A current challenge to alkaline polymer electrolyte fuel cells (APEFCs) is the unexpectedly sluggish kinetics of the hydrogen oxidation reaction (HOR). A recently proposed resolution is to enhance the oxophilicity of the catalyst, so as to remove the H ad intermediate through reacting with OH ad , but this approach is questioned by other researchers.Here we report a clear and convincing test on this problem. By using PtRu/C as the HOR catalyst for APEFC, the peak power density is boosted to 1.0 W/cm 2 , in comparison to 0.6 W/cm 2 when using Pt/C in the anode. Such a remarkable improvement, however, can hardly be explained as an oxophilic effect, because, as monitored by CO stripping, reactive hydroxyl species can generate on certain sites of the Pt surface at more negative potentials than on the PtRu surface in KOH solution. Rather, the incorporation of Ru has posed an electronic effect on weakening the Pt-H ad interaction, as revealed by the voltammetric behavior and from density-functional calculations, which thus benefits the oxidative desorption of H ad , the rate determining step of HOR in alkaline media. These findings further our fundamental understanding of the HOR catalysis, and cast a new light on the exploration of better catalysts for APEFC. 5 process to monitor the generation of reactive hydroxyl species, for the anodic current of CO oxidation has to be triggered by reactive hydroxyl species. 31 As demonstrated in Figure 2, in 0.1 M H 2 SO 4 solution, the CO stripping on Pt/C takes on a single sharp peak at 0.85 V, and, upon alloying with Ru, the CO stripping peak is somewhat broadened and moves negatively by 0.3 V, showing that Ru does accelerate the formation of OH ad in acidic environment.However, the CO stripping on Pt/C behaves rather differently in 0.1 M KOH solution: multiple anodic peaks appear and the onset potential shifts to ~0.2 V, a potential even more negative than the onset of CO stripping on PtRu/C (~0.35 V) in either acid or alkaline media.Such a surprising finding indicates that, in alkaline environment, the reactive hydroxyl species, be it OH ad or OH ad − , can generate on certain sites of the Pt surface more favorably than on the PtRu surface; but when alloyed with Ru, the surface reactivity of Pt is suppressed, thereby no reactive hydroxyl species appearing at the potential region negative to 0.35 V.On the basis of the above observations, the promotion effect of Ru on catalyzing the HOR in alkaline media can hardly be explained as an oxophilic effect. The existence of reactive hydroxyl species on either Pt or PtRu surface at potentials negative to 0.2 V also seems unlikely, as revealed by Figure 2. On the other hand, the Ru has posed an obvious effect on weakening the Pt-H ad interaction, as a consequence of the suppressed surface reactivity of Pt. As illustrated in Figure 3a, in KOH solution, the hydrogen underpotential deposition (H-UPD) and subsequent desorption behavior on PtRu/C is clearly different from that on Pt/C: whereas strong H ad peaks are the major signal for Pt/C...

Increasing evidence suggests that the presence of endotoxemia is of substantial clinical relevance to patients with cirrhosis, but it is unclear whether and how gut-derived LPS amplifies the tumorigenic response of the liver. We found that the circulating levels of LPS were elevated in animal models of carcinogen-induced hepatocarcinogenesis. Reduction of LPS using antibiotics regimen in rats or genetic ablation of its receptor Toll-like receptor 4 (TLR4) in mice prevented excessive tumor growth and multiplicity. Additional investigation revealed that TLR4 ablation sensitizes the liver to carcinogen-induced toxicity via blocking NF-jB activation and sensitizing the liver to reactive oxygen species (ROS)-induced toxicity, but lessens inflammation-mediated compensatory proliferation. Reconstitution of TLR4-expressing myeloid cells in TLR4-deficient mice restored diethylnitrosamine (DEN)-induced hepatic inflammation and proliferation, indicating a paracrine mechanism of LPS in tumor promotion. Meanwhile, deletion of gut-derived endotoxin suppressed DENinduced cytokine production and compensatory proliferation, whereas in vivo LPS prechallenge promotes hepatocyte proliferation. Conclusion: Our data indicate that sustained LPS accumulation represents a pathological mediator of inflammation-associated hepatocellular carcinoma (HCC) and manipulation of the gut flora to prevent pathogenic bacterial translocation and endotoxin absorption may favorably influence liver function in patients with cirrhosis who are at risk of developing HCC. (HEPATOLOGY 2010;52:1322-1333

Adult hepatic progenitor (oval) cells are facultative stem cells in liver, which participate in a range of human liver diseases, including hepatocellular carcinoma (HCC). However, the molecular pathways regulating the expansion and differentiation of these cells are poorly understood. We show that active Wnt/B-catenin signaling occurs preferentially within the oval cell population, and forced expression of constitutively active B-catenin mutant promotes expansion of the oval cell population in the regenerated liver. More importantly, we identify a subpopulation of less differentiated progenitor-like cells in HCC cell lines and primary HCC tissues, which are defined by expression of the hepatic progenitor marker OV6 and endowed with endogenously active Wnt/B-catenin signaling. These OV6 + HCC cells possess a greater ability to form tumor in vivo and show a substantial resistance to standard chemotherapy compared with OV6 À tumor cells. The fraction of tumor cells expressing OV6 is enriched after Wnt pathway activation, whereas inhibition of B-catenin signaling leads to a decrease in the proportion of OV6 + cells. In addition, the chemoresistance of OV6 + HCC progenitor-like cells can be reversed by lentivirus-delivered stable expression of micro-RNA targeting B-catenin. These results highlight the importance of the Wnt/B-catenin pathway in activation and expansion of oval cells in normal rodent models and human HCCs. OV6 + tumor cells may represent the cellular population that confers HCC chemoresistance, and therapies targeted to the Wnt/B-catenin signaling may provide a specific method to disrupt this resistance mechanism to improve overall tumor control with chemotherapy. [Cancer Res 2008;68(11):4287-95]

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The development of frequency-conversion technology in the infrared region is in urgent need of new excellent infrared nonlinear optical (IR NLO) materials. How to achieve a good balance between laser damage threshold (LDT) and NLO coefficient (dij) for new IR NLO candidates is still a challenge. The combination of the highly electropositive alkali metal (Na) and Zn with d(10) electronic configuration into crystal structure affords one new IR NLO material, Na2ZnGe2S6. It exhibits excellent properties including a wide transparent region (0.38-22 μm), large band gap (3.25 eV), and especially a balance between a strong NLO coefficient (30-fold that of KDP) and a high LDT (6-fold that of AgGaS2), indicating a promising application in the IR region. Moreover, novel common-vertex-linked wavelike ∞[GeS3]n chains are interestingly discovered in Na2ZnGe2S6, which rarely exist in the reported thiogermanides containing alkali metals. In addition, calculated SHG density and dipole moment demonstrate that the large NLO response is mainly attributed to the cooperative effects of the [GeS4] and [ZnS4] units.