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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.

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.

The influence of the donor (D) and recipient (R) pre-transplant Epstein-Barr Virus (EBV) serostatus on transplant outcomes (overall survival, relapse-free survival, relapse incidence, non-relapse mortality, acute and chronic GVHD) in 12,931 patients with lymphomas or chronic malignancies undergoing allogeneic hematopoietic cell transplant (allo-HCT) between 1997-2016 was analyzed. In multivariate analysis, the risk of development of chronic GVHD was increased for EBV R+/D+ (HR = 1.26; p = 0.003), R+/D- (HR = 1.21; p = 0.044), and R-/D + (HR = 1.21; p = 0.048) in comparison to R-/D- transplants. No significance was shown for other transplant outcomes; however, in univariate analysis, EBV-seropositive patients receiving grafts from EBV-seropositive donors (EBV R+/D+transplants) had inferior transplant outcomes in comparison to EBV-seronegative recipients of grafts from EBV-seronegative donors (EBV R-/D-): inferior overall survival (59.6% vs 65.9%), inferior relapse-free survival (51.1% vs 57.5%), increased incidence of chronic GVHD (49.5% vs 41.8%), and increased incidence of de novo chronic GVHD (30.5% vs 24.0%). In conclusion, an EBV-negative recipient with lymphoma or chronic malignancy can benefit from selection of an EBV-negative donor in context of chronic GVHD, while there are no preferences in donor EBV serostatus for EBV-seropositive recipient.

We continue the study of a variant of string-objects P systems recently introduced by Krishna and Rama, namely with the possibility to also replicate the strings when rewriting them. The main result of the paper solves an open problem about such P systems: the hierarchy on the number of membranes collapses, systems with six membranes characterize the recursively enumerable languages. We also investigate the power of systems with less than six membranes, in comparison with the families of matrix languages and of E0L and ET0L languages. We close the paper with some remarks about the closure properties of the families of languages generated by P systems with replicated rewriting. Several open problems are also formulated. Journal of Automata, Languages and Combinatorics, Volume 6, Number 3, 2001, 359-374

Mesenchymal stem cells (MSCs) were originally defined by their capacity to differentiate into various connective tissue lineages as well as support hematopoiesis in vitro via the production of various cytokines, chemokines, and adhesion molecules [1, 2]. During the past decade, MSCs have been shown to exhibit angiogenic, trophic, anti-inflammatory, and immunomodulatory activity using a variety of experimental paradigms [3–6]. Together with their easy availability and amenability to large-scale expansion ex vivo, these properties have propelled MSC-based therapies to the forefront of regenerative medicine and immune regulatory cell therapy. Currently, MSCs from a variety of tissue sources are being evaluated in over 200 clinical trials for the treatment of a diverse array of disease indications. Completed Phase I and II clinical trials have reported statistically significant benefits in patients with steroid-resistant graft versus host disease [7], severe systemic lupus erythematosus [8], complex perianal fistulas [9], and ischemic cardiomyopathy [10]. However, not all trials have met their primary endpoint of efficacy and while many factors contribute to suboptimal patient outcomes, key among them are the molecular mechanisms that govern MSC engraftment, homing, and biodistribution in vivo. Indeed, despite rapid progress in describing the therapeutic potency of MSCs in experimental animal models of disease, progress in understanding their biodistribution and mechanism of action in vivo has been slow to develop. For example, robust methodologies to track the fate of MSCs in vivo are critical toward establishing their tissue tropism, duration of engraftment, and rates of clearance. In addition, the identification of endogenous factors that function as chemoattractants and repellents also plays critical roles in directing transplanted cells to sites of tissue injury. Moreover, a clearer understanding of the signaling axes that regulate MSC trafficking in vivo would provide a means to direct cells to specific tissue and organs, thereby increasing overall efficacy of MSC-based therapies. The latter may also provide a means to mobilize endogenous MSCs and enhance their regenerative and immune regulatory properties. Finally, cellular crosstalk and cell-to-cell interactions also likely affect the biodistribution and survival of exogenously administered MSCs, but scant information exists regarding these processes in vivo. In fact, it is a subject of debate whether MSCs localize to tissue due to passive entrapment in small vessels, particularly in lung, or if cells employ active mechanisms similar to leukocytes to home to specific tissues. Therefore, continued study into the mechanism that regulates trafficking of endogenous and transplanted MSCs will shed novel insight into basic MSC biology and lead to the development of more potent cell-based therapies.