Clustering, logistics, and spatial economics

In the last decade, the number of logistic service providers located in clusters across Europe has increased substantially. Because location choice models in logistics studies are not able to give a satisfactory explanation for this phenomenon, various spatial economic concepts are studied in this paper. The main purpose is to provide more insight into the selection of economically attractive locations within these concepts and, more specifically, into the decision of individual firms whether or not to join a cluster. Such insight may lead to an improvement of the existing logistic models. It appears that the spatial economic concepts describe several mechanisms that are relevant to the clustering of logistic service providers. These mechanisms can possibly be incorporated in logistic clustering modelsLocation of Industry;Logistics;Spatial Models;Clusters;business economics

Di-μ-thio­cyanato-bis­[bis­(tri-p-tolyl­phosphine)silver(I)] 0.35-hydrate

In the binuclear centrosymmetric title compound, [Ag2(NCS)2(C21H21P)4]·0.35H2O, a pseudo-polymorph of [Ag2(NCS)2(C21H21P)4]·2CH3CN, the Ag atom is coordinated by two phosphine ligands and two bridging thio­cyanate ligands in a distorted tetra­hedral configuration. The crystal structure exhibits inter­molecular C—H⋯π inter­actions

Beyond the Prevention of Harm: Animal Disease Policy as a Moral Question

European animal disease policy seems to find its justification in a “harm to other” principle. Limiting the freedom of animal keepers—e.g., by culling their animals—is justified by the aim to prevent harm, i.e., the spreading of the disease. The picture, however, is more complicated. Both during the control of outbreaks and in the prevention of notifiable, animal diseases the government is confronted with conflicting claims of stakeholders who anticipate running a risk to be harmed by each other, and who ask for government intervention. In this paper, we first argue that in a policy that aims to prevent animal diseases, the focus shifts from limiting “harm” to weighing conflicting claims with respect to “risks of harm.” Therefore, we claim that the harm principle is no longer a sufficient justification for governmental intervention in animal disease prevention. A policy that has to deal with and distribute conflicting risks of harm needs additional value assumptions that guide this process of assessment and distribution. We show that currently, policies are based on assumptions that are mainly economic considerations. In order to show the limitations of these considerations, we use the interests and position of keepers of backyard animals as an example. Based on the problems they faced during and after the recent outbreaks, we defend the thesis that in order to develop a sustainable animal disease policy other than economic assumptions need to be taken into accoun

Fetal Tachyarrhythmia - Part I: Diagnosis

Fetal tachycardia, first recognized in 1930 by Hyman et al1, is a condition occurring in approximately 0.4-0.6% of all pregnancies2. A subset of these cases with more sustained periods of tachycardia is clinically relevant. The necessity of therapeutic intervention in this condition is still a matter of discussion focused on the natural history of the disease. The spectrum of opinions varies from non-intervention3,4,5 based on a number of cases in which the tachycardia subsided spontaneously6, to aggressive pharmacotherapeutic intervention7,8 based on reports of deterioration of the fetal condition ultimately ending in significant neurological morbidity9,10,11, or fetal demise12,13,14. Prenatal treatment through indirect, maternally administered drug therapy seems to be the preference of most centers15,16,17,18,19,20,21. This matter will be discussed further in Fetal Tachyarrhythmia, Part II, Treatment

Fetal Tachyarrhythmia - Part II: Treatment

The decision to initiate pharmacological intervention in case of fetal tachycardia depends on several factors and must be weighed against possible maternal and/or fetal adverse effects inherent to the use of antiarrhythmics. First, the seriousness of the fetal condition must be recognized. Many studies have shown that in case of fetal tachycardia, there is a significant predisposition to congestive heart failure and subsequent development of fetal hydrops and even sudden cardiac death1,2,3 Secondly, predictors of congestive heart failure have been suggested in several studies, such as the percentage of time that the tachycardia is present, the gestational age at which the tachycardia occurs4, the ventricular rate5 and the site of origin of the tachycardia6. However, the sensitivity of these predictors is low and they are therefore clinically not very useful. In addition, hemodynamic compromise may occur in less than 24 - 48 hours as has been shown in the fetal lamb7 and in tachycardic fetuses8,9. On the other hand, spontaneous resolution of the tachycardia has also been described10. Thirdly, transplacental management of fetuses with tricuspid regurgitation11, congestive heart failure or fetal hydrops is difficult12,13, probably as a result of limited transplacental transfer of the antiarrhythmic drug14,15. In case of fetal hydrops, conversion rates are decreased and time to conversion is increased13. Treatment of sustained fetal tachycardia is therefore to be preferred above expectant management, although some centers oppose this regimen and suggest that in cases with (intermittent) fetal SVT not complicated by congestive heart failure or fetal hydrops, conservative management and close surveillance might be a reasonable alternative16,17,18