Rapporto fra “metodo” e “contenuti matematici” in P. Gesualdo Melacrinò da Reggio Calabria

Summary Father Gesualdo Melacrinò (1725–1803), from Reggio Calabria (Italy), is an unknown Capuchin philosopher and theologian, who produced several works at the time he was teaching (only five years, from 1748–53); these works contained an original approach to the foundations and philosophy of mathematics. His main purpose was to reconciliate the classical traditions with the reality of his time. For him, this included a critical examination of the scholastic curriculum and a new orientation towards the methodological relevance of mathematics for all other sciences, especially for philosophy. Concerning mathematics, he emphasized the necessity of a basic revision and logical reconstruction of its foundations. This paper provides a comparative examination of Melacrinò's work with reference to its cultural and historical environment.     

The role of increasing temperature variability in European summer heatwaves

Instrumental observations and reconstructions of global and hemispheric temperature evolution reveal a pronounced warming during the past approximately 150 years. One expression of this warming is the observed increase in the occurrence of heatwaves. Conceptually this increase is understood as a shift of the statistical distribution towards warmer temperatures, while changes in the width of the distribution are often considered small. Here we show that this framework fails to explain the record-breaking central European summer temperatures in 2003, although it is consistent with observations from previous years. We find that an event like that of summer 2003 is statistically extremely unlikely, even when the observed warming is taken into account. We propose that a regime with an increased variability of temperatures (in addition to increases in mean temperature) may be able to account for summer 2003. To test this proposal, we simulate possible future European climate with a regional climate model in a scenario with increased atmospheric greenhouse-gas concentrations, and find that temperature variability increases by up to 100%, with maximum changes in central and eastern Europe.     

Redescription of Retilaskeya horrida (di Monterosato, 1874) comb. nov. and a re-evaluation of the taxonomic affinity of the genus Retilaskeya (Caenogastropoda: Triphoroidea)

The family Cerithiopsidae H. Adams and A. Adams, 1853 is distributed worldwide, and comprises around 800 extant species divided into ~40 genera. The most speciose genus within the family is Cerithiopsis Forbes and Hanley, 1850, a taxon currently used as a general receptacle rather than as a proper phylogenetic lineage. We hereby redescribe the rare species Cerithiopsis horrida di Monterosato, 1874, review its nomenclature, known material, and distribution as well as figure the entire protoconch, operculum, and radula for the first time. Our results highlight extreme differences between ‘Cerithiopsis’ horrida and the Cerithiopsis type species Cerithiopsis tubercularis (Montagu, 1803) and strong morphological and radular similarities with species belonging to the genus Retilaskeya Marshall, 1978. A wide discussion lists several taxa that might be ascribed to the same group of species, which presumably constitute a different worldwide lineage. Pending relevant molecular phylogenetic studies of the Triphoroidea Gray, 1847, for morphological conformity we suggest transferring ‘Cerithiopsis’ horrida to the genus Retilaskeya, and the same action is presumably appropriate for its possible sister species ‘Cerithiopsis’ leopardus Rolán and Gori, 2013. Finally, Retilaskeya better conforms to Newtoniellidae Korobkov, 1955 than Cerithiopsidae.     

Estrogen receptor alpha (ESR1) gene amplification is frequent in breast cancer

Using an Affymetrix 10K SNP array to screen for gene copy number changes in breast cancer, we detected a single-gene amplification of the ESR1 gene, which encodes estrogen receptor alpha, at 6q25. A subsequent tissue microarray analysis of more than 2,000 clinical breast cancer samples showed ESR1 amplification in 20.6% of breast cancers. Ninety-nine percent of tumors with ESR1 amplification showed estrogen receptor protein overexpression, compared with 66.6% cancers without ESR1 amplification (P < 0.0001). In 175 women who had received adjuvant tamoxifen monotherapy, survival was significantly longer for women with cancer with ESR1 amplification than for women with estrogen receptor-expressing cancers without ESR1 amplification (P = 0.023). Notably, we also found ESR1 amplification in benign and precancerous breast diseases, suggesting that ESR1 amplification may be a common mechanism in proliferative breast disease and a very early genetic alteration in a large subset of breast cancers.     

Hormonal control of Mg2+ transport in the heart

Magnesium is abundant in the mammalian body and the second most abundant cation in cells. Because the concentration of intracellular free Mg2+ is relatively high (0.2-1 mM), Mg2+ is unlikely to act as a second messenger, like Ca2+, by rapidly changing its cytosolic concentration. But changes in Mg2+ do have profound effects on cellular metabolism, structure and bioenergetics. Key enzymes or metabolic pathways, mitochondrial ion transport, Ca2+ channel activities in the plasma membrane and intracellular organelles, ATP-requiring reactions, and structural properties of cells and nucleic acids are modified by changes in Mg2+ concentration. Yet, although some information is available from giant cells and bacteria, little is known about the regulation of intracellular Mg2+ in mammalian cells. Here we report a new transport mechanism for Mg2+ across the sarcolemma of cardiac cells in both intact hearts and dissociated myocytes. We show that noradrenaline, through beta-adrenergic stimulation and increase of cyclic AMP, stimulates a large efflux of Mg2+ from cardiac cells. This transport is of major dimensions and can move up to 20% of total cellular Mg2+ within a few minutes.     

Cavity solitons as pixels in semiconductor microcavities

Cavity solitons are localized intensity peaks that can form in a homogeneous background of radiation. They are generated by shining laser pulses into optical cavities that contain a nonlinear medium driven by a coherent field (holding beam). The ability to switch cavity solitons on and off and to control their location and motion by applying laser pulses makes them interesting as potential 'pixels' for reconfigurable arrays or all-optical processing units. Theoretical work on cavity solitons has stimulated a variety of experiments in macroscopic cavities and in systems with optical feedback. But for practical devices, it is desirable to generate cavity solitons in semiconductor structures, which would allow fast response and miniaturization. The existence of cavity solitons in semiconductor microcavities has been predicted theoretically, and precursors of cavity solitons have been observed, but clear experimental realization has been hindered by boundary-dependence of the resulting optical patterns-cavity solitons should be self-confined. Here we demonstrate the generation of cavity solitons in vertical cavity semiconductor microresonators that are electrically pumped above transparency but slightly below lasing threshold. We show that the generated optical spots can be written, erased and manipulated as objects independent of each other and of the boundary. Numerical simulations allow for a clearer interpretation of experimental results.     

“... in Christophorum Clavium de Contactu Linearum Apologia” Considerazioni attorno alla polemica fra Peletier e Clavio circa l'angolo di contatto (1579–1589)

Summary In this work 1 focus my attention upon the question of the angle of tangency in the XVI^th Century, especially in the polemic between J. Peletier and Chr. Clavius (1579–1589). The interest in the question favored deliberation about the theory of proportions, the principle of Eudoxus-Archimedes and the set of angles of tangency (this is a non-Archimedian set); there were problems about logical proofs and geometrical proofs.

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Memoria presentata da H. Freudenthal     

Defective tryptophan catabolism underlies inflammation in mouse chronic granulomatous disease

Half a century ago, chronic granulomatous disease (CGD) was first described as a disease fatally affecting the ability of children to survive infections. Various milestone discoveries have since been made, from an insufficient ability of patients' leucocytes to kill microbes to the underlying genetic abnormalities. In this inherited disorder, phagocytes lack NADPH oxidase activity and do not generate reactive oxygen species, most notably superoxide anion, causing recurrent bacterial and fungal infections. Patients with CGD also suffer from chronic inflammatory conditions, most prominently granuloma formation in hollow viscera. The precise mechanisms of the increased microbial pathogenicity have been unclear, and more so the reasons for the exaggerated inflammatory response. Here we show that a superoxide-dependent step in tryptophan metabolism along the kynurenine pathway is blocked in CGD mice with lethal pulmonary aspergillosis, leading to unrestrained Vgamma1(+) gammadelta T-cell reactivity, dominant production of interleukin (IL)-17, defective regulatory T-cell activity and acute inflammatory lung injury. Although beneficial effects are induced by IL-17 neutralization or gammadelta T-cell contraction, complete cure and reversal of the hyperinflammatory phenotype are achieved by replacement therapy with a natural kynurenine distal to the blockade in the pathway. Effective therapy, which includes co-administration of recombinant interferon-gamma (IFN-gamma), restores production of downstream immunoactive metabolites and enables the emergence of regulatory Vgamma4(+) gammadelta and Foxp3(+) alphabeta T cells. Therefore, paradoxically, the lack of reactive oxygen species contributes to the hyperinflammatory phenotype associated with NADPH oxidase deficiencies, through a dysfunctional kynurenine pathway of tryptophan catabolism. Yet, this condition can be reverted by reactivating the pathway downstream of the superoxide-dependent step.