To assess healthy-related quality of life and psychosocial adjustment in children with newly diagnosed cancer and their parents immediately and 6 months after diagnosis and treatment of cancer.

A prospective, case control study was conducted on eighty-nine children with newly diagnosed cancer, aged between 6 months to 16.7 years (mean, 8.2 years), and ninety healthy children of matched age group and social background. The children were assessed with the Child Behavior Checklist (CBCL), and the Parenting Stress Index (PSI) and the SF-36 questionnaire were administered to their parents immediately after diagnosis of cancer, 3 months after chemotherapy, and 6 months after chemotherapy.

No matter at the period immediately after diagnosis of cancer, 3 months or 6 months after starting chemotherapy, the parents of children with cancer scored significantly worse on every domains of SF-36 except body pain and every subscales of PSI except distractibility/hyperactivity and attachment when compared with the control group. The cancer group scored consistently lower on all CBCL syndrome scales than the control group, with anxiety, depression and body pain being significantly different. After starting chemotherapy, the parents reported improved scores on quality of life and decreasing parenting stress in both parent and child domains since 3 months or 6 months after starting chemotherapy.

Considerable distress was experienced by both children with newly diagnosed cancer and their parents during the period immediately after diagnosis. However, parents can adjust gradually since 3 months after starting chemotherapy and experience improved quality of life.

The purpose of this study was to predict quality of life (QoL) and associated factors in patients with chronic mental illness (CMI) in Kaohsiung, Taiwan.

Patients (N = 2,023; 52.9% male, 47.1% female) were recruited using cross-sectional and convenience sampling. Structured questionnaires, including a living conditions questionnaire, a psychotic symptom assessment scale, the Caregiver Burden Scale, the 5-item Brief Symptom Rating Scale (BSRS-5), and the Medical Outcomes Study Short Form-12 (MOS SF-12) were used to collect data.

Single-factor analyses showed that those who were single, employed, and younger had better QoL. Additionally, patients who had fewer psychological problems and lower levels of psychological distress reported better QoL. Current psychotic symptoms, especially positive symptoms, were negatively correlated with QoL. For disease factors, schizophrenic patients and hospitalized patients reported better QoL than both bipolar patients and community patients. For family factors, caregiver's attitude and caregiver's burden were negatively correlated with QoL. For social factors, unstable housing and community social dysfunction were negatively correlated with QoL. The results showed that all four dimensions (social, family, disease and personal factors) were significant predictors of the mental component summary (MCS) and physical component summary (PCS) dimensions of QoL.

Personal factors and disease factors were the most important predictors of QoL in CMI patients of this sample. Family factors were more important than social factors in the MCS dimension, but social factors were more important than family factors in the PCS dimension.

Efficacy of conventional repetitive transcranial magnetic stimulation (rTMS) in major depressive disorder (MDD) is limited. The authors report here on an alternative treatment using low energy synchronized TMS (sTMS) at the intrinsic frequency of subjects’ alpha electroencephalogram (EEG).

Establish efficacy and safety profile of sTMS in MDD.

1. (1) Examine the clinical effectiveness of sTMS.

2. (2) Identify adverse effects associated with sTMS.

Fifty-two MDD subjects with 17-item Hamilton Depression Rating Scale (HAMD17) scores >17 were enrolled into a randomized, sham controlled, double-blind trial. Current medication remained unchanged during the trial. Depressive symptoms were evaluated by HAMD17 administered weekly.

EEGs were recorded at baseline to determine the stimulus frequency and at week 4 to evaluate the physiological effect. sTMS was delivered through three 6000-G cylindrical neodymium magnets synchronously rotating at a rate equal to the subject's intrinsic alpha frequency.

Forty-five subjects completed at least 1 week of treatment and were evaluable. Those who received active treatment had superior clinical response to sham (t = 2.54, P = 0.01), where 55.2% in the active treatment group were clinical responders versus 12.5% in sham (X2 = 7.82, P = 0.005). No significant side effects were reported. The clinical improvement was correlated with the degree of EEG improvement (r = .46, P = 0.009).

A therapeutic effect in MDD subjects can be achieved through administration of sTMS at the subject's alpha EEG frequency. Because of minimal side effects, this appears to be a safe and effective treatment option.

To demonstrate whether the communication between two SD rats base on the similar genetic basis or the same living environment, who separated (including visual, auditory, tactile, olfactory and tasting inputs)from each other, occurs.

One SD rat (RECEIVER) was examined by EEG spectral analysis and ECG analysis under anesthesia while the other SD rat (SENDER) received optimal stimuli or malignant stimuli. The course was conducted in the shielded and the unshielded. Compare the EEG and ECG of RECEIVER between the stimulation state and resting state of SENDER.

This study show no significant difference in EEG (index: percentile weight and average weight of EEG on frontal lobe, temporal lobe, hippocampus of each frequency band) and ECG (index: R, PR segment, ST segment, QRS segment, QT segment) of RECEIVER during the time that the SENDER suffered from malignant stimulation, experienced optimal stimulation and of resting state.

The communication of SD rats, not through common five sense organ may not exist, even though the same genetic basis or the common living surrounding.The optimal stimuli and the malignant stimuli of SENDER cannot influence the EEG of Frontal lobe, temporal lobe, hippocampus and ECG on RECEIVER. There is no sufficient evidence for the existence of this communication of animal.

Patients with chronic kidney disease (CKD) have more cognitive impairments. However, the etiologies are not fully clear. Plasma homocysteine levels and vascular burden rise in CKD; meanwhile, high homocysteine levels and vascular factors are known risk factors of dementia in non-CKD patients. Thus, we aimed to investigate the association between homocysteine, vascular burden and cognitive impairment in CKD and to see if the effect of elevated homocysteine on cognitive impairment mediated by vascular factor.

146 patients with CKD and 69 normal comparisons were recruited. Cognitive function was evaluated by comprehensive neuropsychological tests assessing processing speed, executive function, language, visuospatial function, memory, and attention domains. Vascular burden was assessed by Framinghan cardiovascular risk scale (FCRS) which indicates risk of atherosclerotic diseases including stroke.

In controlled analysis, patients with CKD had lower scores in all cognitive domains, and had higher homocysteine levels (18.5±6.4 vs. 9.8±2.9, p< 0.0001) and FCRS(17.0±4.7 vs. 14.0±4.7, p< 0.0001). Among patients with CKD, higher homocysteine levels (p=0.026) were associated with lower score on digit symbol task which is related to processing speed and executive function with controlling for age, sex, education and stage of CKD. The association persisted (p=0.047) after controlling for vascular risks.

Patients with CKD had extensive cognitive impairments. Elevated homocysteine levels may be an risk factor, which is independent of vascular burden, of cognitive impairment on processing speed and executive function. Further studies to investigate if normalization of homocysteine can improve cognitive function will be suggested.

Increasing evidence supports that 5HTTLPR polymorphism of the serotonin transporter gene(5HTTLPR) might associate to bipolar disorder and affective temperaments as measured by TEMPS-A. But the results are discrepant, furthermore, there are no data from Chinese population.

The present study was designed to investigate association between 5HTTLPR and bipolar disorder and affective temperaments of patients with bipolar disorder in the specific Chinese population and add new evidence to the field.

There hundred and five patients with bipolar disorder and 272 normal controls were included in the present case-control study⌧Temperament Evaluation of Memphis, Pisa, Paris and San Diego -autoquestionnaire version (TEMPS-A) in Chinese was used to assess affective temperament. Chi-square test, T test, Nonparametric test and ANOVA were employed to explore association between 5HTTLPR polymorphism and bipolar disorder and affective temperament of patients with bipolar disorder.

5-HTTLPR L/S polymorphism was associated with bipolar disorder in female (genotype χ2 = 6.769⌧P = 0.034⌧allele χ2 = 6.028⌧P = 0.014) and the S allele was associated with anxious temperament (t = 8.248⌧P = 0.005) in patients with bipolar disorder. the LA allele of 5-HTTLPR rs25531 A/G polymorphism was associated with hyperthymic temperament in patients with bipolar disorder (Z = −2.205⌧P = 0.027).

5-HTTLPR might have an effect on the prevalence of bipolar disorder in female and regulate affective temperaments of patients with bipolar disorder in some degree in Chinese population.

Bioinformatic investigations indicate that has-mir-206 (microRNA-206, miRNA-206) could regulate BDNF protein synthesis by interfering with BDNF mRNA translation, which is disrupted in bipolar disorder (BPD).

This study is to investigate whether miRNA-206 gene variants were associated with BPD susceptibility in a Han Chinese population.

342 patients who met DSM-IV criteria for bipolar disorder type I (BPD-I) or type II (BPD-II) and 386 matched health controls were enrolled into this study. the miRNA-206 gene and +/-500bp were selected for gene sequencing. for the case-control genetic comparisons, differences in the genotype and allele distributions between patients and controls were examined using Pearson's χ2 test.

Gene sequencing showed that there are two polymorphisms rs16882131(C/T) and rs62408583 (A/C) located at the upstream of miRNA-206 gene, which are complete linkage disequilibrium. the association analysis showed that there was no significant difference for genotype frequencies (χ2 = 2.075, df = 2, P = 0.354) or for allele frequencies (χ2 = 0.041, df = 1, P = 0.839) between BPD patients and controls. Similarly, no significant difference was found between BPD-I patients and controls (genotype χ2 = 1.411, df = 2, P = 0.494; allele χ2 = 0.380, df = 1, P = 0.538). However, there was significant difference between BPD-II patients and controls (genotype χ2 = 7.933, df = 2, P = 0.019; allele χ2 = 5.403, df = 1, P = 0.020).

Our findings do not support that BPD susceptibility was associated with miRNA-206 gene polymorphisms in the studied Han Chinese population. the association between miRNA-206 gene polymorphisms and bipolar disorder type II is needed to be carefully interpreted. Further studies are necessary to elucidate the involvement miRNA-206 in the pathophysiology of BPD.

Increasing evidence indicates that major depressive disorder (MDD) is associated with cognitive as well as mood disturbances.

To evaluate cognitive function and white matter structure, resting-state brain function in first-episode, treatmentnaive patients with MDD.

To explore brain structure and function mechanisms of cognitive impairment in MDD.

46 Han Chinese MDD patients aged 18–45 year and 46 controls were assessed by a series of validated test procedures.Then, 30 patients and 30 controls were obtained by MRI scan.White matter abnormalities evaluated using diffusion tensor imaging (DTI) were analyzed using tract based spatial statistics (TBSS) and resting-state brain function was evaluated using regional homogeneity (ReHo) analysis.

Cognitive impairment in patients with MDD was demonstrated by reduced accuracy in the Wisconsin Card Sorting test (WSCT) and to a lesser extent the Continuous Performance test (CPT) and Trail Making tests (TMT). White matter abnormalities found in the left cerebellum, and resting-state abnormalities present in the left inferior parietal gyrus, left anterior cingulate nucleus and left hippocampal gyrus were associated with impaired performance in the WSCT and CPT tests. We also showed that poor WSCT performance was associated with increased interconnectivity between the left ventral anterior cingulate nucleus and the medial frontal lobe areas.

The present study indicates cognitive disturbances in patients with MDD are associated with white matter and resting-state changes and altered interconnections in specific brain areas.

The association between gray matter and cognitive dysfunction in young major depression remains unclear.

To investigate the brain gray matter and the correlation with cognitive function in first-episode, treatment-naive patients with major depressive disorder (MDD).

To explore brain structural pathological mechanisms of cognitive impairment in MDD.

46 MDD aged 18-45 year and 46 controls were assessed by Wisconsin Card Sorting Test (WCST) and Trail making test (TMT). Then, 30 patients and 30 controls were obtained by MRI scan.

The total number of errors, number of preservative errors, random errors of WSCT in MDD were significantly more than that in controls, and the completion time in the TMT-A and TMT-B was longer than that in controls. MDD showed significant less gray matter volumns than controls in frontal lobe (right precentral gyrus, bilateral superior frontal gyrus and right middle frontal gyrus), parietal lobe (left postcentral gyrus, left paracentral lobule, and bilateral precuneus), temporal lobe (right superior temporal gyrus), and occipital lobe (left superior occipital gyrus). There was a significant negative correlation between left postcentral gyrus and left superior occipital gyrus gray matter density and the TMT-B completion time (r=-0.462, P=0.017; r=-0.448, P=0.022).

The first-episode MDD patient exhibiteded cognitive impairment and showed significant lower gray matter density than controls in frontal lobe, parietal lobe, temporal lobe, occipital lobe. Decreased gray matter density in left postcentral gyrus and left superior occipital gyrus may be involved in the executive dysfunction.

Antipsychotic drugs (APDs) are the first-line pharmacological treatments for schizophrenia. Recent human studies have found that myelin integrity could be improved by APD treatment in schizophrenia patients. Previous studies indicated that regulation of oligodendrocyte development and function may be a novel target for APDs.

The aim of this current study was to examine the possible effects of the antipsychotic drugs (APDs) haloperidol (HAL), olanzapine (OLA), and quetiapine (QUE) on the development of oligodendroglial lineage cells.

CG4 cells, an oligodendrocyte progenitor cell line, were treated with various concentrations of HAL, OLA, or QUE for specific periods. The proliferation and differentiation of the CG4 cells were measured. The regulation of CG4 cell differentiation by oligodendrocyte lineage transcription factors 1 and 2 (Olig1 and Olig2) was examined.

The APDs used in this study had no effect on the proliferation of CG4 cells. The APDs elevated the expression of 2’,3’-cyclic nucleotide 3’-phosphodiesterase (CNP), a specific marker of oligodendrocytes, and promoted the CG4 cells to differentiate into CNP positive oligodendrocytes. QUE and OLA increased the expression of Olig1 and Olig2 whereas HAL only increased the expression of Olig2.

Our findings suggest that oligodendrocyte development is a target of HAL, OLA, and QUE and provide further evidence of the important role of oligodendrocytes in the pathophysiology and treatment of schizophrenia. They also indicate that the expression level of oligodendrocyte/myelinrelated genes could be profoundly affected by APDs.

To explore the feature of functional connectivity of default mode network (DMN), central-executive network(CEN), and salience network (SN) in patients with schizophrenia during a resting state by functional magnetic resonance imaging (fMRI).

The SPM8, DPARSFA, conn, REST softwares combined with data-driven region of interest analysis were used to compare the functional connectivity (FC) of the DMN, CEN, and SN in 74 patients with schizophrenia(SZ) and 79 age- and gender-matched normal controls(NC). Medial prefrontal cortex(MPFC)was selected as seed region for identifying DMN and CEN; right anterior insula(rAI) for SN.

Compared with NC, SZ showed increased FC with bilateral dorsolateral prefrontal cortex(DLPFC) and bilateral putamen of the MPFC, and increased FC with left middle frontal cortex and precuneus/ posterior cingulate cortex(Pcu/PCC) of the rAI. SZ also showed enhanced interconnectivity strengths of CEN-DMN, CEN-SN, and DMN-SN(p>0.05). Correlation analyses showed that the increased FC between MPFC and left DLPFC significantly negatively correlated with PANSS-negative symptoms(r=-0.224,p=0.030) and increased FC between rAI and Pcu/PCC significantly correlated with PANSS-positve symptoms (r=0.243,p=0.020).

This study provides evidence for resting state functional abnormalities of DMN, CEN, and SN in schizophrenia patients. These aberrant functional connectivities in some key brain regions of the three network could be responsible for the schizophrenic symptoms.

In this study, we aimed to identify protein molecules in the hypothalamus in the female rats injected exogenous androgen before sexual differentiation.

Neonatal female SD rats were randomly divided into two groups: experimental group and control female group. Four neonatal male SD rats were control male group. All animals were subjected to intraperitoneal injection of testosterone propionate as experimental group or aseptic oil as control. The rats were sacrificed 90 days after the injection and the brains were collected. 2-DE were performed in order to establish profiles of proteome from rat hypothalamus and followed by MALDITOF- TOF mass spectrometry was used to identify proteins differentially expressed in rat hypothalamus from experimental group as compared to normal control group.

11 differential spots were cut off from the Silver stained gel, and 9 of the spots were identified, which were Dihydropyrimidinase-like 3 (DPYSL3), heterogeneous nuclear ribonucleoprotein K(hnRNP K), Profilin2, Triosephosphate isomerase 1(Tpi 1), Carbonic anhydrase II(CA II), Annexin A3, Protein disulfide isomerase associated 3 (PDIA3), Creatine kinase-B and Secernin 1.

The results of the present study indicate that the development of sexual differentiation may be associated with the alteration in the expression of a large number of cytosolic proteins in the hypothalamus.