Nonlinear Holomorphic Supersymmetry on Riemann Surfaces

We investigate the nonlinear holomorphic supersymmetry for quantum-mechanical systems on Riemann surfaces subjected to an external magnetic field. The realization is shown to be possible only for Riemann surfaces with constant curvature metrics. The cases of the sphere and Lobachevski plane are elaborated in detail. The partial algebraization of the spectrum of the corresponding Hamiltonians is proved by the reduction to one-dimensional quasi-exactly solvable sl(2,R) families. It is found that these families possess the "duality" transformations, which form a discrete group of symmetries of the corresponding 1D potentials and partially relate the spectra of different 2D systems. The algebraic structure of the systems on the sphere and hyperbolic plane is explored in the context of the Onsager algebra associated with the nonlinear holomorphic supersymmetry. Inspired by this analysis, a general algebraic method for obtaining the covariant form of integrals of motion of the quantum systems in external fields is proposed.Comment: 24 pages, new section and refs added; to appear in Nucl. Phys.

Pericyte FAK negatively regulates Gas6/Axl signalling to suppress tumour angiogenesis and tumour growth

The overexpression of the protein tyrosine kinase, Focal adhesion kinase (FAK), in endothelial cells has implicated its requirement in angiogenesis and tumour growth, but how pericyte FAK regulates tumour angiogenesis is unknown. We show that pericyte FAK regulates tumour growth and angiogenesis in multiple mouse models of melanoma, lung carcinoma and pancreatic B-cell insulinoma and provide evidence that loss of pericyte FAK enhances Gas6-stimulated phosphorylation of the receptor tyrosine kinase, Axl with an upregulation of Cyr61, driving enhanced tumour growth. We further show that pericyte derived Cyr61 instructs tumour cells to elevate expression of the proangiogenic/protumourigenic transmembrane receptor Tissue Factor. Finally, in human melanoma we show that when 50% or more tumour blood vessels are pericyte-FAK negative, melanoma patients are stratified into those with increased tumour size, enhanced blood vessel density and metastasis. Overall our data uncover a previously unknown mechanism of tumour growth by pericytes that is controlled by pericyte FAK

Monitoraggio in area sismica di beni monumentali: tecniche NDT e procedure di verifica

Negli ultimi anni il concetto di vulnerabilità sismica è tristemente entrato a far parte delle conoscenze anche dei non addetti ai lavori. Infatti, gli eventi sismici che hanno interessato dagli inizi del ‘900 il territorio Italiano, hanno sistematicamente messo in risalto l’elevata vulnerabilità sismica del nostro patrimonio edilizio, ivi compresi i beni monumentali, nonché, l’inesistenza di qualsiasi attività di programmazione della manutenzione periodica ordinaria e straordinaria delle strutture sismo-resistenti, che garantiscono nel tempo la conservazione delle loro capacità di risposta alle perturbazioni esterne.Il progetto PON sul Monitoraggio in Area Sismica di SIstemi MOnumentali nasce con la prerogativa di produrre uno strumento dedicato alla tutela di strutture a valenza storico – artistica, attraverso un percorso di catalogazione, di analisi del bene inteso come elemento costituito da elementi resistenti e da materiali, di studio del sito dove la struttura è ubicata e di attività di monitoraggio

The 2013 European Seismic Hazard Model: key components and results

The 2013 European Seismic Hazard Model (ESHM13) results from a community-based probabilistic seismic hazard assessment supported by the EU-FP7 project “Seismic Hazard Harmonization in Europe” (SHARE, 2009–2013). The ESHM13 is a consistent seismic hazard model for Europe and Turkey which overcomes the limitation of national borders and includes a through quantification of the uncertainties. It is the first completed regional effort contributing to the “Global Earthquake Model” initiative. It might serve as a reference model for various applications, from earthquake preparedness to earthquake risk mitigation strategies, including the update of the European seismic regulations for building design (Eurocode 8), and thus it is useful for future safety assessment and improvement of private and public buildings. Although its results constitute a reference for Europe, they do not replace the existing national design regulations that are in place for seismic design and construction of buildings. The ESHM13 represents a significant improvement compared to previous efforts as it is based on (1) the compilation of updated and harmonised versions of the databases required for probabilistic seismic hazard assessment, (2) the adoption of standard procedures and robust methods, especially for expert elicitation and consensus building among hundreds of European experts, (3) the multi-disciplinary input from all branches of earthquake science and engineering, (4) the direct involvement of the CEN/TC250/SC8 committee in defining output specifications relevant for Eurocode 8 and (5) the accounting for epistemic uncertainties of model components and hazard results. Furthermore, enormous effort was devoted to transparently document and ensure open availability of all data, results and methods through the European Facility for Earthquake Hazard and Risk (www.​efehr.​org)

Two-dimensional Schr\"odinger Hamiltonians with Effective Mass in SUSY Approach

The general solution of SUSY intertwining relations of first order for two-dimensional Schr\"odinger operators with position-dependent (effective) mass is built in terms of four arbitrary functions. The procedure of separation of variables for the constructed potentials is demonstrated in general form. The generalization for intertwining of second order is also considered. The general solution for a particular form of intertwining operator is found, its properties - symmetry, irreducibility, separation of variables - are investigated.Comment: 16 page

Cancer associated fibroblast FAK regulates malignant cell metabolism

Abstract: Emerging evidence suggests that cancer cell metabolism can be regulated by cancer-associated fibroblasts (CAFs), but the mechanisms are poorly defined. Here we show that CAFs regulate malignant cell metabolism through pathways under the control of FAK. In breast and pancreatic cancer patients we find that low FAK expression, specifically in the stromal compartment, predicts reduced overall survival. In mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signals that increase malignant cell glycolysis and tumour growth. Proteomic and phosphoproteomic analysis in our mouse model identifies metabolic alterations which are reflected at the transcriptomic level in patients with low stromal FAK. Mechanistically we demonstrate that FAK-depletion in CAFs increases chemokine production, which via CCR1/CCR2 on cancer cells, activate protein kinase A, leading to enhanced malignant cell glycolysis. Our data uncover mechanisms whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations in cancer cells

Cancer associated fibroblast FAK regulates malignant cell metabolism

Abstract: Emerging evidence suggests that cancer cell metabolism can be regulated by cancer-associated fibroblasts (CAFs), but the mechanisms are poorly defined. Here we show that CAFs regulate malignant cell metabolism through pathways under the control of FAK. In breast and pancreatic cancer patients we find that low FAK expression, specifically in the stromal compartment, predicts reduced overall survival. In mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signals that increase malignant cell glycolysis and tumour growth. Proteomic and phosphoproteomic analysis in our mouse model identifies metabolic alterations which are reflected at the transcriptomic level in patients with low stromal FAK. Mechanistically we demonstrate that FAK-depletion in CAFs increases chemokine production, which via CCR1/CCR2 on cancer cells, activate protein kinase A, leading to enhanced malignant cell glycolysis. Our data uncover mechanisms whereby stromal fibroblasts regulate cancer cell metabolism independent of genetic mutations in cancer cells