[Show abstract][Hide abstract] ABSTRACT: Background: Mania and depression in bipolar disorder (BP) manifest two extremes of aberrant emotional, physiologic and behavioral arousal states despite similarities in treatment response and neurocognitive deficits. We used resting-state functional magnetic resonance imaging (rsfMRI) to explore the common and unique abnormal functional connectivity underlying acute manic or depressed state in BP.
Methods: 18 patients with bipolar mania (BM), 10 patients with bipolar depression (BD) and 28 healthy controls underwent resting-state functional magnetic resonance imaging scanning. Left and right amygdala seed-to-voxel based functional connectivity were assessed and compared among the three groups. The relationships between aberrant functional connectivity and the severity of clinical symptoms, number of episodes, illness duration were investigated.
Results: Compared to healthy controls, both BM and BD groups showed reduced functional connectivity between bilateral amygdala and inferior frontal gyrus (orbital), striatum, right lingual gyrus and posterior cerebellar lobe. Furthermore right amygdala-hippocampal connectivity was decreased in BD but increased in BM. No significant correlations were found between strength of abnormal functional connectivity and clinical characteristic in BD or BM.
Limitations: No euthymic subjects were recruited, and the patients in current study were all on medication.
Conclusions: The presence of substantial overlap in the pattern of disturbed connectivity between amygdala and frontal, striatal, lingual and cerebellar regions suggests mood state-independent dysconnectivity. The contrasting pattern of functional connectivity between right amygdala and hippocampus in BD and BM provides a novel lead to the probable mechanistic differences in these two extremes of mood states.
[Show abstract][Hide abstract] ABSTRACT: Background: Schizophrenia is a highly heterogeneous disease. Event-related potentials have been regarded to establish intermediate phenotypes of schizophrenia. Our previous study found that patients with deficit schizophrenia (DS) are relatively homogeneous and show a significantly longer onset latency of contingent negative variation (CNV) expectancy wave. Aims: To further examine CNV in patients with first-episode and drug-naïve DS or bipolar I disorder (BP I) with psychotic features, and also investigate correlations between CNV and clinical characteristics in DS and BP I. Method: We elicited a CNV using an alarm (S1)-imperative (S2) paradigm in 30 DS patients or 33 BP I with psychotic features as well as 40 healthy controls. Results: CNV amplitude was significantly smaller and reaction time significantly longer in the DS and BP I groups than in healthy controls. Post-imperative negative variation (PINV) interval was significantly shorter in the DS group than in healthy controls. The onset latency of CNV expectancy wave was significantly longer and PINV area significantly smaller in the DS group than in the other groups. In the DS group, CNV amplitude and PINV interval correlated negatively with the subscale of negative symptoms on the Positive and Negative Syndrome Scale (PANSS); CNV amplitude also correlated negatively with disease duration. In the BP I group, CNV amplitude and reaction time showed no correlation with clinical features. Conclusions: CNV amplitude is a common trait marker for psychosis. The onset latency of CNV expectancy wave appears to be a specific trait marker and may be used to identify candidate genes for DS.
[Show abstract][Hide abstract] ABSTRACT: Studies have shown that minor physical anomalies (MPAs) may be associated with schizophrenia. However, it remains unclear whether any items of MPAs are more associated with schizophrenia than the others. We aimed to examine which specific MPAs are more associated with schizophrenia than others. A total of 154 patients with schizophrenia and 152 healthy controls were assessed using candidate MPAs items along with items from the Waldrop scale. Significant differences were found between the patients and controls in inner canthal distance, epicanthus, adherent ear lobe, cuspidal ear and length difference from section index to ring finger (2D:4D length difference) as well as gap between the first and the second toes. These six items were selected by the logistic regression model, which correctly classified 89.0% of patients with schizophrenia (sensitivity) and 96.7% of healthy controls (specificity). The overall classification success rate was 92.8%. MPAs are associated with neurodevelopment, especially 2D:4D associated with cerebral lateralisation. Hence, our present findings support that it is necessary to evaluate MPAs beyond the Waldrop scale, as some item, such as 2D:4D length difference may reflect the more detailed aberrant neurodevelopment of schizophrenia.
Psychiatry Research 08/2012; 200(2-3). DOI:10.1016/j.psychres.2012.07.022 · 2.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The study analyzed the effect of dopamine 2 receptor gene (DRD2) polymorphism on the risk for major depressive disorder (MDD) and the response to selective serotonin reuptake inhibitors (SSRIs). The results suggest that the DRD2 gene may play a role on MDD susceptibility and the onset-time of antidepressant response.
Psychiatry Research 07/2012; 200(2-3). DOI:10.1016/j.psychres.2012.06.024 · 2.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We previously reported the potential of a novel small molecule 3-amino-6-(3-methoxyphenyl)thieno[2.3-b]pyridine-2-carboxamide (SKLB70326) as an anticancer agent. In the present study, we investigated the anticancer effects and possible mechanisms of SKLB70326 in vitro. We found that SKLB70326 treatment significantly inhibited human hepatic carcinoma cell proliferation in vitro, and the HepG2 cell line was the most sensitive to its treatment. The inhibition of cell proliferation correlated with G(0)/G(1) phase arrest, which was followed by apoptotic cell death. The SKLB70326-mediated cell-cycle arrest was associated with the downregulation of cyclin-dependent kinase (CDK) 2, CDK4 and CDK6 but not cyclin D1 or cyclin E. The phosphorylation of the retinoblastoma protein (Rb) was also observed. SKLB70326 treatment induced apoptotic cell death via the activation of PARP, caspase-3, caspase-9 and Bax as well as the downregulation of Bcl-2. The expression levels of p53 and p21 were also induced by SKLB70326 treatment. Moreover, SKLB70326 treatment was well tolerated. In conclusion, SKLB70326, a novel cell-cycle inhibitor, notably inhibits HepG2 cell proliferation through the induction of G(0)/G(1) phase arrest and subsequent apoptosis. Its potential as a candidate anticancer agent warrants further investigation.
Biochemical and Biophysical Research Communications 04/2012; 421(4):684-9. DOI:10.1016/j.bbrc.2012.04.062 · 2.30 Impact Factor