In recent studies, numerous anomalies against the weak and semi-strong-forms of efficient market hypothesis have been found insignificant after controlling the small-firm effect. We investigate whether the insider trading anomaly, a major anomaly against the strong-form of EMH, can survive after excluding small firms with a novel data set and document several new findings. We find a substantially larger number of insider purchases than sales, while the average volume of insider sales is much higher than the average volume of insider (...) purchases. Echoing recent US studies, we find that insider sales generate more abnormal returns than insider purchases do. We find much lower abnormal returns from insider trading than documented in the literature and the associated trading costs, which suggests that the market efficiency of individual stocks may depend on their sizes, and even the strong-form of EMH holds to a larger extent than previously recognized. (shrink)

This paper concentrates on the event-triggered H ∞ filter design for the discrete-time Markovian jump neural networks under random missing measurements and cyber attacks. Considering that the controlled system and the filtering can exchange information over a shared communication network which is vulnerable to the cyber attacks and has limited bandwidth, the event-triggered mechanism is proposed to relieve the communication burden of data transmission. A variable conforming to Bernoulli distribution is exploited to describe the stochastic phenomenon since the missing measurements (...) occur with random probability. Furthermore, seeing that the communication networks are vulnerable to external malicious attacks, the transferred information via the shared communication network may be changed by the injected false information from the attackers. Based on the above consideration, sufficient conditions for the filtering error system to maintain asymptotically stable are provided with predefined H ∞ performance. In the end, three numerical examples are given to verify the proposed theoretical results. (shrink)

Several functional magnetic resonance imaging studies have demonstrated abnormalities in static intra- and interhemispheric functional connectivity among diverse brain regions in patients with major depressive disorder. However, the dynamic changes in intra- and interhemispheric functional connectivity patterns in patients with MDD remain unclear. Fifty-eight first-episode, drug-naive patients with MDD and 48 age-, sex-, and education level-matched healthy controls underwent resting-state fMRI. Whole-brain functional connectivity, analyzed using the functional connectivity density approach, was decomposed into ipsilateral and contralateral functional connectivity. We computed (...) the intra- and interhemispheric dynamic FCD using a sliding window analysis to capture the dynamic patterns of functional connectivity. The temporal variability in functional connectivity was quantified as the variance of the dFCD over time. In addition, intra- and interhemispheric static FCD patterns were calculated. Associations between the dFCD variance and sFCD in abnormal brain regions and the severity of depressive symptoms were analyzed. Compared to HCs, patients with MDD showed lower interhemispheric dFCD variability in the inferior/middle frontal gyrus and decreased sFCD in the medial prefrontal cortex/anterior cingulate cortex and posterior cingulate cortex/precuneus in both intra- and interhemispheric comparisons. No significant correlations were found between any abnormal dFCD variance or sFCD at the intra- and interhemispheric levels and the severity of depressive symptoms. Our results suggest intra- and interhemispheric functional connectivity alterations in the dorsolateral prefrontal cortex and default mode network regions involved in cognition, execution and emotion. Furthermore, our study emphasizes the essential role of altered interhemispheric communication dynamics in the DLPFC in patients with MDD. These findings contribute to our understanding of the pathophysiology of MDD. (shrink)

BackgroundTemporal lobe epilepsy is the most prevalent refractory focal epilepsy and is more likely accompanied by cognitive impairment. The fully understanding of the neuronal activity underlying TLE is of great significance.ObjectiveThis study aimed to comprehensively explore the potential brain activity abnormalities affected by TLE and detect whether the changes were associated with cognition.MethodsSix static intrinsic brain activity indicators [amplitude of low-frequency fluctuation, fractional ALFF, regional homogeneity, degree centrality, global signal correlation, and voxel-mirrored homotopic connectivity ] and their corresponding dynamic indicators, (...) such as dynamic ALFF, dynamic fALFF, dynamic ReHo, dynamic DC, dynamic VMHC, and dynamic GSCorr, in 57 patients with unilateral TLE and 42 healthy volunteers were compared. Correlation analyses were also performed between these indicators in areas displaying group differences and cognitive function, epilepsy duration, and severity.ResultsMarked overlap was present among the abnormal brain regions detected using various static and dynamic indicators, primarily including increased ALFF/dALFF/fALFF in the bilateral medial temporal lobe and thalamus, decreased ALFF/dALFF/fALFF in the frontal lobe contralateral to the epileptogenic side, decreased fALFF, ReHo, dReHo, DC, dDC, GSCorr, dGSCorr, and VMHC in the temporal neocortex ipsilateral to the epileptogenic foci, decreased dReHo, dDC, dGSCorr, and dVMHC in the occipital lobe, and increased ALFF, fALFF, dfALFF, ReHo, and DC in the supplementary motor area ipsilateral to the epileptogenic foci. Furthermore, most IBA indicators in the abnormal brain region significantly correlated with the duration of epilepsy and several cognitive scale scores.ConclusionThe combined application of static and dynamic IBA indicators could comprehensively reveal more real abnormal neuronal activity and the impairment and compensatory mechanisms of cognitive function in TLE. Moreover, it might help in the lateralization of epileptogenic foci and exploration of the transmission and inhibition pathways of epileptic activity. (shrink)