Construction and Validation of the Postgraduate Research Innovation Ability Scale (PRIAS): A Three-Dimensional Structural Model Based on Componential Theory of Creativity.

Purpose: To explore the structure of postgraduate research innovation ability and verify the Postgraduate Research Innovation Ability Scale. Patients and Methods: This study was based on the componential theory of creativity. First, we drafted an item pool from the literature review, semi-structured interviews, and group discussions. A total of 125 postgraduates were selected for the pre-test. After item selection and exploratory factor analysis, an 11-item, 3-factor postgraduate research innovation ability scale was formed. The scale was applied to a sample of 330 postgraduates from various domestic universities. Exploratory factor analysis and confirmatory factor analysis were used to examine the factor structure of the scales. Results: The results support a three-factor model including creativity-relevant processes, domain-relevant skills, and intrinsic motivation for the Postgraduate Research Innovation Ability Scale. The scale showed good internal consistency (α =0.89) and test-retest reliability (r=0.86). Exploratory factor analysis showed that the KMO value was 0.87, and the Bartlett's sphericity test results were significant. Confirmatory factor analysis confirmed that the three-factor construct demonstrated a good model fit (χ2/df=1.945, GFI=0.916, CFI=0.950, RMSEA=0.076). Conclusion: The Postgraduate Research Innovation Ability Scale has good reliability and validity, and it can be used for future research in related fields.

Self-Handicapping in Chinese Medical Students During the COVID-19 Pandemic: The Role of Academic Anxiety, Procrastination and Hardiness.

Background: In the face of the 2019 Coronavirus Disease (COVID-19) outbreak, Chinese medical students worried about their future studies which might make them more susceptible to academic anxiety. Previous studies have shown that academic anxiety is an important risk factor for self-handicapping, but there are few studies to explore the relationship between the two which may be mediated or moderated by other variables. Therefore, this study investigated how Chinese medical students' academic anxiety is correlated to their self-handicapping in time of COVID-19 epidemic, and explored the moderating and mediating effects of hardiness and procrastination. Methods: In this study, 320 Chinese medical students' psychological traits were measured with Academic Anxiety Questionnaire, Self-Handicapping Scale, General Procrastination Scale and Hardiness Scale to explore the potential associations between these variables. Results: The most obvious finding to emerge from this study was that self- handicapping had a positive correlation with academic anxiety and procrastination, but had a negative correlation with hardiness; hardiness had a negative association with academic anxiety and procrastination; and academic anxiety and procrastination were positively correlated. In addition, the relationship between academic anxiety and self-handicapping of Chinese medical students was not only partially mediated by procrastination, but also moderated by hardiness. Furthermore, medical students who had lower hardiness had stronger direct effect, while the indirect effect was strong at high and low conditions of hardiness. Conclusion: In time of the COVID-19 epidemic, the academic anxiety and self-handicapping of medical students are influenced by procrastination and hardiness to a great extent. Thus, in addition to suggesting that more attention should be paid to the academic anxiety and procrastination of medical students, in the future, more attention should be paid to cultivating the hardiness of medical students and exerting its interventional role in self-handicapping.

Synapse-associated protein 90/postsynaptic density-95-associated protein (SAPAP) is expressed differentially in phencyclidine-treated rats and is increased in the nucleus accumbens of patients with schizophrenia.

Phencyclidine (PCP) induces a psychotomimetic state that closely resembles schizophrenia. Therefore, PCP-treated animals can provide a model for schizophrenia. Using differential display, we identified a gene regulated by the delayed action of PCP in rat nucleus accumbens (NAcs). Sequence analysis showed that the cDNA clone obtained was identical to rat synapse-associated protein 90/postsynaptic density-95-associated protein 1 (SAPAP1). Quantitative reverse transcriptase (RT)-PCR analysis showed that SAPAP1 mRNA had increased significantly in rat NAc (P<0.0001) and hippocampus (P<0.01) 24 h after a PCP (10 mg/kg) injection as compared to the controls. Immunoquantification using an anti-SAPAP1 antibody indicated that immunoreactivity for SAPAP1 increased significantly (P&<0.05) in the NAcs of unmedicated patients with schizophrenia, as compared to the control subjects and medicated patients with schizophrenia. Our findings support the hypothesis that there is abnormal glutamatergic neurotransmission in schizophrenia and show evidence of abnormalities in the intracellular signal transduction via N-methyl-D-aspartate (NMDA) receptors.

Decreased calcineurin and increased phosphothreonine-DARPP-32 in the striatum of rats behaviorally sensitized to methamphetamine.

We investigated changes in signal transduction via calcineurin (CaN) in the striatum of rats behaviorally sensitized to methamphetamine (Meth). The rats were injected with Meth (4 mg/kg, s.c.) five times a week for 3 weeks and then were given a challenge dose of Meth (2 mg/kg, s.c.). Seven days after the challenge test, we determined the levels of CaN Aalpha and Abeta by Western blotting. We further immunoquantified DARPP-32 (dopamine- and cAMP-regulated phosphoprotein, mw 32,000) and phosphothreonine-DARPP-32, which can be dephosphorylated at threonine sites by CaN. We found that both CaN Aalpha and Abeta were significantly decreased in the particulate fractions but were not changed in the soluble fractions from the striatum of Meth-sensitized rats as compared with control rats. The same findings were observed in the striatum of rats 6 h after the injection of PCP (10 mg/kg, s.c.). In the striatum of Meth-sensitized rats, phosphothreonine-DARPP-32 immunoreactivities significantly increased, but DARPP-32 immunoreactivities were not significantly different from those of the control rats. These results indicate that the activity of signal transduction via CaN is functionally decreased in the striatum of Meth-sensitized rats.

Differential changes in glutamatergic transmission via N-methyl-D-aspartate receptors in the hippocampus and striatum of rats behaviourally sensitized to methamphetamine.

We searched for changes in glutamatergic transmission via N-methyl-D-aspartate (NMDA) receptors in the hippocampus and striatum of rats behaviourally sensitized to methamphetamine (Meth). Prior to being given a challenge dose of Meth (2 mg/kg, s.c.), the rats were given Meth (4 mg/kg, s.c.) five times a week for 3 wk. Seven days after the challenge test, we examined glutamate (Glu) release from hippocampal and striatal slices evoked by 30 mm KCl, and NMDA-evoked dopamine (DA) release from striatal slices. We further immunoquantified NMDAR1, R2A and R2B receptors as well as the fodrin alpha-subunit, a 240 kDa cytoskeletal protein that is cleaved to form 150 kDa limited proteolytic fragments by NMDA receptor stimulation. In the study of KCl-evoked Glu release, Glu release from the hippocampus was 31% lower in the Meth-sensitized rats than in the control rats, while Glu release from the striatum was 34% higher in the Meth-sensitized rats. NMDAR1, R2A and R2B immunoreactivities in the striatum were significantly lower in the Meth-sensitized rats (by 12, 13 and 12%, respectively) than those in the control rats. However, no differences in the immunoreactivities were found for the hippocampus. Immunoquantification of the fodrin alpha-subunit in the hippocampus revealed that 150 kDa fragments were significantly lower (by 10%) in the Meth-sensitized rats than in the control rats. In contrast to the control rats, NMDA-evoked DA release from the striatum was diminished in the Meth-sensitized rats. These results indicate that the activity of the Glu system is functionally decreased in the hippocampus of Meth-sensitized rats, whereas the Glu system in the striatum of Meth- sensitized rats shows adaptive and functional changes in the receptors in response to the increased Glu release.