Froberger in Rome: From Frescobaldi's Craftsmanship to Kircher's Compositional Secrets

If the lack of information on Froberger's life is undeniable, so too is the lack of scholarly research in this area. Indeed, all the documents concerning his two visits to Rome were found accidentally by scholars researching other subjects. One such example is the financial records testifying to Froberger's service at the Viennese court. What has enabled reference books to tell us that he studied in Rome with Frescobaldi between September 1637 and April 1641 is the disappearance of his name from the Viennese records during that time. However, the records in question were discovered more than a century ago, not by a Froberger biographer but by a scholar researching the history of the imperial music chapel in Vienna-Ludwig von Kochel, author of the Mozart catalogue. Another example is the two extant letters from Froberger to Athanasius Kircher, a learned German Jesuit living in Rome who included Froberger's fantasy super ut re mi fa solla for harpsichord in his gigantic musical treatise Musurgia universalis (1650). From a biographical standpoint, these letters are of critical importance, as they testify that another extended absence of the musician from the imperial music chapel between October 1645 and April 1653 included many trips to Italy, Germany, France, England, and the Netherlands and that one of these journeys led him back to Rome before September 1649. These letters, however, were discovered and first interpreted by a scholar interested not in Froberger's life but in Kircher's theories of music-Ulf Scharlau-who concluded from the first letter, if with some caution, that Froberger spent his second stay in the papal city studying with Giacomo Carissimi, an interpretation that has been adopted in a number of summaries of Froberger's life in dictionaries, monographs, and editions of his music

Polypyrrole modified with sulfated β-cyclodextrin: characterization and application in the sensing of viologens

In this thesis a conducting polypyrrole (ppy) matrix doped with the anionic sulfated β-cyclodextrin (sβ-CD) was electrosynthesized and characterized. This modified polymer, ppysβ-CD, was used as a sensor for the detection of three compounds, methyl, ethyl and benzyl viologen. Methyl viologen is commonly known as paraquat and it is one of the most commonly used herbicides worldwide. The sβ-CD was permanently immobilized within the ppy backbone during the potentiostatic growth of the polymer. The incorporation of the macrocycle was confirmed by means of cyclic voltammetry (CV), quartz crystal microbalance (QCM) and differential scanning calorimetry (DSC). The large dopant was found not to significantly alter certain properties of the polymer such as diffusion of a probe analyte to the surface and charge transfer rate constant. The cyclodextrin modified polymer was shown to have cation exchange properties and this characteristic was used towards the sensing of the three electroactive viologen compounds. The three viologens were detected by means of differential pulse voltammetry (DPV), while for methyl viologen constant potential amperometry (CPA) experiments were also performed. These techniques gave a good linear response for the current measured at the polymer surface, as a function of the viologen concentration. Detection limits of 1.00 x 10-4 M for ethyl viologen (DPV), 2.50 x 10-5 M for benzyl viologen (DPV) and 1.56 x 10-5 M for methyl viologen (CPA) were measured experimentally. A detailed analysis was performed on the interaction of the sβ-CD with methyl, ethyl and benzyl viologen, using both electrochemistry (CV and RDV) and spectroscopy (UV-Vis, 1H NMR). It was established that a 1:1 interaction occurs between the sβ-CD and each of the viologens. The formation of inclusion complexes was verified not to occur. The generation of association complexes was instead suggested. These complexes result from an ion pairing interaction between the sβ-CD and the viologens, either in their dication state or in their radical state

Economic and environmental assessment of thermal insulation. A case study in the Italian context

Abstract An analysis of the state of the art has shown how current European policy underpins the importance of assessing the impact of different energy efficiency strategies during the life cycle of buildings. In this study a framework is developed for the identification of the optimal material to be used to achieve the highest level of energy efficiency in building retrofits, taking into account environmental and economic elements and comparing different scenarios. For each of these scenarios the Life Cycle Cost Analysis was applied together with related environmental analysis in terms of the production of CO2. The research was applied to an industrial factory in Italy. Results showed that, among ten material with different origin, namely plant, animal, mineral and fossil origin, the optimal thickness varied between 0.023 m of the line fiber, and 0.082 m of the rock wool. From the economic point of view, saving was between 1.58 €/m2 with the linen fiber, and 9.63 €/m2 with the rock wool. Finally, considering the environmental aspect, savings in terms of CO2 was possible only for three of the ten materials, namely cork, sheep wool and fiber glass, respectively equal to 0.14 Kg/m2, 0.65 Kg/m2 and 0.34 Kg/m2. The study has important implications mainly regarding the issue of energy efficiency. Specifically, the opportunity to analyse and compare economic and environmental aspects of a series of alternative materials to improve energy efficiency may provide stakeholders with calculated and objective input for the support of sustainable actions. Sum up, this research has identified a "result oriented" methodology comparing traditional and sustainable materials and measuring the benefits from the correct insulation of a building. These benefits are mainly of an economic and environmental nature and, in this regard, the study helps to strengthen the leadership of the EU for a sustainable use of natural resources within an efficient bioeconomy, essential to achieve Sustainable Development Goals

RelA/NF-kappaB recruitment on the bax gene promoter antagonizes p73-dependent apoptosis in costimulated T cells

The balance between antiapoptotic and proapoptotic proteins of the Bcl-2 family is critical in determining the fate of T cells in response to death stimuli. Proapoptotic genes, such as bax, are generally regulated by the p53 family of transcription factors, whereas NF-kappaB subunits can activate the transcription of antiapoptotic Bcl-2 members. Here, we show that CD28 activation protects memory T cells from irradiation-induced apoptosis by both upregulating bcl-xL and inhibiting bax gene expression. We found that p73, but not p53, binds to and trans-activates the bax gene promoter in irradiated T cells. The activation of RelA/NF-kappaB subunit in CD28 costimulated T cells and its binding onto the bax gene promoter results in suppression of bax transcription and decrease in both p73 and RNA polymerase II recruitment in vivo. RelA recruitment on the bax gene promoter is also accompanied by the lost of p300 binding and the parallel appearance of histone deacetylase-1-containing complexes. These findings identify RelA/NF-kappaB as a critical regulator of T-cell survival by affecting the balance of Bcl-2 family members

Tumor sensitizing function and mechanism of action of a RasGAP derived peptide

Cancer is the second cause of death after cardio-vascular diseases in economically developed countries. Two of the most commonly used anti-cancer therapies are chemo and radiotherapy. Despite the remarkable advances made in term of delivery and specificity of these two anti-tumor regimens, their toxicity towards healthy tissue remains a limitation. A promising approach to overcome this obstacle would be the utilization of therapeutic peptides that specifically augment the sensitivity of tumoral cells to treatments. Lower therapeutical doses would then be required to kill malignant cells, limiting toxic effects on healthy tissues. It was previously shown in our laboratory that the caspase-3 generated fragment N2 of RasGAP is able to potentiate the genotoxin-induced apoptosis selectively in cancer cells. In this work we show that fragment N2 strictly requires a cytoplasmic localization to deliver its pro-apoptotic effect in genotoxin-treated cancer cells. The tumor sensitizing capacity of fragment N2 was found to reside within the 10 amino acid sequence 317-326. Our laboratory earlier demonstrated that a peptide corresponding to amino acids 317 to 326 of RasGAP fused to the TAT cell permeable moiety, called TAT-RasGAP317.326, is able to sensitize cancer cells, but not normal cells, to genotoxin-induced apoptosis. In the present study we describe the capacity of TAT-RasGAP 317.326 to sensitize tumors to both chemo and radiotherapy in an in vivo mouse model. The molecular mechanism underlying the TAT-RasGAP 317.326-mediated sensitization starts now to be elucidated. We demonstrate that G3BP1, an endoribonuclease binding to amino acids 317-326 of RasGAP, is not involved in the sensitization mechanism. We also provide evidence showing that TAT-RasGAP3 17-326 potentiates the genotoxin-mediated activation of Bax in a tBid-dependent manner. Altogether our results show that TAT-RasGAP 317.326 could be potentially used in cancer therapy as sensitizer, in order to improve the efficacy of chemo and radiotherapy and prolong the life expectancy of cancer patients. Moreover, the understanding of the TAT-RasGAP317.326 mode of action might help to unravel the mechanisms by which cancer cells resist to chemo and radiotherapy and therefore to design more targeted and efficient anti-tumoral strategies

Solar Photovoltaic Optimal Tilt Angles in Public Building

Abstract The reduction of the consumption of fossil fuels that cause climate change and the encouragement of the use of cleaner renewable sources, appears to be a fundamental objective for achieving the climate aims agreed in Paris. Moreover, the sustainability of the implementation of solutions for energy efficiency in public administration buildings has played a fundamental role in recent years, strengthened also by the regulatory context of energy and environmental policies of European countries. The research fits into this context and it intends to promote a methodology that is able to evaluate the economic and environmental performance of a photovoltaic system applied in a school located in Italy when only the roof inclination angle changes. The economic and environmental performances are evaluated respectively through Life Cycle Cost Analysis and the avoided CO2 emissions. The results show that although the case study does not present the optimal roof inclination angle, there are economic and environmental advantages. Furthermore, the research notes that, considering the characteristics of the photovoltaic system concerned, the optimal roof inclination angle is equal to 40 degrees from an economic and environmental point of view. This methodology could easily support the decision-making process of designers and administrators to make the energy upgrading choices for the promotion of renewable sources. It was applied to a case study, that is a school located in Italy, in the Abruzzo region, in the province of L'Aquila, but it could be easily replicated in other existing public buildings in different locations

Revisiting G3BP1 as a RasGAP binding protein: sensitization of tumor cells to chemotherapy by the RasGAP 317-326 sequence does not involve G3BP1.

RasGAP is a multifunctional protein that controls Ras activity and that is found in chromosomal passenger complexes. It also negatively or positively regulates apoptosis depending on the extent of its cleavage by caspase-3. RasGAP has been reported to bind to G3BP1 (RasGAP SH3-domain-binding protein 1), a protein regulating mRNA stability and stress granule formation. The region of RasGAP (amino acids 317-326) thought to bind to G3BP1 corresponds exactly to the sequence within fragment N2, a caspase-3-generated fragment of RasGAP, that mediates sensitization of tumor cells to genotoxins. While assessing the contribution of G3BP1 in the anti-cancer function of a cell-permeable peptide containing the 317-326 sequence of RasGAP (TAT-RasGAP₃₁₇₋₃₂₆), we found that, in conditions where G3BP1 and RasGAP bind to known partners, no interaction between G3BP1 and RasGAP could be detected. TAT-RasGAP₃₁₇₋₃₂₆ did not modulate binding of G3BP1 to USP10, stress granule formation or c-myc mRNA levels. Finally, TAT-RasGAP₃₁₇₋₃₂₆ was able to sensitize G3BP1 knock-out cells to cisplatin-induced apoptosis. Collectively these results indicate that G3BP1 and its putative RasGAP binding region have no functional influence on each other. Importantly, our data provide arguments against G3BP1 being a genuine RasGAP-binding partner. Hence, G3BP1-mediated signaling may not involve RasGAP

Energy Improvement in the Building Sector: An Economic Analysis Relating to the Most Common Italian Masonry

The construction sector is a major contributor to total energy consumption, therefore, it is crucial to adopt energy efficiency strategies capable of reducing energy impact in buildings. Among these strategies, exterior wall insulation is one of the most cost-effective options to achieve energy savings for both newly constructed and renovated buildings. In this paper, based on an economic analysis, we aim to determine the economically optimal thickness of insulation material to be used for retrofit interventions of masonry structures. The study analyzes 10 different insulating materials and 5 masonry structures widespread in Italy. The results show that each masonry structure requires a careful evaluation of the thickness of the insulating material to be applied in retrofit operations. Moreover, varying the type of insulating material used, even if applied to the same wall structure, there are different levels of thickness to be applied in order to optimize the performance of the structure

Sustainability of Biogas Based Projects: Technical and Economic Analysis

Biomethane is a renewable gas produced by the transformation of organic matter. It can lead to emissions reduction and it contributes to increasing methane production. Incentive policies favour its development and for this reason, the objective of this paper is to investigate the economic performance of biomethane plants and their process monitoring by electronic systems. Mathematical modeling is here presented to study the financial feasibility of biomethane plants in function of the size (100 m3/h, 250 m3/h, 500 m3/h, 1000 m3/h), the feedstock used (organic fraction of municipal solid waste and a mixture of 30% maize and 70% manure residues on a weight basic) and the destination for final use (fed into the grid, destined for cogeneration or sold as vehicle fuel). From an economic point of view the plant performance is studied by economic tools as Net Present Value and Discounted Payback Time and the uncertainty analysis is implemented using Monte Carlo method. Moreover, from a technical point of view, process monitoring is analyzed to understand what happens in a biomethane plant and help to maintain a stable process. The results show that the profitability of biomethane plants is verified in several scenarios presenting losses only if subsidies were removed

Checkpoints in TNF-Induced Cell Death: Implications in Inflammation and Cancer.

Tumor necrosis factor (TNF) is a proinflammatory cytokine that coordinates tissue homeostasis by regulating cytokine production, cell survival, and cell death. However, how life and death decisions are made in response to TNF is poorly understood. Many inflammatory pathologies are now recognized to be driven by aberrant TNF-induced cell death, which, in most circumstances, depends on the kinase Receptor-interacting serine/threonine-protein kinase 1 (RIPK1). Recent advances have identified ubiquitin (Ub)-mediated phosphorylation of RIPK1 as belonging to crucial checkpoints for cell fate in inflammation and infection. A better understanding of these checkpoints might lead to new approaches for the treatment of chronic inflammatory diseases fueled by aberrant RIPK1-induced cell death, and/or reveal novel strategies for anticancer immunotherapies, harnessing the ability of RIPK1 to trigger immunogenic cell death