The Historical Turn in Democratization Studies: A New Research Agenda for Europe and Beyond. CES Working Paper Series No. 177, 2010

The paper lays the theoretical and methodological foundations of a new historically-minded approach to the comparative study of democratization, centered on the analysis of the creation, development and interaction of democratic institutions. Historically, democracy did not emerge as a singular coherent whole but rather as a set of different institutions, which resulted from conflicts across multiple lines of social and political cleavage that took place at different moments in time. The theoretical advantage of this approach is illustrated by highlighting the range of new variables that come into focus in explaining democracy's emergence. Rather than class being the single variable that explains how and why democracy came about, we can see how religious conflict, ethnic cleavages, and the diffusion of ideas played a much greater role in Europe's democratization than has typically been appreciated. Above all, we argue that political parties were decisive players in how and why democracy emerged in Europe and should be at the center of future analyses

Trying perpetrators: denazification trials and support for democracy in West Germany

We study the effects of transitional justice (TJ) programs that punish large numbers of human rights violators through the lenses of social psychology theories on how individuals respond to punishment in allocative situations, including how defendants in court trials evaluate their verdicts. We analyze subnational variation in procedures and outcomes of denazification trials in West Germany during 1946-47. Consistently with established findings in social psychology, we find that procedural justice and the distributive fairness of outcomes can compensate for the anti-democratic attitudinal effects of being a defendant in a TJ trial. We also find evidence that procedural justice influences the democratic attitudes of family members of TJ defendants. The study has implications for contemporary cases of TJ programs that affect large numbers of perpetrators

S100B inhibitor pentamidine attenuates reactive gliosis and reduces neuronal loss in a mouse model of Alzheimer's disease

Among the different signaling molecules released during reactive gliosis occurring in Alzheimer’s disease (AD), the astrocytederived S100B protein plays a key role in neuroinflammation, one of the hallmarks of the disease. The use of pharmacological tools targeting S100B may be crucial to embank its effects and some of the pathological features of AD. The antiprotozoal drug pentamidine is a good candidate since it directly blocks S100B activity by inhibiting its interaction with the tumor suppressor p53. We used a mouse model of amyloid beta- (A-) induced AD, which is characterized by reactive gliosis and neuroinflammation in the brain, and we evaluated the effect of pentamidine on the main S100B-mediated events. Pentamidine caused the reduction of glial fibrillary acidic protein, S100B, and RAGE protein expression, which are signs of reactive gliosis, and induced p53 expression in astrocytes. Pentamidine also reduced the expression of proinflammatory mediators and markers, thus reducing neuroinflammation in AD brain. In parallel, we observed a significant neuroprotection exerted by pentamidine on CA1 pyramidal neurons. We demonstrated that pentamidine inhibits A-induced gliosis and neuroinflammation in an animal model of AD, thus playing a role in slowing down the course of the disease

To Witness, To Practise, To Recognise: We see water system

The goal of this concept research is to enhance works of art made by Gian Lorenzo Bernini for Piazza Navona, Piazza di Spagna and Piazza Barberini in the city of Rome (Italy) with a vision of care and knowledge for the water entity. This design proposal hopes to create a link and a dialogue between two dimensions: the artistic works, represented by Bernini’s fountains inside the architectonic spaces of these plazas on one side, and the dimension of common good environmental heritage of the element water that lives inside the shapes and art of the Bernini’s fountains. This design scenario is a macro design system that has been developed with first-year Master’s students in Systemic Design

Formal Versus Functional Method in Comparative Constitutional Law

In the field of comparative constitutional law, the dominant approach to concept formation and research design is formal. That is, comparative projects generally identify what counts as the supreme law that can be enforced against all other sources of law based on the “constitutional” label of the positive law (written constitutions and the jurisprudence of constitutional courts) and the law books. This formal method, however, has significant limitations when compared with the functional method used in the field of comparative law more generally speaking. After a brief exposition of the functional method, this article explores the advantages of the functional method as applied to comparative constitutional law with the problem of judicial review (based on the supreme law) of social and economic policy-making in France, the United States, and Germany. Only in Germany is this law contained in constitutional law. In France, the supreme law is to be found largely in administrative law, because the constitutional court faces an institutional competitor, some would say superior, in the highest administrative court (Conseil d’État). In the United States, the supreme law is to be found in administrative law because economic and social rights—the rights that most directly affect this area of state activity—have largely been read out of constitutional law. Based on the functional method, the article proceeds to identify the similarities that unite the law of France and Germany and that set it apart from the law of the United States. It also outlines the important avenues of theoretical inquiry triggered by these similarities and differences in judicial review. The article concludes by sketching a functional agenda for empirical research in comparative constitutional law

Enteric glia: A new player in inflammatory bowel diseases

In addition to the well-known involvement of macrophages and neutrophils, other cell types have been recently reported to substantially contribute to the onset and progression of inflammatory bowel diseases (IBD). Enteric glial cells (EGC) are the equivalent cell type of astrocyte in the central nervous system (CNS) and share with them many neurotrophic and neuro-immunomodulatory properties. This short review highlights the role of EGC in IBD, describing the role played by these cells in the maintenance of gut homeostasis, and their modulation of enteric neuronal activities. In pathological conditions, EGC have been reported to trigger and support bowel inflammation through the specific over-secretion of S100B protein, a pivotal neurotrophic factor able to induce chronic inflammatory changes in gut mucosa. New pharmacological tools that may improve the current therapeutic strategies for inflammatory bowel diseases (IBD), lowering side effects (i.e. corticosteroids) and costs (i.e. anti-TNFα monoclonal antibodies) represent a very important challenge for gastroenterologists and pharmacologists. Novel drugs capable to modulate enteric glia reactivity, limiting the pro-inflammatory release of S100B, may thus represent a significant innovation in the field of pharmacological interventions for inflammatory bowel diseases

Rifaximin improves Clostridium difficile toxin A-induced toxicity in Caco-2 cells by the PXR-dependent TLR4/MyD88 /NF-?B pathway

Background: Clostridium difficile infections (CDIs) caused by Clostridium difficile toxin A (TcdA) lead to severe ulceration, inflammation and bleeding of the colon, and are difficult to treat. Aim: The study aimed to evaluate the effect of rifaximin on TcdA-induced apoptosis in intestinal epithelial cells and investigate the role of PXR in its mechanism of action. Methods: Caco‐2 cells were incubated with TcdA and treated with rifaximin (0.1−10 μM) with or without ketoconazole (10 μM). The transepithelial electrical resistance (TEER) and viability of the treated cells was determined. Also, the expression of zona occludens‐1 (ZO‐1), toll‐like receptor 4 (TLR4), Bcl‐2‐associated X protein (Bax), transforming growth factor‐β‐activated kinase‐1 (TAK1), myeloid differentiation factor 88 (MyD88) and nuclear factor‐kappaB (NF‐κB) was determined. Results Rifaximin treatment (0.1, 1.0 and 10 μM) caused a significant and concentration-dependent increase in the TEER of Caco-2 cells (360%, 480% and 680% vs TcdA treatment) 24 hours after the treatment and improved their viability (61%, 79% and 105%). Treatment also concentration-dependently decreased the expression of Bax protein (–29%, –65% and –77%) and increased the expression of ZO-1 (25%, 54% and 87%) and occludin (71%, 114% and 262%) versus TcdA treatment. The expression of TLR4 (–33%, –50% and –75%), MyD88 (–29%, –60% and –81%) and TAK1 (–37%, –63% and –79%) were also reduced with rifaximin versus TcdA treatment. Ketoconazole treatment inhibited these effects. Conclusions: Rifaximin improved TcdA‐induced toxicity in Caco‐2 cells by the PXR‐dependent TLR4/MyD88/NF‐κB pathway mechanism, and may be useful in the treatment of CDIs