Uqosp(2,2)U_q osp(2,2) Lattice Models

In this paper I construct lattice models with an underlying $U_q osp(2,2)$ superalgebra symmetry. I find new solutions to the graded Yang-Baxter equation. These {\it trigonometric} $R$-matrices depend on {\it three} continuous parameters, the spectral parameter, the deformation parameter $q$ and the $U(1)$ parameter, $b$, of the superalgebra. It must be emphasized that the parameter $q$ is generic and the parameter $b$ does not correspond to the `nilpotency' parameter of \cite{gs}. The rational limits are given; they also depend on the $U(1)$ parameter and this dependence cannot be rescaled away. I give the Bethe ansatz solution of the lattice models built from some of these $R$-matrices, while for other matrices, due to the particular nature of the representation theory of $osp(2,2)$, I conjecture the result. The parameter $b$ appears as a continuous generalized spin. Finally I briefly discuss the problem of finding the ground state of these models.Comment: 19 pages, plain LaTeX, no figures. Minor changes (version accepted for publication

Dispersive shock waves in partially ionised plasmas

Compressional waves propagating in the partially ionised solar lower atmospheric plasmas can easily steepen into nonlinear waves, including shocks. Here we investigate the effect of weak dispersion generated by Hall currents perpendicular to the ambient magnetic field on the characteristics of shock waves. Our study will also focus on the interplay between weak dispersion and partial ionisation of the plasma. Using a multiple scale technique we derive the governing equation in the form of a Korteweg-de Vries-Burgers equation. The effect of weak dispersion on shock waves is obtained using a perturbation technique. The secular behaviour of second order terms is addressed with the help of a renormalisation technique. Our results show that dispersion modifies the characteristics of shock waves and this change is dependent also on the ionisation degree of the plasma. Dispersion can create short lived oscillations in the shocked plasma. The shock fronts become wider with the increase in the number of neutrals in the plasma

Clinical chemistry, haematology, immune response and histological evaluation of rabbits after immunisation and challenge with rabbit haemorrhagic disease (RHD) virus

[EN] Following their immunisation and infection with a VSHI-CN-6 viral strain, a group of 15 rabbits were examined in a study of Rabbit Haemorrhagic Disease (RHD). Serum samples were collected from the external ear vein at 0, 15, 30 and 60 days post-immunisation. The recorded platelet numbers were closer to the lower physiological limit, indicating a mild thrombocytopenia, with values ranging from 26.6 to 30.43×104/mm3. The phagocytic index revealed significant differences (P<0.001) between the mean values obtained before vaccination (day 0) and the 3 post-vaccination measurements, confirming the increase in phagocytic capacity after immunisation. Additionally, the serum lysozyme average value equalled 9.14 mg/mL post-vaccination. The analysis of variance revealed significant statistical differences (P<0.05) between the average values obtained before vaccination (0) and the post-vaccination values, measured on day 14 and 30, respectively. The morphology of the samples collected from the main organs involved in immune protection, spleen and gastric and portal lymph nodes highlighted changes corresponding to the post-vaccination immunological response. The white pulp of the spleen appeared as a diffuse lymphoid tissue, presenting with primary and secondary lymphoid follicles. The ratio of white/red pulp was in favour of the white pulp and multiple lymphoid follicles were present, indicating their reactivation. In the medullary area of gastric and portal lymph nodes, narrow lymphoid cords, circumscribed by relatively large lymphatic sinuses, and well defined lymphocytolysis were observed. Moreover, the exudate and lymphoid follicles during activation were noted in the cortical area. Furthermore, the inflammatory processes were identified, morphologically manifested by the thickening of connective tissue in the lymph node capsule, dilacerations of the connective fibres and the presence of light acidophilic serous exudate with rare inflammatory cells (serous lymphoreticulitis).Stancu, CA.; Cărpinișan, L.; Ghișe, A.; Marcu, A.; Pentea, MC.; Dumitrescu, E.; Muselin, F.... (2017). Clinical chemistry, haematology, immune response and histological evaluation of rabbits after immunisation and challenge with rabbit haemorrhagic disease (RHD) virus. World Rabbit Science. 25(4):357-365. doi:10.4995/wrs.2017.7500SWORD35736525

217 MECHANISMS OF ACTION OF ESE1, A NOVEL TRANSCRIPTIONAL REGULATOR OF CARTILAGE REMODELING, IN MMP-13 REGULATION

Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K-Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3K alpha isoform in cardioprotection Pharmacological PI3K alpha inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3K alpha inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol. These results were confirmed in an in vivo model. Moreover, pharmacological PI3K alpha activation by insulin at reperfusion was sufficient to confer cardioprotection against IRI. In addition, PI3K alpha was shown to be expressed and activated in mouse cardiomyocytes, mouse cardiac endothelial cells, as well as in mouse and human heart tissue. Furthermore, PI3K alpha was shown to mediate its effect though the inhibition of mitochondrial permeability transition pore opening. In conclusion, PI3K alpha activity is required during the early reperfusion phase to reduce myocardial infarct size. This suggests that strategies specifically enhancing the alpha isoform of PI3K at reperfusion promote tissue salvage and as such, and could provide a direct target for clinical treatment of IRI.Fundacion Rafael del Pino FONDECYT 3160298 British Heart Foundation Cancer Research UK C23338/A15965 UK NIHR University College London Hospitals Biomedical Research Centr

Predictive models of tumour response to treatment using functional imaging techniques

Editorial, abstract not included.Loredana G. Marcu, Eva Bezak, Iuliana Toma-Dasu, and Alexandru Das

Basal and IL-1β enhanced chondrocyte chemotactic activity on monocytes are co-dependent on both IKKα and IKKβ NF-κB activating kinases

IKKα and IKKβ are essential kinases for activating NF-κB transcription factors that regulate cellular differentiation and inflammation. By virtue of their small size, chemokines support the crosstalk between cartilage and other joint compartments and contribute to immune cell chemotaxis in osteoarthritis (OA). Here we employed shRNA retroviruses to stably and efficiently ablate the expression of each IKK in primary OA chondrocytes to determine their individual contributions for monocyte chemotaxis in response to chondrocyte conditioned media. Both IKKα and IKKβ KDs blunted both the monocyte chemotactic potential and the protein levels of CCL2/MCP-1, the chemokine with the highest concentration and the strongest association with monocyte chemotaxis. These findings were mirrored by gene expression analysis indicating that the lowest levels of CCL2/MCP-1 and other monocyte-active chemokines were in IKKαKD cells under both basal and IL-1β stimulated conditions. We find that in their response to IL-1β stimulation IKKαKD primary OA chondrocytes have reduced levels of phosphorylated NFkappaB p65pSer536 and H3pSer10. Confocal microscopy analysis revealed co-localized p65 and H3pSer10 nuclear signals in agreement with our findings that IKKαKD effectively blunts their basal level and IL-1β dependent increases. Our results suggest that IKKα could be a novel OA disease target