Deliberating foreign policy: perceptions and effects of citizen participation in Germany

Citizen participation has been a popular format in policy fields like environmental and climate policies for many years. More recently, however, it has extended to issues of foreign policy which has long been considered as a prerogative of the executive in democratic systems. This paper analyses citizen participation in German foreign policy by comparing deliberative-participatory processes implemented by the German Federal Foreign Office (AA) and the Ministry for the Environment, Nature Conservation, and Nuclear Safety (BMU). We draw on recent scholarship in the field of deliberative democracy in order to gain a better understanding how the two ministries understand citizen participation, how they implement these processes, and what effects they have on formal decision-making. Using interviews, participant observation, and document analysis, we investigate two processes of citizen participation in depth. We argue that ministerial understandings of citizen participation determine how they design formats in their respective field. This leads to quite divergent implementations and results of deliberative-participatory formats in the field of foreign policy, depending on whether the AA or the BMU initiates them

Die Agenda 2010 und die Armutsgefährdung

Die Zahl der von Armut gefährdeten Personen in Deutschland lag im Jahr 2006 mit rund 14 Millionen um rund eine Million niedriger als 2005. Der Abbau der Armutsgefährdung verlief parallel mit dem Rückgang der Arbeitslosigkeit, der wegen der Agenda 2010 im letzten Boom allein in Westdeutschland um eine Million Menschen größer war, als man es bei einer Fortsetzung früherer Entwicklungsmuster hätte erwarten können. Der im Zuge der Agenda 2010 gewachsene Niedriglohnsektor ist kein Problem, sondern ein Erfolg der deutschen Politik. Denn selbst bei sehr schlecht bezahlten Stellen kommt man durch eine Vollzeitbeschäftigung über die Armutsgefährdungsgrenze, weil ein Lohnzuschusssystem eingeführt wurde, das verhindert, dass Geringqualifizierte allein von ihrer Hände Arbeit leben müssen. Das hat Implikationen für die Mindestlohndebatte. Politisch verursachte Lohnerhöhungen, die über das Marktergebnis hinaus führen, bedrohen einen Teil der Menschen, den man helfen will, mit Armut. Sie vernichten Stellen und drücken das Einkommen der Arbeitslosen nach Auslaufen des Arbeitslosengeldes auf das Hartz-IV-Niveau und damit unter die Armutsgefährdungsschwelle. Der Verzicht auf Mindestlöhne verringert hingegen den Anteil der von Armut gefährdeten Menschen, weil er den bislang arbeitslosen Hartz-IV-Empfängern bezuschusste Arbeit verschafft und ihr Nettoeinkommen damit über die Armutsgefährdungsschwelle hebt.Arbeitsmarktpolitik, Sozialreform, Armutspolitik, Arbeitslosigkeit, Deutschland

Das Bundesverfassungsgerichtsurteil zu den Hartz-IV-Regelsätzen: Hintergrund und Bedeutung

Am 9. Februar 2010 hat das Bundesverfassungsgericht die Berechnung der Hartz-IV-Regelsätze für nicht konform mit der Verfassung der Bundesrepublik Deutschland befunden. In diesem Artikel wird die aktuelle Hartz-IV-Gesetzeslage dargelegt, die Kritik des Bundesverfassungsgerichts zusammengefasst, die alternativen Berechnungs- und Auszahlungsmodalitäten im bestehenden System aufgezeigt und Verbesserungsmöglichkeiten diskutiert.Arbeitsrecht, Soziale Sicherung, Verfassung, Existenzminimum, Sozialhilfe, Deutschland, Hartz-Reform

Persistent neurocognitive deficits in cognitively impaired survivors of sepsis are explained by reductions in working memory capacity

IntroductionSepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Mounting evidence suggests that many cognitively impaired sepsis survivors show long-term neurocognitive deficits in neuropsychological tasks. To date, the underlying mechanisms of these deficits are insufficiently understood. Based on previous evaluations we hypothesized that visual attention and working memory may be affected in a sample of cognitively impaired sepsis survivors.MethodsWe utilized psychophysical whole-and partial-report paradigms based on the computational theory of visual attention (TVA) to determine (i) whether sepsis survivors show changes in basic parameters of visual attention and working memory, (ii) whether the affected parameters are related to neuropsychological test results in a standard battery in sepsis survivors and matched healthy control participants, (iii) whether between-group differences in these basic parameters of visual attention could account for underperformance of sepsis survivors in neuropsychological tests when adjusting for potentially relevant clinical variables.ResultsWe showed that, in sepsis survivors, the maximum number of elements consciously maintained in an instant, i.e. the working memory storage capacity K, is reduced (sepsis survivors: M = 3.0; healthy controls: M = 3.4). Moreover, K explained variance in neurocognitive outcomes –17% in attentional and 16 % in executive functions – in a standard neuropsychological battery. The association remained stable when adjusting for clinical variables.DiscussionThus, in our sample of cognitively impaired sepsis survivors, a reduction in working memory capacity seems to be a critical determinant of the neurocognitive sequelae. It should be the subject of future work on mechanisms but may also serve as surrogate outcome measure in interventional studies

Video Tutorial for Clinical Flap-Monitoring in Plastic Surgery

Free tissue transfer is a well-established technique in the field of plastic reconstructive surgery. Despite great progress being made in relation to technical issues and the anatomical understanding of free flap transfers, a loss rate of between 2% and 5% remains.1–5 The main reasons for free flap failure are vascular problems, such as vascular thrombosis (venous and arterial), arterial insufficiency, active bleeding or hematoma, and venous congestion.1–4 Many studies have demonstrated that the salvage rate for flaps is inversely related to the time between the onset of vascular compromise and surgical intervention.6,7 To guarantee an immediate reaction in case of perfusion problems in free flap surgery, a continuous and sufficient flap monitoring is indispensable. Although there are numerous techniques to assess flap vitality, clinical examination remains the gold standard.8 Besides this preferred method, a handheld and implantable Doppler, microdialysis, video-based application, real-time measurement of oxygen saturation, fluorescence angiography, spectroscopy, contrast-enhanced duplex, and activated clotting time have been proposed as alternative modalities for monitoring, though none of these has provided better results than clinical examination.9,10 The postoperative clinical examination and monitoring of flaps is frequently delegated to nurses and paramedics. Thus, there is often a high variation in skill level due to the lack of clinical experience needed to assess flap vitality.11 When asked, even young plastic surgeons often admit uncertainty when it comes to assessing postoperative flap vitality. To guarantee a high level of monitoring quality, constant training is indispensable. As mentioned above, perfusion compromise—being of arterial or venous origin—emerges rarely and is hard to include consistently within a training program. Therefore, educational material that clearly elucidates different qualities in vascular compromise in flaps is highly desirable

Métodos de reconocimiento del subsuelo

The aim of this workshop is to present the main methods of subsoil studies (namely mechanical and geophysical methods) to the Earth Sciences professorate. These methods frequently involve the use of specific material. The different methods are usually taught in the classroom where there is no real contact between the students and the equipment. Several activities, all of them taking place in surrounding areas of the university campus of Girona, will provide the assistants to the workshop with the opportunity of making measurements with different equipment. These activities will be made in the field so as to contribute to the resolution of a problem which will have been previously proposed. The problems presented are situations, most of them real, when subsoil investigation techniques are usually used. These cases have been employed as teaching-learning strategies with university and second grade students in the area of Girona. Finally, some examples of exercises involving the treatment of data obtained through subsoil investigation techniques are also presented to complement the workshopEl taller tiene como objeto principal facilitar al profesorado de Ciencias de la Tierra el contacto directo con los principales tipos de métodos que se utilizan en el estudio del subsuelo. Éstos comprenden un conjunto de equipos que generalmente son explicados en el aula sin que haya habido un contacto directo con los mismos (los sondeos mecánicos de reconocimiento y los instrumentos geofísicos son los casos más habituales). A través de diversas actividades, ubicadas en el entorno del campus universitario de Girona, los asistentes participan en la realización de las mediciones mediante equipos diversos. Estas actividades se desarrollan en campo con el objeto de contribuir a la resolución de una problemática concreta planteada. Se trata de situaciones, reales en su mayoría, en las cuales suele ser habitual la utilización de métodos de reconocimiento del subsuelo. Los casos presentados han sido utilizados como estrategias de enseñanza-aprendizaje con estudiantes universitarios y de secundaria de nuestro entorno. El taller se complementa con la presentación de varios ejemplos de una tipología de ejercicios que incluyen el tratamiento de datos obtenidos mediante métodos de reconocimiento del subsuel

LGI1 antibodies alter Kv1.1 and AMPA receptors changing synaptic excitability, plasticity and memory

Leucine-rich glioma-inactivated 1 (LGI1) is a secreted neuronal protein that forms a trans-synaptic complex that includes the presynaptic disintegrin and metalloproteinase domain-containing protein 23 (ADAM23), which interacts with voltage-gated potassium channels Kv1.1, and the postsynaptic ADAM22, which interacts with AMPA receptors. Human autoantibodies against LGI1 associate with a form of autoimmune limbic encephalitis characterized by severe but treatable memory impairment and frequent faciobrachial dystonic seizures. Although there is evidence that this disease is immune-mediated, the underlying LGI1 antibody-mediated mechanisms are unknown. Here, we used patient-derived immunoglobulin G (IgG) antibodies to determine the main epitope regions of LGI1 and whether the antibodies disrupt the interaction of LGI1 with ADAM23 and ADAM22. In addition, we assessed the effects of patient-derived antibodies on Kv1.1, AMPA receptors, and memory in a mouse model based on cerebroventricular transfer of patient-derived IgG. We found that IgG from all patients (n = 25), but not from healthy participants (n = 20), prevented the binding of LGI1 to ADAM23 and ADAM22. Using full-length LGI1, LGI3, and LGI1 constructs containing the LRR1 domain (EPTP1-deleted) or EPTP1 domain (LRR3-EPTP1), IgG from all patients reacted with epitope regions contained in the LRR1 and EPTP1 domains. Confocal analysis of hippocampal slices of mice infused with pooled IgG from eight patients, but not pooled IgG from controls, showed a decrease of total and synaptic levels of Kv1.1 and AMPA receptors. The effects on Kv1.1 preceded those involving the AMPA receptors. In acute slice preparations of hippocampus, patch-clamp analysis from dentate gyrus granule cells and CA1 pyramidal neurons showed neuronal hyperexcitability with increased glutamatergic transmission, higher presynaptic release probability, and reduced synaptic failure rate upon minimal stimulation, all likely caused by the decreased expression of Kv1.1. Analysis of synaptic plasticity by recording field potentials in the CA1 region of the hippocampus showed a severe impairment of long-term potentiation. This defect in synaptic plasticity was independent from Kv1 blockade and was possibly mediated by ineffective recruitment of postsynaptic AMPA receptors. In parallel with these findings, mice infused with patient-derived IgG showed severe memory deficits in the novel object recognition test that progressively improved after stopping the infusion of patient-derived IgG. Different from genetic models of LGI1 deficiency, we did not observe aberrant dendritic sprouting or defective synaptic pruning as potential cause of the symptoms. Overall, these findings demonstrate that patient-derived IgG disrupt presynaptic and postsynaptic LGI1 signalling, causing neuronal hyperexcitability, decreased plasticity, and reversible memory deficits

Glycine receptor autoantibody binding to the extracellular domain is independent from receptor glycosylation

Glycine receptor (GlyR) autoantibodies are associated with stiff-person syndrome and the life-threatening progressive encephalomyelitis with rigidity and myoclonus in children and adults. Patient histories show variability in symptoms and responses to therapeutic treatments. A better understanding of the autoantibody pathology is required to develop improved therapeutic strategies. So far, the underlying molecular pathomechanisms include enhanced receptor internalization and direct receptor blocking altering GlyR function. A common epitope of autoantibodies against the GlyRα1 has been previously defined to residues 1 A- 33 G at the N-terminus of the mature GlyR extracellular domain. However, if other autoantibody binding sites exist or additional GlyR residues are involved in autoantibody binding is yet unknown. The present study investigates the importance of receptor glycosylation for binding of anti-GlyR autoantibodies. The glycine receptor α1 harbors only one glycosylation site at the amino acid residue asparagine 38 localized in close vicinity to the identified common autoantibody epitope. First, non-glycosylated GlyRs were characterized using protein biochemical approaches as well as electrophysiological recordings and molecular modeling. Molecular modeling of non - glycosylated GlyRα1 did not show major structural alterations. Moreover, non-glycosylation of the GlyRα1 N38Q did not prevent the receptor from surface expression. At the functional level, the non-glycosylated GlyR demonstrated reduced glycine potency, but patient GlyR autoantibodies still bound to the surface-expressed non-glycosylated receptor protein in living cells. Efficient adsorption of GlyR autoantibodies from patient samples was possible by binding to native glycosylated and non-glycosylated GlyRα1 expressed in living not fixed transfected HEK293 cells. Binding of patient-derived GlyR autoantibodies to the non-glycosylated GlyRα1 offered the possibility to use purified non-glycosylated GlyR extracellular domain constructs coated on ELISA plates and use them as a fast screening readout for the presence of GlyR autoantibodies in patient serum samples. Following successful adsorption of patient autoantibodies by GlyR ECDs, binding to primary motoneurons and transfected cells was absent. Our results indicate that the glycine receptor autoantibody binding is independent of the receptor’s glycosylation state. Purified non-glycosylated receptor domains harbouring the autoantibody epitope thus provide, an additional reliable experimental tool besides binding to native receptors in cell-based assays for detection of autoantibody presence in patient sera

Peripherally-derived LGI1-reactive monoclonal antibodies cause epileptic seizures in vivo

One striking clinical hallmark in patients with autoantibodies to leucine-rich glioma inactivated 1 (LGI1) is the very frequent focal seizure semiologies, including faciobrachial dystonic seizures (FBDS), in addition to the amnesia. Polyclonal serum IgGs have successfully modelled the cognitive changes in vivo but not seizures. Hence, it remains unclear whether LGI1-autoantibodies are sufficient to cause seizures. We tested this with the molecularly precise monoclonal antibodies directed against LGI1 (LGI1-mAbs), derived from patient circulating B cells. These were directed towards both major domains of LGI1, LRR and EPTP and infused intracerebroventricularly over 7 days into juvenile male Wistar rats using osmotic pumps. Continuous wireless EEG was recorded from a depth electrode placed in hippocampal CA3 plus behavioural tests for memory and hyperexcitability were performed. Following infusion completion (Day 9), post-mortem brain slices were studied for antibody binding and effects on Kv1.1. The LGI1-mAbs bound most strongly in the hippocampal CA3 region and induced a significant reduction in Kv1.1 cluster number in this subfield. By comparison to control-Ab injected rats video-EEG analysis over 9 days revealed convulsive and non-convulsive seizure activity in rats infused with LGI1-mAbs, with a significant number of ictal events. Memory was not impaired in the novel object recognition test. Peripherally-derived human LGI1-mAbs infused into rodent CSF provide strong evidence of direct in vivo epileptogenesis with molecular correlations. These findings fulfill criteria for LGI1-antibodies in seizure causation