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The medical field is facing a physician‐scientist shortage, threatening future medical research and development. Medical institutions can contribute to developing physician‐scientists by stimulating students' involvement in research. In this study, a medical undergraduate teaching module to develop research skills and encourage interest in research was held in Chongqing, China. Undergraduate medical students at Chongqing Medical University completed research skills training. Before and after the training, an online, anonymous, self‐reported questionnaire was administered. The self‐reported questionnaire investigated students' demographic characteristics, students' perception of attitudes toward conducting research, research skills (e.g., identifying and utilizing information, critical appraisal of literature, paper writing, and understanding of research), and feedback on scientific research training. The module was implemented with 25 students from July 2019 to October 2019, and 96.0% (N = 24) of participants responded to the questionnaire both prior to and after the training. In the evaluation of research skills, results showed that use of appropriate tools for research (Z = −3.340, p < 0.01), students' ability to undertake a focused literature search (Z = −3.40, p < 0.01), identifying and utilizing information (Z = −3.34, p < 0.01), and paper‐writing skills (Z = −3.49, p < 0.01) were significantly improved after the undergraduates participated in the scientific research training. A qualitative analysis of the feedback showed that students found that the training helped to enhance their knowledge, improve their study scores, and motivate them to conduct research in the future. Early scientific research ability training strengthened the research skills of medical undergraduates and motivated them to pursue research. [ABSTRACT FROM AUTHOR]

Influenza A virus (IAV) is a negative-sense single-stranded RNA virus that causes acute lung injury and acute respiratory distress syndrome, posing a serious threat to both animal and human health. N6-methyladenosine (m 6 A), a prevalent and abundant post-transcriptional methylation of RNA in eukaryotes, plays a crucial regulatory role in IAV infection by altering viral RNA and cellular transcripts to affect viral infection and the host immune response. This review focuses on the molecular mechanisms underlying m 6 A modification and its regulatory function in the context of IAV infection and the host immune response. This will provide a better understanding of virus-host interactions and offer insights into potential anti-IAV strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Liu, Chen, Li and Sheng.)

JOURNAL/nrgr/04.03/01300535-202502000-00031/figure1/v/2024-05-28T214302Z/r/image-tiff Transforming growth factor-beta 1 (TGF-β1) has been extensively studied for its pleiotropic effects on central nervous system diseases. The neuroprotective or neurotoxic effects of TGF-β1 in specific brain areas may depend on the pathological process and cell types involved. Voltage-gated sodium channels (VGSCs) are essential ion channels for the generation of action potentials in neurons, and are involved in various neuroexcitation-related diseases. However, the effects of TGF-β1 on the functional properties of VGSCs and firing properties in cortical neurons remain unclear. In this study, we investigated the effects of TGF-β1 on VGSC function and firing properties in primary cortical neurons from mice. We found that TGF-β1 increased VGSC current density in a dose- and time-dependent manner, which was attributable to the upregulation of Nav1.3 expression. Increased VGSC current density and Nav1.3 expression were significantly abolished by preincubation with inhibitors of mitogen-activated protein kinase kinase (PD98059), p38 mitogen-activated protein kinase (SB203580), and Jun NH2-terminal kinase 1/2 inhibitor (SP600125). Interestingly, TGF-β1 significantly increased the firing threshold of action potentials but did not change their firing rate in cortical neurons. These findings suggest that TGF-β1 can increase Nav1.3 expression through activation of the ERK1/2-JNK-MAPK pathway, which leads to a decrease in the firing threshold of action potentials in cortical neurons under pathological conditions. Thus, this contributes to the occurrence and progression of neuroexcitatory-related diseases of the central nervous system., (Copyright © 2025 Copyright: © 2025 Neural Regeneration Research.)

Traumatic brain injury (TBI) is a leading cause of disability and death in adolescents, and there is a lack of effective methods of treatment. The neuroprotective effects exerted by TGF-β1 can ameliorate a range of neuronal lesions in multiple central nervous system diseases. In this study, we used an in-vitro TBI model of mechanical injury on murine primary cortical neurons and the neuro-2a cell line to investigate the neuroprotective role played by TGF-β1 in cortical neurons in TBI. Our results showed that TGF-β1 significantly increased neuronal viability and inhibited apoptosis for 24 h after trauma. The expression of Ca v 1.2, an L-type calcium channel (LTCC) isoform, decreased significantly after trauma injury, and this change was reversed by TGF-β1. Nimodipine, a classic LTCC blocker, abolished the protective effect of TGF-β1 on trauma-induced neuronal apoptosis. The knockdown of Ca v 1.2 in differentiated neuro-2a cells significantly inhibited the anti-apoptosis effect of TGF-β1 exerted on injured neuro-2a cells. Moreover, TGF-β1 rescued and enhanced the trauma-suppressed neuro-2a intracellular Ca 2+ concentration, while the effect of TGF-β1 was partially inhibited by nimodipine. TGF-β1 significantly upregulated the expression of Ca v 1.2 by activating the p38 MAPK pathway and by inhibiting trauma-induced neuronal apoptosis. In conclusion, TGF-β1 increased trauma-injured murine cortical neuronal activity and inhibited apoptosis by upregulating Cav1.2 channels via activating the p38 MAPK pathway. Therefore, the TGF-β1/p38 MAPK/Ca v 1.2 pathway has the potential to be used as a novel therapeutic target for TBI., (Copyright © 2022 IBRO. Published by Elsevier Ltd. All rights reserved.)

Background: Available evidence on the comparative efficacy and acceptability of psychotherapies for post-traumatic stress disorder (PTSD) in children and adolescents remains uncertain., Objective: We aimed to compare and rank the different types and formats of psychotherapies for PTSD in children and adolescents., Methods: We searched eight databases and other international registers up to 31 December 2020. The pairwise meta-analyses and frequentist network meta-analyses estimated pooled standardised mean differences (SMDs) and ORs with random-effects model. Efficacy at post-treatment and follow-up, acceptability, depressive and anxiety symptoms were measured., Findings: We included 56 randomised controlled trials with 5327 patients comparing 14 different types of psychotherapies and 3 control conditions. For efficacy, cognitive processing therapy (CPT), behavioural therapy (BT), individual trauma-focused cognitive-behavioural therapy (TF-CBT), eye movement desensitisation and reprocessing, and group TF-CBT were significantly superior to all control conditions at post-treatment and follow-up (SMDs between -2.42 and -0.25). Moreover, CPT, BT and individual TF-CBT were more effective than supportive therapy (SMDs between -1.92 and -0.49). Results for depressive and anxiety symptoms were similar to the findings for the primary outcome. Most of the results were rated as 'moderate' to 'very low' in terms of confidence of evidence., Conclusions: CPT, BT and individual TF-CBT appear to be the best choices of psychotherapy for PTSD in young patients. Other types and different ways of delivering psychological treatment can be alternative options. Clinicians should consider the importance of each outcome and the patients' preferences in real clinical practice., Competing Interests: Competing interests: AC has received research and consultancy fees from INCiPiT (Italian Network for Paediatric Trials), CARIPLO Foundation and Angelini Pharma. JRW reported support from unrelated grants from the National Institute of Mental Health and the Institute of Education Sciences, US Department of Education; he also receives royalties for books and honoraria for various invited presentations. PC reported support for unrelated grants from the European Commission, and ZonMw, for being Chair of the Mental Health Priority Area of the Wellcome Trust in London, UK; and he receives royalties for books, and for occasional workshops and invited addresses. DC reported past consultation for or the receipt of honoraria from Otsuka, Shire, Lundbeck, Roche, Janssen and Biocodex. XZ reported receiving lecture fees from Janssen Pharmaceutica and Lundbeck. PX reported receiving lecture fees from Eli Lilly and Company, Janssen Pharmaceutica, Lundbeck and Pfizer. No other disclosures were reported., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)