Charged pion production in 4496^{96}_{44}Ru+4496^{96}_{44}Ru collisions at 400A and 1528A MeV

We present transverse momentum and rapidity spectra of charged pions in central Ru + Ru collisions at 400$A$ and 1528$A$ MeV. The data exhibit enhanced production at low transverse momenta compared to the expectations from the thermal model that includes the decay of $\Delta(1232)$-resonances and thermal pions. Modification of the $\Delta$-spectral function and the Coulomb interaction are necessary to describe the detailed shape of the transverse momentum spectra. Within the framework of the thermal model, the freeze-out radii of pions are similar at both beam energies. The IQMD model reproduces the shapes of the transverse momentum and rapidity spectra of pions, but the predicted absolute yields are larger than in the measurements, especially at lower beam energy.Comment: 12 pages, 11 figure

Cell genesis and dendritic plasticity: a neuroplastic pas de deux in the onset and remission from depression

Brain neuroplasticity is increasingly considered to be an important component of both the pathology and treatment of depressive spectrum disorders. Recent studies shed light on the relevance of hippocampal cell genesis and cortico-limbic dendritic plasticity for the development and remission from depressive-like behavior. However, the neurobiological significance of neuroplastic phenomena in this context is still controversial. Here we summarize recent developments in this topic and propose an integrative interpretation of data gathered so far

Identification of baryon resonances in central heavy-ion collisions at energies between 1 and 2 AGeV

The mass distributions of baryon resonances populated in near-central collisions of Au on Au and Ni on Ni are deduced by defolding the $p_t$ spectra of charged pions by a method which does not depend on a specific resonance shape. In addition the mass distributions of resonances are obtained from the invariant masses of $(p, \pi^{\pm})$ pairs. With both methods the deduced mass distributions are shifted by an average value of -60 MeV/c$^2$ relative to the mass distribution of the free $\Delta(1232)$ resonance, the distributions descent almost exponentially towards mass values of 2000 MeV/c^2. The observed differences between $(p, \pi^-)$ and $(p, \pi^+)$ pairs indicate a contribution of isospin $I = 1/2$ resonances. The attempt to consistently describe the deduced mass distributions and the reconstructed kinetic energy spectra of the resonances leads to new insights about the freeze out conditions, i.e. to rather low temperatures and large expansion velocities.Comment: 30 pages, 13 figures, Latex using documentstyle[12pt,a4,epsfig], to appear in Eur. Phys. J.

Excitation function of elliptic flow in Au+Au collisions and the nuclear matter equation of state

We present measurements of the excitation function of elliptic flow at midrapidity in Au+Au collisions at beam energies from 0.09 to 1.49 GeV per nucleon. For the integral flow, we discuss the interplay between collective expansion and spectator shadowing for three centrality classes. A complete excitation function of transverse momentum dependence of elliptic flow is presented for the first time in this energy range, revealing a rapid change with incident energy below 0.4 AGeV, followed by an almost perfect scaling at the higher energies. The equation of state of compressed nuclear matter is addressed through comparisons to microscopic transport model calculations.Comment: 10 pages, 4 eps figures, submitted for publication. Data files will be available at http://www.gsi.de/~fopiwww/pub

Isospin-tracing: A probe of non-equilibrium in central heavy-ion collisions

Four different combinations of $^{96}_{44}$Ru and $^{96}_{40}$Zr nuclei, both as projectile and target, were investigated at the same bombarding energy of 400$A$ MeV using a $4 \pi$ detector. The degree of isospin mixing between projectile and target nucleons is mapped across a large portion of the phase space using two different isospin-tracer observables, the number of measured protons and the ${\rm t}/^{3}{\rm He}$ yield ratio. The experimental results show that the global equilibrium is not reached even in the most central collisions. Quantitative measures of stopping and mixing are extracted from the data. They are found to exhibit a quite strong sensitivity to the in-medium (n,n) cross section used in microscopic transport calculations.Comment: 4 pages RevTeX, 3 figures (ps files), submitted to Phys. Rev. Let

Morphometric evidence for neuronal and glial prefrontal cell pathology in major depression

Background: This report provides histopathological evidence to support prior neuroimaging findings of decreased volume and altered metabolism in the frontal cortex in major depressive disorder. Methods: Computer-assisted three-dimensional cell counting was used to reveal abnormal cytoarchitecture in left rostral and caudal orbitofrontal and dorsolateral prefrontal cortical regions in subjects with major depression as compared to psychiatrically normal controls. Results: Depressed subjects had decreases in cortical thickness, neuronal sizes, and neuronal and glial densities in the upper (II–IV) cortical layers of the rostral orbitofrontal region. In the caudal orbitofrontal cortex in depressed subjects, there were prominent reductions in glial densities in the lower (V–VI) cortical layers that were accompanied by small but significant decreases in neuronal sizes. In the dorsolateral prefrontal cortex of depressed subjects marked reductions in the density and size of neurons and glial cells were found in both supra- and infragranular layers. Conclusions: These results reveal that major depression can be distinguished by specific histopathology of both neurons and glial cells in the prefrontal cortex. Our data will contribute to the interpretation of neuroimaging findings and identification of dysfunctional neuronal circuits in major depression

Impaired Brain Dopamine and Serotonin Release and Uptake in Wistar Rats Following Treatment with Carbotplatin

Chemotherapy-induced cognitive impairment, known also as “chemobrain”, is a medical complication of cancer treatment that is characterized by a general decline in cognition affecting visual and verbal memory, attention, complex problem solving skills, and motor function. It is estimated that one-third of patients who undergo chemotherapy treatment will experience cognitive impairment. Alterations in the release and uptake of dopamine and serotonin, central nervous system neurotransmitters that play important roles in cognition, could potentially contribute to impaired intellectual performance in those impacted by chemobrain. To investigate how chemotherapy treatment affects these systems, fast-scan cyclic voltammetry (FSCV) at carbon-fiber microelectrodes was used to measure dopamine and serotonin release and uptake in coronal brain slices containing the striatum and dorsal raphe nucleus, respectively. Measurements were taken from rats treated weekly with selected doses of carboplatin and from control rats treated with saline. Modeling the stimulated dopamine release plots revealed an impairment of dopamine release per stimulus pulse (80% of saline control at 5 mg/kg and 58% at 20 mg/kg) after 4 weeks of carboplatin treatment. Moreover, Vmax, the maximum uptake rate of dopamine, was also decreased (55% of saline control at 5 mg/kg and 57% at 20 mg/kg). Nevertheless, overall dopamine content, measured in striatal brain lysates by high performance liquid chromatography, and reserve pool dopamine, measured by FSCV after pharmacological manipulation, did not significantly change, suggesting that chemotherapy treatment selectively impairs the dopamine release and uptake processes. Similarly, serotonin release upon electrical stimulation was impaired (45% of saline control at 20 mg/kg). Measurements of spatial learning discrimination were taken throughout the treatment period and carboplatin was found to alter cognition. These studies support the need for additional neurochemical and behavioral analyses to identify the underlying mechanisms of chemotherapy-induced cognitive disorders

Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers

Quantitative Analysis of Focused A-To-I RNA Editing Sites by Ultra-High-Throughput Sequencing in Psychiatric Disorders

A-to-I RNA editing is a post-transcriptional modification of single nucleotides in RNA by adenosine deamination, which thereby diversifies the gene products encoded in the genome. Thousands of potential RNA editing sites have been identified by recent studies (e.g. see Li et al, Science 2009); however, only a handful of these sites have been independently confirmed. Here, we systematically and quantitatively examined 109 putative coding region A-to-I RNA editing sites in three sets of normal human brain samples by ultra-high-throughput sequencing (uHTS). Forty of 109 putative sites, including 25 previously confirmed sites, were validated as truly edited in our brain samples, suggesting an overestimation of A-to-I RNA editing in these putative sites by Li et al (2009). To evaluate RNA editing in human disease, we analyzed 29 of the confirmed sites in subjects with major depressive disorder and schizophrenia using uHTS. In striking contrast to many prior studies, we did not find significant alterations in the frequency of RNA editing at any of the editing sites in samples from these patients, including within the 5HT2C serotonin receptor (HTR2C). Our results indicate that uHTS is a fast, quantitative and high-throughput method to assess RNA editing in human physiology and disease and that many prior studies of RNA editing may overestimate both the extent and disease-related variability of RNA editing at the sites we examined in the human brain