Fiasco: a multidetector optimized for semiperipheral heavy ion collisions at Fermi energies

The Fiasco multidetector is a low-threshold apparatus, optimized for the investigation of peripheral to semi-central collisions in heavy ion reactions at Fermi energies. It consists of three types of detectors. The first detector layer is a shell of 24 position-sensitive Parallel Plate Avalanche Detectors (PPADs), covering about 70% of the forward hemisphere, which measure the velocity vectors of the heavy ðZ\10Þ reaction products. Below and around the grazing angle, behind the most forward PPADs, there are 96 DE–E silicon telescopes (with thickness of 200 and 500 mm; respectively); they are mainly used to measure the energy of the projectile-like fragment and to identify its charge and, via the time-of-flight of the PPADs, also its mass. Finally, behind most of the PPADs there are 158 (or 182, depending on the configuration) scintillation detectors, mostly of the phoswich type, which cover 25–30% of the forward hemisphere; they identify both light charged particles ðZ ¼ 1; 2Þ and intermediate mass fragments ð3pZt20Þ; measuring also their time-of-flight. r 2003 Elsevier B.V. All rights reserved

Poly[ADP-Ribose] Polymerase-1 Expression Is Related To Cold Ischemia, Acute Tubular Necrosis, and Delayed Renal Function In Kidney Transplantation

Cold ischemia time especially impacts on outcomes of expanded-criteria donor (ECD) transplantation. Ischemia-reperfusion (IR) injury produces excessive poly[ADP-Ribose] Polymerase-1 (PARP-1) activation. The present study explored the hypothesis that increased tubular expression of PARP-1 contributes to delayed renal function in suboptimal ECD kidney allografts and in non-ECD allografts that develop posttransplant acute tubular necrosis (ATN)

Coalition Formation and the Ancillary Benefits of Climate Policy

Several studies found ancillary benefits of environmental policy to be of considerable size. These additional private benefits imply not only higher cooperative but also noncooperative abatement targets. However, beyond these largely undisputed important quantitative effects, there are qualitative and strategic implications associated with ancillary benefits: climate policy is no longer a pure but an impure public good. In this paper, we investigate these implications in a setting of non-cooperative coalition formation. In particular, we address the following questions. 1) Do ancillary benefits increase participation in international environmental agreements? 2) Do ancillary benefits raise the success of these treaties in welfare terms

The Association of PNPLA3 Variants with Liver Enzymes in Childhood Obesity Is Driven by the Interaction with Abdominal Fat

BACKGROUND AND AIMS: A polymorphism in adiponutrin/patatin-like phospholipase-3 gene (PNPLA3), rs738409 C->G, encoding for the I148M variant, is the strongest genetic determinant of liver fat and ALT levels in adulthood and childhood obesity. Aims of this study were i) to analyse in a large group of obese children the role of the interaction of not-genetic factors such as BMI, waist circumference (W/Hr) and insulin resistance (HOMA-IR) in exposing the association between the I148M polymorphism and ALT levels and ii) to stratify the individual risk of these children to have liver injury on the basis of this gene-environment interaction. METHODS: 1048 Italian obese children were investigated. Anthropometric, clinical and metabolic data were collected and the PNPLA3 I148M variant genotyped. RESULTS: Children carrying the 148M allele showed higher ALT and AST levels (p = 0.000006 and p = 0.0002, respectively). Relationships between BMI-SDS, HOMA-IR and W/Hr with ALT were analysed in function of the different PNPLA3 genotypes. Children 148M homozygous showed a stronger correlation between ALT and W/Hr than those carrying the other genotypes (p: 0.0045) and, therefore, 148M homozygotes with high extent of abdominal fat (W/Hr above 0.62) had the highest OR (4.9, 95% C. I. 3.2-7.8, p = 0.00001) to develop pathologic ALT. CONCLUSIONS: We have i) showed for the first time that the magnitude of the association of PNPLA3 with liver enzymes is driven by the size of abdominal fat and ii) stratified the individual risk to develop liver damage on the basis of the interaction between the PNPLA3 genotype and abdominal fat