Internet Banking in Europe: a comparative analysis.

A key strategic issue for banks is the implementation of internet banking. The ‘click and mortar’ model that complements classical branch banking with online facilities is competing with pure internet banks. The objective of this paper is to compare the performance of these two models across countries, so as to examine the role of differences in the banking system and technological progress. A fuzzy cluster analysis on the performance of banks in Finland, Spain, Italy and the UK shows that internet banks are hard to distinguish from banks that follow a click and mortar strategy; country borders are more important. We therefore explain bank performance by a group of selected bank features, country-specific economic and IT indicators over the period 1995-2004. We find that the strategy of banking groups to incorporate internet banks reflects some competitive edge that these banks have in their business models. Extensive technological innovation boosts internet banking.Banks, Internet, Innovation.

Internet Banking in Europe: a comparative analysis

A key strategic issue for banks is the implementation of internet banking. The ‘click and mortar’ model that complements classical branch banking with online facilities is competing with pure internet banks. The objective of this paper is to compare the performance of these two models across countries, so as to examine the role of differences in the banking system and technological progress. A fuzzy cluster analysis on the performance of banks in Finland, Spain, Italy and the UK shows that internet banks are hard to distinguish from banks that follow a click and mortar strategy; country borders are more important. We therefore explain bank performance by a group of selected bank features, country-specific economic and IT indicators over the period 1995-2004. We find that the strategy of banking groups to incorporate internet banks reflects some competitive edge that these banks have in their business models. Extensive technological innovation boosts internet banking

The Institute for Religious Works: key features of financial intermediation

Corresponding author: F. Arnaboldi, email: [email protected]. While the paper is the result of intense collaboration between the two authors, sections 3 is attributable to F. Arnaboldi and section 1 and 2 to B. Rossignoli. Section 4 is a joint effort. The authors wish to thank P. Mottura and two anonymous referees for their valuable comments. All errors are ours.  Article peer reviewed.SUMMARY: 1. Introduction – 2. Background to anti-money laundering – 3. Financial intermediation, 2011–2014 – 4. Conclusion

Board Diversity Reforms: Do they Matter for EU Bank Performance?

We examine the impact of governance reforms related to board diversity on the performance of EU banks. Using a difference-in-difference approach, we document that reforms increase bank stock returns and their volatility within the first three years after their enactment. The type of reform matters, with quotas increasing return volatility more compared to affirmative actions. The effectiveness of reforms depends on a country's institutional environment. The impact on volatility is lower in countries more open to diversity, with common law system and with higher economic freedom. Finally, reforms play a bigger role in banks that have ex-ante less heterogeneous boards

Expression of TLR7 in the murine eye during the embryonic period and in the adult animal

In the present study, we evaluated Toll-like receptor 7 (TLR7) expression at different stages of the murine eye development and in the adult organ. In mammals, TLRs are best known for their immunitary function, however data from the literature are demonstrating that in analogy to their Drosophila homologue Toll, they also participate in developmental mechanisms (Okun, Griffioen and Mattson 2011, Shechter et al. 2008). Immunohistochemistry for TLR7 and double immunofluorescence for TLR7/PCNA were performed on E12, E14 and E16 formalin-fixed paraffin-embedded mouse heads and on eyes enucleated from 3 months adult mice Results of experiments indicate that TLR7 expression is present in different compartments of the mouse eye (cornea, pigmented epithelium, neural retina, and lens) during gestation both in proliferating and differentiating cells and that such expression persists also in the adult organ. These observations indicate that besides being involved in protective mechanisms in the adult eye, TLR7 is also likely involved in the morphogenetic processes of this complex organ to which cells and tissues of different embryological origin contribute

Expression of Toll-like receptors 4 and 7 in the embryonic and adult pancreas, liver and adrenal gland of the mouse

The role of Toll protein in development and immunity is very well understood in Drosophila melanogaster (Anderson et al.,1985). Conversely, the contribution of Tolllike receptors (TLRs) in mammalian development is just beginning to be revealed. In this study, we evaluated the expression of TLR4 and TLR7 by immunohistochemistry on paraffin-embedded tissue in the adrenal gland, liver and pancreas of mouse embryos from stages E12, E14 and E16 and in the adult organs. Results show that TLR4 and TLR7 start to be detectable during embryonic development already at the first stage examined (E12). This expression follows the maturation of the organs and is still present in the adult with a different distribution pattern. Before this study no data in the literature were present on TLR4 and 7 expression in mammalian splanchnic organs development and in the adult no localization studies were available for TLR7. A possible interpretation of the results suggests that, besides their immunitary function, TLRs might be involved in a shared mechanism that regulates proliferation and differentiation both in embryonic organs and adult organs (Sato et al., 2009). These results also suggest that the contribution of TLRs in the context of carcinogenesis should be investigated not only in relation to chronic inflammation and tissue damage but also in relation to their contribution to the process of organogenesis

Structural and ultrastructural evaluation of the effects induced by IL-22 alone or in combination with psoriatic cytokines in an ex-vivo human skin model

L-22 is a pro-inflammatory cytokine playing a crucial role in the pathogenesis of psoriasis, an autoimmune chronic inflammatory skin disease. The immunological acti- vation during the progression of the psoriatic lesion is driven by IL-22 together with other cytokines, such as (TNF)-alpha and interleukin (IL)-17 [1]. The aim of our study was to evaluate the early, direct, and specific effect of IL-22 alone or in combination with TNF-alpha and IL-17 by immunofluorescence on i) the molecular composition of intercellular junctions (desmocollin (DSC)1, E-cadherin, and occludin), ii) keratin(K) 10 and 17 expression, iii) keratinocyte proliferation, and, by transmission electron micros- copy (TEM), on the ultrastructural morphology of the skin. An innovative model of human skin culture standardized in our laboratory, in which a psoriatic microenviron- ment was reproduced, was used [2]. Skin explants obtained from plastic surgery of healthy 20-40 year-old women (n = 7) after informed consent were cultured overnight in Dulbecco’s modified Eagle’s medium, divided before adding IL-22 or a combination of the three cytokines, and harvested 24, 48, and 72 hours after cytokine incubation.Interestingly, keratinocyte proliferation was inhibited after exposure to the combi- nation of cytokines while was not affected by IL-22 incubation. In both experimental groups, starting from T24, occludin immunostaining was non homogeneously distrib- uted, K10 immunostaining gradually decreased in scattered clusters in the spinous layer, while K17 expression was induced and progressively increased with time in the suprabasal layers of epidermis. By TEM, after IL-22 incubation we observed keratin aggregates in the perinuclear cytoplasm of cells, while the combination of the three cytokines induced an enlargement of intercellular spaces.Altogether, our results suggest that IL-22 mainly affects keratinocyte terminal dif- ferentiation, whereas, for inducing an impairment in cell proliferation, a more com- plex psoriatic-like microenvironment is needed.

A proinflammatory microenvironment induces NFkB activation and beta-defensin expression through specific Toll Like Receptors in a 3D human skin model

Psoriasis is an autoimmune skin disease characterized by the formation and the progression of silvery plaques on the extensory surfaces of our body. Proinflammatory cytokines as Tumor Necrosis Factor (TNF)-alpha, interleukin (IL)-17, IL-22 and IL-23 represent for the normal skin a psoriatic microenvironment. In the 3D human skin model standardized in our lab in the last decade, we were able to dissect the events in which each cytokine exerts a specific effect, e.g. keratinocyte proliferation, Langerhans cell activation, cytoskeleton arrangement, and, more recently, the epidermal expression of Toll like Receptors (TLRs) 2, 7, 9. Several experimental studies reported that in psoriasis TLRs are expressed and their activation triggers i) NFkB translocation from the cytoplasm to the nucleus and ii) the release of beta defensins (HBDs). The present study was aimed at investigating the intracellular NFkB activation and HBD1 and HBD2 expression induced by a cytokine mix (TNF-alpha, IL-17, IL-22, IL-23) by indirect immunofluorescence. Bioptic samples of normal human skin were obtained after aesthetic surgery of young healthy informed women (n=7). After overnight incubation to reduce mechanical and termical stress, skin fragments were incubated in a Transwell system for 5 (T5), 24 (T24), and 48 (T48) hours with the cytokine mix. Parallel control samples were carried out and each patient was represented at all time points. In controls at all time-points NFkB was localized only in the cytoplasm, while, starting from T5, scattered basal nuclei were observed in the cytokine-incubated samples. At later time points, in the upper spinous and granular layers, NFkB nuclear immunostaining was evident. HBD2 expression was affected after cytokine mix exposure, while HBD1 distribution was similar to controls. Thanks to this simple but effective model, a deep knowledge of the early events occurring in the normal epidermis exposed to cytokines can be achieved, excluding the contribution of the blood and lymphatic vessels herein absent. This basic research can thus represent an important tool for targeting and counteracting single phenomenon leading to the formation/progression with the most innovative biological drugs

Effect of TNF-alpha and IL-17 on TLR expression and Langerhans cells phenotype in a three-dimensional model of normal human skin: a morphological study

Toll-like receptors (TLRs) are essential for innate immunity and contribute to create the skin barrier. Their abnormal stimulation is involved in the development of several dermatological diseases, among which psoriasis. Tumor Necrosis Factor (TNF)-alpha and interleukin (IL)-17 play a pivotal role in the pathogenesis of psoriatic plaques and their proinflammatory activity can affect Langerhans cell (LC) phenotype. In a well characterized three-dimensional model of organotypic cultures of normal human skin [1-3] we evaluated the effect of TNF-alpha and IL-17 on the expression of TLR2 and 9 by immunofluorescence, on the ultrastructural morphology of keratinocytes and LCs by transmission electron microscopy (TEM). Human skin explants (n=7) were cultured at the air-liquid interface overnight in a Transwell system and exposed to 50 ng/ml IL-17 or 100 ng/ml TNF-alpha or a combination of both cytokines. Samples were harvested 24 (T24) and 48h (T48) after cytokines incubation. After incubation with IL-17 and IL-17+TNF-alpha, TLR2 immunostaining was not detectable in the basal layer, differently from controls and TNF-alpha-treated samples. Conversely, TLR9 expression was progressively induced in granular keratinocytes in all cytokine-exposed groups. By TEM, enlargements of intercellular spaces were evident especially and, after IL-17 treatment, LCs showed an activated phenotype. At T24 LCs number increased indicating that TNF-alpha and IL-17+TNF-alpha exert a chemoattractant activity, while at T48 only IL-17+TNF-alpha maintained this effect on trapping LCs in epidermis. TNF-alpha and IL-17 differently affect LCs behaviour and TLR expression, with a specific contribution to the inflammatory loop underlying the lesion formation. These results suggest that the simultaneous inhibition of the effect of different cytokines with a defined role in the pathogenesis of psoriasis could improve psoriasis treatment