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A novel super ink jet printing (SIJP) system was used to fabricate 3D zinc-silver microbatteries directly on a substrate. The SIJP provides a simple and flexible method to deposit interesting 2D and 3D structures of varying morphologies without the waste and large energy inputs typical of standard microfabrication technologies. The system deposited symmetric silver electrodes on glass substrates, and the battery self assembles during the first charge. Using an aqueous electrolyte solution of KOH with dissolved ZnO, the SIJP printed structures showed similar electrochemical behavior to batteries made of foil electrodes. For a sparse array of pillars (~2.5% footprint area of each electrode pad occupied by pillars), a capacity increase of 60% for a given area was measured in comparison to a cell with thin film electrodes. The cycle performance of the printed structures was poor and likely due to the stress induced on the negative electrode upon initial zinc electrodeposition during the first charge cycle.

We have developed an ink-jet system which allows arrangements of dots with a submicron minimum size. Using an ultra-fine silver paste, we achieved the direct print of metallic wires of only a few micrometers in width without any pre-patterning treatment of the substrate, hydrophobic/hydrophilic patterning, bank patterning etc. We also propose an application, such as direct printing of ultra-fine redistribution wiring for a build-up board and/or package. Since all of these processes can be carried out at atmospheric pressure on the desktop without special treatment of the substrate. The direct fabrication process using ink-jet printing can be expected to be a powerful tool for both nanotechnology research and applications such as micro electronics, etc.

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Hall resistivity ρ H has been investigated for single crystals of pyrochlore molybdate Nd 2 Mo 2 O 7 . With decreasing temperature T , the anomalous Hall effect appears at around the Curie temperature T C (∼95 K). In the relatively high temperature region (T > 60 K), ρ H can be described by the ell-known equation ρ H = R 0 H + 4πR s M , where R 0 and R s are the and anomalous Hall coefficients, respectively, and M is the net magnetization predominantly contributed by the Mo spins. With further decreasing T , the ordering of the Nd moments, which is confirmed by neutron diffraction studies carried out by the present authors' group, induces marked change in the behavior of the anomalous part of ρ H . The behavior in the low temperature region has been found to be simply described by the equation ρ H = R 0 H + 4πR s M Mo + 4πR s M Nd , where M Mo and M Nd are the net magnetizations of the Mo-and Nd-moments, respectively. This result and the T -dependence of R s and R s are quite different from those known for ordinary ferromagnets and might be related to the nonzero spin chirality observed in the present system.

The decision between survival and death in cells exposed to TNF relies on a highly regulated equilibrium between proapoptotic and antiapoptotic factors. The TNF-activated antiapoptotic response depends on several transcription factors, including NF-κB and its RelA/p65 subunit, that are activated through phosphorylation-mediated degradation of IκB inhibitors, a process controlled by the IκB kinase complex. Genetic studies in mice have identified the IκB kinase-related kinase TANK-binding kinase 1 (TBK1; also called NAK or T2K) as an additional regulatory molecule that promotes survival downstream of TNF, but the mechanism through which TBK1 exerts its survival function has remained elusive. Here we show that TBK1 triggers an antiapoptotic response by controlling a specific RelA/p65 phosphorylation event. TBK1-induced RelA phosphorylation results in inducible expression of plasminogen activator inhibitor-2 (PAI-2), a member of the serpin family with known antiapoptotic activity. PAI-2 limits caspase-3 activation through stabilization of transglutaminase 2 (TG2), which cross-links and inactivates procaspase-3. Importantly, Tg2 −/− mice were found to be more susceptible to apoptotic cell death in two models of TNF-dependent acute liver injury. Our results establish PAI-2 and TG2 as downstream mediators in the antiapoptotic response triggered upon TBK1 activation.

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Cancer cells often develop drug resistance. In cisplatin-resistant HeLa cisR cells, fibroblast growth factor 13 (FGF13/FHF2) gene and protein expression was strongly upregulated, and intracellular platinum concentrations were kept low. When the FGF13 expression was suppressed, both the cells' resistance to platinum drugs and their ability to keep intracellular platinum low were abolished. Overexpression of FGF13 in parent cells led to greater resistance to cisplatin and reductions in the intracellular platinum concentration. These cisplatin-resistant cells also showed increased resistance to copper. In preoperative cervical cancer biopsy samples from poor prognoses patients after cisplatin chemoradiotherapy, FGF13-positive cells were detected more abundantly than in the biopsy samples from patients with good prognoses. These results suggest that FGF13 plays a pivotal role in mediating resistance to platinum drugs, possibly via a mechanism shared by platinum and copper. Our results point to FGF13 as a novel target and useful prognostic guide for cancer therapy.