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Background: Migraine is a disabling chronic episodic disorder. Attack frequency progressively increases in some patients. Incremental cortical excitability has been implicated as a mechanism underlying progression. Cortical spreading depression (CSD) is the electrophysiological event underlying migraine aura, and a headache trigger .We hypothesized that CSD events during frequent migraine attacks condition the cortex to increase the susceptibility to further attacks. Methods: A single daily CSD was induced for 1 or 2 weeks in mouse frontal cortex; contralateral hemisphere served as sham control. At the end of CSD conditioning, occipital CSD susceptibility was determined by measuring the frequency of CSDs evoked by topical KCl application. Results: Sham hemispheres developed 8.4 ± 0.3 CSDs/hour, and did not significantly differ from naïve controls without prior cranial surgery (9.3 ± 0.4 CSDs/hour). After 2 but not 1 week of daily CSD conditioning, CSD frequency (4.9± 0.3 CSDs/hour) as well as the duration and propagation speed were reduced significantly in the conditioned hemispheres. Histopathological examination revealed marked reactive astrocytosis without neuronal injury throughout the conditioned cortex after 2 weeks, temporally associated with CSD susceptibility. Conclusions: These data do not support the hypothesis that frequent migraine attacks predispose the brain to further attacks by enhancing tissue susceptibility to CSD. [ABSTRACT FROM AUTHOR]

Myocardin is a remarkably potent transcriptional coactivator expressed specifically in cardiac muscle lineages and smooth muscle cells during postnatal development. Myocardin shares homology with myocardin-related transcription factor-A (MRTF-A), which are expressed in a broad range of embryonic and adult tissues. Our previous results show that myocardin induces cardiac hypertrophy. However, the effects of MRTF-A in cardiac hypertrophy remain poorly understood. Our present work further demonstrates that myocardin plays an important role in inducing hypertrophy. At the same time, we find that overexpression of MRTF-A in neonatal rat cardiomyocytes might induce cardiomyocyte hypertrophy. Furthermore, MRTF-A expression is induced in phenylephrine, angiotensin-II, and transforming growth factor-β-stimulated cardiac hypertrophy, whereas a dominant-negative form of MRTF-A or MRTF-A siRNA strongly inhibited upregulation of hypertrophy genes in response to hypertrophic agonists in neonatal rat cardiomyocytes. Our studies indicate that besides myocardin, MRTF-A might play an important role in cardiac hypertrophy. Our findings provide novel evidence for the future studies to explore the roles of MRTFs in cardiac hypertrophy. © 2011 IUBMB IUBMB Life, 63(1):54-61, 2011. [ABSTRACT FROM AUTHOR]

Complement component C4 mediates C3-dependent tissue damage after systemic ischemia–reperfusion injury. Activation of C3 also contributes to the pathogenesis of experimental and human traumatic brain injury (TBI); however, few data exist regarding the specific pathways (classic, alternative, and lectin) involved. Using complement knockout mice and a controlled cortical impact (CCI) model, we tested the hypothesis that the classic pathway mediates secondary damage after TBI. After CCI, C4c and C3d immunostaining were detected in cortical vascular endothelial cells in wild-type (WT) mice; however, C4c and C3d immunostaining were also detected in C1q−/− mice, and C3d immunostaining was detected in C4−/− mice. After CCI, WT and C1q−/− mice had similar motor deficits, Morris water maze performance, and brain lesion size. Naive C4−/− and WT mice did not differ in baseline motor performance, but C4−/− mice had reduced postinjury motor deficits (days 1 to 7, P<0.05) and decreased brain tissue damage (days 14 and 35, P<0.05) versus WT. Reconstitution of C4−/− mice with human C4 (hC4) reversed their protection against postinjury motor deficits (P<0.05 versus vehicle), but administration of hC4 did not impair postinjury motor performance (versus vehicle) in WT mice. The protective effects of C4−/− were functionally distinct from the classic pathway and terminal complement, as C1q−/− and C3−/− mice had postinjury tissue damage and motor dysfunction similar to WT. Thus, C4 contributes to motor deficits and brain tissue damage after CCI by mechanism(s) fundamentally different from those involved in experimental systemic ischemia–reperfusion injury.Journal of Cerebral Blood Flow & Metabolism (2007) 27, 1954–1964; doi:10.1038/sj.jcbfm.9600497; published online 25 April 2007 [ABSTRACT FROM AUTHOR]

Neuregulin-1 is a pleiotropic endogenous growth factor that is neuroprotective in experimental models of cerebral ischemia. We tested the hypothesis that pretreatment with neuregulin-1 would be similarly protective after traumatic brain injury in mice. Mice were administered neuregulin-1 or equal amounts of vehicle intravenously immediately before controlled cortical impact. Injured mice were subjected to motor and cognitive testing, and brain tissue loss was quantitated at 4 weeks. Compared to vehicle, pretreatment with neuregulin-1 had no effect on brain tissue loss, motor function, or acquisition of a spatial learning task. However, neuregulin-1 treated mice showed improved retention of spatial memory versus vehicle-treated mice in subsequent probe trials (p< 0.05). These proof-of-principle data suggest that neuregulin-1 may improve some functional outcomes after brain trauma. Further studies are therefore warranted to more carefully explore molecular mechanisms, dose-responses, and relationships between morphological outcome and long-term recovery. [ABSTRACT FROM AUTHOR]

Multiclass classification has been investigated for many years in the literature. Recently, the scales of real-world multiclass classification applications have become larger and larger. For example, there are hundreds of thousands of categories employed in the Open Directory Project (ODP) and the Yahoo! directory. In such cases, the scalability of classification methods turns out to be a major concern. To tackle this problem, hierarchical classification is proposed and widely adopted to get better trade-off between effectiveness and efficiency. Unfortunately, many data sets are not explicitly organized in hierarchical forms and, therefore, hierarchical classification cannot be used directly. In this paper, we propose a novel algorithm to automatically mine a hierarchical structure from the flat taxonomy of a data corpus as a preparation for the adoption of hierarchical classification. In particular, we first compute matrices to represent the relations among categories, documents, and terms. And, then, we cocluster the three substances at different scales through consistent bipartite spectral graph copartitioning, which is formulated as a generalized singular value decomposition problem. At last, a hierarchical taxonomy is constructed from the category clusters. Our experiments showed that the proposed algorithm could discover very reasonable taxonomy hierarchy and help improve the classification accuracy. [ABSTRACT FROM AUTHOR]

Decision-making plays an essential role in the interpersonal interactions and cognitive processing of individuals. There has been increasing interest in being able to predict an individual's decision-making response (i.e., acceptance or rejection). We proposed an electroencephalogram (EEG)-based computational intelligence framework to predict individual responses. Specifically, the discriminative spatial network pattern (DSNP), a supervised learning approach, was applied to single-trial EEG data to extract the DSNP feature from the single-trial brain network. A linear discriminate analysis (LDA) trained on the DSNP features was then used to predict the individual response trial-by-trial. To verify the performance of the proposed DSNP, we recruited two independent subject groups, and recorded the EEGs using two types of EEG systems. The performances of the trial-by-trial predictors achieved an accuracy of 0.88 ± 0.09 for the first dataset, and 0.90 ± 0.10 for the second dataset. These trial-by-trial prediction performances suggested that individual responses could be predicted trial-by-trial by using the specific pattern of single-trial EEG networks, and our proposed method has the potential to establish the biologically inspired artificial intelligence decision system. • A single-trial EEG based approach is developed to predict individual decision-making response. • A supervised learning approach is developed to extract the discriminative spatial network pattern. • The proposed approach achieves the high prediction performances (over 0.88) for two independent EEG datasets. [ABSTRACT FROM AUTHOR]

One novel cyanide-bridged mixed-valence {FeIII 2 (μ -CN) 4 FeII 2 } square cluster exhibits thermally-induced, reversible, complete spin transition behaviour at two out of four metal centers. • One novel cyano-bridged mixed-valence bimetallic {FeIII 2 (μ -CN) 4 FeII 2 } cluster has been prepared. • The square cluster exhibits thermally-induced, reversible, complete spin transition behavior. One novel cyano-bridged mixed-valence bimetallic {FeIII 2 (μ -CN) 4 FeII 2 } cluster, {[(Tp)FeIII(CN) 3 ] 2 [FeII(Py 2 N 2)] 2 }·(PF 6) 2 (1), has been synthesized (Tp = hydrotris(pyrazolyl)borate, Py 2 N 2 = N,N'-bis(2-pyridylmethyl)-N,N'-bis(4-benzyl)-1,2-ethanediamine). The molecular structure has been determined by single-crystal X-ray diffraction. Compound 1 exhibit temperature driven Fe(II) spin crossover behaviour (SCO) associated with the high-spin (HS) ↔ low-spin (LS) transition with the transition temperature of 130 K at two out of four metal centers. The evolution of HS and LS Fe(II) ions with temperature was followed by FT-IR, X-ray crystallography, the variable temperature magnetic susceptibility. [ABSTRACT FROM AUTHOR]

After publication of the article [1], it has been brought to our attention that an author's name was spelt incorrectly in the original published article. Yonghua Wang was previously spelt "Yonghua Wan". This has now been corrected in the revised version of the article. [ABSTRACT FROM AUTHOR]

The article presents a study which tested the therapeutic effects of fingolimod (FTY720) in rodent models of cerebral ischemia. It evaluates the long-term behavioral outcome of fingolimod, and whether delayed treatment is still effective. The study utilized mouse models of middle cerebral artery occlusion and cell-culture models of neurotoxicity and inflammation. The results showed that fingolimod decreased infarct size and edema, and neuroprotection was associated with reduced inflammation.