Neural correlates of prediction error in patients with schizophrenia: evidence from an fMRI meta-analysis.

Abnormal processes of learning from prediction errors, i.e. the discrepancies between expectations and outcomes, are thought to underlie motivational impairments in schizophrenia. Although dopaminergic abnormalities in the mesocorticolimbic reward circuit have been found in patients with schizophrenia, the pathway through which prediction error signals are processed in schizophrenia has yet to be elucidated. To determine the neural correlates of prediction error processing in schizophrenia, we conducted a meta-analysis of whole-brain neuroimaging studies that investigated prediction error signal processing in schizophrenia patients and healthy controls. A total of 14 studies (324 schizophrenia patients and 348 healthy controls) using the reinforcement learning paradigm were included. Our meta-analysis showed that, relative to healthy controls, schizophrenia patients showed increased activity in the precentral gyrus and middle frontal gyrus and reduced activity in the mesolimbic circuit, including the striatum, thalamus, amygdala, hippocampus, anterior cingulate cortex, insula, superior temporal gyrus, and cerebellum, when processing prediction errors. We also found hyperactivity in frontal areas and hypoactivity in mesolimbic areas when encoding prediction error signals in schizophrenia patients, potentially indicating abnormal dopamine signaling of reward prediction error and suggesting failure to represent the value of alternative responses during prediction error learning and decision making.

Suppression of excitatory synaptic transmission in the centrolateral amygdala via presynaptic histamine H3 heteroreceptors.

The central histaminergic system has a pivotal role in emotional regulation and psychiatric disorders, including anxiety, depression and schizophrenia. However, the effect of histamine on neuronal activity of the centrolateral amygdala (CeL), an essential node for fear and anxiety processing, remains unknown. Here, using immunostaining and whole-cell patch clamp recording combined with optogenetic manipulation of histaminergic terminals in CeL slices prepared from histidine decarboxylase (HDC)-Cre rats, we show that histamine selectively suppresses excitatory synaptic transmissions, including glutamatergic transmission from the basolateral amygdala, on both PKC-δ- and SOM-positive CeL neurons. The histamine-induced effect is mediated by H3 receptors expressed on VGLUT1-/VGLUT2-positive presynaptic terminals in CeL. Furthermore, optoactivation of histaminergic afferent terminals from the hypothalamic tuberomammillary nucleus (TMN) also significantly suppresses glutamatergic transmissions in CeL via H3 receptors. Histamine neither modulates inhibitory synaptic transmission by presynaptic H3 receptors nor directly excites CeL neurons by postsynaptic H1, H2 or H4 receptors. These results suggest that histaminergic afferent inputs and presynaptic H3 heteroreceptors may hold a critical position in balancing excitatory and inhibitory synaptic transmissions in CeL by selective modulation of glutamatergic drive, which may not only account for the pathophysiology of psychiatric disorders but also provide potential psychotherapeutic targets. KEY POINTS: Histamine selectively suppresses the excitatory, rather than inhibitory, synaptic transmissions on both PKC-δ- and SOM-positive neurons in the centrolateral amygdala (CeL). H3 receptors expressed on VGLUT1- or VGLUT2-positive afferent terminals mediate the suppression of histamine on glutamatergic synaptic transmission in CeL. Optogenetic activation of hypothalamic tuberomammillary nucleus (TMN)-CeL histaminergic projections inhibits glutamatergic transmission in CeL via H3 receptors.

Pretreatment Pan-Immune-Inflammation Value (PIV) in Predicting Therapeutic Response and Clinical Outcomes of Neoadjuvant Immunochemotherapy for Esophageal Squamous Cell Carcinoma.

PURPOSE: The pan-immune-inflammation value (PIV), which reflects the balance between the host immune and inflammatory status, is a readily available index for evaluating cancer outcomes. Until now, however, no study has demonstrated the clinical response of PIV to neoadjuvant immunochemotherapy (NICT) in esophageal squamous cell carcinoma (ESCC). METHODS: This retrospective study included 218 patients with ESCC who underwent NICT. The relationship between PIV and therapeutic response (pathological complete response [PCR]) and clinical outcomes (overall survival [OS] and disease-free survival [DFS]) was examined. Cox proportional, hazard-regression analyses and the Kaplan-Meier method were used for survival analyses. Recursive partitioning analysis (RPA) was used to establish a novel risk stratification model. RESULTS: Sixty-six patients (30.3%) achieved PCR after NICT. Using PCR as the endpoint of interest, patients were compared in groups based on the optimal threshold. PIV was closely related to PCR (odds ratio [OR] 0.311, 95% confidence interval [CI] 0.140-0.690, P = 0.004). Compared with patients in the low PIV cohort, patients with high PIV had worse 3-year OS (58.7% vs. 83.6%, P < 0.001) and DFS (51.9% vs. 79.1%, P < 0.001). PIV was an independent predictor of OS (hazard ratio [HR] 2.364, 95% CI 1.183-4.724, P = 0.015) and DFS (HR 1.729, 95% CI 1.026-2.913, P = 0.040). Three risk groups with varied DFS and OS were staged by using an RPA method, and the prognostication accuracy was considerably improved. CONCLUSIONS: Pretreatment PIV can predict the therapeutic efficacy of NICT for ESCC. Because of better prognostic stratification, pretreatment PIV is a novel, sensitive, and effective indicator in ESCC receiving NICT. The prognostic results of PIV need to be verified in additional prospective studies.

A novel NIR fluorescent probe inhibits melanoma progression through apoptosis and ERK/DRP1-mediated mitochondrial fission.

Melanoma, a highly metastatic malignant tumour, necessitated early detection and intervention. This study focuses on a hemicyanine fluorescent probe activated by near-infrared (NIR) light for bioimaging and targeted mitochondrial action in melanoma cells. IR-418, our newly designed hemicyanine-based NIR fluorescent probe, demonstrated effective targeting of melanoma cell mitochondria for NIR imaging. In vitro and in vivo experiments revealed IR-418's inhibition of melanoma growth through the promotion of mitochondrial apoptosis (Bax/Bcl-2/Cleaved Caspase pathway). Moreover, IR-418 inhibited melanoma metastasis by inhibiting mitochondrial fission through the ERK/DRP1 pathway. Notably, IR-418 mitigated abnormal ATL and ASL elevations caused by tumours without inflicting significant organ damage, indicating its high biocompatibility. In conclusion, IR-418, a novel hemicyanine-based NIR fluorescent probe targeting the mitochondria, exhibits significant fluorescence imaging capability, anti-melanoma proliferation, anti-melanoma lung metastasis activities and high biosafety. Therefore, it has significant potential in the early diagnosis and treatment of melanoma.

Altered single-subject gray matter structural networks in social anxiety disorder.

Previous fMRI studies have reported more random brain functional graph configurations in social anxiety disorder (SAD). However, it is still unclear whether the same configurations would occur in gray matter (GM) graphs. Structural MRI was performed on 49 patients with SAD and on 51 age- and gender-matched healthy controls (HC). Single-subject GM networks were obtained based on the areal similarities of GM, and network topological properties were analyzed using graph theory. Group differences in each topological metric were compared, and the structure-function coupling was examined. These network measures were further correlated with the clinical characteristics in the SAD group. Compared with controls, the SAD patients demonstrated globally decreased clustering coefficient and characteristic path length. Altered topological properties were found in the fronto-limbic and sensory processing systems. Altered metrics were associated with the illness duration of SAD. Compared with the HC group, the SAD group exhibited significantly decreased structural-functional decoupling. Furthermore, structural-functional decoupling was negatively correlated with the symptom severity in SAD. These findings highlight less-optimized topological configuration of the brain structural networks in SAD, which may provide insights into the neural mechanisms underlying the excessive fear and avoidance of social interactions in SAD.

Disrupted brain gray matter connectome in social anxiety disorder: a novel individualized structural covariance network analysis.

Phenotyping approaches grounded in structural network science can offer insights into the neurobiological substrates of psychiatric diseases, but this remains to be clarified at the individual level in social anxiety disorder (SAD). Using a recently developed approach combining probability density estimation and Kullback-Leibler divergence, we constructed single-subject structural covariance networks (SCNs) based on multivariate morphometry (cortical thickness, surface area, curvature, and volume) and quantified their global/nodal network properties using graph-theoretical analysis. We compared network metrics between SAD patients and healthy controls (HC) and analyzed the relationship to clinical characteristics. We also used support vector machine analysis to explore the ability of graph-theoretical metrics to discriminate SAD patients from HC. Globally, SAD patients showed higher global efficiency, shorter characteristic path length, and stronger small-worldness. Locally, SAD patients showed abnormal nodal centrality mainly involving left superior frontal gyrus, right superior parietal lobe, left amygdala, right paracentral gyrus, right lingual, and right pericalcarine cortex. Altered topological metrics were associated with the symptom severity and duration. Graph-based metrics allowed single-subject classification of SAD versus HC with total accuracy of 78.7%. This finding, that the topological organization of SCNs in SAD patients is altered toward more randomized configurations, adds to our understanding of network-level neuropathology in SAD.

Casticin induces apoptosis and cytoprotective autophagy while inhibiting stemness involving Akt/mTOR and JAK2/STAT3 pathways in glioblastoma.

Glioblastoma (GBM) is the most common malignant glioma. However, the current systemic drugs cannot completely cure GBM. Casticin is a methoxylated flavonol compound isolated from a traditional Chinese medicine Vitex rotundifolia L.f. and exhibits a strong antitumor activity in multiple human malignancies. This study was aimed to explore the effects and underlying mechanisms of casticin in GBM. The MTT assay and colony formation was used to evaluate the casticin-induced cell viability in GBM cells. Apoptosis was assessed by ANNEXIV/PI staining assay. Autophagy was analyzed by transmission electron microscopy and immunofluorescence assays. GBM stem cell (GSC) was analyzed by tumor-sphere formation assay and ALDEFLUOR assay. The anti-GBM effect of casticin was also determined by the U87MG xenograft model. Casticin inhibited tumor cell growth in vitro and in vivo, as well as significantly induced apoptosis and autophagy. Autophagy inhibition augmented casticin-induced apoptosis. Casticin also reduced the GSC population by suppressing Oct4, Nanog, and Sox2. Mechanistically, casticin inhibited Akt/mTOR and JAK2/STAT3 signal pathways. The antitumor effect of casticin in GBM was demonstrated by inducing apoptosis, autophagy, and reducing population of GSCs; thus, it may be a potential GBM therapeutic agent for future clinical usage.

Mapping the hotspots and future trends of electrical stimulation for peripheral nerve injury: A bibliometric analysis from 2002 to 2023.

Peripheral nerve injuries often result in severe personal and social burden, and even with surgical treatment, patients continue to have poor clinical outcomes. Over the past two decades, electrical stimulation has been shown to promote axonal regeneration and alleviate refractory neuropathic pain. The aim of this study was to analyse this field using a bibliometric approach. Literature was searched through Web of Science Core Collection (WOSCC) for the years 2002-2023. Literature analysis included: (1) Describing publication trends in the field. (2) Exploring collaborative network relationships. (3) Finding research advances and research hotspots in the field. (4) Summarizing research trends in the field. With the number of studies in this field still increasing, a total of 693 publications were included in the analysis. This field of research is interdisciplinary in nature. Research hotspots include peripheral nerve regeneration, the treatment of neuropathic pain, materials for nerve injury repair, and the restoration of sensory function in patients with peripheral nerve injury. Correspondingly, the development of nerve conduits and systems for peripheral nerve electrical stimulation, clinical trials of peripheral nerve electrical stimulation, and tactile recovery and movement for amputees have shown significant promise as future research trends in this field.

A meta-analysis of the neural substrates of monetary reward anticipation and outcome in alcohol use disorder.

The capacity to anticipate and detect rewarding outcomes is fundamental for the development of adaptive decision-making and goal-oriented behavior. Delineating the neural correlates of different stages of reward processing is imperative for understanding the neurobiological mechanism underlying alcohol use disorder (AUD). To examine the neural correlates of monetary anticipation and outcome in AUD patients, we performed two separate voxel-wise meta-analyses of functional neuroimaging studies, including 12 studies investigating reward anticipation and 7 studies investigating reward outcome using the monetary incentive delay task. During the anticipation stage, AUD patients displayed decreased activation in response to monetary cues in mesocortical-limbic circuits and sensory areas, including the ventral striatum (VS), insula, hippocampus, inferior occipital gyrus, supramarginal gyrus, lingual gyrus and fusiform gyrus. During the outcome stage, AUD patients exhibited reduced activation in the dorsal striatum, VS and insula, and increased activation in the orbital frontal cortex and medial temporal area. Our findings suggest that different activation patterns are associated with nondrug rewards during different reward processing stages, potentially reflecting a changed sensitivity to monetary reward in AUD.

A Meta-Analysis of Neural Correlates of Reward Anticipation in Individuals at Clinical Risk for Schizophrenia.

BACKGROUND: Aberrant striatal responses to reward anticipation have been observed in schizophrenia. However, it is unclear whether these dysfunctions predate the onset of psychosis and whether reward anticipation is impaired in individuals at clinical high risk for schizophrenia (CHR). METHODS: To examine the neural correlates of monetary anticipation in the prodromal phase of schizophrenia, we performed a whole-brain meta-analysis of 13 functional neuroimaging studies that compared reward anticipation signals between CHR individuals and healthy controls (HC). Three databases (PubMed, Web of Science, and ScienceDirect) were systematically searched from January 1, 2000, to May 1, 2022. RESULTS: Thirteen whole-brain functional magnetic resonance imaging studies including 318 CHR individuals and 426 HC were identified through comprehensive literature searches. Relative to HC, CHR individuals showed increased brain responses in the medial prefrontal cortex and anterior cingulate cortex and decreased activation in the mesolimbic circuit, including the putamen, parahippocampal gyrus, insula, cerebellum, and supramarginal gyrus, during reward anticipation. CONCLUSIONS: Our findings in the CHR group confirmed the existence of abnormal motivational-related activation during reward anticipation, thus demonstrating the pathophysiological characteristics of the risk populations. These results have the potential to lead to the early identification and more accurate prediction of subsequent psychosis as well as a deeper understanding of the neurobiology of high-risk state of psychotic disorder.

Chiral-Flux-Phase-Based Topological Superconductivity in Kagome Systems with Mixed Edge Chiralities.

Recent studies have attracted intense attention on the quasi-2D kagome superconductors AV_{3}Sb_{5} (A=K, Rb, and Cs) where the unexpected chiral flux phase (CFP) associates with the spontaneous time-reversal symmetry breaking in charge density wave states. Here, commencing from the 2-by-2 charge density wave phases, we bridge the gap between topological superconductivity and time-reversal asymmetric CFP in kagome systems. Several chiral topological superconductor (TSC) states featuring distinct Chern numbers emerge for an s-wave or a d-wave superconducting pairing symmetry. Importantly, these CFP-based TSC phases possess unique gapless edge modes with mixed chiralities (i.e., both positive and negative chiralities), but with the net chiralities consistent with the Bogoliubov-de Gennes Chern numbers. We further study the transport properties of a two-terminal junction, using Chern insulator or normal metal leads via atomic Green's function method with Landauer-Büttiker formalism. In both cases, the normal electron tunneling and the crossed Andreev reflection oscillate as the chemical potential changes, but together contribute to plateau transmissions (1 and 3/2, respectively) that exhibit robustness against disorder. These behaviors can be regarded as the signature of a TSC hosting edge states with mixed chiralities.

Large-scale brain functional network abnormalities in social anxiety disorder.

BACKGROUND: Although aberrant brain regional responses are reported in social anxiety disorder (SAD), little is known about resting-state functional connectivity at the macroscale network level. This study aims to identify functional network abnormalities using a multivariate data-driven method in a relatively large and homogenous sample of SAD patients, and assess their potential diagnostic value. METHODS: Forty-six SAD patients and 52 demographically-matched healthy controls (HC) were recruited to undergo clinical evaluation and resting-state functional MRI scanning. We used group independent component analysis to characterize the functional architecture of brain resting-state networks (RSNs) and investigate between-group differences in intra-/inter-network functional network connectivity (FNC). Furtherly, we explored the associations of FNC abnormalities with clinical characteristics, and assessed their ability to discriminate SAD from HC using support vector machine analyses. RESULTS: SAD patients showed widespread intra-network FNC abnormalities in the default mode network, the subcortical network and the perceptual system (i.e. sensorimotor, auditory and visual networks), and large-scale inter-network FNC abnormalities among those high-order and primary RSNs. Some aberrant FNC signatures were correlated to disease severity and duration, suggesting pathophysiological relevance. Furthermore, intrinsic FNC anomalies allowed individual classification of SAD v. HC with significant accuracy, indicating potential diagnostic efficacy. CONCLUSIONS: SAD patients show distinct patterns of functional synchronization abnormalities both within and across large-scale RSNs, reflecting or causing a network imbalance of bottom-up response and top-down regulation in cognitive, emotional and sensory domains. Therefore, this could offer insights into the neurofunctional substrates of SAD.

Impact of non-pharmaceutical interventions during COVID-19 on future influenza trends in Mainland China.

BACKGROUND: Influenza is a common illness for its high rates of morbidity and transmission. The implementation of non-pharmaceutical interventions (NPIs) during the COVID-19 pandemic to manage its dissemination could affect the transmission of influenza. METHODS: A retrospective analysis, between 2018 and 2023, was conducted to examine the incidence of influenza virus types A and B among patients in sentinel cities located in North or South China as well as in Wuhan City. For validations, data on the total count of influenza patients from 2018 to 2023 were collected at the Central Hospital of Wuhan, which is not included in the sentinel hospital network. Time series methods were utilized to examine seasonal patterns and to forecast future influenza trends. RESULTS: Northern and southern cities in China had earlier outbreaks during the NPIs period by about 8 weeks compared to the 2018-2019. The implementation of NPIs significantly reduced the influenza-like illness (ILI) rate and infection durations. Influenza B Victoria and H3N2 were the first circulating strains detected after the relaxation of NPIs, followed by H1N1 across mainland China. The SARIMA model predicted synchronized H1N1 outbreak cycles in North and South China, with H3N2 expected to occur in the summer in southern cities and in the winter in northern cities over the next 3 years. The ILI burden is expected to rise in both North and South China over the next 3 years, with higher ILI% levels in southern cities throughout the year, especially in winter, and in northern cities mainly during winter. In Wuhan City and the Central Hospital of Wuhan, influenza levels are projected to peak in the winter of 2024, with 2 smaller peaks expected during the summer of 2023. CONCLUSIONS: In this study, we report the impact of NPIs on future influenza trends in mainland China. We recommend that local governments encourage vaccination during the transition period between summer and winter to mitigate economic losses and mortality associated with influenza.

Diagnostic signature composed of seven genes in HIF-1 signaling pathway for preeclampsia.

PURPOSE: In this study, we explored the relationship of genes in HIF-1 signaling pathway with preeclampsia and establish a logistic regression model for diagnose preeclampsia using bioinformatics analysis. METHOD: Two microarray datasets GSE75010 and GSE35574 were downloaded from the Gene Expression Omnibus database, which was using for differential expression analysis. DEGs were performed the Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene set enrichment analysis (GSEA). Then we performed unsupervised consensus clustering analysis using genes in HIF-1 signaling pathway, and clinical features and immune cell infiltration were compared between these clusters, as well as the least absolute shrinkage and selection operator (LASSO) method to screened out key genes to constructed logistic regression model, and receiver operating characteristic (ROC) curve was plotted to evaluate the accuracy of the model. RESULTS: 57 DEGs were identified, of which GO, KEGG and analysis GSEA showed DEGs were mostly involved in HIF-1 signaling pathway. Two subtypes were identified of preeclampsia and 7 genes in HIF1-signaling pathway were screened out to establish the logistic regression model for discrimination preeclampsia from controls, of which the AUC are 0.923 and 0.845 in training and validation datasets respectively. CONCLUSION: Seven genes (including MKNK1, ARNT, FLT1, SERPINE1, ENO3, LDHA, BCL2) were screen out to build potential diagnostic model of preeclampsia.

Efficacy of Pneumatic Retinopexy Preceding Pars Plana Vitrectomy in Managing Combined Retinal and Choroidal Detachment: A Retrospective Study of 64 Patients.

BACKGROUND Combined retinal and choroidal detachment (RD-CD) poses significant challenges in ophthalmic treatment, often requiring surgical intervention for optimal outcomes. The selection of the appropriate surgical procedure is crucial for ensuring visual restoration and overall eye health. This study delves into the therapeutic benefits and outcomes of two distinct surgical approaches for RD-CD: pneumatic retinopexy (PR) followed by pars plana vitrectomy (PPV) and PPV alone, in an attempt to guide optimal clinical decision-making. MATERIAL AND METHODS We retrospectively analyzed data from 64 consecutive patients diagnosed with RD-CD. They were categorized into two groups: Group A consisted of 34 patients (34 eyes) who underwent PR as an initial treatment and subsequently received PPV, while Group B, serving as a control, comprised 30 patients (30 eyes) treated solely with PPV. RESULTS The application of PR in Group A notably accelerated intraocular pressure (IOP) increase (P.

Emotional intelligence mediates the protective role of the orbitofrontal cortex spontaneous activity measured by fALFF against depressive and anxious symptoms in late adolescence.

As a stable personality construct, trait emotional intelligence (TEI) refers to a battery of perceived emotion-related skills that make individuals behave effectively to adapt to the environment and maintain well-being. Abundant evidence has consistently shown that TEI is important for the outcomes of many mental health issues, particularly depression and anxiety. However, the neural substrates involved in TEI and the underlying neurobehavioral mechanism of how TEI reduces depression and anxiety symptoms remain largely unknown. Herein, resting-state functional magnetic resonance imaging and a group of behavioral measures were applied to examine these questions among a large sample comprising 231 general adolescent students aged 16-20 years (52% female). Whole-brain correlation analysis and prediction analysis demonstrated that TEI was negatively linked with spontaneous activity (measured with the fractional amplitude of low-frequency fluctuations) in the bilateral medial orbitofrontal cortex (OFC), a critical site implicated in emotion-related processes. Furthermore, structural equation modeling analysis found that TEI mediated the link of OFC spontaneous activity to depressive and anxious symptoms. Collectively, the current findings present new evidence for the neurofunctional bases of TEI and suggest a potential "brain-personality-symptom" pathway for alleviating depressive and anxious symptoms among students in late adolescence.

Ga2O3-Based Solar-Blind Position-Sensitive Detector for Noncontact Measurement and Optoelectronic Demodulation.

As a kind of photodetector, position-sensitive-detectors (PSDs) have been widely used in noncontact photoelectric positioning and measurement. However, fabrications and applications of solar-blind PSDs remain yet to be harnessed. Herein, we demonstrate a solar-blind PSD developed from a graphene/Ga2O3 Schottky junction with a 25-nanometer-thick Ga2O3 film, in which the absorption of the nanometer-thick Ga2O3 is enhanced by multibeam interference. The graphene/Ga2O3 junction exhibits a responsivity of 48.5 mA/W and a rise/decay time of 0.8/99.8 µs at zero bias. Moreover, the position of the solar-blind spot can be determined by the output signals of the PSD. Using the device as a sensor of noncontact test systems, we demonstrate its application in measurement of angular, displacement, and light trajectory. In addition, the position-sensitive outputs have been used to demodulate optical signals into electrical signals. The results may prospect the application of solar-blind PSDs in measurement, tracking, communication, and so on.

X-ray inhibits FUT4-mediated proliferation in A549 cells by downregulating SP1 expression.

Objective: To identify the mechanism of down-regulation of Lewis Y antigen caused by X-ray irradiation. METHODS: The present original research study was conducted at Zhejiang University City College, Hangzhou, Republic of China, from 2020 to 2022. Western blotting, Co-immunoprecipitation (CO-IP), electrophoretic mobility shift assay and Cell Counting Kit-8 (CCK8) were performed to confirm the effect of X-ray irradiation on A549 cell proliferation and its mechanism. Data was analysed using Statistical Package for Social Sciences (SPSS) 11.5. RESULTS: The expressions of fucosyltransferase IV and Lewis Y were decreased after X-ray irradiation, thus inhibiting the proliferation of A549 lung cancer cells. Deoxyribonucleic acid damage caused by the irradiation caused higher level of poly- adenosinediphosphate-ribosylated Specific Protein 1(SP1), and translocation of SP1 from the nucleus, decreasing the expression of fucosyltransferase IV and Lewis Y. Conclusion: There was a significant role of glycosylation in radiation therapy for lung cancer.

Clinical significance of Osaka prognostic score based on nutritional and inflammatory status in patients with esophageal squamous cell carcinoma.

BACKGROUND: It has been reported that Osaka prognostic score (OPS), based on C-reactive protein (CRP), total lymphocyte counts (TLC) and albumin (ALB), was relevant to prognosis in colorectal cancer. However, the role of OPS regarding prognosis in patients with esophageal squamous cell carcinoma (ESCC) has not been reported. The current study aimed to explore the clinical outcome of OPS and establish and validate a nomogram for survival prediction in ESCC after radical resection. METHODS: This retrospective study included 395 consecutive ESCC patients with radical resection. Then patients were randomly divided into two cohorts: training cohort (276) and validation cohort (119). The OPS, based on TLC, CRP and ALB, was constructed to verify the prognostic value by Kaplan-Meier curves and Cox analyses. A nomogram model for prognosis prediction of cancer-specific survival (CSS) was developed and validated in two cohorts. RESULTS: Kaplan-Meier curves regarding the 5-year CSS for the groups of OPS 0, 1, 2 and 3 were 55.3, 30.6, 17.3 and 6.7% (P < 0.001) in the training cohort and 52.6, 33.3, 15.8 and 9.1% (P < 0.001) in the validation cohort, respectively. Then the OPS score in multivariate Cox analysis was confirmed to be a useful independent score. Finally, a predictive OPS-based nomogram was developed and validated with a C-index of 0.68 in the training cohort and 0.67 in the validation cohort, respectively. All above results indicated that the OPS-based nomogram can accurately and effectively predict survival in ESCC after radical resection. CONCLUSION: The OPS serves as a novel, convenient and effective predictor in ESCC after radical resection. The OPS-based nomogram has potential independent prognostic value, which can accurately and effectively predict individual CSS in ESCC after radical resection.

Neurofunctional mapping of reward anticipation and outcome for major depressive disorder: a voxel-based meta-analysis.

Aberrations in how people form expectations about rewards and how they respond to receiving rewards are thought to underlie major depressive disorder (MDD). However, the underlying mechanism linking the appetitive reward system, specifically anticipation and outcome, is still not fully understood. To examine the neural correlates of monetary anticipation and outcome in currently depressed subjects with MDD, we performed two separate voxel-wise meta-analyses of functional neuroimaging studies using the monetary incentive delay task. During reward anticipation, the depressed patients exhibited an increased response in the bilateral middle cingulate cortex (MCC) extending to the anterior cingulate cortex, the medial prefrontal cortex, the left inferior frontal gyrus (IFG), and the postcentral gyrus, but a reduced response in the mesolimbic circuit, including the left striatum, insula, amygdala, right cerebellum, striatum, and IFG, compared to controls. During the outcome stage, MDD showed higher activity in the left inferior temporal gyrus, and lower activity in the mesocortical pathway, including the bilateral MCC, left caudate nucleus, precentral gyrus, thalamus, cerebellum, right striatum, insula, IFG, middle frontal gyrus, and temporal pole. Our findings suggest that cMDD may be characterised by state-dependent hyper-responsivity in cortical regions during the anticipation phase, and hypo-responsivity of the mesocortico-limbic circuit across the two phases of the reward response. Our study showed dissociable neural circuit responses to monetary stimuli during reward anticipation and outcome, which help to understand the dysfunction in different aspects of reward processing, particularly motivational v. hedonic deficits in depression.