Alveolar-arterial oxygen gradient: An early marker to predict the severity of community-acquired pneumonia in children.

To study the clinical significance of alveolar-arterial oxygen gradient (PA-aO2) for children with community-acquired pneumonia (CAP). A prospective study was carried out from January 2020 to June 2023, Overall, 100 patients were included in the study, 35 had severe pneumonia, whereas, 65 had non-severe pneumonia. Clinical and laboratory data were retrospectively collected at the time of hospital admission and during hospitalization. Patients were divided into severe and non-severe groups. PA-aO2 was significantly higher among children with severe pneumonia, as determined by WHO, PRESS (P < .001). PA-aO2 was significantly higher among children with mechanical ventilation, shock, sepsis, and mortality. Receiver operating characteristic curve (ROC) analysis for PA-aO2 showed that the area under the curve was 0.76 (P value < .05), with a sensitivity of 84.3% and a specificity of 67.9%. Our study suggests that PA-aO2 level has a predictive value for detecting community-acquired pneumonia severity in children.

Social excluder's face reduces gaze-triggered attention orienting.

Social ostracism, a negative affective experience in interpersonal interactions, is thought to modulate the gaze-cueing effect (GCE). However, it is unclear whether the impact of social exclusion on the GCE is related to the identity of the cueing face. Therefore, the present study employed a two-phase paradigm to address this issue. In the first phase, two groups of participants were instructed to complete a Cyberball game with two virtual avatars to establish a binding relationship between a specific face's identity and the emotions of social exclusion or inclusion. In the second phase, these two virtual avatars (exclusion faces/inclusion faces) and two new faces (control faces) were used as cueing faces in the gaze-cueing task. The results found that, for the exclusion group, the magnitudes of the GCEs for the exclusion and exclusion-control faces were similar in the 200 ms stimulus onset asynchrony (SOA) condition, while the exclusion face's GCE was significantly smaller than that of the exclusion-control face in the 700 ms SOA condition. In contrast, for the inclusion group, the GCEs for inclusion and inclusion-control faces in both the 200 ms SOA and 700 ms SOA conditions did not significantly differ. This study reveals that the effect of social exclusion on the GCE is related to the identity of the cueing face, with individuals more reluctant to follow the gaze direction of excluder and shift their attention and provides experimental evidence that the perception of higher social relations can exert a top-down impact on the processing of social spatial cues.

Protocol to monitor cardiac function and hemodynamics in septic rodents.

Septic cardiomyopathy is associated with high mortality in septic patients, characterized by reversible systolic and diastolic dysfunction. It is essential to monitor cardiac function and hemodynamic changes in septic animals. Here, we present a protocol to monitor cardiac function and hemodynamics in septic rodents. We describe steps for performing cecal ligation and puncture on rodents to induce sepsis, acquiring two-dimensional echocardiographic and M-mode ultrasonic images, and assessing mean arterial pressure in septic animals. For complete details on the use and execution of this protocol, please refer to Zhang et al.1.

Prefrontal cortical dopamine deficit may cause impaired glucose metabolism in schizophrenia.

The brain neurotramsmitter dopamine may play an important role in modulating systemic glucose homeostasis. In seven hundred and four drug- naïve patients with first-episode schizophrenia, we provide robust evidence of positive associations between negative symptoms of schizophrenia and high fasting blood glucose. We then show that glucose metabolism and negative symptoms are improved when intermittent theta burst stimulation (iTBS) on prefrontal cortex (PFC) is performed in patients with predominantly negative symptoms of schizophrenia. These findings led us to hypothesize that the prefrontal cortical dopamine deficit, which is known to be associated with negative symptoms, may be responsible for abnormal glucose metabolism in schizophrenia. To explore this, we optogenetically and chemogenetically inhibited the ventral tegmental area (VTA)-medial prefrontal cortex (mPFC) dopamine projection in mice and found both procedures caused glucose intolerance. Moreover, microinjection of dopamine two receptor (D2R) neuron antagonists into mPFC in mice significantly impaired glucose tolerance. Finally, a transgenic mouse model of psychosis named Disc1tr exhibited depressive-like symptoms, impaired glucose homeostasis, and compared to wild type littermates reduced D2R expression in prefrontal cortex.

Extracellular proteins as potential biomarkers in Sepsis-related cerebral injury.

Background: Sepsis can cause brain damage known as septic encephalopathy (SAE), which is linked to higher mortality and poorer outcomes. Objective clinical markers for SAE diagnosis and prognosis are lacking. This study aimed to identify biomarkers of SAE by investigating genes and extracellular proteins involved in sepsis-induced brain injury. Methods: Extracellular protein differentially expressed genes (EP-DEGs) from sepsis patients' brain tissue (GSE135838) were obtained from Gene Expression Omnibus (GEO) and evaluated by protein annotation database. The function and pathways of EP-DEGs were examined using GO and KEGG. Protein-protein interaction (PPI) networks were built and crucial EP-DEGs were screened using STRING, Cytoscape, MCODE, and Cytohubba. The diagnostic and prognostic accuracy of key EP-DEGs was assessed in 31 sepsis patients' blood samples and a rat cecal ligation and puncture (CLP)-induced sepsis model. Cognitive and spatial memory impairment was evaluated 7-11 days post-CLP using behavioral tests. Blood and cerebrospinal fluid from 26 rats (SHAM n=14, CLP n=12) were collected 6 days after CLP to analyze key EP-DEGs. Results: Thirty-one EP-DEGs from DEGs were examined. Bone marrow leukocytes, neutrophil movement, leukocyte migration, and reactions to molecules with bacterial origin were all enhanced in EP-DEGs. In comparison to the sham-operated group, sepsis rats had higher levels of MMP8 and S100A8 proteins in their venous blood (both p<0.05) and cerebrospinal fluid (p=0.0506, p<0.0001, respectively). Four important extracellular proteins, MMP8, CSF3, IL-6, and S100A8, were identified in clinical peripheral blood samples. MMP8 and S100A8 levels in the peripheral blood of sepsis patients were higher in SAE than in non-SAE. In comparison to MMP8, S100A8 had a higher area under the curve (AUC: 0.962, p<0.05) and a higher sensitivity and specificity (80% and 100%, respectively) than MMP8 (AUC: 0.790, p<0.05). High levels of S100A8 strongly correlated with 28-day mortality and the Glasgow Coma Scale (GCS) scores. Conclusion: The extracellular proteins MMP8, CSF3, IL-6, and S100A8 may be crucial in the pathophysiology of SAE. S100A8 and MMP8 are possible biomarkers for SAE's onset and progression. This research may help to clarify the pathogenesis of SAE and improve the diagnosis and prognosis of the disease.

Decoding molecular signature on heart of septic mice with distinct left ventricular ejection fraction.

Dysregulated cardiac function after sepsis in intensive care unit is known to predict poor long-term outcome and increase mortality. Their pathological feature and molecular mechanism remain unclear. We observed that septic patients with depressed left ventricular ejection fraction (LVEF) have the highest in-hospital and 28 days mortality comparing to patients with hyperdynamic LVEF or with heart failure with preserved LVEF. Echocardiograms reveal that survivors post cecum ligation and puncture (CLP) on rodents have stable LVEF and non-survivors have fluctuated LVEF at CLP early phase. CLP-induced mice fall into three groups based on LVEF 24 h post-surgery: high-, low-, and normal-LVEF. Transcriptomic and proteomic analyses identify jointly and distinctively changed genes, proteins and biologically essential pathways in left ventricles from three CLP groups. Notably, transmission electron microscopy shows different mitochondrial and sarcomere defects associated with LVEF variances. Together, this study systematically characterizes the molecular, morphological, and functional alterations in CLP-induced cardiac injury.

Face mask reduces gaze-cueing effect.

Recent studies have found that face masks affect social cognition and behaviour in the context of the novel coronavirus (COVID-19) pandemic. The eyes, the only part of the face not covered by face masks, are an important spatial attention cue that can trigger social attention orienting. Here, we adopted a spatial gaze-cueing task to investigate whether face masks affect social attention orienting triggered by eye gaze cues. In Experiment 1, participants were asked to determine the orientation of a target line under two types of cues-masked and non-masked faces-and two stimulus onset asynchrony (SOA) conditions (300 ms and 1000 ms). The results showed that masked faces induced a smaller gaze-cueing effect (GCE) compared to non-masked faces at 300 ms SOA, while two face types induced similar GCEs at 1000 ms SOA. Experiment 2 used mouth-obscured faces and non-masked faces as cues and found that no significant difference in GCE between the two types at either 300 ms or 1000 ms SOA, indicating that the reduction of GCE caused by the masked face was due to the social meaning expressed by the mask rather than a physical effect of masking. The present study extends previous findings to support the idea that high-level social information affects the processing of eye gaze direction and provides evidence that face masks affect social cognition and behaviour in the context of COVID-19.

Research on route planning for solar UAV based on the intelligent optimization algorithm.

The solar unmanned aerial vehicle (UAV) route planning needs to comprehensively consider the conversion efficiency of solar cells under the influence of solar ground reflection radiation and sky scattering radiation. On the one hand, it is necessary to consider the cost of radar threat, mileage energy consumption, mountain impact and other costs. On the other hand, it is also necessary to consider the influence of high threat, mountain shadow occlusion cost, and cloud shading cost on solar photovoltaic conversion efficiency. The above problem was solved through using the ant colony intelligent optimization algorithm. By constructing ant colony paths rationally, models of mountain impact cost, high threat, mountain shadow shelter cost, and cloud shading cost were established. The constraints such as the maximum action distance, solar irradiation angle and effective action distance of various costs were introduced into the cost model and exploration factor calculation, and the comprehensive optimization problem of solar UAV route was solved. Finally, the simulation results show that the algorithm path structure is reasonable; the target node can be found independently; the convergence speed can meet the requirements of route planning; the generated route cost is small; the algorithm is reasonable and effective.

Insights into the mechanism of growth and fat deposition by feeding different levels of lipid provided by transcriptome analysis of swamp eel (Monopterus albus, Zuiew 1793) liver.

Lipid is an important source of energy in fish feeds, and the appropriate fat content can improve the efficiency of protein utilization. However, excessive lipid content in the feed can lead to abnormal fat deposition in fish, which has a negative effect on the growth of fish. Therefore, the effects of feed lipid levels on swamp eel were studied. Essential functional genes were screened using transcriptomics. We divided 840 fish into seven groups (four replicates). A mixture of fish and soybean oils (1:4), 0%, 2%, 4%, 6%, 8%, 10%, and 12% was added to the basic feed were named groups one to seven (L1-L7), respectively. Isonitrogenous diets were fed swamp eel for 10 weeks. Growth performance, visceral index, nutritional components, and biochemical indexes were measured and analyzed. Livers of the 0%, 6%, and 12% groups were subjected to transcriptome sequencing analysis. The results of our study showed that: the suitable lipid level for the growth of swamp eel was 7.03%; the crude fat content of whole fish, liver, intestine, muscle, and skin increased with the increase of lipid level, with some significant difference, and excess fat was deposited in skin tissue; triglyceride, total cholesterol, and free fatty acid contents increased with the increase of feed lipid level. High-density lipoprotein levels in the L3 and L4 groups were higher than in the other groups. Blood glucose concentrations in the L5, L6, and L7 groups increased; the liver tissue structure was damaged when the lipid level was too high. two-hundred-and-twenty-eight differentially expressed genes were found. Several critical pathways regulating glucose metabolism and energy balance (e.g., glycerolipid metabolism, glycolysis synthesis, degradation of ketone bodies, and Janus Kinase/Signal Transducer and Activator of Transcription signaling pathway) were enriched in swamp eel compared with the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Suitable lipid levels (7.03%) can promote the growth of swamp eel, and excessive lipid levels can cause elevated blood lipids and lead to liver cell damage. Regulatory mechanisms may involve multiple metabolic pathways for glucose and lipid metabolism in eels. This study provides new insights to explain the mechanism of fat deposition due to high levels of lipid and provides a basis for the production of efficient and environmentally friendly feed for swamp eel.

Synaptic plasticity in schizophrenia pathophysiology.

Schizophrenia is a severe neuropsychiatric syndrome with psychotic behavioral abnormalities and marked cognitive deficits. It is widely accepted that genetic and environmental factors contribute to the onset of schizophrenia. However, the etiology and pathology of the disease remain largely unexplored. Recently, the synaptopathology and the dysregulated synaptic plasticity and function have emerging as intriguing and prominent biological mechanisms of schizophrenia pathogenesis. Synaptic plasticity is the ability of neurons to change the strength of their connections in response to internal or external stimuli, which is essential for brain development and function, learning and memory, and vast majority of behavior responses relevant to psychiatric diseases including schizophrenia. Here, we reviewed molecular and cellular mechanisms of the multiple forms synaptic plasticity, and the functional regulations of schizophrenia-risk factors including disease susceptible genes and environmental alterations on synaptic plasticity and animal behavior. Recent genome-wide association studies have provided fruitful findings of hundreds of risk gene variances associated with schizophrenia, thus further clarifying the role of these disease-risk genes in synaptic transmission and plasticity will be beneficial to advance our understanding of schizophrenia pathology, as well as the molecular mechanism of synaptic plasticity.

Guilt-inducing interaction with others modulates subsequent attentional orienting via their gaze.

Gaze direction can trigger social attentional orientation, characterised by a speeded reaction time in detecting targets appearing in a gazed-at location compared with those appearing in other locations. This is called the 'gaze-cueing effect' (GCE). Here, we investigated whether a feeling of guilt established through prior interaction with a cueing face could modulate the gaze-cueing effect. Participants first completed a guilt-induction task using a modified dot-estimation paradigm to associate the feeling of guilt with a specific face, after which the face that had established the binding relationship was used as the stimulus in a gaze-cueing task. The results showed that guilt-directed faces and control faces induce equal magnitudes of gaze-cueing effect in 200 ms of stimulus onset asynchrony (SOA), while guilt-directed faces induce a smaller gaze-cueing effect than control faces in 700 ms SOA. These findings provide preliminary evidence that guilt may modulate social attention triggered by eye gaze at a later stage of processing but not in the earlier stages.

Masked face is looking at me: Face mask increases the feeling of being looked at during the COVID-19 pandemic.

Background: As the COVID-19 global pandemic unfolded, governments recommended wearing face masks as a protective measure. Recent studies have found that a face mask influences perception; but how it affects social perception, especially the judgment of being looked at, is still unknown. This study investigated how wearing a mask influences the judgment of gaze direction by conducting a cone of direct gaze (CoDG) task. Methods: In Experiment 1, three types of masked faces were considered to investigate whether the effect of masks on CoDG is modulated by mask types. Experiment 2 was to further validate the results of Experiment 1 by adding a learning phase to help participants better distinguish N95 and surgical masks. Furthermore, to investigate whether the effect of masks derives from its social significance, a face with only the eye-region (a mouth-cut face) was used as the stimuli in Experiment 3. Results: The results of Experiment 1 found that wearing masks widens the CoDG, irrespective of the mask type. Experiment 2 replicated the results of Experiment 1. Experiment 3 found that the CoDG of N95-masked faces was wider than the mouth-cut and non-masked faces, while no significant difference existed between the CoDG of mouth-cut and non-masked faces, illustrating that the influence of wearing masks on CoDG was due to high-level social significance rather than low-level facial feature information. Conclusion: The results show that face mask increases the feeling of being looked at during the COVID-19 Pandemic. The present findings are of significance for understanding the impact of wearing masks on human social cognition in the context of COVID-19.

Association of variants in the KIF1A gene with amyotrophic lateral sclerosis.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a devastating progressive neurodegenerative disease that affects neurons in the central nervous system and the spinal cord. As in many other neurodegenerative disorders, the genetic risk factors and pathogenesis of ALS involve dysregulation of cytoskeleton and neuronal transport. Notably, sensory and motor neuron diseases such as hereditary sensory and autonomic neuropathy type 2 (HSAN2) and spastic paraplegia 30 (SPG30) share several causative genes with ALS, as well as having common clinical phenotypes. KIF1A encodes a kinesin 3 motor that transports presynaptic vesicle precursors (SVPs) and dense core vesicles and has been reported as a causative gene for HSAN2 and SPG30. METHODS: Here, we analyzed whole-exome sequencing data from 941 patients with ALS to investigate the genetic association of KIF1A with ALS. RESULTS: We identified rare damage variants (RDVs) in the KIF1A gene associated with ALS and delineated the clinical characteristics of ALS patients with KIF1A RDVs. Clinically, these patients tended to exhibit sensory disturbance. Interestingly, the majority of these variants are located at the C-terminal cargo-binding region of the KIF1A protein. Functional examination revealed that the ALS-associated KIF1A variants located in the C-terminal region preferentially enhanced the binding of SVPs containing RAB3A, VAMP2, and synaptophysin. Expression of several disease-related KIF1A mutants in cultured mouse cortical neurons led to enhanced colocalization of RAB3A or VAMP2 with the KIF1A motor. CONCLUSIONS: Our study highlighted the importance of KIF1A motor-mediated transport in the pathogenesis of ALS, indicating KIF1A as an important player in the oligogenic scenario of ALS.

Interaction dynamics of optical dark bound solitons for a defocusing Lakshmanan-Porsezian-Daniel equation.

We investigate the propagation and interaction dynamics of the optical dark bound solitons for the defocusing Lakshmanan-Porsezian-Daniel equation, which is a physically relevant generalization of the nonlinear Schrödinger equation involving the higher-order effects. Explicit N-dark soliton solutions in the compact determinant form are constructed via the binary Darboux transformation method. Bound states of the dark solitons are discussed when the incoherent solitons have the same velocity. We find an interesting phenomenon that dark soliton molecules and double-valley dark solitons (DVDSs) can be obtained by controlling the interval of the bound state dark solitons, and abundant interaction modalities between them can be formed. Moreover, dark soliton molecules always undergo elastic interactions with other solitons, while interactions for the DVDSs are usually inelastic, and special parameter conditions for elastic interaction of DVDSs through asymptotic analysis are obtained. Numerical simulations are employed to verify the stability of the bound state dark solitons. Analytical results obtained in this paper are expected to be useful for the experimental realization of bound-state dark solitons in optical fibers with higher-order effects and a further understanding of their optical transmission properties..

Dietary Macroalgae Saccharina japonica Ameliorates Liver Injury Induced by a High-Carbohydrate Diet in Swamp Eel (Monopterus albus).

A high-carbohydrate diet lowers the rearing cost and decreases the ammonia emission into the environment, whereas it can induce liver injury, which can reduce harvest yields and generate economic losses in reared fish species. Macroalgae Saccharina japonica (SJ) has been reported to improve anti-diabetic, but the protective mechanism of dietary SJ against liver injury in fish fed a high-carbohydrate diet has not been studied. Therefore, a 56-day nutritional trial was designed for swamp eel Monopterus albus, which was fed with the normal diet [20% carbohydrate, normal carbohydrate (NC)], a high carbohydrate diet (32% carbohydrate, HC), and a HC diet supplemented with 2.5% SJ (HC-S). The HC diet promoted growth and lowered feed coefficient (FC), whereas it increased hepatosomatic index (HSI) when compared with the NC diet in this study. However, SJ supplementation increased iodine contents in muscle, reduced HSI, and improved liver injury, such as the decrease of glucose (GLU), total bile acid (TBA), and alanine aminotransferase (ALT) in serum, and glycogen and TBA in the liver. Consistently, histological analysis showed that SJ reduced the area of lipid droplet, glycogen, and collagen fiber in the liver (p < 0.05). Thoroughly, the underlying protective mechanisms of SJ supplementation against HC-induced liver injury were studied by liver transcriptome sequencing coupled with pathway analysis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the differentially expressed genes (DEGs), such as the acetyl-coenzyme A synthetase (acss1), alcohol dehydrogenase (adh), interferon-induced protein with tetratricopeptide repeats 1 (ifit1), aldo-keto reductase family 1 member D1 (akr1d1), cholesterol 7-alpha-monooxygenase (cyp7a1), and UDP-glucuronosyltransferase (ugt), indicated that the pathway of glycolysis/gluconeogenesis was the main metabolic pathway altered in the HC group compared with the NC group. Meanwhile, hepatitis C, primary BA biosynthesis, and drug metabolism-cytochrome P450 were the three main metabolic pathways altered by SJ supplementation when compared with the HC group. Moreover, the BA-targeted metabolomic analysis of the serum BA found that SJ supplementation decreased the contents of taurohyocholic acid (THCA), taurochenodeoxycholic acid (TCDCA), taurolithocholic acid (TLCA), nordeoxycholic acid (NorDCA), and increased the contents of ursocholic acid (UCA), allocholic acid (ACA), and chenodeoxycholic acid (CDCA). In particular, the higher contents of UCA, ACA, and CDCA regulated by SJ were associated with lower liver injury. Overall, these results indicate that the 2.5% supplementation of SJ can be recommended as a functional feed additive for the alleviation of liver injury in swamp eel-fed high-carbohydrate diets.

Recurrent de novo single point variant on the gene encoding Na+/K+ pump results in epilepsy.

The etiology of epilepsy remains undefined in two-thirds of patients. Here, we identified a de novo variant of ATP1A2 (c.2426 T > G, p.Leu809Arg), which encodes the α2 subunit of Na+/K+-ATPase, from a family with idiopathic epilepsy. This variant caused epilepsy with hemiplegic migraine in the study patients. We generated the point variant mouse model Atp1a2L809R, which recapitulated the epilepsy observed in the study patients. In Atp1a2L809R/WT mice, convulsions were observed and cognitive and memory function was impaired. This variant affected the potassium binding function of the protein, disabling its ion transport ability, thereby increasing the frequency of nerve impulses. Valproate (VPA) and Carbamazepine (CBZ) have limited therapeutic efficacy in ameliorating the epileptic syndromes of Atp1a2L809R/WT mice. Our work revealed that ATP1A2L809R variants cause a predisposition to epilepsy. Moreover, we provide a point variant mouse model for epilepsy research and drug screening.

PINK1-mediated Drp1S616 phosphorylation modulates synaptic development and plasticity via promoting mitochondrial fission.

Dynamic change of mitochondrial morphology and distribution along neuronal branches are essential for neural circuitry formation and synaptic efficacy. However, the underlying mechanism remains elusive. We show here that Pink1 knockout (KO) mice display defective dendritic spine maturation, reduced axonal synaptic vesicles, abnormal synaptic connection, and attenuated long-term synaptic potentiation (LTP). Drp1 activation via S616 phosphorylation rescues deficits of spine maturation in Pink1 KO neurons. Notably, mice harboring a knockin (KI) phosphor-null Drp1S616A recapitulate spine immaturity and synaptic abnormality identified in Pink1 KO mice. Chemical LTP (cLTP) induces Drp1S616 phosphorylation in a PINK1-dependent manner. Moreover, phosphor-mimetic Drp1S616D restores reduced dendritic spine localization of mitochondria in Pink1 KO neurons. Together, this study provides the first in vivo evidence of functional regulation of Drp1 by phosphorylation and suggests that PINK1-Drp1S616 phosphorylation coupling is essential for convergence between mitochondrial dynamics and neural circuitry formation and refinement.

Phenotypes, mechanisms and therapeutics: insights from bipolar disorder GWAS findings.

Genome-wide association studies (GWAS) have reported substantial genomic loci significantly associated with clinical risk of bipolar disorder (BD), and studies combining techniques of genetics, neuroscience, neuroimaging, and pharmacology are believed to help tackle clinical problems (e.g., identifying novel therapeutic targets). However, translating findings of psychiatric genetics into biological mechanisms underlying BD pathogenesis remains less successful. Biological impacts of majority of BD GWAS risk loci are obscure, and the involvement of many GWAS risk genes in this illness is yet to be investigated. It is thus necessary to review the progress of applying BD GWAS risk genes in the research and intervention of the disorder. A comprehensive literature search found that a number of such risk genes had been investigated in cellular or animal models, even before they were highlighted in BD GWAS. Intriguingly, manipulation of many BD risk genes (e.g., ANK3, CACNA1C, CACNA1B, HOMER1, KCNB1, MCHR1, NCAN, SHANK2 etc.) resulted in altered murine behaviors largely restoring BD clinical manifestations, including mania-like symptoms such as hyperactivity, anxiolytic-like behavior, as well as antidepressant-like behavior, and these abnormalities could be attenuated by mood stabilizers. In addition to recapitulating phenotypic characteristics of BD, some GWAS risk genes further provided clues for the neurobiology of this illness, such as aberrant activation and functional connectivity of brain areas in the limbic system, and modulated dendritic spine morphogenesis as well as synaptic plasticity and transmission. Therefore, BD GWAS risk genes are undoubtedly pivotal resources for modeling this illness, and might be translational therapeutic targets in the future clinical management of BD. We discuss both promising prospects and cautions in utilizing the bulk of useful resources generated by GWAS studies. Systematic integrations of findings from genetic and neuroscience studies are called for to promote our understanding and intervention of BD.

The impact of retro-cue validity on working memory representation: Evidence from electroencephalograms.

Visual working memory (VWM) performance can be improved by retrospectively cueing an item. The validity of retro-cues has an impact on the mechanisms underlying the retro-cue effect, but how non-cued representations are handled under different retro-cue validity conditions is not yet clear. Here, we used electroencephalograms to investigate whether retro-cue validity can affect the fate of non-cued representations in VWM. The participants were required to perform a change-detection task using a retro-cue with 80% or 20% validity. Contralateral delay activity and the lateralized alpha power were used to assess memory storage and selective attention, respectively. The retro-cue could redirect selective attention to the cued item under both validity conditions; however, the participants maintained the non-cued representations under the low-validity condition but dropped them from VWM under the high-validity condition. These results suggest that the maintenance of non-cued representations in VWM is affected by the expectation of cue validity and may be partially strategically driven.

Synaptic plasticity in schizophrenia pathophysiology.

Schizophrenia is a severe neuropsychiatric syndrome with psychotic behavioral abnormalities and marked cognitive deficits. It is widely accepted that genetic and environmental factors contribute to the onset of schizophrenia. However, the etiology and pathology of the disease remain largely unexplored. Recently, the synaptopathology and the dysregulated synaptic plasticity and function have emerging as intriguing and prominent biological mechanisms of schizophrenia pathogenesis. Synaptic plasticity is the ability of neurons to change the strength of their connections in response to internal or external stimuli, which is essential for brain development and function, learning and memory, and vast majority of behavior responses relevant to psychiatric diseases including schizophrenia. Here, we reviewed molecular and cellular mechanisms of the multiple forms synaptic plasticity, and the functional regulations of schizophrenia-risk factors including disease susceptible genes and environmental alterations on synaptic plasticity and animal behavior. Recent genome-wide association studies have provided fruitful findings of hundreds of risk gene variances associated with schizophrenia, thus further clarifying the role of these disease-risk genes in synaptic transmission and plasticity will be beneficial to advance our understanding of schizophrenia pathology, as well as the molecular mechanism of synaptic plasticity.