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PHGDH attaches importance to serine biosynthesis in cancer cells and maintaining mitochondrial redox homeostasis. However, the role of PHGDH inhibitor CBR-5884 in cell ROS level and its downstream pathways has not been explored in epithelial ovarian cancer. Thus, we investigated the function and possible mechanism of PHGDH inhibitor CBR-5884 on epithelial ovarian cancer in vitro and in vivo. A2780, OVCAR3, and ES-2 were treated with CBR-5884 at different concentrations or different time points. Results showed that CBR-5884 inhibited epithelial ovarian cancer cell proliferation, migration, and invasion and increases cell ROS level. Meanwhile, CBR-5884 exerts antitumor effect through activating ROS/Wnt/

Ovarian cancer is the second common cancer among the gynecological tumors. It is difficult to be found and diagnosed in the early stage and easy to relapse due to chemoresistance and deficiency in choices of treatment. Therefore, future exploring the biomarkers for diagnosis, treatment, and prognosis prediction of ovarian cancer is significant to women in the world. We downloaded data from TCGA and GTEx and used R “limma” package for analyzing the differentially expressed immune-related lncRNA in ovarian cancer and finally got 7 downregulated and 171 upregulated lncRNA. Then, we paired the differentially expressed immune-related lncRNA and constructed a novel lncRNA pairing model containing 7 lncRNA pairs. Based on the cut-off point with the highest AUC value, 102 patients were selected in high-risk group and 272 in low-risk group. The KM analysis suggested that the patients in the low-risk group had a longer overall survival. Future analysis showed the correlations between risk scores and clinicopathological parameters and infiltrating immune cells. In conclusion, we identified an immune-related lncRNA pairing model for predicting the prognosis and immune-infiltrating cell condition in human ovarian cancer, which thus further can instruct immunotherapy.

Accumulating evidence suggests that neural abnormalities in conduct disorder (CD) may be subject to genetic influences, but few imaging studies have taken genetic variants into consideration. The Val66Met polymorphism of brain-derived neurotrophic factor (BDNF) has emerged as a high-interest genetic variant due to its importance in cortical maturation, and several studies have implicated its involvement in neurodevelopmental disorders. Thus, it is unclear how this polymorphism may influence brain anatomy and aberrant behaviors in CD. A total of 65 male adolescents with CD and 69 gender-, IQ- and socioeconomic status-matched healthy controls (HCs) (age range 13-17 years) were enrolled in this study. Analyses of variance (ANOVAs) were used to assess the main effects of CD diagnosis, BDNF genotype, and diagnosis-genotype interactions on brain anatomy and behaviors. We detected a significant main effect of BDNF genotype on temporal gyrification and antisocial behaviors, but not on CD symptoms. Diagnosis-genotype interactive effects were found for cortical thickness of the superior temporal and adjacent areas. These results suggest that the BDNF Val66Met polymorphism may exert its influence both on neural alterations and delinquent behaviors in CD patients. This initial evidence highlights the importance of elucidating potentially different pathways between BDNF genotype and cortical alterations or delinquent behaviors in CD patients.

Objective Identification of state-independent and -dependent neural biomarkers may provide insight into the pathophysiology and effective treatment of major depressive disorder (MDD), therefore we aimed to investigate the state-independent and -dependent topological alterations of MDD. Method Brain resting-state functional magnetic resonance imaging (fMRI) data were acquired from 59 patients with unmedicated first episode current MDD (cMDD), 48 patients with remitted MDD (rMDD) and 60 demographically matched healthy controls (HCs). Using graph theory, we systematically studied the topological organization of their whole-brain functional networks at the global and nodal level. Results At a global level, both patient groups showed decreased normalized clustering coefficient in relative to HCs. On a nodal level, both patient groups showed decreased nodal centrality, predominantly in cortex-mood-regulation brain regions including the dorsolateral prefrontal cortex, posterior parietal cortex and posterior cingulate cortex. By comparison to cMDD patients, rMDD group had a higher nodal centrality in right parahippocampal gyrus. Limitations The present study, an exploratory analysis, may require further confirmation with task-based and experimental studies. Conclusions Deficits in the topological organization of the whole brain and cortex-mood-regulation brain regions in both rMDD and cMDD represent state-independent biomarkers.

Background It has been proposed that state-independent, or trait, neurobiological alterations across illness phases may contribute to the high recurrence of major depressive disorder (MDD). Although intrinsic brain network abnormalities have been implicated consistently in MDD neuropathology, MDD state-independent and -dependent resting-state network alterations have not been clearly studied. Methods Resting-state functional magnetic resonance imaging (fMRI) data were collected from 57 medication-naive first-episode current MDD patients, 35 remitted MDD patients, and 66 healthy controls (HCs). Independent component analysis (ICA) was used to extract subnetworks of the default mode network (DMN), central executive network (CEN), and salience network (SN). Results Relative to HCs, the current MDD and remitted MDD groups had decreased intra-intrinsic functional connectivity (iFC) in the dorsal lateral prefrontal cortex (dlPFC) of the left CEN, increased inter-FC between the SN and right CEN (rCEN), and decreased inter-FC between the anterior DMN (aDMN) and rCEN. The altered intra-iFC in the left CEN were correlated negatively with the depressive level in the remitted MDD. Conclusions Hypoactivity of the dlPFC in the left CEN, increased inter-FC between the SN and rCEN, and decreased inter-FC between the aDMN and rCEN may reflect state-independent biomarkers of MDD.

Background: Obsessive-compulsive personality disorder (OCPD) is one of the most prevalent personality disorders in general population. However, neural mechanisms underlying OCPD remain elusive. The aim of this study is to use functional magnetic resonance imaging (fMRI) to examine whether OCPD patients will exhibit altered spontaneous brain activity as compared to healthy controls (HC). Methods: Resting-state fMRI data were acquired in 37 OCPD patients and 37 matched HC. Amplitudes of low-frequency fluctuation (ALFF) were calculated and compared between the two groups. Correlation analysis was performed between regional ALFF values and OCPD severity scores. Results: Significant group differences in regional ALFF were found in multiple brain regions. Compared to HCs, OCPD subjects had increased ALFF in bilateral caudate, left precuneus, left insula, and left medial superior frontal gyrus, and decreased ALFF in the right fusiform gyrus and left lingual gyrus. The ALFF values in the left precuneus correlated with OCPD severity scores. Limitations: We excluded patients with comorbidity and did not conduct cognitive function assessments. Our findings are also limited to cross-sectional analysis. Conclusions: OCPD patients exhibit altered spontaneous neural activity as compared to healthy controls in multiple brain regions, which may reflect different characteristic symptoms of OCPD pathophysiology, including cognitive inflexibility, excessive self-control, lower empathy, and visual attention bias. Keywords: Obsessive-compulsive personality disorder, Resting-state functional MRI, Amplitude of low-frequency fluctuation, Spontaneous neuronal activity

Stress is a strong risk factor for major depressive disorder, while sensitization to stress in remitted individuals plays a key role in depression recurrence. The present study explored the state-independent (trait) and dependent (state) neural responses to psychosocial stress in major depressive disorder.Thirty-six patients with medication-naive first-episode current depression, 33 patients with remitted depression, and 36 demographically matched healthy control participants were administered the Montreal Imaging Stress Task during functional MRI. One-way analyses of variance were used to assess differences in stress responses in the three groups.Both currently depressed and remitted patients exhibited higher stress levels and cortisol responses than control subjects. Compared with control subjects, both depressed and remitted patients exhibited reduced activation in the ventromedial prefrontal cortex and increased activation in the precuneus. The stress-induced ventromedial prefrontal cortex activation changes negatively correlated with cortisol increases in all three groups. Additional increased activations were found in the dorsolateral prefrontal cortex and bilateral striatum in remitted patients compared with control subjects, and activation in these regions correlated inversely with depressive symptoms in the remitted group.These findings provide novel evidence regarding the trait and state markers of depression on neural responses to psychosocial stress. Regional activation changes in the ventromedial prefrontal cortex and precuneus may reflect the trait markers of depression. Hyperactivation in the dorsolateral prefrontal cortex and striatum may represent a state-dependent compensatory mechanism during depression remission.

Individuals with higher neuroticism are vulnerable to stress and are prone to develop depression, however, the neural mechanisms underlying it have not been clarified clearly.The Montreal Imaging Stress Task (MIST) was administered to 148 healthy adults during functional magnetic resonance imaging (fMRI). Whole-brain voxel-wise regression analyses were used to detect associations of neuroticism with neural activity involved in perceiving and processing psychosocial stress. In addition, two-sample t-tests were conducted between the high-neurotic and low-neurotic group in order to supplement the results found in regression analyses.Higher neuroticism scores were associated with higher activities in the posterior cingulate cortex (PCC)/precuneus and thalamus (p0.05, false discovery rate correction). Moreover, two sample t-tests also revealed that the high-neurotic group had higher neural stress responses in precuneus and bilateral thalamus in comparison to the low-neurotic group (p0.05, false discovery rate correction).Our study mainly recruited young adults, which may limit the generalizability of our findings.Our findings highlight the crucial role of PCC/precuneus and thalamus in the association between neuroticism and stress and may provide insight into the cognitive model of depression.

As key post-transcriptional regulators, microRNAs (miRNAs) play an indispensable role in skeletal muscle development. Our previous study suggested that miR-34b-5p and IGFBP2 could have a potential role in skeletal muscle growth. Our goal in this study is to explore the function and regulatory mechanism of miR-34b-5p and IGFBP2 in myogenesis. In this study, the dual-luciferase reporter assay and Western blot analysis showed that IGFBP2 is a direct target of miR-34b-5p. Flow cytometric analysis and EdU assay showed that miR-34b-5p could repress the cell cycle progression of myoblasts, and miR-34b-5p could promote the formation of myotubes by promoting the expression of MyHC. On the contrary, the overexpression of IGFBP2 significantly facilitated the proliferation of myoblasts and hampered the formation of myotubes. Together, our results indicate that miR-34b-5p could mediate the proliferation and differentiation of myoblasts by targeting IGFBP2.

Background The hopelessness theory of depression posits that individuals with negative cognitive styles are at risk of developing depression following negative life events. The purpose of this work was to examine whether individuals with cognitive vulnerability to depression (CVD) exhibit similar spontaneous brain activity patterns as compared to patients with major depressive disorder (MDD). Methods Subjects with CVD (N=32), drug-naive first-episode patients with major depressive disorder (N=32), and sex-, age- and education-matched healthy controls (HCs; N=35) were subjected to resting state functional magnetic resonance imaging (RS-fMRI) and amplitudes of low-frequency fluctuation (ALFF) was compared between the groups. Pearson correlation analysis was performed between regional ALFFs and psychometric scores, namely the Cognitive Style Questionnaire (CSQ) and the Center for Epidemiologic Studies Depression (CES-D) scale scores. Results Significant group differences in ALFF values were observed bilaterally in the orbitofrontal cortex (OFC) and insular cortex (IC), and in the left fusiform gyrus (FFG). Compared to HCs, CVD subjects had reduced ALFFs in the bilateral OFC and increased ALFF in the bilateral IC and the left FFG, which were similar to the differences observed between the HCs and MDD patients. Compared to MDD patients, CVD subjects showed significant reduced ALFF values in right IC. Additionally, CSQ scores for the CVD group correlated with ALFF values in the left IC. Limitations We did not conduct a longitudinal study. Our findings were limited in cross-sectional analysis. Conclusions A hypoactive OFC and hyperactive IC in a resting-state may underlie an imbalance in the spontaneous brain activity in orbitofrontal-insular circuits, and these differences may represent a trait-related marker of vulnerability to depression.

The Balloon Analogue Risk Task (BART) provides a reliable and ecologically valid model for the assessment of individual risk-taking propensity and is frequently used in neuroimaging and developmental research. Although the test-retest reliability of risk-taking behavior during the BART is well established, the reliability of brain activation patterns in response to risk-taking during the BART remains elusive. In this study, we used functional magnetic resonance imaging (fMRI) and evaluated the test-retest reliability of brain responses in 34 healthy adults during a modified BART by calculating the intraclass correlation coefficients (ICC) and Dice’s similarity coefficients (DSC). Analyses revealed that risk-induced brain activation patterns showed good test-retest reliability (median ICC ​= ​0.62) and moderate to high spatial consistency, while brain activation patterns associated with win or loss outcomes only had poor to fair reliability (median ICC ​= ​0.33 for win and 0.42 for loss). These findings have important implications for future utility of the BART in fMRI to examine brain responses to risk-taking and decision-making.

Background there has been a recent increase in the use of connectome-based multivariate pattern analysis (MVPA) of resting-state functional magnetic resonance imaging (fMRI) data aimed at distinguishing patients with major depressive disorder (MDD) from healthy controls (HCs). However, the validity of this method needs to be confirmed in independent samples. Method we used resting-state fMRI to explore whole-brain functional connectivity (FC) patterns characteristic of MDD and to confirm the effectiveness of MVPA in distinguishing MDD versus HC groups in two independent samples. The first sample set included 29 MDD patients and 33 HCs and second sample set included 46 MDD patients and 57 HCs. Results for the first sample, we obtained a correct classification rate of 91.9% with a sensitivity of 89.6% and specificity of 93.9%. For the second sample, we observed a correct classification rate of 86.4% with a sensitivity of 84.8% and specificity of 87.7%. With both samples, we found that the majority of consensus FCs used for MDD identification were located in the salience network, default mode network, the cerebellum, visual cortical areas, and the affective network. Limitation we did not analyze potential structural differences between the groups. Conclusion results suggest that whole-brain FC patterns can be used to differentiate depressed patients from HCs and provide evidence for the potential use of connectome-based MVPA as a complementary tool in the clinical diagnosis of MDD.

Background There are limited data on neurobiological correlates of poor insight in obsessive-compulsive disorder (OCD). This study explored whether specific changes occur in small-world network (SWN) properties in the brain functional network of OCD patients with poor insight. Method Resting-state electroencephalograms (EEGs) were recorded for 12 medication-free OCD patients with poor insight, 50 medication-free OCD patients with good insight, and 36 healthy controls. Results Both of the OCD groups exhibited topological alterations in the brain functional network characterized by abnormal small-world parameters at the beta band. However, the alterations at the theta band only existed in the OCD patients with poor insight. Limitations A relatively small sample size. Subjects were naive to medications and those with Axis I comorbidity were excluded, perhaps limiting generalizability. Conclusions Disrupted functional integrity at the beta bands of the brain functional network may be related to OCD, while disrupted functional integrity at the theta band may be associated with poor insight in OCD patients, thus this study might provide novel insight into our understanding of the pathophysiology of OCD.

Regional abnormalities in brain structure and function, as well as disrupted connectivity, have been found repeatedly in adolescents with conduct disorder (CD). Yet, the large-scale brain topology associated with CD is not well characterized, and little is known about the systematic neural mechanisms of CD. We employed graphic theory to investigate systematically the structural connectivity derived from cortical thickness correlation in a group of patients with CD (N = 43) and healthy controls (HCs, N = 73). Nonparametric permutation tests were applied for between-group comparisons of graphical metrics. Compared with HCs, network measures including global/local efficiency and modularity all pointed to hypo-functioning in CD, despite of preserved small-world organization in both groups. The hubs distribution is only partially overlapped with each other. These results indicate that CD is accompanied by both impaired integration and segregation patterns of brain networks, and the distribution of highly connected neural network ‘hubs’ is also distinct between groups. Such misconfiguration extends our understanding regarding how structural neural network disruptions may underlie behavioral disturbances in adolescents with CD, and potentially, implicates an aberrant cytoarchitectonic profiles in the brain of CD patients.

The present study examines the inhibitory function of patients with obsessive-compulsive disorder (OCD) involved in semantic conflict using event-related potentials (ERPs). EPRs were recorded in a group of 18 medicine-free OCD patients and 18 normal controls using a modified Stroop paradigm in which the participants were asked to make a judgment of congruent or incongruent stimuli. The reaction time to color-word incongruent stimuli in the OCD group was significantly longer than the reaction time to congruent stimuli. In the OCD group, a significant negativity shift was discovered in P350 amplitude and N450 amplitude in response to incongruent stimuli, a shift not present in the control group. The amplitude of difference waveform was significantly higher for OCD than for control subjects. The findings probably revealed an inhibitory deficit in patients with OCD when performing semantic conflict tasks. The results suggest that this type of inhibitory deficit may be the cause of increased Stroop effects in patients with OCD, and one of contributors to the pathophysiology of OCD.

Functional magnetic resonance imaging (fMRI) studies have revealed abnormal neural activity in several brain regions of adolescents with conduct disorder (CD) performing various tasks. However, little is known about the spontaneous neural activity in people with CD in a resting state. The aims of this study were to investigate CD-associated regional activity abnormalities and to explore the relationship between behavioral impulsivity and regional activity abnormalities. Resting-state fMRI (rs-fMRI) scans were administered to 28 adolescents with CD and 28 age-, gender-, and IQ-matched healthy controls (HCs). The rs-fMRI data were subjected to regional homogeneity (ReHo) analysis. ReHo can demonstrate the temporal synchrony of regional blood oxygen level-dependent signals and reflect the coordination of local neuronal activity facilitating similar goals or representations. Compared to HCs, the CD group showed increased ReHo bilaterally in the insula as well as decreased ReHo in the right inferior parietal lobule, right middle temporal gyrus and right fusiform gyrus, left anterior cerebellum anterior, and right posterior cerebellum. In the CD group, mean ReHo values in the left and the right insula correlated positively with Barratt Impulsivity Scale (BIS) total scores. The results suggest that CD is associated with abnormal intrinsic brain activity, mainly in the cerebellum and temporal–parietal-limbic cortices, regions that are related to emotional and cognitive processing. BIS scores in adolescents with CD may reflect severity of abnormal neuronal synchronization in the insula.

The aim of the current study was to examine the association between age at symptom onset and action cancelation in adults with obsessive-compulsive disorder (OCD). Performance on the stop-signal task was compared among adult patients with early-onset OCD (n=63, onset age ≤19), late-onset OCD (n=33, onset age ≥20), and healthy controls (n=51). Stop-signal reaction time (SSRT) was significantly longer in both OCD groups compared to the control group. However, no significant differences were found between the two OCD groups. In addition, age at symptom onset was not associated with response inhibition performance in adults with OCD. The study findings support the existence of reduced performance on action cancelation in patients with OCD compared to healthy controls with no difference between early- and late-onset OCD subtypes.

It has been generally acknowledged that the diagnosis, treatment and prognosis evaluation of leukemia largely rely on an adequate identification of genetic abnormalities. A systemic analysis of genetic aberrations was performed in a cohort of 1346 patients with newly diagnosed acute lymphoblastic leukemia (ALL) in China. The pediatric patients had higher incidence of hyperdiploidy and t(12;21) (p13;q22)/ETV6–RUNX1 than adults (P

Background The hopelessness theory of depression posits that individuals with negative cognitive styles are at an increased risk for depression following negative life events. In neuroimaging studies, brain gray matter volume abnormalities correlate with the presence of depressive disorders. However, it is unknown whether changes in gray matter volume also appear in healthy individuals with cognitive vulnerability to depression (CVD). Methods 30 subjects diagnosed with CVD, 33 first-episode patients with major depressive disorder (MDD), and 32 healthy controls were examined using voxel-based morphometry following magnetic resonance imaging (MRI). Results We found significant volumetric differences between three groups in the left precentral gyrus, right fusiform gyrus and the right thalamus. In these regions, compared to controls, CVD subjects showed reduced gray matter volumes in the left precentral gyrus and right fusiform gyrus. MDD patients demonstrated reduced gray matter volume in the left precentral gyrus and increased gray matter volume in the right thalamus. Additionally, CVD individuals had significantly smaller right fusiform gyrus and right thalamus than MDD patients. The weakest-link scores on CSQ were negatively correlated with gray matter volumes in the left precentral gyrus. Conclusions Reductions in brain gray matter volume exist widely in individuals with CVD. In addition, there exist similar abnormalities in gray matter volume in both CVD subjects and MDD patients. Reductions of gray matter volume in the left precentral gyrus might be correlated to the negative cognitive styles, as well as an increased risk for depression.

To evaluate the value of modified early warning score ( MEWS ) in predicting mortality of critically ill patients admitted to emergency department.A prospective cohort study was conducted. Clinical data of emergency patients admitted to resuscitation room of Peking Union Medical College Hospital from Feburary 13rd, 2014 to April 20th, 2014 were collected, and their MEWS were calculated based on medical records and their clinical outcomes was followed. Incidence of primary outcome ( 3-day mortality ) and secondary outcome [ all deaths and composite outcome of intensive care unit ( ICU ) transfer, cardio-pulmonary resuscitation, and death ] were compared between MEWS positive ( MEWS≥5 ) or negative ( MEWS 0-4 ) patients, and multi-regression logistic analysis was done to look for the impact factors of primary outcome in these patients.176 patients, among them 98 ( 55.68% ) were male, were enrolled in the study. Their mean age was ( 56.86±21.46 ) years old. Mean MEWS was 4.30±2.74. There was 74 cases in MEWS positive group, and 102 in negative group. Primary endpoint occurred in 41 patients, and the 3-days mortality in MEWS positive group was significantly higher than that in MEWS negative group [ 37.84 ( 28/74) vs. 12.74% ( 13/102 ), odds ratio ( OR ) = 4.167, 95% confidence interval ( 95%CI ) = 1.973-8.804, P0.001 ]. At the meantime, incidence of all death [ 54.05% ( 40/74 ) vs. 17.65% ( 18/102 ), OR = 5.490, 95%CI = 2.770-10.883, P0.001 ] and the incidence of ICU transfer, cardio-pulmonary resuscitation and death [ 64.86% ( 48/74 ) vs. 25.49% ( 26/102 ), OR = 5.396, 95%CI = 2.809-10.366, P0.001 ] were also significantly higher in MEWS positive group as compared with negative group. Multi-regression logistic showed abnormal mental status ( OR = 3.606, 95%CI = 1.541-8.436, P = 0.003 ) but not MEWS ≥5 ( OR = 1.672, 95%CI = 0.622-4.494, P = 0.308 ) was the predictor of 3-day mortality in emergency admitted critically ill patients.Although the incidence of severe adverse events is significantly increased in patients with MEWS ≥5 compared with those with MEWS 0-4, MEWS≥5 cannot be an efficient predictor for 3-day mortality. Abnormal mental status shows some predictive value for early mortality in critically ill patients seen in emergency department.

Impaired response inhibition has been consistently reported in patients diagnosed with obsessive-compulsive disorder (OCD). This clinically heterogeneous disorder is characterized by several symptom dimensions that may have distinct, but partially overlapping, neural correlates. The present study examined whether alterations in response inhibition may be related to symptom severity and symptom dimensions. Event-related potentials (ERPs) were recorded in a group of 42 medication-free OCD patients as well as 42 healthy controls during a stop-signal task. Symptom dimension scores were obtained using the Yale-Brown Obsessive Compulsive Scale symptom checklist. OCD patients showed longer stop-signal reaction times (SSRT, p p

The scaffolding adapter protein Gab2 (Grb2-associated binder) participates in the signaling response evoked by various growth factors and cytokines. Gab2 is overexpressed in several human malignancies, including breast cancer, and was shown to promote mammary epithelial cell migration. The role of Gab2 in the activation of different signaling pathways is well documented, but less is known regarding the feedback mechanisms responsible for its inactivation. We now demonstrate that activation of the Ras/mitogen-activated protein kinase (MAPK) pathway promotes Gab2 phosphorylation on basic consensus motifs. More specifically, we show that RSK (p90 ribosomal S6 kinase) phosphorylates Gab2 on three conserved residues, both in vivo and in vitro. Mutation of these phosphorylation sites does not alter Gab2 binding to Grb2, but instead, we show that Gab2 phosphorylation inhibits the recruitment of the tyrosine phosphatase Shp2 in response to growth factors. Expression of an unphosphorylatable Gab2 mutant in mammary epithelial cells promotes an invasion-like phenotype and increases cell motility. Taken together, these results suggest that RSK is part of a negative-feedback loop that restricts Gab2-dependent epithelial cell motility. On the basis of the widespread role of Gab2 in receptor signaling, these findings also suggest that RSK plays a regulatory function in diverse receptor systems.

The aim of this study was to examine cognitive emotion regulation strategies in adult outpatients with major depressive disorder (MDD). A clinical sample of 191 MDD outpatients and a non-clinical sample of 267 general adults were recruited. Nine cognitive emotion regulation strategies were assessed in all participants (aged 21–65 years). Results showed that MDD participants had significantly higher scores on the following strategies: self-blame, acceptance, rumination, catastrophizing, and blaming others, but lower scores on positive refocusing, refocus on planning, positive reappraisal, and putting in perspective strategies than general populations. In addition, self-blame, acceptance, and catastrophizing positively correlated and positive reappraisal negatively correlated with depressive symptoms in MDD populations. Further logistic regression analyses indicated that five strategies have significant and independent contributions to the prediction of MDD group membership (a higher reported use of self-blame, catastrophizing, and acceptance, and a lower reported use of positive refocusing, and putting in perspective). The results suggest that cognitive emotion regulation strategies may be a useful target for psychological assessment and treatment in patients with MDD.

Background Major depressive disorder (MDD) has been associated with abnormal structure and function of the brain's affective network, including the amygdala and orbitofrontal cortex (OFC). However, it is unclear if alterations of resting-state function in this affective network are present at the initial onset of MDD. Aims To examine resting-state function of the brain's affective network in first-episode, medication-naive patients with MDD compared to healthy controls (HCs). Methods Resting-state functional magnetic resonance imaging (rs-fMRI) was performed on 32 first-episode, medication-naive young adult patients with MDD and 35 matched HCs. The amplitude of low-frequency fluctuations (ALFF) of the blood oxygen level-dependent (BOLD) signal and amygdala-seeded functional connectivity (FC) were investigated. Results Compared to HC, MDD patients showed reduced ALFF in the bilateral OFC and increased ALFF in the bilateral temporal lobe extending to the insular and left fusiform cortices. Enhanced anti-correlation of activity between the left amygdala seed and the left OFC was found in MDD patients but not in HCs. Conclusions Reduced ALFF in the OFC suggests hypo-functioning of emotion regulation in the affective network. Enhanced anti-correlation of activity between the amygdala and OFC may reflect dysfunction of the amygdala-OFC network and additionally represent a pathological process of MDD.