The Mediating Role of Cognitive Flexibility in the Influence of Counter-Stereotypes on Creativity

The aim of this study is to explore the relationship between counter-stereotypes and creativity, and further explore the mechanism underlying the impact of priming counter-stereotypic information on individual creativity. More importantly, here we have proposed cognitive and emotional dual processing pathways, which may mediate the influences of counter-stereotypes on creativity. Two experiments examined how counter-stereotypes impacted creativity through the dual processing pathways. A total of 152 university students were recruited to test their creativity performance. In Experiment 1, we replicated results of past studies. Participants were randomly allocated to different priming conditions (stereotype or counter-stereotype), in which descriptions of male governors and female nurses served as priming of stereotypes, whereas descriptions of male nurses and female governors served as priming of counter-stereotypes. Measurements of creativity were based on the poster paradigm. The poster paradigm required participants to design a poster for a college fellowship party. In Experiment 2, we recruited 104 participants to examine the mediating roles of emotions and cognitive flexibility. The procedure of Experiment 2 was similar to that of Experiment 1, except for the measurement of creativity, which was Chinese idiom riddle test. Participants who selected more creative answers were more creative, based on the criteria of our experimental design. Also, we included measurements of emotions (i.e., surprise and delight) and cognitive flexibility (using the Cognitive Flexibility Scale) after priming of stereotypes and counter-stereotypes in Experiment 2. We also verified the credibility of our counter-stereotype measurements. The results of Experiment 1—which replicated previous studies—demonstrated that priming of counter-stereotypes promoted creative performance compared with priming of stereotypes in the poster paradigm. However, our proposed dual processing pathways were not fully verified by Experiment 2. The results of this experiment showed that neither surprising nor delighted emotion mediated the influence of counter-stereotypes on creativity, whereas cognitive flexibility did. In conclusion, our current study reveals a mechanism of creative performance in terms of cognitive flexibility, and further inspires us to focus on the positive influence of counter-stereotypes on creativity

Coherent Fano resonances in a plasmonic nanocluster enhance optical four-wave mixing

Plasmonic nanoclusters, an ordered assembly of coupled metallic nanoparticles, support unique spectral features known as Fano resonances due to the coupling between their subradiant and superradiant plasmon modes. Within the Fano resonance, absorption is significantly enhanced, giving rise to highly localized, intense near fields with the potential to enhance nonlinear optical processes. Here, we report a structure supporting the coherent oscillation of two distinct Fano resonances within an individual plasmonic nanocluster. We show how this coherence enhances the optical four-wave mixing process in comparison with other doubleresonant plasmonic clusters that lack this property. A model that explains the observed four-wave mixing features is proposed, which is generally applicable to any third-order process in plasmonic nanostructures. With a larger effective susceptibility χ (3) relative to existing nonlinear optical materials, this coherent double-resonant nanocluster offers a strategy for designing high-performance thirdorder nonlinear optical media

PO-204 Effects of hypoxia and/or endurance exercise on autophagy of skeletal muscle in rats with nutritional obesity: There is no full text article associated whit this abstract

  Objective The globalization of obesity has become an important factor threatening human health, and the rational health of the solution has driven the exploration of experts and scholars. For this reason, this experiment uses hypoxia and exercise as interventions for 8 weeks. Changes of autophagy-related factors LC3 mRNA, p62 mRNA and energy regulation factor AMPKα2 mRNA, and cell stress-inducing factor Sestrin2 mRNA after hypoxia and/or combined endurance exercise, and explored the effect of hypoxia endurance exercise on autophagy of skeletal muscle cells To provide a reasonable experimental basis for exploring hypoxic exercise to lose weight and to prevent or reduce autophagy-related diseases. Methods  First, a nutritional obese rat model fed with high-fat diet for 8 weeks was constructed and randomly divided into 8 groups: the normoxia group (A), the normoxic group (AE), and 16.3%. Oxygen quiet group (B) and 16.3% hypoxic exercise group (BE), 13.3% hypoxic quiet group (C), 13.3% hypoxic exercise group (CE), 11.3% hypoxic quiet group (D), 11.3% low Oxygen exercise group (DE), 10 in each group, and continued to feed with high fat diet. Secondly, establish a hypoxic and/or endurance exercise model, and the experimental experiment is expected. The rat training program is as follows: the normoxia quiet group does not perform any endurance exercise and other interventions under normoxia; the normoxic exercise group is large. The rats underwent a medium-intensity endurance exercise with a running speed of 20 m/min in a normal oxygen environment for 40 min. Similarly, rats in the hypoxic quiet group underwent continuous hypoxia intervention for 12h in the corresponding hypoxic environment; the hypoxic-binding endurance exercise group was based on the intervention of the hypoxic-quiet group, with a time of 40 min and a running speed of 20 m/ Min's medium-intensity endurance exercise. The frequency of exercise is 5 times a week (every Monday to Friday) for 8 weeks. After the last training, fasting for 24 hours, the rats were sacrificed and sampled. Biochemical indicators were used to measure blood lipids and blood glucose concentration; real-time quantitative PCR was used to detect the expression of autophagy regulators Sestrin2, AMPKɑ2 and autophagy Beclin1 and LC3II mRNA. Results 1.Nutritional obesity rat model: After 8 weeks of high-fat feeding, the body weight, Lee's index, BG, TC, TG and LDL-c concentrations in the high-fat group were significantly increased (P<0.05) 2.Changes in morphology and blood lipids of rats: Compared with group A, the body weight, BG, TC, TG, LDL-c concentrations in the AE group were significantly decreased (P<0.05), and the HDL-c concentration was significantly increased (P<0.05). LDL-c in group D, TG and BD concentrations in group B, group C and group D were significantly decreased (P<0.05), and HDL-c concentrations in groups C and D were significantly increased (P<0.05); Compared with the group, the LDL-c and TG concentrations in the DE group were significantly lower (P<0.05), the BG concentrations in the CE group and the DE group were significantly lower (P<0.05), and the HDL-c concentration in the DE group was significantly increased (P<0.05). ). 3.Real-time quantitative PCR showed that compared with group A, the expression of Sestrin2, Beclin1 and LC3II mRNA in skeletal muscle cells of AE group, C group and D group was significantly increased (P<0.05), and the expression of AMPKɑ2 mRNA in group D was significantly increased. Compared with AE group, the expressions of Beclin1, LC3II and AMPKɑ2 mRNA in CE group and DE group were significantly increased (P<0.05), and the expression of Sestrin2 mRNA in DE group was significantly increased (P<0.05). Conclusions   1.Three different concentrations of hypoxia and / or combined endurance exercise can reduce the body weight of obese rats, improve the blood sugar, blood lipids, hypoxia and exercise in obese rats, the effect of weight loss, blood sugar and blood lipids is more obvious. 2.Endurance exercise, hypoxic exposure, hypoxia combined with endurance exercise can induce autophagy in skeletal muscle cells; and the cumulative stimulation effect of exercise and hypoxia is more prominent than simple endurance exercise and hypoxia exposure. 3.Three different concentrations of hypoxia and/or combined endurance exercise can up-regulate the expression of Sestrin2, AMPKɑ2, Beclin1, and LC3II mRNA, thereby effectively activating and enhancing the autophagy level of skeletal muscle cells in obese rats, especially 11.3% hypoxia. The endurance exercise group has a more pronounced effect

A phase I study of ridaforolimus in adult Chinese patients with advanced solid tumors

PURPOSE: Ridaforolimus (AP23573, MK-8669 or deforolimus) is an inhibitor of mammalian target of rapamycin (mTOR), an important regulator in the cell survival pathway. This open-label, single center phase I study aimed to investigate the pharmacokinetic (PK) and safety profiles of ridaforolimus in Chinese patients with treatment-refractory advanced or relapsed solid tumors. The PK data generated from these Chinese patients were further compared with those previously reported in Caucasian and Japanese patient populations. EXPERIMENTAL DESIGN: The patients were given an oral dose of 40 mg of ridaforolimus on Day 1 of the study. On Day 8, patients were initiated on a treatment regimen that comprised a once daily dose of 40 mg of ridaforolimus for five consecutive days, followed by a 2-day off-drug interval. Patients repeated this regimen until disease progression or intolerance. Blood samples were collected at specific times pre- and post-treatment to establish the PK profile of ridaforolimus in all patients. RESULTS: Fifteen patients were given at least one dose of 40 mg of ridaforolimus. The median absorption lag-time was 2 hours, the median T(max) was 4 hours and the mean elimination half-life was 53 hours. The accumulation ratio for AUC(0-24hr) was 1.3 on day 19 (steady state)/day 1 (after a single dose). The most common drug-related adverse events (AEs) that occurred in ≥40% of patients were stomatitis, proteinuria, leukopenia, hyperglycemia, and pyrexia. Grade 3/4 drug-related AEs were anemia, stomatitis, fatigue, thrombocytopenia, constipation, gamma glutamyltransferase increase, and proteinuria. All 11 evaluable patients achieved stable disease. CONCLUSIONS: Oral ridaforolimus at a daily dose of 40 mg were generally well tolerated in Chinese patients with advanced or refractory solid tumors. Adverse events and PK profiles of ridaforolimus in this study were similar to those from Caucasian and Japanese patients reported previously

Delineating the role of FANCA in glucose-stimulated insulin secretion in β cells through its protein interactome

Hyperinsulinemia affects 72% of Fanconi anemia (FA) patients and an additional 25% experience lowered glucose tolerance or frank diabetes. The underlying molecular mechanisms contributing to the dysfunction of FA pancreas β cells is unknown. Therefore, we sought to evaluate the functional role of FANCA, the most commonly mutated gene in FA, in glucosestimulated insulin secretion (GSIS). This study reveals that FANCA or FANCB knockdown impairs GSIS in human pancreas β cell line EndoC-βH3. To identify potential pathways by which FANCA might regulate GSIS, we employed a proteomics approach to identify FANCA protein interactions in EndoC-βH3 differentially regulated in response to elevated glucose levels. Glucose-dependent changes in the FANCA interaction network were observed, including increased association with other FA family proteins, suggesting an activation of the DNA damage response in response to elevated glucose levels. Reactive oxygen species increase in response to glucose stimulation and are necessary for GSIS in EndoC-βH3 cells. Glucose-induced activation of the DNA damage response was also observed as an increase in the DNA damage foci marker γ-H2AX and dependent upon the presence of reactive oxygen species. These results illuminate the role of FANCA in GSIS and its protein interactions regulated by glucose stimulation that may explain the prevalence of β cell-specific endocrinopathies in FA patients

Dcf1 Deficiency Attenuates the Role of Activated Microglia During Neuroinflammation

Microglia serve as the principal immune cells and play crucial roles in the central nervous system, responding to neuroinflammation via migration and the execution of phagocytosis. Dendritic cell-derived factor 1 (Dcf1) is known to play an important role in neural stem cell differentiation, glioma apoptosis, dendritic spine formation, and Alzheimer’s disease (AD), nevertheless, the involvement of the Dcf1 gene in the brain immune response has not yet been reported. In the present paper, the RNA-sequencing and function enrichment analysis suggested that the majority of the down-regulated genes in Dcf1-/- (Dcf1-KO) mice are immune-related. In vivo experiments showed that Dcf1 deletion produced profound effects on microglial function, increased the expression of microglial activation markers, such as ionized calcium binding adaptor molecule 1 (Iba1), Cluster of Differentiation 68 (CD68) and translocator protein (TSPO), as well as certain proinflammatory cytokines (Cxcl1, Ccl7, and IL17D), but decreased the migratory and phagocytic abilities of microglial cells, and reduced the expression levels of some other proinflammatory cytokines (Cox-2, IL-1β, IL-6, TNF-α, and Csf1) in the mouse hippocampus. Furthermore, in vitro experiments revealed that in the absence of lipopolysaccharide (LPS), the majority of microglia were ramified and existed in a resting state, with only approximately 10% of cells exhibiting an amoeboid-like morphology, indicative of an activated state. LPS treatment dramatically increased the ratio of activated to resting cells, and Dcf1 downregulation further increased this ratio. These data indicated that Dcf1 deletion mediates neuroinflammation and induces dysfunction of activated microglia, preventing migration and the execution of phagocytosis. These findings support further investigation into the biological mechanisms underlying microglia-related neuroinflammatory diseases, and the role of Dcf1 in the immune response

Study on pathological and clinical characteristics of chronic HBV infected patients with HBsAg positive, HBV DNA negative, HBeAg negative

AimsStudy of clinical characteristics of hepatitis B virus deoxyribonucleic acid (HBV DNA)-negative, hepatitis B surface antigen (HBsAg)-positive, hepatitis B e antigen (HBeAg)-negative patients based on liver histopathology.MethodsWe retrospectively enrolled patients with chronic HBV infection diagnosis at Beijing Ditan Hospital from May 2008 to November 2020. To study the differences between patients with significant hepatic histopathology and those without significant hepatic histopathology. And to study the independent factors of significant hepatic histopathology.Results85 HBV DNA-negative and HBeAg-negative patients were 37.90 ± 10.30 years old, 23.50% of patients with grade of inflammation (G) >1, 35.30% of patients with liver fibrosis stage (S) >1, 44.70% patients were diagnosed with significant hepatic histopathology. Compared to the no significant hepatic histopathology group, another group had older age (41.70 ± 10.70 vs 34.80 ± 8.87 years, t=-3.28, P=0.002), higher total bilirubin (TBIL) [14.9(10.3, 22.4) vs 11(8.9, 14.4) μmol/L, z=-2.26, P=0.024], lower cholinesterase (CHE) (t=-2.86, P=0.005, 7388.00 ± 2156.00 vs 8988.00 ± 2823.00 U/L) and lower platelet (PLT) (t=2.75, P=0.007, 157.00 ± 61.40 vs 194.00 ± 61.00 10^9/L). Abnormal ALT patients are more likely to have significant hepatic histopathology (z=5.44, P=0.020, 66.70% vs 337.50%). G had significant correlation with CHE (P=0.008, r=-0.23), alanine aminotransferase (ALT) (P=0.041, r=0.18), aspartate aminotransferase (AST) (P=0.001, r=0.29). S had significant correlation with TBIL (P = 0.008, r = 0.23), age (P < 0.001, r = 0.32), international normalized ratio (INR) (P = 0.04, r = 0.23), CHE (P < 0.001, r = -0.30), PLT (P < 0.001, r = -0.40) and prothrombin time activity (PTA) (P = 0.046, r = -0.22). Multivariate logistic analysis indicated only age (95%CI=1.014~1.130, OR=1.069, P=0.013) was an impact factor for significant hepatic histopathology. The cutoff point of age was 34.30 years.ConclusionsA large proportion of chronic HBV infection patients with HBeAg-negative and HBV DNA-negative still have chronic hepatitis. Age is an independent factor for significant hepatic histopatholog