The professionals speak: Practitioners’ perspectives on professional election campaigning

Faced with some fundamental changes in the socio-cultural, political and media environment, political parties in post-industrialized democracies have started to initiate substantial transformations of both their organizational structures and communicative practices. Those innovations, described as professionalization, become most obvious during election campaigns. In recent times, the number of empirical studies measuring the degree of political parties’ campaign professionalism has grown. They have relied on a broad spectrum of indicators derived from theory which have not been tested for their validity. For the first time, we put these indicators to a ‘reality check’ by asking top-ranked party secretaries and campaign managers in 12 European countries to offer their perceptions of professional election campaigning. Furthermore, we investigate whether any differences in understanding professionalism among party campaign practitioners can be explained by macro (country) and meso (party) factors. By and large, our results confirm the validity of most indicators applied in empirical studies on campaign professionalism so far. There are some party- and country-related differences in assessing campaign professionalism too, but the influence of most factors on practitioners’ evaluations is weak. Therefore, we conclude that largely there is a far-reaching European Union-wide common understanding of professional election campaigning

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

Nicotinic receptors

Regulation of normal or abnormal behaviour is critically controlled by the central serotonergic systems. Recent evidence has suggested that serotonin (5-HT) neurotransmission dysfunction contributes to a variety of pathological conditions, including depression, anxiety, schizophrenia and Parkinson’s disorders. There is also a great amount of evidence indicating that 5-HT signalling may affect the reinforcing properties of drugs of abuse by the interaction and modulation of dopamine (DA) function. This chapter is focused on one of the more addictive drugs, nicotine. It is widely recognised that the effects of nicotine are strongly associated with the stimulatory action it exhibits on mesolimbic DAergic function. We outline the role of 5-HT and its plethora of receptors, focusing on 5-HT2 subtypes with relation to their involvement in the neurobiology of nicotine addiction. We also explore the novel pharmacological approaches using 5-HT agents for the treatment of nicotine dependence. Compelling evidence shows that 5-HT2C receptor agonists may be possible therapeutic targets for smoking cessation, although further investigation is required.peer-reviewe

Using C. elegans to decipher the cellular and molecular mechanisms underlying neurodevelopmental disorders

Prova tipográfica (uncorrected proof)Neurodevelopmental disorders such as epilepsy, intellectual disability (ID), and autism spectrum disorders (ASDs) occur in over 2 % of the population, as the result of genetic mutations, environmental factors, or combination of both. In the last years, use of large-scale genomic techniques allowed important advances in the identification of genes/loci associated with these disorders. Nevertheless, following association of novel genes with a given disease, interpretation of findings is often difficult due to lack of information on gene function and effect of a given mutation in the corresponding protein. This brings the need to validate genetic associations from a functional perspective in model systems in a relatively fast but effective manner. In this context, the small nematode, Caenorhabditis elegans, presents a good compromise between the simplicity of cell models and the complexity of rodent nervous systems. In this article, we review the features that make C. elegans a good model for the study of neurodevelopmental diseases. We discuss its nervous system architecture and function as well as the molecular basis of behaviors that seem important in the context of different neurodevelopmental disorders. We review methodologies used to assess memory, learning, and social behavior as well as susceptibility to seizures in this organism. We will also discuss technological progresses applied in C. elegans neurobiology research, such as use of microfluidics and optogenetic tools. Finally, we will present some interesting examples of the functional analysis of genes associated with human neurodevelopmental disorders and how we can move from genes to therapies using this simple model organism.The authors would like to acknowledge Fundação para a Ciência e Tecnologia (FCT) (PTDC/SAU-GMG/112577/2009). AJR and CB are recipients of FCT fellowships: SFRH/BPD/33611/2009 and SFRH/BPD/74452/2010, respectively

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

The Many Faces of Fear: Comparing the Pathways and Impacts of Nonconsumptive Predator Effects on Prey Populations

Background: Most ecological models assume that predator and prey populations interact solely through consumption: predators reduce prey densities by killing and consuming individual prey. However, predators can also reduce prey densities by forcing prey to adopt costly defensive strategies. Methodology/Principal Findings: We build on a simple Lotka-Volterra predator-prey model to provide a heuristic tool for distinguishing between the demographic effects of consumption (consumptive effects) and of anti-predator defenses (nonconsumptive effects), and for distinguishing among the multiple mechanisms by which anti-predator defenses might reduce prey population growth rates. We illustrate these alternative pathways for nonconsumptive effects with selected empirical examples, and use a meta-analysis of published literature to estimate the mean effect size of each pathway. Overall, predation risk tends to have a much larger impact on prey foraging behavior than measures of growth, survivorship, or fecundity. Conclusions/Significance: While our model provides a concise framework for understanding the many potential NCE pathways and their relationships to each other, our results confirm empirical research showing that prey are able to partially compensate for changes in energy income, mitigating the fitness effects of defensive changes in time budgets. Distinguishing the many facets of nonconsumptive effects raises some novel questions, and will help guide both empirica

Factorial validity and internal consistency of the PRAFAB questionnaire in women with stress urinary incontinence

<p>Abstract</p> <p>Background</p> <p>To investigate the factor structure, dimensionality and construct validity of the (5-item) PRAFAB questionnaire score in women with stress urinary incontinence (stress UI).</p> <p>Methods</p> <p>A cross validation study design was used in a cohort of 279 patients who were randomly divided into Sample A or B. Sample A was used for preliminary exploratory factor analyses with promax rotation. Sample B provided an independent sample for confirming the premeditated and proposed factor structure and item retention. Internal consistency, item-total and subscale correlations were determined to assess the dimensionality. Construct validity was assessed by comparing factor-based scale means by clinical characteristics based on known relationships.</p> <p>Results</p> <p>Factor analyses resulted in a two-factor structure or subscales: items related to 'leakage severity' (protection, amount and frequency) and items related to its 'perceived symptom impact' or consequences of stress UI on the patient's life (adjustment and body (or self) image). The patterns of the factor loadings were fairly identical for both study samples. The two constructed subscales demonstrated adequate internal consistency with Cronbach's alphas in a range of 0.78 and 0.84 respectively. Scale scores differed by clinical characteristics according to the expectations and supported the construct validity of the scales.</p> <p>Conclusion</p> <p>The findings suggest a two-factorial structure of the PRAFAB questionnaire. Furthermore the results confirmed the internal consistency and construct validity as demonstrated in our previous study. The best description of the factorial structure of the PRAFAB questionnaire was given by a two-factor solution, measuring the stress UI leakage severity items and the perceived symptom impact items. Future research will be necessary to replicate these findings in different settings, type of UI and non-white women and men.</p

Measurement of the Branching Fraction for τ→ρν

This Letter presents a measurement of the decay τ-→ρ-ντ using data obtained with the Mark II detector at SPEAR. In the center-of-mass energy region 4.5&lt;~Ec.m.&lt;~6.0 GeV 85 events are observed in which a charged ρ was found in coincidence with either an electron or a muon. It was determined that B(τ-→ρ-ντ)=(20.5±4.1)% and the ratio B(τ-→ρ-ντ)B(τ-→e-ντν̄e)=1.11± 0.23. © 1979 The American Physical Society

Precise Measurement of the Tau Lifetime

The τ lifetime was measured with the Mark II vertex detector at the storage ring PEP. ττ=(3.20±0.41±0.35)×10-13 sec was found, which agrees well with e-μ-τ university. © 1983 The American Physical Society

Ubiquitous molecular substrates for associative learning and activity-dependent neuronal facilitation.

Recent evidence suggests that many of the molecular cascades and substrates that contribute to learning-related forms of neuronal plasticity may be conserved across ostensibly disparate model systems. Notably, the facilitation of neuronal excitability and synaptic transmission that contribute to associative learning in Aplysia and Hermissenda, as well as associative LTP in hippocampal CA1 cells, all require (or are enhanced by) the convergence of a transient elevation in intracellular Ca2+ with transmitter binding to metabotropic cell-surface receptors. This temporal convergence of Ca2+ and G-protein-stimulated second-messenger cascades synergistically stimulates several classes of serine/threonine protein kinases, which in turn modulate receptor function or cell excitability through the phosphorylation of ion channels. We present a summary of the biophysical and molecular constituents of neuronal and synaptic facilitation in each of these three model systems. Although specific components of the underlying molecular cascades differ across these three systems, fundamental aspects of these cascades are widely conserved, leading to the conclusion that the conceptual semblance of these superficially disparate systems is far greater than is generally acknowledged. We suggest that the elucidation of mechanistic similarities between different systems will ultimately fulfill the goal of the model systems approach, that is, the description of critical and ubiquitous features of neuronal and synaptic events that contribute to memory induction