817 research outputs found
Isolation, identification and continuous culture of coronary endothelial cells from guinea pig hearts
Coulomb field of an accelerated charge: physical and mathematical aspects
The Maxwell field equations relative to a uniformly accelerated frame, and
the variational principle from which they are obtained, are formulated in terms
of the technique of geometrical gauge invariant potentials. They refer to the
transverse magnetic (TM) and the transeverse electric (TE) modes. This gauge
invariant "2+2" decomposition is used to see how the Coulomb field of a charge,
static in an accelerated frame, has properties that suggest features of
electromagnetism which are different from those in an inertial frame. In
particular, (1) an illustrative calculation shows that the Larmor radiation
reaction equals the electrostatic attraction between the accelerated charge and
the charge induced on the surface whose history is the event horizon, and (2) a
spectral decomposition of the Coulomb potential in the accelerated frame
suggests the possibility that the distortive effects of this charge on the
Rindler vacuum are akin to those of a charge on a crystal lattice.Comment: 27 pages, PlainTex. Related papers available at
http://www.math.ohio-state.edu/~gerlac
Support Vector Machine Analysis of Functional Magnetic Resonance Imaging of Interoception Does Not Reliably Predict Individual Outcomes of Cognitive Behavioral Therapy in Panic Disorder with Agoraphobia
Background: The approach to apply multivariate pattern analyses based on neuro
imaging data for outcome prediction holds out the prospect to improve
therapeutic decisions in mental disorders. Patients suffering from panic
disorder with agoraphobia (PD/AG) often exhibit an increased perception of
bodily sensations. The purpose of this investigation was to assess whether
multivariate classification applied to a functional magnetic resonance imaging
(fMRI) interoception paradigm can predict individual responses to cognitive
behavioral therapy (CBT) in PD/AG. Methods: This analysis is based on
pretreatment fMRI data during an interoceptive challenge from a multicenter
trial of the German PANIC-NET. Patients with DSM-IV PD/AG were dichotomized as
responders (n = 30) or non-responders (n = 29) based on the primary outcome
(Hamilton Anxiety Scale Reduction ≥50%) after 6 weeks of CBT (2 h/week). fMRI
parametric maps were used as features for response classification with linear
support vector machines (SVM) with or without automated feature selection.
Predictive accuracies were assessed using cross validation and permutation
testing. The influence of methodological parameters and the predictive ability
for specific interoception-related symptom reduction were further evaluated.
Results: SVM did not reach sufficient overall predictive accuracies
(38.0–54.2%) for anxiety reduction in the primary outcome. In the exploratory
analyses, better accuracies (66.7%) were achieved for predicting
interoception-specific symptom relief as an alternative outcome domain. Subtle
information regarding this alternative response criterion but not the primary
outcome was revealed by post hoc univariate comparisons. Conclusion: In
contrast to reports on other neurofunctional probes, SVM based on an
interoception paradigm was not able to reliably predict individual response to
CBT. Results speak against the clinical applicability of this technique
A53T-alpha-synuclein overexpression impairs dopamine signaling and striatal synaptic plasticity in old mice
BACKGROUND: Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or the A53T missense mutation of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. METHODOLOGY/PRINCIPAL FINDINGS: Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. To characterize the progression, we employed young adult as well as old mice. Analysis of striatal neurotransmitter content demonstrated that dopamine (DA) levels correlated directly with the level of expression of SNCA, an observation also made in SNCA-deficient (knockout, KO) mice. However, the elevated DA levels in the striatum of old A53T-SNCA overexpressing mice may not be transmitted appropriately, in view of three observations. First, a transcriptional downregulation of the extraneural DA degradation enzyme catechol-ortho-methytransferase (COMT) was found. Second, an upregulation of DA receptors was detected by immunoblots and autoradiography. Third, extensive transcriptome studies via microarrays and quantitative real-time RT-PCR (qPCR) of altered transcript levels of the DA-inducible genes Atf2, Cb1, Freq, Homer1 and Pde7b indicated a progressive and genotype-dependent reduction in the postsynaptic DA response. As a functional consequence, long term depression (LTD) was absent in corticostriatal slices from old transgenic mice. CONCLUSIONS/SIGNIFICANCE: Taken together, the dysfunctional neurotransmission and impaired synaptic plasticity seen in the A53T-SNCA overexpressing mice reflect early changes within the basal ganglia prior to frank neurodegeneration. As a model of preclinical stages of PD, such insights may help to develop neuroprotective therapeutic approaches
Posttraumatische Belastungsstörung infolge eines Suizidversuchs
Zusammenfassung:Hintergrund: Erste Studien legen nahe, dass ein selbstdurchgeführter Suizidversuch überraschend häufig eine PTBS-Symptomatik verursachen könnte. Die berichteten Prävalenzangaben der Studien variieren jedoch erheblich. Methode: In der vorliegenden Online-Studie wurden N = 50 Suizidversuchsüberlebenden zu suizidversuchsbezogenen PTBS-Symptomen und gegenwärtigen Suizidgedanken befragt. Zur Falldefinition diente eine modifizierte Version der Posttraumatischen Checkliste für DSM-5 (PCL-5) entweder auf Basis eines Cut-off Wertes oder auf Syndrom-Basis. Ergebnisse: In Abhängigkeit von der Falldefinition wurden 52 % (n = 26) bzw. 42 % (n = 21) der Teilnehmenden als Personen identifiziert, welche potenziell die Diagnosekriterien einer PTBS infolge eines eigenen Suizidversuchs erfüllten. Teilnehmende mit suizidversuchsbezogener PTBS-Symptomatik berichteten teilweise über mehr gegenwärtige Suizidgedanken. Schlussfolgerung: Die Ergebnisse legen nahe, dass Personen nach einem selbstdurchgeführten Suizidversuch eine PTBS-Symptomatik entwickeln. Aufgrund der Relevanz dieser Ergebnisse für eine wirksame Behandlung von Suizidversuchsüberlebenden sind weitere Studien an größeren deutschen Stichproben und unter Nutzung klinischer Interviews zu empfehlen
Dynamics on expanding spaces: modeling the emergence of novelties
Novelties are part of our daily lives. We constantly adopt new technologies,
conceive new ideas, meet new people, experiment with new situations.
Occasionally, we as individuals, in a complicated cognitive and sometimes
fortuitous process, come up with something that is not only new to us, but to
our entire society so that what is a personal novelty can turn into an
innovation at a global level. Innovations occur throughout social, biological
and technological systems and, though we perceive them as a very natural
ingredient of our human experience, little is known about the processes
determining their emergence. Still the statistical occurrence of innovations
shows striking regularities that represent a starting point to get a deeper
insight in the whole phenomenology. This paper represents a small step in that
direction, focusing on reviewing the scientific attempts to effectively model
the emergence of the new and its regularities, with an emphasis on more recent
contributions: from the plain Simon's model tracing back to the 1950s, to the
newest model of Polya's urn with triggering of one novelty by another. What
seems to be key in the successful modelling schemes proposed so far is the idea
of looking at evolution as a path in a complex space, physical, conceptual,
biological, technological, whose structure and topology get continuously
reshaped and expanded by the occurrence of the new. Mathematically it is very
interesting to look at the consequences of the interplay between the "actual"
and the "possible" and this is the aim of this short review.Comment: 25 pages, 10 figure
Dimensional structure of bodily panic attack symptoms and their specific connections to panic cognitions, anxiety sensitivity and claustrophobic fears
This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.Background.
Previous studies of the dimensional structure of panic attack symptoms have mostly identified a respiratory and a vestibular/mixed somatic dimension. Evidence for additional dimensions such as a cardiac dimension and the allocation of several of the panic attack symptom criteria is less consistent. Clarifying the dimensional structure of the panic attack symptoms should help to specify the relationship of potential risk factors like anxiety sensitivity and fear of suffocation to the experience of panic attacks and the development of panic disorder.
Method.
In an outpatient multicentre study 350 panic patients with agoraphobia rated the intensity of each of the ten DSM-IV bodily symptoms during a typical panic attack. The factor structure of these data was investigated with nonlinear confirmatory factor analysis (CFA). The identified bodily symptom dimensions were related to panic cognitions, anxiety sensitivity and fear of suffocation by means of nonlinear structural equation modelling (SEM).
Results.
CFA indicated a respiratory, a vestibular/mixed somatic and a cardiac dimension of the bodily symptom criteria. These three factors were differentially associated with specific panic cognitions, different anxiety sensitivity facets and suffocation fear.
Conclusions.
Taking into account the dimensional structure of panic attack symptoms may help to increase the specificity of the associations between the experience of panic attack symptoms and various panic related constructs.Peer Reviewe
A53T-Alpha-Synuclein Overexpression Impairs Dopamine Signaling and Striatal Synaptic Plasticity in Old Mice
Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or the A53T missense mutation of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons.Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. To characterize the progression, we employed young adult as well as old mice. Analysis of striatal neurotransmitter content demonstrated that dopamine (DA) levels correlated directly with the level of expression of SNCA, an observation also made in SNCA-deficient (knockout, KO) mice. However, the elevated DA levels in the striatum of old A53T-SNCA overexpressing mice may not be transmitted appropriately, in view of three observations. First, a transcriptional downregulation of the extraneural DA degradation enzyme catechol-ortho-methytransferase (COMT) was found. Second, an upregulation of DA receptors was detected by immunoblots and autoradiography. Third, extensive transcriptome studies via microarrays and quantitative real-time RT-PCR (qPCR) of altered transcript levels of the DA-inducible genes Atf2, Cb1, Freq, Homer1 and Pde7b indicated a progressive and genotype-dependent reduction in the postsynaptic DA response. As a functional consequence, long term depression (LTD) was absent in corticostriatal slices from old transgenic mice.Taken together, the dysfunctional neurotransmission and impaired synaptic plasticity seen in the A53T-SNCA overexpressing mice reflect early changes within the basal ganglia prior to frank neurodegeneration. As a model of preclinical stages of PD, such insights may help to develop neuroprotective therapeutic approaches
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