Health care as a team sport? - Studying athletics to improve interprofessional collaboration

Organizations value teamwork and collaboration as they strive to build culture and attain their goals and objectives. Sports provide a useful and easily accessible means to study teamwork. Interprofessional collaborative practice (IPCP) has been identified as a means of improving patient and population health outcomes. Principles of teamwork in sports can inform health professionals and organizations regarding possible improvement strategies and barriers in the optimization of IPCP. Twenty-eight delegates from the 2017 All Together Better Health Conference in Oxford, UK participated in a World Café to discuss the how teamwork in sports can inform IPCP in healthcare and sports medicine. These discussions were captured, transcribed and coded using the domains developed by the Interprofessional Education Collaborative (IPEC) along with extrapersonal or interpersonal loci. Extrapersonal factors regarding structure of leadership, roles and organizational commitment can be positive factors to promote teamwork. However, interpersonal factors affecting communication, values and lack of commitment to collaboration can serve as barriers. Athletic trainers and other sports medicine professionals can serve as valuable members of interprofessional teams and teamwork is essential in the field of sports medicine

Enhancement of vaccinia virus based oncolysis with histone deacetylase inhibitors

Histone deacetylase inhibitors (HDI) dampen cellular innate immune response by decreasing interferon production and have been shown to increase the growth of vesicular stomatitis virus and HSV. As attenuated tumour-selective oncolytic vaccinia viruses (VV) are already undergoing clinical evaluation, the goal of this study is to determine whether HDI can also enhance the potency of these poxviruses in infection-resistant cancer cell lines. Multiple HDIs were tested and Trichostatin A (TSA) was found to potently enhance the spread and replication of a tumour selective vaccinia virus in several infection-resistant cancer cell lines. TSA significantly decreased the number of lung metastases in a syngeneic B16F10LacZ lung metastasis model yet did not increase the replication of vaccinia in normal tissues. The combination of TSA and VV increased survival of mice harbouring human HCT116 colon tumour xenografts as compared to mice treated with either agent alone. We conclude that TSA can selectively and effectively enhance the replication and spread of oncolytic vaccinia virus in cancer cells. © 2010 MacTavish et al

Развитие альтернативной энергетики Германии

В данной статье рассмотрены последние тенденции развития альтернативной энергетики Германии. Приведены некоторые причины выбора политики, направленной на столь стремительную интеграцию технологий, использующих возобновляемые источники энергии. Проведено сравнение Германии с другими странами Евросоюза по динамике использования возобновляемой энергии

Stimulated amplification of propagating spin waves

Spin-wave amplification techniques are key to the realization of magnon-based computing concepts. We introduce a novel mechanism to amplify spin waves in magnonic nanostructures. Using the technique of rapid cooling, we create a non-equilibrium state in excess of high-energy magnons and demonstrate the stimulated amplification of an externally seeded, propagating spin wave. Using an extended kinetic model, we qualitatively show that the amplification is mediated by an effective energy flux of high energy magnons into the low energy propagating mode, driven by a non-equilibrium magnon distribution

Control of the Bose-Einstein Condensation of Magnons by the Spin-Hall Effect

Previously, it has been shown that rapid cooling of yttrium-iron-garnet (YIG)/platinum (Pt) nano structures, preheated by an electric current sent through the Pt layer, leads to overpopulation of a magnon gas and to subsequent formation of a Bose-Einstein condensate (BEC) of magnons. The spin Hall effect (SHE), which creates a spin-polarized current in the Pt layer, can inject or annihilate magnons depending on the electric current and applied field orientations. Here we demonstrate that the injection or annihilation of magnons via the SHE can prevent or promote the formation of a rapid cooling induced magnon BEC. Depending on the current polarity, a change in the BEC threshold of -8% and +6% was detected. These findings demonstrate a new method to control macroscopic quantum states, paving the way for their application in spintronic devices

Stabilization of a nonlinear bullet coexisting with a Bose-Einstein condensate in a rapidly cooled magnonic system driven by a spin-orbit torque

We have recently shown that injection of magnons into a magnetic dielectric via the spin-orbit torque (SOT) effect in the adjacent layer of a heavy metal subjected to the action of short (0.1 $\mu$s) current pulses allows for control of a magnon Bose-Einstein Condensate (BEC). Here, the BEC was formed in the process of rapid cooling (RC), when the electric current heating the sample is abruptly terminated. In the present study, we show that the application of a longer (1.0 $\mu$s) electric current pulse triggers the formation of a nonlinear localized magnonic bullet below the linear magnon spectrum. After pulse termination, the magnon BEC, as before, is formed at the bottom of the linear spectrum, but the nonlinear bullet continues to exist, stabilized for additional 30 ns by the same process of RC-induced magnon condensation. Our results suggest that a stimulated condensation of excess magnons to all highly populated magnonic states occurs

Interleukin 10 inhibits pro-inflammatory cytokine responses and killing of Burkholderia pseudomallei.

Melioidosis, caused by Burkholderia pseudomallei, is endemic in northeastern Thailand and Northern Australia. Severe septicemic melioidosis is associated with high levels of pro-inflammatory cytokines and is correlated with poor clinical outcomes. IL-10 is an immunoregulatory cytokine, which in other infections can control the expression of pro-inflammatory cytokines, but its role in melioidosis has not been addressed. Here, whole blood of healthy seropositive individuals (n = 75), living in N. E. Thailand was co-cultured with B. pseudomallei and production of IL-10 and IFN-γ detected and the cellular sources identified. CD3- CD14+ monocytes were the main source of IL-10. Neutralization of IL-10 increased IFN-γ, IL-6 and TNF-α production and improved bacteria killing. IFN-γ production and microbicidal activity were impaired in individuals with diabetes mellitus (DM). In contrast, IL-10 production was unimpaired in individuals with DM, resulting in an IL-10 dominant cytokine balance. Neutralization of IL-10 restored the IFN-γ response of individuals with DM to similar levels observed in healthy individuals and improved killing of B. pseudomallei in vitro. These results demonstrate that monocyte derived IL-10 acts to inhibit potentially protective cell mediated immune responses against B. pseudomallei, but may also moderate the pathological effects of excessive cytokine production during sepsis

Identification of Motifs of <em>Burkholderia pseudomallei</em> BimA Required for Intracellular Motility, Actin Binding, and Actin Polymerization

Actin-based motility of the melioidosis pathogen Burkholderia pseudomallei requires BimA (Burkholderia intracellular motility A). The mechanism by which BimA mediates actin assembly at the bacterial pole is ill-defined. Toward an understanding of the regions of B. pseudomallei BimA required for intracellular motility and the binding and polymerization of actin, we constructed plasmid-borne bimA variants and glutathione-S-transferase fusion proteins with in-frame deletions of specific motifs. A 13-amino-acid direct repeat and IP(7) proline-rich motif were dispensable for actin binding and assembly in vitro, and expression of the mutated proteins in a B. pseudomallei bimA mutant restored actin-based motility in J774.2 murine macrophage-like cells. However, two WASP homology 2 (WH2) domains were found to be required for actin binding, actin assembly, and plaque formation. A tract of five PDASX direct repeats influenced the polymerization of pyrene-actin monomers in vitro and was required for actin-based motility and intercellular spread, but not actin binding. None of the mutations impaired surface expression or polar targeting of BimA. The number of PDASX repeats varied in natural isolates from two to seven. Such repeats acted additively to promote pyrene-actin polymerization in vitro, with stepwise increases in the rate of polymerization as the number of repeats was increased. No differences in the efficiency of actin tail formation could be discerned between strains expressing BimA variants with two, five, or seven PDASX repeats. The data provide valuable new insights into the role of conserved and variable motifs of BimA in actin-based motility and intercellular spread of B. pseudomallei

Viral-mediated oncolysis is the most critical factor in the late-phase of the tumor regression process upon vaccinia virus infection

<p>Abstract</p> <p>Background</p> <p>In principle, the elimination of malignancies by oncolytic virotherapy could proceed by different mechanisms - e.g. tumor cell specific oncolysis, destruction of the tumor vasculature or an anti-tumoral immunological response. In this study, we analyzed the contribution of these factors to elucidate the responsible mechanism for regression of human breast tumor xenografts upon colonization with an attenuated vaccinia virus (VACV).</p> <p>Methods</p> <p>Breast tumor xenografts were analyzed 6 weeks post VACV infection (p.i.; regression phase) by immunohistochemistry and mouse-specific expression arrays. Viral-mediated oncolysis was determined by tumor growth analysis combined with microscopic studies of intratumoral virus distribution. The tumor vasculature was morphologically characterized by diameter and density measurements and vessel functionality was analyzed by lectin perfusion and extravasation studies. Immunological aspects of viral-mediated tumor regression were studied in either immune-deficient mouse strains (T-, B-, NK-cell-deficient) or upon cyclophosphamide-induced immunosuppression (MHCII⁺-cell depletion) in nude mice.</p> <p>Results</p> <p>Late stage VACV-infected breast tumors showed extensive necrosis, which was highly specific to cancer cells. The tumor vasculature in infected tumor areas remained functional and the endothelial cells were not infected. However, viral colonization triggers hyperpermeability and dilatation of the tumor vessels, which resembled the activated endothelium in wounded tissue. Moreover, we demonstrated an increased expression of genes involved in leukocyte-endothelial cell interaction in VACV-infected tumors, which orchestrate perivascular inflammatory cell infiltration. The immunohistochemical analysis of infected tumors displayed intense infiltration of MHCII-positive cells and colocalization of tumor vessels with MHCII⁺/CD31⁺vascular leukocytes. However, GI-101A tumor growth analysis upon VACV-infection in either immunosuppressed nude mice (MHCII⁺-cell depleted) or in immune-deficient mouse strains (T-, B-, NK-cell-deficient) revealed that neither MHCII-positive immune cells nor T-, B-, or NK cells contributed significantly to VACV-mediated tumor regression. In contrast, tumors of immunosuppressed mice showed enhanced viral spreading and tumor necrosis.</p> <p>Conclusions</p> <p>Taken together, these results indicate that VACV-mediated oncolysis is the primary mechanism of tumor shrinkage in the late regression phase. Neither the destruction of the tumor vasculature nor the massive VACV-mediated intratumoral inflammation was a prerequisite for tumor regression. We propose that approaches to enhance viral replication and spread within the tumor microenvironment should improve therapeutical outcome.</p