The Method of Combinatorial Telescoping

We present a method for proving q-series identities by combinatorial telescoping, in the sense that one can transform a bijection or a classification of combinatorial objects into a telescoping relation. We shall illustrate this method by giving a combinatorial proof of Watson's identity which implies the Rogers-Ramanujan identities.Comment: 11 pages, 5 figures; to appear in J. Combin. Theory Ser.

The class I PI3K/Akt pathway is critical for cancer cell survival in dogs and offers an opportunity for therapeutic intervention

<p>Abstract</p> <p>Background</p> <p>Using novel small-molecular inhibitors, we explored the feasibility of the class I PI3K/Akt/mTORC1 signaling pathway as a therapeutic target in canine oncology either by using pathway inhibitors alone, in combination or combined with conventional chemotherapeutic drugs <it>in vitro</it>.</p> <p>Results</p> <p>We demonstrate that growth and survival of the cell lines tested are predominantly dependent on class I PI3K/Akt signaling rather than mTORC1 signaling. In addition, the newly developed inhibitors ZSTK474 and KP372-1 which selectively target pan-class I PI3K and Akt, respectively, and Rapamycin which has been well-established as highly specific mTOR inhibitor, decrease viability of canine cancer cell lines. All inhibitors demonstrated inhibition of phosphorylation of pathway members. Annexin V staining demonstrated that KP372-1 is a potent inducer of apoptosis whereas ZSTK474 and Rapamycin are weaker inducers of apoptosis. Simultaneous inhibition of class I PI3K and mTORC1 by ZSTK474 combined with Rapamycin additively or synergistically reduced cell viability whereas responses to the PI3K pathway inhibitors in combination with conventional drug Doxorubicin were cell line-dependent.</p> <p>Conclusion</p> <p>This study highlighted the importance of class I PI3K/Akt axis signaling in canine tumour cells and identifies it as a promising therapeutic target.</p

Lattice Anharmonicity in Defect-Free Pd Nanowhiskers

We have investigated anharmonic behavior of Pd by applying systematic nanoscale tensile testing to near defect-free nanowhiskers offering a large range of elastic strain. We measured size-dependent deviations from bulk elastic behavior in nanowhiskers with diameters as small as ∼30  nm. In addition to size-dependent variations in Young’s modulus in the small strain limit, we measured nonlinear elasticity at strains above ∼1%. Both phenomena are attributed to higher-order elasticity in the bulklike core upon being biased from its equilibrium configuration due to the role of surface stresses in small volumes. Quantification of the size-dependent second- and third-order elastic moduli allows for calculation of intrinsic material nonlinearity parameters, e.g., δ. Comparison of the size-independent values of δ in our nanowhiskers with studies on bulk fcc metals lends further insight into the role of length scales on both elastic and plastic mechanical behavior

Differentiation, Distribution and γδ T Cell-Driven Regulation of IL-22-Producing T Cells in Tuberculosis

Differentiation, distribution and immune regulation of human IL-22-producing T cells in infections remain unknown. Here, we demonstrated in a nonhuman primate model that M. tuberculosis infection resulted in apparent increases in numbers of T cells capable of producing IL-22 de novo without in vitro Ag stimulation, and drove distribution of these cells more dramatically in lungs than in blood and lymphoid tissues. Consistently, IL-22-producing T cells were visualized in situ in lung tuberculosis (TB) granulomas by confocal microscopy and immunohistochemistry, indicating that mature IL-22-producing T cells were present in TB granuloma. Surprisingly, phosphoantigen HMBPP activation of Vγ2Vδ2 T cells down-regulated the capability of T cells to produce IL-22 de novo in lymphocytes from blood, lung/BAL fluid, spleen and lymph node. Up-regulation of IFNγ-producing Vγ2Vδ2 T effector cells after HMBPP stimulation coincided with the down-regulated capacity of these T cells to produce IL-22 de novo. Importantly, anti-IFNγ neutralizing Ab treatment reversed the HMBPP-mediated down-regulation effect on IL-22-producing T cells, suggesting that Vγ2Vδ2 T-cell-driven IFNγ-networking function was the mechanism underlying the HMBPP-mediated down-regulation of the capability of T cells to produce IL-22. These novel findings raise the possibility to ultimately investigate the function of IL-22 producing T cells and to target Vγ2Vδ2 T cells for balancing potentially hyper-activating IL-22-producing T cells in severe TB