Synthetic models of distribution networks based on open data and georeferenced information

Many planning and operation studies that aim at fully assessing and optimizing the performance of the distribution grids, in response to the current trends, cannot ignore grid limitations. Modelling the distribution system, by including the electrical characteristics of the network (e.g., topology) and end user behaviors, has become complex, but essential, for all conventional and emerging actors/players of power systems (i.e., system and market operators, regulators, new market parties as service providers, aggregators, researchers, etc.). This paper deals with a methodology that, starting from publicly available open data on the energy consumption of a region or wider area, is capable to obtain reasonable load and generation profiles for the network supplied by each primary substation in the region/area. Furthermore, by combining these profiles with territorial and socio-economic information, the proposed methodology is able to model the network in terms of lines, conductors, loads and generators. The results of this procedure are the synthetic networks of the real distribution networks, that do not correspond exactly to the actual networks, but can characterize them in a realistic way. Such models can be used for all the kind of optimization studies that need to check the grid limitations. Results derived from Italian test cases are presented and discussed

Resummation of fermionic in-medium ladder diagrams to all orders

A system of fermions with a short-range interaction proportional to the scattering length $a$ is studied at finite density. At any order $a^n$, we evaluate the complete contributions to the energy per particle $\bar E(k_f)$ arising from combined (multiple) particle-particle and hole-hole rescatterings in the medium. This novel result is achieved by simply decomposing the particle-hole propagator into the vacuum propagator plus a medium-insertion and correcting for certain symmetry factors in the $(n-1)$-th power of the in-medium loop. Known results for the low-density expansion up to and including order $a^4$ are accurately reproduced. The emerging series in $a k_f$ can be summed to all orders in the form of a double-integral over an arctangent function. In that representation the unitary limit $a\to \infty$ can be taken and one obtains the value $\xi= 0.5067$ for the universal Bertsch parameter. We discuss also applications to the equation of state of neutron matter at low densities and mention further extensions of the resummation method.Comment: 12 pages, 7 figures, submitted to Nuclear Physics

The JAK inhibitor tofacitinib suppresses synovial JAK1-STAT signalling in rheumatoid arthritis.

ObjectiveTofacitinib is an oral Janus kinase (JAK) inhibitor for the treatment of rheumatoid arthritis (RA). The pathways affected by tofacitinib and the effects on gene expression in situ are unknown. Therefore, tofacitinib effects on synovial pathobiology were investigated.MethodsA randomised, double-blind, phase II serial synovial biopsy study (A3921073; NCT00976599) in patients with RA with an inadequate methotrexate response. Patients on background methotrexate received tofacitinib 10 mg twice daily or placebo for 28 days. Synovial biopsies were performed on Days -7 and 28 and analysed by immunoassay or quantitative PCR. Clinical response was determined by disease activity score and European League Against Rheumatism (EULAR) response on Day 28 in A3921073, and at Month 3 in a long-term extension study (A3921024; NCT00413699).ResultsTofacitinib exposure led to EULAR moderate to good responses (11/14 patients), while placebo was ineffective (1/14 patients) on Day 28. Tofacitinib treatment significantly reduced synovial mRNA expression of matrix metalloproteinase (MMP)-1 and MMP-3 (p<0.05) and chemokines CCL2, CXCL10 and CXCL13 (p<0.05). No overall changes were observed in synovial inflammation score or the presence of T cells, B cells or macrophages. Changes in synovial phosphorylation of signal transducer and activator of transcription 1 (STAT1) and STAT3 strongly correlated with 4-month clinical responses (p<0.002). Tofacitinib significantly decreased plasma CXCL10 (p<0.005) at Day 28 compared with placebo.ConclusionsTofacitinib reduces metalloproteinase and interferon-regulated gene expression in rheumatoid synovium, and clinical improvement correlates with reductions in STAT1 and STAT3 phosphorylation. JAK1-mediated interferon and interleukin-6 signalling likely play a key role in the synovial response.Trial registration numberNCT00976599