The redox kinetics of VO 2? /VO 2 ? and V 3? / V 2? couples on a carbon paper (CP, HCP030 N, Shanghai Hesen, Ltd., China) electrode were investigated in terms of their standard rate constant (k 0 ) and reaction mechanism. The values determined for k 0 for VO 2? ? VO 2 ? and V 3? ? V 2? using the CP electrode are 1.0 9 10 -3 and 1.1 9 10 -3 cm s -1 , respectively. The value of k 0 increases by one or two order(s) of magnitude compared with values obtained using electrodes composed of pyrolytic graphite and glassy carbon. The acceleration of the redox kinetics of vanadium ions is a result of the large surface area of the CP electrode. An inner-sphere mechanism for the reaction on the surface of the electrode is proposed. The kinetic features of vanadium redox reactions on the CP electrode reveal that CP is suitable for use as the electrodes in vanadium redox-flow batteries.

Solid pseudopapillary neoplasms can be treated by complete tumor resection with limited resection or a minimally invasive approach when applicable. The combination of surgical resection and chemotherapy may therefore prolong survival, even in malignant cases.

Hepatectomy is a standard therapy that allows liver cancer patients to achieve long-term survival. Preceding hepatectomy, portal vein embolization (PVE) is frequently performed to increase the remnant liver size and reduce complications. Although the clinical importance of PVE is widely accepted, molecular mechanisms by which PVE leads to compensatory hypertrophy of nonembolized lobes remain elusive. We hypothesized that NF-E2-related factor 2 (Nrf2), a master regulator of cytoprotection, promotes compensatory liver hypertrophy after PVE. To address this hypothesis, we utilized three mouse lines and the portal vein branch ligation (PVBL) technique, which primarily induces the redistribution of the portal bloodstream in liver in a manner similar to PVE. PVBL was conducted in Kelch-like ECH-associated protein 1 (Keap1) conditional knockout (Keap1-CKO) mice in which Nrf2 is constitutively activated, along with Nrf2-deficient (Nrf2-KO) mice. We found that hypertrophy of nonligated lobes after PVBL was enhanced and limited in Keap1-CKO and Nrf2-KO mice, respectively, compared to wild-type mice. In Keap1-CKO mice, Nrf2 activity was increased, consistent with transient activation of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, and reactive hepatocyte proliferation was significantly prolonged after PVBL. Importantly, Nrf2 activation by a chemical inducer was also effective for enhancement of hypertrophy after PVBL. Conclusion: Nrf2 supports compensatory liver hypertrophy after PVBL. This finding is particularly intriguing, because the primary effect of PVBL is limited to the alteration of bloodstream; this effect is much milder than changes resulting from hepatectomy, in which intrahepatic bloodstream and bile production cease. Our results suggest that premedication with an Nrf2 inducer may be a promising strategy to improve the outcome of PVE; this approach expands the indication of hepatectomy to patients with poorer liver function. (HEPATOLOGY 2014;59:2371-2382 A n increasing number of patients suffer from primary liver cancers and metastatic liver cancers in both developing and developed countries. Hepatectomy is a standard curative therapy that allows for the long-term survival of liver cancer patients.2 In spite of the technical advancements, major hepatectomy still places patients at risk for complications caused by liver failure. The liver volume that remains after surgery has been shown to be a strong predictor of postoperative complications.3 Portal vein embolization (PVE), developed by Makuuchi et al., 4 is a preoperative treatment designed to prevent postoperative liver failure resulting from insufficient remnant liver mass. Selective PVE produces the atrophy of the embolized lobe and the compensatory hypertrophy of the contralateral lobe, which increases the remnant Abbreviations: Akt, protein kinase B; ALB, albumin; ALT, alanine aminotransferase; AST, aspartate aminotransferase; bTrCP, b-transducin repeat-containing protein; CDDO-Im, 2-cyano-3,12 dioxooleana-1,9-dien-28-imidazolide;...

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BackgroundPancreatic cancer is among the most lethal malignancies worldwide. This study aimed to identify a novel prognostic biomarker, facilitating treatment selection, using mass spectrometry (MS)-based proteomic analysis with formalin-fixed paraffin-embedded (FFPE) tissue.ResultsThe two groups with poor prognosis (n = 4) and with better prognosis (n = 4) had been carefully chosen among 96 resected cases of pancreatic cancer during 1998 to 2007 in Tohoku University Hospital. Although those 2 groups had adjusted background (UICC-Stage IIB, Grade2, R0, gemcitabine adjuvant), there was a significant difference in postoperative mean survival time (poor 21.0 months, better 58.1 months, P = 0.0067). Cancerous epithelial cells collected from FFPE tissue sections by laser micro-dissection (LMD) were processed for liquid chromatography-tandem mass spectrometry (LC-MS/MS). In total, 1099 unique proteins were identified and 6 proteins showed different expressions in the 2 groups by semi-quantitative comparison. Among these 6 proteins, we focused on Nm23/Nucleoside Diphosphate Kinase A (NDPK-A) and immunohistochemically confirmed its expression in the cohort of 96 cases. Kaplan-Meier analysis showed high Nm23/NDPK-A expression to correlate with significantly worse overall survival (P = 0.0103). Moreover, in the multivariate Cox regression model, Nm23/NDPK-A over-expression remained an independent predictor of poor survival with a hazard ratio of 1.97 (95% CI 1.16-3.56, P = 0.0110).ConclusionsWe identified 6 candidate prognostic markers for postoperative pancreatic cancer using FFPE tissues and immunohistochemically demonstrated high Nm23/NDPK-A expression to be a useful prognostic marker for pancreatic cancer.