Proline hydroxylation of CREB-regulated transcriptional coactivator 2 controls hepatic glucose metabolism.

Prolyl hydroxylase domain (PHD) enzymes change HIF activity according to oxygen signal; whether it is regulated by other physiological conditions remains largely unknown. Here, we report that PHD3 is induced by fasting and regulates hepatic gluconeogenesis through interaction and hydroxylation of CRTC2. Pro129 and Pro615 hydroxylation of CRTC2 following PHD3 activation is necessary for its association with cAMP-response element binding protein (CREB) and nuclear translocation, and enhanced binding to promoters of gluconeogenic genes by fasting or forskolin. CRTC2 hydroxylation-stimulated gluconeogenic gene expression is independent of SIK-mediated phosphorylation of CRTC2. Liver-specific knockout of PHD3 (PHD3 LKO) or prolyl hydroxylase-deficient knockin mice (PHD3 KI) show attenuated fasting gluconeogenic genes, glycemia, and hepatic capacity to produce glucose during fasting or fed with high-fat, high-sucrose diet. Importantly, Pro615 hydroxylation of CRTC2 by PHD3 is increased in livers of fasted mice, diet-induced insulin resistance or genetically obese ob/ob mice, and humans with diabetes. These findings increase our understanding of molecular mechanisms linking protein hydroxylation to gluconeogenesis and may offer therapeutic potential for treating excessive gluconeogenesis, hyperglycemia, and type 2 diabetes.

Intrahepatic osteopontin signaling by CREBZF defines a checkpoint for steatosis-to-NASH progression.

BACKGROUND AND AIMS: NASH has emerged as a leading cause of chronic liver disease. However, the mechanisms that govern NASH fibrosis remain largely unknown. CREBZF is a CREB/ATF bZIP transcription factor that causes hepatic steatosis and metabolic defects in obesity. APPROACH AND RESULTS: Here, we show that CREBZF is a key mechanism of liver fibrosis checkpoint that promotes hepatocyte injury and exacerbates diet-induced NASH in mice. CREBZF deficiency attenuated liver injury, fibrosis, and inflammation in diet-induced mouse models of NASH. CREBZF increases HSC activation and fibrosis in a hepatocyte-autonomous manner by stimulating an extracellular matrix protein osteopontin, a key regulator of fibrosis. The inhibition of miR-6964-3p mediates CREBZF-induced production and secretion of osteopontin in hepatocytes. Adeno-associated virus -mediated rescue of osteopontin restored HSC activation, liver fibrosis, and NASH progression in CREBZF-deficient mice. Importantly, expression levels of CREBZF are increased in livers of diet-induced NASH mouse models and humans with NASH. CONCLUSIONS: Osteopontin signaling by CREBZF represents a previously unrecognized intrahepatic mechanism that triggers liver fibrosis and contributes to the severity of NASH.

Registered report "Categorical perception of facial expressions of anger and disgust across cultures".

Previous research has demonstrated that individuals from Western cultures exhibit categorical perception (CP) in their judgments of emotional faces. However, the extent to which this phenomenon characterises the judgments of facial expressions among East Asians remains relatively unexplored. Building upon recent findings showing that East Asians are more likely than Westerners to see a mixture of emotions in facial expressions of anger and disgust, the present research aimed to investigate whether East Asians also display CP for angry and disgusted faces. To address this question, participants from Canada and China were recruited to discriminate pairs of faces along the anger-disgust continuum. The results revealed the presence of CP in both cultural groups, as participants consistently exhibited higher accuracy and faster response latencies when discriminating between-category pairs of expressions compared to within-category pairs. Moreover, the magnitude of CP did not vary significantly across cultures. These findings provide novel evidence supporting the existence of CP for facial expressions in both East Asian and Western cultures, suggesting that CP is a perceptual phenomenon that transcends cultural boundaries. This research contributes to the growing literature on cross-cultural perceptions of facial expressions by deepening our understanding of how facial expressions are perceived categorically across cultures.

Salt-Induced Hepatic Inflammatory Memory Contributes to Cardiovascular Damage Through Epigenetic Modulation of SIRT3.

BACKGROUND: High salt intake is the leading dietary risk factor for cardiovascular diseases. Although clinical evidence suggests that high salt intake is associated with nonalcoholic fatty liver disease, which is an independent risk factor for cardiovascular diseases, it remains elusive whether salt-induced hepatic damage leads to the development of cardiovascular diseases. METHODS: Mice were fed with normal or high-salt diet for 8 weeks to determine the effect of salt loading on liver histological changes and blood pressure, and salt withdrawal and metformin treatment were also conducted on some high-salt diet-fed mice. Adeno-associated virus 8, global knockout, or tissue-specific knockout mice were used to manipulate the expression of some target genes in vivo, including SIRT3 (sirtuin 3), NRF2 (NF-E2-related factor 2), and AMPK (AMP-activated protein kinase). RESULTS: Mice fed with a high-salt diet displayed obvious hepatic steatosis and inflammation, accompanied with hypertension and cardiac dysfunction. All these pathological changes persisted after salt withdrawal, displaying a memory phenomenon. Gene expression analysis and phenotypes of SIRT3 knockout mice revealed that reduced expression of SIRT3 was a chief culprit responsible for the persistent inflammation in the liver, and recovering SIRT3 expression in the liver effectively inhibits the sustained hepatic inflammation and cardiovascular damage. Mechanistical studies reveal that high salt increases acetylated histone 3 lysine 27 (H3K27ac) on SIRT3 promoter in hepatocytes, thus inhibiting the binding of NRF2, and results in the sustained inhibition of SIRT3 expression. Treatment with metformin activated AMPK, which inhibited salt-induced hepatic inflammatory memory and cardiovascular damage by lowering the H3K27ac level on SIRT3 promoter, and increased NRF2 binding ability to activate SIRT3 expression. CONCLUSIONS: This study demonstrates that SIRT3 inhibition caused by histone modification is the key factor for the persistent hepatic steatosis and inflammation that contributes to cardiovascular damage under high salt loading. Avoidance of excessive salt intake and active intervention of epigenetic modification may help to stave off the persistent inflammatory status that underlies high-salt-induced cardiovascular damage in clinical practice.

Molecular insight of p53/Sp1/MUC5AC axis in the tumorigenesis and progression of lung adenocarcinoma.

The aberrant expression of secretory mucin MUC5AC has been documented during the tumourigenesis and progression of various cancers. However, little is currently known on the function of MUC5AC in lung adenocarcinoma. The present study focused on the tumour-promoting role of MUC5AC and its regulatory mechanisms in lung adenocarcinoma. Firstly, MUC5AC expression was evaluated in NSCLC tissue microarrays by immunohistochemistry. Kaplan-Meier analysis were used to clarify the prognostic value of MUC5AC. Subsequently, small interfering RNA and small hairpin RNA were used to knockdown MUC5AC in lung ADC cell lines to elucidate its role in tumorigenesis and progression of lung adenocarcinoma via in vitro functional assays and xenograft mouse models. Finally, the regulatory mechanisms underlying p53/Sp1/MUC5AC axis were identified through dual-luciferase report. We found that MUC5AC was upregulated in lung ADC tissues and cell lines, especially in KRAS-mutant cases and correlated with poor prognosis. MUC5AC gene silencing resulted in reduced cell proliferation, invasion and migration. Furthermore, knockdown of MUC5AC led to reversion of the epithelial-mesenchymal transition. Additionally, downregulation of MUC5AC reduced tumourigenesis in mouse models. Finally, we found an antagonistic role between Sp1 and p53 in the regulation of MUC5AC gene expression. Our findings suggest that high MUC5AC expression promotes tumourigenesis and progression of lung ADC. Both p53 gene inactivation and Sp1 overexpression in lung ADC may enhance MUC5AC expression, especially in KRAS-mutated cases. Given the paucity of efficient drug-targeted approaches of KRAS-driven lung ADCs, therapies directed at downstream effectors such as MUC5AC could have huge prospects.

What music makes us feel: At least 13 dimensions organize subjective experiences associated with music across different cultures.

What is the nature of the feelings evoked by music? We investigated how people represent the subjective experiences associated with Western and Chinese music and the form in which these representational processes are preserved across different cultural groups. US (n = 1,591) and Chinese (n = 1,258) participants listened to 2,168 music samples and reported on the specific feelings (e.g., "angry," "dreamy") or broad affective features (e.g., valence, arousal) that they made individuals feel. Using large-scale statistical tools, we uncovered 13 distinct types of subjective experience associated with music in both cultures. Specific feelings such as "triumphant" were better preserved across the 2 cultures than levels of valence and arousal, contrasting with theoretical claims that valence and arousal are building blocks of subjective experience. This held true even for music selected on the basis of its valence and arousal levels and for traditional Chinese music. Furthermore, the feelings associated with music were found to occupy continuous gradients, contradicting discrete emotion theories. Our findings, visualized within an interactive map (https://www.ocf.berkeley.edu/∼acowen/music.html) reveal a complex, high-dimensional space of subjective experience associated with music in multiple cultures. These findings can inform inquiries ranging from the etiology of affective disorders to the neurological basis of emotion.

Circulating chemerin levels in metabolic-associated fatty liver disease: a systematic review and meta-analysis.

BACKGROUND AND OBJECTIVES: Chemerin is a brand-new adipokine that has been linked to both inflammation and metabolic dysfunction. Even though a rising number of studies have connected chemerin to metabolic-associated fatty liver disease (MAFLD), formerly referred to as non-alcoholic fatty liver disease (NAFLD), this association has been controversial. METHODS: A comprehensive literature search was undertaken up to February 1, 2022, in the PubMed, Embase, Web of Science, CNKI, WANFANG, and CBM library databases. Circulating chemerin levels were obtained and summarized using the standardized mean difference (SMD) and 95% confidence interval (CI). Subgroup and meta-regression analyses were conducted to examine the possibility of heterogeneity. RESULTS: A total of 17 studies involving 2580 participants (1584 MAFLD patients and 996 controls) evaluated circulating chemerin levels in patients with MAFLD. The present study showed that higher chemerin levels were found in patients with MAFLD (SMD: 1.32; 95% CI: 0.29, 2.35) and nonalcoholic fatty liver (NAFL) (SMD: 0.75; 95% CI: 0.01, 1.50) compared to controls. However, circulating chemerin levels did not differ significantly in the following comparisons: nonalcoholic steatohepatitis (NASH) patients and controls (SMD: 0.75; 95% CI: -0.52, 2.03); NASH patients and NAFL patients (SMD: 0.16; 95% CI: -0.39, 0.70); moderate to severe steatosis and mild steatosis (SMD: 0.55; 95% CI: -0.59, 1.69); present liver fibrosis and absent liver fibrosis (SMD: 0.66; 95% CI: -0.42, 1.74); present lobular inflammation and absent lobular inflammation (SMD: 0.45; 95% CI: -0.53, 1.42); and present portal inflammation and absent portal inflammation (SMD: 1.92; 95% CI: -0.85, 4.69). CONCLUSIONS: Chemerin levels were considerably greater in patients with MAFLD than in controls, despite the fact that they were not significantly linked to different liver tissue lesions of MAFLD. In different subtypes of MAFLD, in comparison to healthy controls, the chemerin levels of NAFL patients were higher, whereas, there was no obvious difference in chemerin levels between NASH patients and controls. It is possible that chemerin will be used as a biomarker in the future to track the development and progression of MAFLD.

A potential model of systemic sclerosis with pulmonary hypertension induced by monocrotaline plus bleomycin.

OBJECTIVE: The lack of a well-established animal model limits the clarification of the detailed mechanisms of the pathogenesis of systemic sclerosis with pulmonary hypertension (SSc-PH) and the development of effective treatments for it. METHODS: In this study, New Zealand rabbits were injected with monocrotaline (MCT), bleomycin (BLM), and MCT plus BLM, respectively. Three and six weeks after the first injection, the mean pulmonary artery pressure (mPAP) was measured. Skin and lung samples were isolated and the histological changes were analyzed by hematoxylin and eosin staining or Masson's trichrome staining. RESULTS: All groups of rabbits showed an increased mean mPAP compared with the saline-injected rabbits. The high mPAP persisted until week six only in the MCT and MCT + BLM groups. Furthermore, persistent high Fulton's indices were found in the MCT and MCT + BLM groups, indicating that these treatments successfully induced right ventricular hypertrophy. The rabbits in the MCT + BLM group developed severe lung inflammation, as evidenced by a high level of neutrophil infiltration in the pulmonary interstitium. Importantly, pathological changes of the skin in the MCT + BLM group were observed, and further damage to the skin was caused by additional exposure to MCT plus BLM. Meanwhile, an excessive production of cytokines, including tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1 (TGF-ß1), were detected in the MCT + BLM group. CONCLUSION: These data indicate that SSc-PH induced by co-injection with MCT plus BLM shows persistent fibrosis and progressive PH, constituting a potential study model for SSc-PH.

Low serum Maresin-1 levels are associated with non-alcoholic fatty liver disease: a cross-sectional study.

BACKGROUND: Maresin-1 (MaR1) is an anti-inflammatory pro-resolving mediator and is considered a potential regulator of metabolic diseases. Non-alcoholic fatty liver disease (NAFLD) is a very common metabolic liver disease. However, little information is available on the relationship between MaR1 and NAFLD in humans. Therefore, the study explored the association between serum MaR1 levels and NAFLD. METHODS: A cross-sectional study was conducted in 240 Chinese people, including 116 non-NAFLD subjects and 124 NAFLD patients. Serum MaR1 levels were determined by enzyme-linked immunosorbent assay (ELISA). The association between MaR1 and NAFLD was assessed. RESULTS: Circulating MaR1 levels in NAFLD patients were markedly lower than those in non-NAFLD subjects (63.63 [59.87-73.93] vs 73.11 [65.12-84.50] pg/mL, P = 0.000). The percentages of patients with NAFLD gradually decreased with the increase of MaR1 quartiles (P < 0.001). Furthermore, serum MaR1 levels were positively associated with aspartate aminotransferase/alanine aminotransferase (AST/ALT), albumin, the albumin-globulin-ratio, and high-density lipoprotein cholesterol (HDL-C) (all P < 0.05) and negatively associated with body mass index (BMI), waist circumference, hip circumference, the waist-to-hip ratio, ALT, gamma-glutamyl transpeptidase (GGT), uric acid, triglyceride (TG), and fasting blood glucose (FBG) (all P < 0.05) after adjusting for sex and age. Binary logistic regression analysis revealed that serum MaR1 levels were significantly associated with NAFLD. CONCLUSIONS: Circulating MaR1 levels were decreased in patients with NAFLD, and a negative correlation was identified between NAFLD and serum MaR1 concentrations. Decreased MaR1 might be involved in the development of NAFLD.

One-step synthesis of golf ball-like thiol-functionalized silica particles.

There is increasing interest in the synthesis of golf ball-like particles. Most of the reports on golf ball-like particles have focused on polymer particles, while relatively few are concerned with inorganic particles. In this work, golf ball-like thiol-functionalized silica particles were synthesized for the first time by a one-step sol-gel reaction using 3-mercaptopropyl trimethoxysilane (MPTMS) and tetraethoxysilane (TEOS) as the precursors. The particle growth with time was monitored by SEM and a particle formation mechanism was proposed. The effects of different reaction parameters including the TEOS/MPTMS molar ratio, the NH4OH concentration, and the stirring rate on the morphology and size of the golf ball-like organosilica particles were studied. Given that the thiol groups have versatile functionalities, golf ball-like thiol-functionalized silica particle is a useful model for academic studies.

HIMF (Hypoxia-Induced Mitogenic Factor) Signaling Mediates the HMGB1 (High Mobility Group Box 1)-Dependent Endothelial and Smooth Muscle Cell Crosstalk in Pulmonary Hypertension.

OBJECTIVE: HIMF (hypoxia-induced mitogenic factor; also known as FIZZ1 [found in inflammatory zone-1] or RELM [resistin-like molecule-α]) is an etiological factor of pulmonary hypertension (PH) in rodents, but its underlying mechanism is unclear. We investigated the immunomodulatory properties of HIMF signaling in PH pathogenesis. Approach and Results: Gene-modified mice that lacked HIMF (KO [knockout]) or overexpressed HIMF human homolog resistin (hResistin) were used for in vivo experiments. The pro-PH role of HIMF was verified in HIMF-KO mice exposed to chronic hypoxia or sugen/hypoxia. Mechanistically, HIMF/hResistin activation triggered the HMGB1 (high mobility group box 1) pathway and RAGE (receptor for advanced glycation end products) in pulmonary endothelial cells (ECs) of hypoxic mouse lungs in vivo and in human pulmonary microvascular ECs in vitro. Treatment with conditioned medium from hResistin-stimulated human pulmonary microvascular ECs induced an autophagic response, BMPR2 (bone morphogenetic protein receptor 2) defects, and subsequent apoptosis-resistant proliferation in human pulmonary artery (vascular) smooth muscle cells in an HMGB1-dependent manner. These effects were confirmed in ECs and smooth muscle cells isolated from pulmonary arteries of patients with idiopathic PH. HIMF/HMGB1/RAGE-mediated autophagy and BMPR2 impairment were also observed in pulmonary artery (vascular) smooth muscle cells of hypoxic mice, effects perhaps related to FoxO1 (forkhead box O1) dampening by HIMF. Experiments in EC-specific hResistin-overexpressing transgenic mice confirmed that EC-derived HMGB1 mediated the hResistin-driven pulmonary vascular remodeling and PH. CONCLUSIONS: In HIMF-induced PH, HMGB1-RAGE signaling is pivotal for mediating EC-smooth muscle cell crosstalk. The humanized mouse data further support clinical implications for the HIMF/HMGB1 signaling axis and indicate that hResistin and its downstream pathway may constitute targets for the development of novel anti-PH therapeutics in humans.

High Expression Levels of Long Noncoding RNA Small Nucleolar RNA Host Gene 18 and Semaphorin 5A Indicate Poor Prognosis in Multiple Myeloma.

BACKGROUND: The aim of this study was to detect the expression of long noncoding RNA small nucleolar RNA host gene 18 (SNHG18) andsemaphorin 5A (SEMA5A) genes in multiple myeloma (MM) patients and to explore the correlation of the expression of these genes with the clinical characteristics and prognosis of MM patients. METHODS: Forty-seven newly diagnosed MM, 18 complete remission MM, 13 refractory/relapse MM, and 22 iron deficiency anemia (serving as control) samples were extracted at the Department of Hematology, Second Affiliated Hospital of Xian Jiaotong University between January 2015 and December 2016. The clinical features of the MM patients are summarized. Real-time quantitative PCR was performed to analyze the relative expression levels of the SNHG18 and SEMA5Agenes. The clinical characteristics and overall survival (OS) of the MM patients were statistically analyzed while measuring different levels of SNHG18 and SEMA5Agene expression. At the same time, the correlation between the expression of SNHG18 and SEMA5A was also analyzed. RESULTS: The analysis confirmed that SNHG18 and its possible target gene SEMA5A were both highly expressed in newly diagnosed MM patients. After analyzing the clinical significance of SNHG18 and SEMA5A in MM patients, we found that the expression of SNHG18 and SEMA5A was related to the Durie-Salmon (DS), International Staging System (ISS), and Revised International Staging System (R-ISS) classification systems, and the Mayo Clinic Risk Stratification for Multiple Myeloma (mSMART; p < 0.05). Moreover, we observed a significant difference in OS between the SNHG18/SEMA5A high expression group and the low expression group. We found a positive correlation between SNHG18 and SEMA5A expression (r = 0.709, p < 0.01). Surprisingly, the expected median OS times of both the SNHG18 and SEMA5Ahigh expression groups were significantly decreased, which was in contrast to those of both the SNHG18 and SEMA5Alow expression groups and the single-gene high expression group (p < 0.05). CONCLUSION: High expression of both SNHG18 and SEMA5A is associated with poor prognosis in patients with MM.

A Double-Branch Surface Detection System for Armatures in Vibration Motors with Miniature Volume Based on ResNet-101 and FPN.

In this paper, a complete system based on computer vision and deep learning is proposed for surface inspection of the armatures in a vibration motor with miniature volume. A device for imaging and positioning was designed in order to obtain the images of the surface of the armatures. The images obtained by the device were divided into a training set and a test set. With continuous experimental exploration and improvement, the most efficient deep-network model was designed. The results show that the model leads to high accuracy on both the training set and the test set. In addition, we proposed a training method to make the network designed by us perform better. To guarantee the quality of the motor, a double-branch discrimination mechanism was also proposed. In order to verify the reliability of the system, experimental verification was conducted on the production line, and a satisfactory discrimination performance was reached. The results indicate that the proposed detection system for the armatures based on computer vision and deep learning is stable and reliable for armature production lines.

An Industrial Micro-Defect Diagnosis System via Intelligent Segmentation Region.

In the field of machine vision defect detection for a micro workpiece, it is very important to make the neural network realize the integrity of the mask in analyte segmentation regions. In the process of the recognition of small workpieces, fatal defects are always contained in borderline areas that are difficult to demarcate. The non-maximum suppression (NMS) of intersection over union (IOU) will lose crucial texture information especially in the clutter and occlusion detection areas. In this paper, simple linear iterative clustering (SLIC) is used to augment the mask as well as calibrate the score of the mask. We propose an SLIC head of object instance segmentation in proposal regions (Mask R-CNN) containing a network block to learn the quality of the predict masks. It is found that parallel K-means in the limited region mechanism in the SLIC head improved the confidence of the mask score, in the context of our workpiece. A continuous fine-tune mechanism was utilized to continuously improve the model robustness in a large-scale production line. We established a detection system, which included an optical fiber locator, telecentric lens system, matrix stereoscopic light, a rotating platform, and a neural network with an SLIC head. The accuracy of defect detection is effectively improved for micro workpieces with clutter and borderline areas.

High Circulating Alarin Levels Are Associated with Presence of Metabolic Syndrome.

BACKGROUND/AIMS: Alarin has been reported to be related with increased food intake and body weight. The relationship of circulating Alarin with insulin resistance or metabolic syndrome (MetS), however, is unknown. This study aimed to investigate the physiological role of Alarin and its association with MetS in humans. METHODS: Newly diagnosed MetS patients (n=237) and age-matched healthy subjects (n=192) were recruited for this study. Oral glucose tolerance test, treadmill exercise, lipid infusions and euglycemic-hyperinsulinemic clamp (EHCs) were performed. Circulating Alarin and TNFα levels were measured by ELISA. RESULTS: Circulating Alarin levels were significantly higher in MetS patients compared with healthy subjects (0.46 ± 0.22 vs. 0.41 ± 0.14 µg/L, P < 0.01). In all studied subjects, circulating Alarin levels were positively correlated with WC, blood pressure, FBG, triglyceride, HbA1c, HOMA-IR, AUCglucose, and TNFα (P < 0.05 or P < 0.01). Multivariate logistic regression analyses revealed that circulating Alarin levels were correlated with MetS and insulin resistance. There was no significant change of circulating Alarin levels in the subjects with treadmill exercise for 45 min. In healthy individuals, however, glucose challenge, acute hyperglycemia and lipid infusions resulted in increased circulating Alarin levels, while acute hyperinsulinaemia transiently decreased circulating Alarin levels. CONCLUSION: The present study provides the evidence that circulating Alarin levels are associated with MetS and insulin resistance.

Synthesis of Acyl Azides from 1,3-Diketones via Oxidative Cleavage of Two C-C Bonds.

A metal-free PhI(OAc)2-mediated method for the synthesis of acyl azides through oxidative cleavage of 1,3-diketones is described. This method is shown to have a broad substrate scope, providing a useful tool for multiproduct synthesis in a single procedure. A possible reaction pathway is proposed based on mechanistic studies.

Comparison of combined anterior-posterior approach versus posterior-only approach in neuromuscular scoliosis: a systematic review and meta-analysis.

PURPOSE: Neuromuscular scoliosis (NS) is a complicated spinal disorder, and it could be treated through posterior-only approach (POA) or combined anterior-posterior approach (APA), which one is better and how to choose the surgical tactic is still in controversy. So comparing POA with APA parameters in the treatment of NS is meaningful. METHODS: Database of PubMed, Embase and Cochrane Library was systematically searched, and the studies, which focus on the comparisons of POA and APA in the treatment of NS, were included. The meta-analysis was performed by RevMan 5.3. RESULTS: Seven retrospective studies with 602 patients were included in meta-analysis. In previous analysis, statistically significant differences were observed in the major parameters between APA and POA. However, the results of subgroup meta-analysis, which focused on the correction angle and loss angle to eliminate the influence of different preoperative angles, were tend to no difference between two groups, except loss angle of scoliosis (MD, 6.4; 95% CI - 0.19 to 13) and correction angle of pelvic obliquity (MD, - 3.44; 95% CI - 6.71 to - 0.17). CONCLUSIONS: Our meta-analysis suggested that POA was similar to APA in the correction of scoliosis in coronal and sagittal planes. However, APA had advantages in the correction of pelvic obliquity and decreasing the loss of angle between postoperation and follow-up in main scoliosis, whereas POA had advantages in operative time, blood loss, duration of hospital stay and complications. LEVEL OF EVIDENCE: Level II. These slides can be retrieved under Electronic Supplementary Material.

Person perception from changing emotional expressions: primacy, recency, or averaging effect?

Dynamic changes in emotional expressions are a valuable source of information in social interactions. As the expressive behaviour of a person changes, the inferences drawn from the behaviour may also change. Here, we test the possibility that dynamic changes in emotional expressions affect person perception in terms of stable trait attributions. Across three experiments, we examined perceivers' inferences about others' personality traits from changing emotional expressions. Expressions changed from one emotion ("start emotion") to another emotion ("end emotion"), allowing us to disentangle potential primacy, recency, and averaging effects. Drawing on three influential models of person perception, we examined perceptions of dominance and affiliation (Experiment 1a), competence and warmth (Experiment 1b), and dominance and trustworthiness (Experiment 2). A strong recency effect was consistently found across all trait judgments, that is, the end emotion of dynamic expressions had a strong impact on trait ratings. Evidence for a primacy effect was also observed (i.e. the information of start emotions was integrated), but less pronounced, and only for trait ratings relating to affiliation, warmth, and trustworthiness. Taken together, these findings suggest that, when making trait judgements about others, observers weigh the most recently displayed emotion in dynamic expressions more heavily than the preceding emotion.

Seeing Mixed Emotions: The Specificity of Emotion Perception From Static and Dynamic Facial Expressions Across Cultures.

Although perceivers often agree about the primary emotion that is conveyed by a particular expression, observers may concurrently perceive several additional emotions from a given facial expression. In the present research, we compared the perception of two types of nonintended emotions in Chinese and Dutch observers viewing facial expressions: emotions which were morphologically similar to the intended emotion and emotions which were morphologically dissimilar to the intended emotion. Findings were consistent across two studies and showed that (a) morphologically similar emotions were endorsed to a greater extent than dissimilar emotions and (b) Chinese observers endorsed nonintended emotions more than did Dutch observers. Furthermore, the difference between Chinese and Dutch observers was more pronounced for the endorsement of morphologically similar emotions than of dissimilar emotions. We also obtained consistent evidence that Dutch observers endorsed nonintended emotions that were congruent with the preceding expressions to a greater degree. These findings suggest that culture and morphological similarity both influence the extent to which perceivers see several emotions in a facial expression.

CD244 maintains the proliferation ability of leukemia initiating cells through SHP-2/p27kip1 signaling.

Targeting leukemia initiating cells is considered to be an effective way to cure leukemia, for which it is critical to identify novel therapeutic targets. Herein, we demonstrate that CD244, which was initially reported as a key regulator for natural killer cells, is highly expressed on both mouse and human leukemia initiating cells. Upon CD244 knockdown, human leukemia cell lines and primary leukemia cells have markedly impaired proliferation abilities both in vitro and in vivo Interestingly, the repopulation ability of both mouse and human hematopoietic stem cells is not impaired upon CD244 knockdown. Using an MLL-AF9-induced murine acute myeloid leukemia model, we show that leukemogenesis is dramatically delayed upon CD244 deletion, together with remarkably reduced Mac1+/c-Kit+ leukemia cells (enriched for leukemia initiating cells). Mechanistically, we reveal that CD244 is associated with c-Kit and p27 except for SHP-2 as previously reported. CD244 co-operates with c-Kit to activate SHP-2 signaling to dephosphorylate p27 and maintain its stability to promote leukemia development. Collectively, we provide intriguing evidence that the surface immune molecule CD244 plays an important role in the maintenance of stemness of leukemia initiating cells, but not in hematopoietic stem cells. CD244 may represent a novel therapeutic target for the treatment of acute myeloid leukemia.