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This study investigates the emotional responses and engagement levels of Chinese university students enrolled in Ideological and Political Theory Courses (IPTCs), with particular attention to how curriculum design influences students’ attitudes and feelings. Using the IPTCSSE scale, a quantitative analysis was conducted to measure multiple dimensions of emotional engagement. A total of 3,992 valid questionnaires were collected. Based on the emotional engagement subscale, exploratory and confirmatory factor analyses identified seven underlying factors: interest and belonging, classmates and peers, family and curriculum, emotions and feelings, sense of identification, teacher support and influence, and sense of achievement in courses. Descriptive statistics indicated that students generally evaluated all seven factors positively, and all factors were significantly and positively correlated. Among them, sense of achievement in courses received the highest score, while classmates and peers scored the lowest. Correlation and linear regression analyses further showed that each factor positively predicted emotional engagement in IPTCs. Interest and belonging emerged as the strongest predictor, whereas sense of achievement exerted the smallest predictive effect. Drawing on these findings, the study discusses how emotional engagement can be strategically emphasized to improve the pedagogical effectiveness of IPTCs. The results highlight the importance of fostering interest, belonging, supportive teacher-student relationships, and positive emotional experiences to enhance students’ overall engagement with ideological and political education in China’ s higher education context.

Immune-checkpoint inhibitors (ICBs), in addition to targeting CTLA-4, PD-1, and PD-L1, novel targeting LAG-3 drugs have also been approved in clinical application. With the widespread use of the drug, we must deeply analyze the dilemma of the agents and seek a breakthrough in the treatment prospect. Over the past decades, these agents have demonstrated dramatic efficacy, especially in patients with melanoma and non-small cell lung cancer (NSCLC). Nonetheless, in the field of a broad concept of solid tumours, non-specific indications, inseparable immune response and side effects, unconfirmed progressive disease, and complex regulatory networks of immune resistance are four barriers that limit its widespread application. Fortunately, the successful clinical trials of novel ICB agents and combination therapies, the advent of the era of oncolytic virus gene editing, and the breakthrough of the technical barriers of mRNA vaccines and nano-delivery systems have made remarkable breakthroughs currently. In this review, we enumerate the mechanisms of each immune checkpoint targets, associations between ICB with tumour mutation burden, key immune regulatory or resistance signalling pathways, the specific clinical evidence of the efficacy of classical targets and new targets among different tumour types and put forward dialectical thoughts on drug safety. Finally, we discuss the importance of accurate triage of ICB based on recent advances in predictive biomarkers and diagnostic testing techniques.

Dielectric materials with good thermal transport performance and desirable dielectric properties have significant potential to address the critical challenges of heat dissipation for microelectronic devices and power equipment under high electric field. This work reported the role of synergistic effect and interface on through-plane thermal conductivity and dielectric properties by intercalating the hybrid fillers of the alumina and boron nitride nanosheets (BNNs) into epoxy resin. For instance, epoxy composite with hybrid fillers at a relatively low loading shows an increase of around 3 times in through-plane thermal conductivity and maintains a close dielectric breakdown strength compared to pure epoxy. Meanwhile, the epoxy composite shows extremely low dielectric loss of 0.0024 at room temperature and 0.022 at 100 ℃ and 10 −1  Hz. And covalent bonding and hydrogen-bond interaction models were presented for analyzing the thermal conductivity and dielectric properties.

The treatment of diabetic wounds faces enormous challenges due to complex wound environments, such as infected biofilms, excessive inflammation, and impaired angiogenesis. The critical role of the microenvironment in the chronic diabetic wounds has not been addressed for therapeutic development. Herein, we develop a microneedle (MN) bandage functionalized with dopamine-coated hybrid nanoparticles containing selenium and chlorin e6 (SeC@PA), which is capable of the dual-directional regulation of reactive species (RS) generation, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), in response to the wound microenvironment. The SeC@PA MN bandage can disrupt barriers in wound coverings for efficient SeC@PA delivery. SeC@PA not only depletes endogenous glutathione (GSH) to enhance the anti-biofilm effect of RS, but also degrades GSH in biofilms through cascade reactions to generate more lethal RS for biofilm eradication. SeC@PA acts as an RS scavenger in wound beds with low GSH levels, exerting an anti-inflammatory effect. SeC@PA also promotes the M2-phenotype polarization of macrophages, accelerating wound healing. This self-enhanced, catabolic and dynamic therapy, activated by the wound microenvironment, provides an approach for treating chronic wounds. The treatment of diabetic wounds tends to be hindered by complex wound environments, and the critical role of the microenvironment in the chronic diabetic wounds has not been explored for therapeutic development. Here, the authors develop a wound microenvironment-responsive microneedle bandage to achieve self-enhanced, catabolic and dynamic therapy of chronic wounds.

Background A self-reported life satisfaction question is routinely used as an indicator of societal well-being. Several studies support that mental illness is an important determinant for life satisfaction and improvement of mental healthcare access therefore could have beneficial effects on a population’s life satisfaction. However, only a few studies report the relationship between subjective mental health and life satisfaction. Subjective mental health is a broader concept than the presence or absence of psychopathology. In this study, we examine the strength of the association between a self-reported mental health question and self-reported life satisfaction, taking into account other relevant factors. Methods We conducted this analysis using successive waves of the Canadian Community Health Survey (CCHS) collected between 2003 and 2012. Respondents included more than 400,000 participants aged 12 and over. We extracted information on self-reported mental health, socio-demographic and other factors and examined correlation with self-reported life satisfaction using a proportional ordered logistic regression. Results Life satisfaction was strongly associated with self-reported mental health, even after simultaneously considering factors such as income, general health, and gender. The poor-self-reported mental health group had a particularly low life satisfaction. In the fair-self-reported mental health category, the odds of having a higher life satisfaction were 2.35 (95% CI 2.21 to 2.50) times higher than the odds in the poor category. In contrast, for the “between 60,000 CAD and 79,999 CAD” household income category, the odds of having a higher life satisfaction were only 1.96 (95% CI 1.90 to 2.01) times higher than the odds in the “less than 19,999 CAD” category. Conclusions Subjective mental health contributes highly to life satisfaction, being more strongly associated than other selected previously known factors. Future studies could be useful to deepen our understanding of the interplay between subjective mental health, mental illness and life satisfaction. This may be beneficial for developing public health policies that optimize mental health promotion, illness prevention and treatment of mental disorders to enhance life satisfaction in the general population.

Continuous cell division is a hallmark of cancer, and the underlying mechanism is tumor genomics instability. Cell cycle checkpoints are critical for enabling an orderly cell cycle and maintaining genome stability during cell division. Based on their distinct functions in cell cycle control, cell cycle checkpoints are classified into two groups: DNA damage checkpoints and DNA replication stress checkpoints. The DNA damage checkpoints (ATM-CHK2-p53) primarily monitor genetic errors and arrest cell cycle progression to facilitate DNA repair. Unfortunately, genes involved in DNA damage checkpoints are frequently mutated in human malignancies. In contrast, genes associated with DNA replication stress checkpoints (ATR-CHK1-WEE1) are rarely mutated in tumors, and cancer cells are highly dependent on these genes to prevent replication catastrophe and secure genome integrity. At present, poly (ADP-ribose) polymerase inhibitors (PARPi) operate through “synthetic lethality” mechanism with mutant DNA repair pathways genes in cancer cells. However, an increasing number of patients are acquiring PARP inhibitor resistance after prolonged treatment. Recent work suggests that a combination therapy of targeting cell cycle checkpoints and PARPs act synergistically to increase the number of DNA errors, compromise the DNA repair machinery, and disrupt the cell cycle, thereby increasing the death rate of cancer cells with DNA repair deficiency or PARP inhibitor resistance. We highlight a combinational strategy involving PARP inhibitors and inhibition of two major cell cycle checkpoint pathways, ATM-CHK2-TP53 and ATR-CHK1-WEE1. The biological functions, resistance mechanisms against PARP inhibitors, advances in preclinical research, and clinical trials are also reviewed.

Over the last decade, adipose‐derived stem cells (ADSCs) have attracted increasing attention in the field of regenerative medicine. ADSCs appear to be the most advantageous cell type for regenerative therapies owing to their easy accessibility, multipotency, and active paracrine activity. This review highlights current challenges in translating ADSC‐based therapies into clinical settings and discusses novel strategies to overcome the limitations of ADSCs. To further establish ADSC‐based therapies as an emerging platform for regenerative medicine, this review also provides an update on the advancements in this field, including fat grafting, wound healing, bone regeneration, skeletal muscle repair, tendon reconstruction, cartilage regeneration, cardiac repair, and nerve regeneration. ADSC‐based therapies are expected to be more tissue‐specific and increasingly important in regenerative medicine. Adipose‐derived stem cells (ADSCs) serve as an ideal candidate for regenerative medicine owing to their ability to differentiate into multilineages, facilitate angiogenesis, suppress apoptosis, and participate in immunoregulation. Numerous preclinical studies and clinical trials have demonstrated the therapeutic potential of ADSCs in fat grafting, wound healing, bone regeneration, skeletal muscle repair, tendon reconstruction, cartilage regeneration, cardiac repair, and nerve regeneration.

Maternal RNA degradation is critical for embryogenesis and is tightly controlled by maternal RNA-binding proteins. Fragile X mental-retardation protein (FMR1) binds target mRNAs to form ribonucleoprotein (RNP) complexes/granules that control various biological processes, including early embryogenesis. However, how FMR1 recognizes target mRNAs and how FMR1-RNP granule assembly/disassembly regulates FMR1-associated mRNAs remain elusive. Here we show that Drosophila FMR1 preferentially binds mRNAs containing m6A-marked “AGACU” motif with high affinity to contributes to maternal RNA degradation. The high-affinity binding largely depends on a hydrophobic network within FMR1 KH2 domain. Importantly, this binding greatly induces FMR1 granule condensation to efficiently recruit unmodified mRNAs. The degradation of maternal mRNAs then causes granule de-condensation, allowing normal embryogenesis. Our findings reveal that sequence-specific mRNAs instruct FMR1-RNP granules to undergo a dynamic phase-switch, thus contributes to maternal mRNA decay. This mechanism may represent a general principle that regulated RNP-granules control RNA processing and normal development. Maternal RNA degradation is critical for embryogenesis and is tightly controlled by maternal RNA-binding proteins. Here the authors show that a subset of m6A-modified mRNAs regulates the dynamics of RNA-granules, thus contributes to maternal mRNA decay.

The CRISPR (clustered regularly interspaced short palindromic repeats) system has emerged as a revolutionary gene-editing tool with immense potential in gene therapy, functional genomics, and beyond. However, achieving precise spatiotemporal control of gene editing in specific cells and tissues while effectively mitigating potential risks, such as off-target effects, remains a key challenge for its clinical translation. To overcome these limitations, researchers have developed innovative strategies based on chemical modifications of oligonucleotides to enhance the precision, efficiency, and controllability of CRISPR/Cas9-mediated gene editing. By introducing conditional responsive elements, such as photosensitive groups, small-molecule responsive units, and supramolecular structures, they have successfully achieved precise spatiotemporal and dose-dependent regulation of CRISPR/Cas9 function. This review provides a comprehensive overview of recent advancements in gRNA regulation strategies based on chemical modifications of oligonucleotides, discussing their applications in improving the efficiency, specificity, and controllability of CRISPR/Cas9 editing. We also highlight the challenges associated with the conditional control of gRNA and offer insights into future directions for the chemical regulation of gRNA to further advance CRISPR/Cas9 technology.

Altered cholesterol metabolism has been linked to a poor prognosis in various types of cancer. Cholesterol oxidation can lead to lipid peroxidation, membrane damage, and cell death. Ferroptosis is a regulated form of cell death characterized by the accumulation of lipid peroxides, which significantly inhibits the growth of ovarian cancer cells. SQLE is the primary enzyme responsible for catalyzing cholesterol lipid synthesis and is notably expressed in ovarian cancer tissues and cells. This study aims to investigate the role of squalene monooxygenase (SQLE) in ferroptosis in ovarian cancer. The protein and mRNA expression of SQLE was assessed using qRT-PCR, Western Blot, and immunohistochemistry. The association between SQLE and ferroptosis was demonstrated through analysis of TCGA and GTEx databases, TMT protein sequencing, as well as validation by qRT-PCR, Western Blot, immunofluorescence, ROS detection, and lipid peroxide detection. Animal experiments further confirmed the relationship between SQLE and ferroptosis in ovarian cancer. The protein and mRNA expression of SQLE was found to be upregulated in both ovarian cancer tissues and cell lines. Decreased SQLE expression led to ferroptosis in ovarian cancer cells, thereby increasing their sensitivity to ferroptosis inducers. Our research demonstrates that SQLE is significantly upregulated in both ovarian cancer tissues and cells. The overexpression of SQLE in ovarian cancer may facilitate tumorigenesis by conferring resistance to ferroptosis, thus shedding light on potential novel therapeutic strategies for ovarian cancer.