HGF ; and median, 397.5 versus 245.6 pg/ml (p=0.0003) for VEGF. We found a significant correlation between serum level of HGF and clinical stage and tumor grade. Survival of patients with high serum HGF ( 1150 pg/ml) was significantly reduced compared to patients with low serum HGF concentrations (p=0.0044). In patients with nuclear grade 2 or high stage RCC, the higher serum HGF group exhibited significantly lower cause-specific survival (p= 0.0087 and p 0.05, respectively). No significant difference was observed between serum VEGF levels and cause-specific survival rate. Serum HGF might be a diagnostic and prognostic indicator in clear cell RCC, especially for patients with grade 2 or high stage RCC.

The influence of the console surgeon on the feasibility and outcome of various robot-assisted surgeries has been evaluated. These variables may be partially affected by the skills of the patient-side surgeon (PSS), but this has not been evaluated using objective data. This study aimed to describe the surgical techniques of the PSS in robot-assisted radical cystectomy (RARC) and intracorporeal ileal conduit (ICIC) urinary diversion and objectively examine the changes in surgical outcomes with increasing PSS experience. During a 3-year period, 28 men underwent RARC and ICIC urinary diversion. Clinical characteristics and surgical outcomes were compared between patients who underwent surgery early (first half group) or late in the study period (second half group). The pre-docking incision enabled easy specimen removal. The glove port technique widened the working space of the PSS. The stay suture allowed the PSS to control the distal portion of the conduit, facilitating the passage of the ureteral stents. During stoma creation, pneumoperitoneum pressure was lost by opening the abdominal cavity. To overcome this problem, the robotic arm was used to lift the abdominal wall to maintain the surgical field and facilitate the PSS procedure. Compared with the first half group, the second half group had significantly shorter times for urinary diversion (202 min vs 148 min, p < 0.001), ileal isolation and anastomosis (73 min vs 45 min, p < 0.001), and stenting (23.0 min vs 6.5 min, p < 0.001). As the experience of the PSS increased, the time of the PSS procedures decreased.