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Aim:We utilized single-voxel 1 H magnetic resonance spectroscopy to determine biochemical abnormalities related to major depressive disorder (MDD) in the bilateral dorsolateral prefrontal cortex, anterior cingulate cortex (ACC), and cerebellar hemisphere before and after antidepressant treatment. Methods:Fifteen adult MDD patients and 15 ageand sex-matched healthy controls were involved. Magnetic resonance spectroscopy of the brain was conducted in all subjects at the beginning of the study and the depressed subjects were reassessed after 8 weeks of antidepressant treatment.Results: At baseline, N-acetyl aspartate (NAA), total glutamine plus glutamate (Glx) and myo-inositol (MI) levels in the bilateral ACC were significantly lower in MDD patients than in controls (P < 0.05/3). MI in the bilateral cerebellar hemisphere were also decreased in patients compared with controls. After the treatment, the lower NAA, Glx and MI in ACC were normalized in MDD patients and the NAA and Glx increased compared to baseline values. The MI levels in the bilateral cerebellar hemisphere were also normalized in patients. MI and choline levels in the right cerebellar hemisphere were elevated compared to those at baseline. Conclusion:Our study suggests that metabolic abnormalities in the ACC and cerebellar hemisphere are implicated in MDD. Antidepressants may alter the local metabolic abnormalities in these areas.

Attention-deficit hyperactivity disorder (ADHD) is a frequent childhood-onset psychiatric condition and categorized into three subtypes of predominantly inattentive (ADHD-I), hyperactive impulsive (ADHD-H), and combined (ADHD-C). The prevalence and subtypes of ADHD vary considerably. The primary aim of this study was to provide a prevalence estimate of ADHD in elementary school students living in Shantou, a district of China, and in addition to examine the influence of informants, age, and gender on the prevalence. A total of 3,497 students aged 7–12 years were enrolled by random and stratified sampling. In stage I, teachers and parents of all participating students in randomly selected schools were asked to complete Chinese versions of the Conners’ 10-item scale. In stage II, students with high scores (>15) were interviewed by a psychiatrist for a diagnosis with or without ADHD. Parents rated many more students with high scores than teachers did in stage I. The prevalence of ADHD determined by Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) was 5.91% (5.27%–6.55%), which is comparable to the rates reported in previous studies with Chinese children. This hits the low border of the ADHD prevalence range from 5.9 to 7.1% worldwide, and is lower than that of Chinese children living in Hong Kong, suggesting an important influence of Chinese culture on the diagnosis of ADHD. The constituent ratios of ADHD-I, ADHD-C, and ADHD-H subtypes were 67.43, 24.57, and 8.00%, respectively. The rate of ADHD-H decreased with age, whereas that of ADHD-I remained at the highest levels in all age groups, suggesting that symptoms in the inattention domain are the most persistent and refractory.

An Fe3O4 nanotube array was successfully prepared in pores of an anodic aluminium oxide (AAO) template. Fe3O4 nanotubes and the nanotube array were characterized by transmission and scanning electron microscopy. The average diameter of the nanotubes was about 200 nm, and the length was more than 10 µm. The static distribution of the magnetic moments was investigated by means of magnetostatic energy analysis and Mössbauer spectrum measurement. The resulting Mössbauer spectrum shows that the distribution of the magnetic moments in the Fe3O4 nanotube array is spatially isotropic. However, macroscopic magnetic measurement shows the Fe3O4 nanotube array to have obvious anisotropy, and the easy axis is parallel to the nanotube axis. These magnetic behaviours are discussed on the basis of analysis of the magnetostatic energy.

These results add to the evidence of brain metabolite differences in brains of patients with UD and BD which may be of help in differentiating these two mood disorders.

BackgroundThe objective of this study was to investigate relationships among family environmental characteristics, behavior problems, and social function impairments in children with ADHD.MethodsAmong children from four primary schools in Shantou city of China, 132 who were diagnosed with ADHD were selected and 138 typically developing children were recruited from the same schools. These children were evaluated using the self-designed questionnaire, FES-CV, CPRS, CTRS, and WFIRS-P for familial environment, behavioral problems, and social function impairment measures. In addition, children’s behavioral problems and functional impairments were evaluated using self-established field behavior observation method. Logistic regression model was used to estimate ORs and 95% CIs for ADHD risk with family environmental factors.ResultsIn the unconditional logistic model, ADHD risk in children was increased with parents’ worse educational level, occupational status, and emotional stability with trend. Children with ADHD had lower scores on most subscales of FES-CV (P<0.01) but higher scores on Conflict subscale (P<0.001). Children with ADHD showed impairments on all the six WFIRS-P subscales tests (all P<0.001), and higher scores on the CPRS and CTRS scale subscales representing behavioral symptoms (all P<0.001 except Somatic Complaints), and more behavioral problems and functional impairments.ConclusionCompared with typically developing children, children with ADHD had worse family environment. Family characteristics especially parents’ emotional unstability, lower education levels, and worse occupation status may increase ADHD risk in children. In addition, the behavioral problems and social functional impairments may interact with adverse family environmental factors in children with ADHD. Therefore, early interventions with focus onto the compromising factors can be useful for improving the social-behavioral functions of children with ADHD.

The present study investigated the effect of early life stress in adolescent rats on brain metabolites, serum corticosterone, and depressive-like behavior. A group of rats were subject to early life stress from postnatal day (PND) 1 to 14. A matched control group was studied. Behavioral tests, serum corticosterone and high-resolution proton magnetic resonance spectroscopy were conducted between PND 30 and 40. In this study, adolescent rats exposed to early life stress demonstrated depressive-like behavior and increased serum corticosterone during adolescence. They also showed reduced glutamate, glutamine, and N-acetyl aspartate (NAA) levels in the prefrontal cortex. A reduced myo-inositol level, consistent with astroglial deficits, was observed but was not statistically significant. Together, these findings characterize the effect of early life stress on adolescent animals and underscore the long-lasting and detrimental effects of childhood adversities.

To investigate the changes of LTP in hippocampal CA1 region induced by chronic stress and the effect of phenytoin on them, thirty-two adult male Sprague-Dawley rats were randomly divided equally into four groups: control group, control-phenytoin group, stress-saline group and stress-phenytoin group. Isolated hippocampal slices of rats were used to observe the changes of long-term potentiation (LTP) in hippocampal CA1 field using electrophysiological technique. Amplitude of population spike (PS) and field excitatory postsynaptic potentials (fEPSPs) slope were used to indicate the changes of LTP. High-frequency stimulation (HFS) was applied to Schaffer collaterals of hippocampal CA3 field, and the changes of PS amplitude and fEPSPs slope in CA1 field were observed. The results showed that the LTP induction rate, the increases of PS amplitude and fEPSPs slope after HFS in control and stress-phenytoin groups were significantly greater than those in stress-saline group (P<0.05). There were no significant differences between control group and stressphenytoin group or between control and control-phenytoin groups in these indexes (P>0.05). It is suggested that chronic stress can damage the development of LTP in hippocampal CA1 field, while phenytoin can protect the LTP of stressed hippocampal slices in normal state. Key wordsphenytoin; long-term potentiation; hippocampus; stress Stress is the response to stimulation from inside and outside with complicated effects on organisms. Appropriate stressful reactions are helpful in resisting diseases by activating unspecific modulation system, while severe or prolonged stresses are harmful and even induce mental and physical disorders such as recurrent depression, posttraumatic stress disorder (PTSD), Alzheimer's disease and epilepsy [1]. Hippocampus, a main brain region of key importance for learning, memory and emotion, is the target of stressful hormone and mediates stress response. It has plasticity and is liable to be impaired during chronic stress and participates in the pathology of some stress-related diseases that markedly affect memory and other cognitive functions [2,3]. Exploring the effects of stress on hippocampal functions can help to reveal pathogenesis of stress-related disorders.Long-term potentiation (LTP), a persistent increase in the efficacy of synaptic connections induced by high-frequency stimulation (HFS), has been regarded as a model of synapse plasticity. LTP in the hippocampus is especially related to learning and memory. Most scholars consider that Ca 2+ entering into the postsynaptic cells triggers the development of LTP [4][5][6]. Excitation of presynapses induces release of excitatory amino acid (EAA), which facilitates the Ca provokes a series of physiochemical reactions and induces LTP. It has been reported that exposure to stressful event can impair the induction of LTP in the hippocampus [7][8][9]. However, the mechanisms of LTP suppression under stress have not been fully elucidated.Phenytoin, an anti-epileptic drug, can decrease the...