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An extensive literature has focused on the impact of new public management (NPM) oriented structural changes on academics’ practice and identity. These critical studies have been resolute in concluding that NPM inevitably leads to a degeneration of academics’ ethos and values. Drawing from the moral philosophy of Alasdair MacIntyre, we argue that these previous analyses have overlooked the moral agency of the academics and their role in ‘moralizing’ and consequently shaping the ethical nature of their practices. The paper provides a new theoretical understanding of NPM-oriented reforms in light of the virtue ethics approach, thereby directing the attention to the moral character and moral agency of academics. Our analysis of interviews collected in the business department of a Danish university provides an example of how individuals have divergent ethical understandings of these structural changes and enact/resist pre-defined social roles in different ways. While in some cases the NPM agenda of the institutions has triggered internal moral conflict and a crisis of moral character, in other cases the new logic resonates with academics’ values and evaluative standards. Partially departing from the theoretical ground of MacIntyre (1981), we conclude that academics can play a crucial role in shaping the morality of NPM-oriented institutions and in transforming these settings into suitable contexts for the cultivation of virtues.

We present a novel approach to computing Hamming distance and its kernelisation within Topological Quantum Computation. This approach is based on an encoding of two binary strings into a topological Hilbert space, whose inner product yields a natural Hamming distance kernel on the two strings. Kernelisation forges a link with the field of Machine Learning, particularly in relation to binary classifiers such as the Support Vector Machine (SVM). This makes our approach of potential interest to the quantum machine learning community.

Downy mildew resistance is a quantitative trait in grapevines of the genus Vitis. The grapevine 'Bianca' has retained resistance, originally present in its North American ancestors, through several cycles of backcrossing with susceptible cultivars of Vitis vinifera followed by phenotypic selection. The genetic control of the trait was studied using 116 full-siblings from the cross 'Chardonnay' x 'Bianca' and parental genetic maps consisting of 298 and 312 markers, respectively. Ratings of resistance and histological identification of the stage of interaction, when pathogen development is impaired in resistant individuals, were performed using leaf disc inoculation assays with two isolates of Plasmopara viticola collected in Italian and French vineyards. 'Bianca' and 59% of its offspring were heterozygous for a dominant gene, located in a 2.9 cM interval at the Rpv3 locus on chromosome 18, responsible for the onset of a hypersensitive response (HR) at the infection sites within 2 days post inoculation (dpi). Localised necrosis was the earliest phenotypic difference compared to susceptible individuals, it did not halt pathogen growth, but it was associated with a significant reduction of pathogen performance and disease symptoms from 3 to 6 dpi. QTL peaks for quantitative ratings revealed the strongest effects being caused by the Rpv3 locus: extent of mesophyll colonisation (LOD 3.1, percentage of explained phenotypic variance 16.2%), sporulation density (29.7, 74.3%), and symptom severity expressed by the OIV452 descriptor recommended by the Office International de la Vigne et du Vin (28.3, 74.6%). Strong correlation was observed between the ability of a seedling to mount an HR under controlled experimental conditions and quantitative resistance of the adult plant exposed to natural infections in the field, which was expressed by the number of leaves with fungal sporulation, in two consecutive years of observations.

La malattia di von Hippel-Lindau e una sindrome neoplastica multisistemica a trasmissione autosomica dominante, penetranza completa ed espressivita variabile causata da un difetto del gene VHL. La mancanza o l’insufficienza del prodotto proteico del gene VHL, attraverso la mancata distruzione di HIF e la conseguente iperespressione di geni coinvolti nell’angiogenesi, conduce allo sviluppo di svariati tumori, benigni o maligni, e cisti in molti sistemi ed apparati. Gli individui affetti ereditano la predisposizione allo sviluppo di lesioni al SNC quali emangioblastomi cerebellari, spin ali, del tronco cerebrale, delle radici nervose e sopratentoriali, ed inoltre emangioblastomi retinici e tumori del sacco endolinfatico. Le lesioni viscerali includono carcinomi renali a cellule chiare, feocromocitomi, cisti renali e pancreatiche, tumori endocrini del pancreas, cistoadenomi papillari dell’epididimo e del legamento largo, emangiomi del fegato e del polmone. Quindi nella malattia di von Hippel- Lindau vi sono almeno due neoplasie di ghiandole endocrine, la midollare del surrene e l’insula pancreatica. Inoltre, anche paragangliomi della testa e del collo sono stati descritti in pazienti con malattia di VHL. Le varie lesioni tipich e del von Hippel- Lindau mostrano una costante progressione nel tempo per cui, in questi pazienti, risulta fondamentale un follow-up clinico volto alla prevenzione delle complicanze. L’unica terapia attualmente disponibile e quella chirurgica ma sono in corso di valutazione trattamenti farmacologici con inibitori delle kinasi.