Objective: To review the relationship between 24 hour movement behaviors and physical and mental health among college students, in order to provide evidence to support health promotion and further research in universities. Methods: Following the Joanna Briggs Institude(JBI) scoping review guidelines, relevant studies published in databases from inception date to December 26, 2025 were searched, including PubMed, Embase, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI) and Wanfang Data. For studies meeting the inclusion and exclusion criteria, a descriptive analysis was conducted to summarize the measurement tools used, adherence rates with guidelines, and the relationship between physical and mental health. Results: A total of 30 studies were included. Measurement tools exhibited a high heterogeneity, with questionnaires being the primary method. The rate of full adherence with 24 hour movement behaviors among college students was less than 30%. Moderate to vigorous physical activity and high quality sleep were associated with improvements in physical fitness, cardiopulmonary function, and mental health, while prolonged sitting was negatively associated with obesity and depression. Equivalent time substitution analysis indicated that increasing moderate to vigorous physical activity and reducing prolonged sitting could significantly improve health outcomes. Conclusions The adherence rate for 24 hour movement behaviors among college students is low and it is closely associated with physical and mental health. Future studies should standardize measurement tools, and implement targeted interventions based on the optimization of daily activity patterns.

The incomplete degradation of tumour cells by macrophages(Mφ)is a contributing factor to tumour progression and metastasis,and the degradation function of Mφ is mediated through phagosomes and lysosomes.In our preliminary experiments,we found that overactivation of NADPH oxidase 2(NOX2)reduced the ability of Mφ to degrade engulfed tumour cells.Above this,we screened out liquiritin from Glycyrrhiza uralensis Fisch,which can significantly inhibit NOX2 activity and inhibit tumours,to elucidate that suppressing NOX2 can enhance the ability of Mφ to degrade tumour cells.We found that the tumour environment could activate the NOX2 activity in Mφ phagosomes,causing Mφ to produce excessive reactive oxygen species(ROS),thus prohibiting the formation of phagolysosomes before degradation.Conversely,inhibiting NOX2 in Mφ by liquiritin can reduce ROS and promote phagosome-lysosome fusion,therefore improving the enzymatic degradation of tumour cells after phagocytosis,and subse-quently promote T cell activity by presenting antigens.We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox,blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox,thereby inhibiting the activity of NOX2.This study elucidates the specific mechanism by which Mφ cannot degrade tumour cells after phagocytosis,and indicates that liquiritin can promote the ability of Mφ to degrade tumour cells by suppressing NOX2.

The incomplete degradation of tumour cells by macrophages (Mϕ) is a contributing factor to tumour progression and metastasis, and the degradation function of Mϕ is mediated through phagosomes and lysosomes. In our preliminary experiments, we found that overactivation of NADPH oxidase 2 (NOX2) reduced the ability of Mϕ to degrade engulfed tumour cells. Above this, we screened out liquiritin from Glycyrrhiza uralensis Fisch, which can significantly inhibit NOX2 activity and inhibit tumours, to elucidate that suppressing NOX2 can enhance the ability of Mϕ to degrade tumour cells. We found that the tumour environment could activate the NOX2 activity in Mϕ phagosomes, causing Mϕ to produce excessive reactive oxygen species (ROS), thus prohibiting the formation of phagolysosomes before degradation. Conversely, inhibiting NOX2 in Mϕ by liquiritin can reduce ROS and promote phagosome-lysosome fusion, therefore improving the enzymatic degradation of tumour cells after phagocytosis, and subsequently promote T cell activity by presenting antigens. We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox, blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox, thereby inhibiting the activity of NOX2. This study elucidates the specific mechanism by which Mϕ cannot degrade tumour cells after phagocytosis, and indicates that liquiritin can promote the ability of Mϕ to degrade tumour cells by suppressing NOX2.

Gastroesophageal reflux disease(GERD)is a chronic recurrent disorder characterized by typical symptoms such as acid regurgitation and heartburn.Its high recurrence rate and long-term complications not only significantly impact patients' quality of life but also impose a heavy healthcare burden.Traditional proton pump inhibitors(PPIs),as first-line therapeutic agents,are often inadequate for long-term maintenance therapy of GERD due to shortcomings such as short half-life,susceptible to genetic polymorphisms,and nocturnal acid breakthrough.Recently,the potassium-competitive acid blocker(P-CAB)vonoprazan has demonstrated advantages increasingly in the maintenance therapy of GERD.This article reviewed the research progress on vonoprazan in the maintenance therapy of GERD,aiming to provide a reference for optimizing the long-term management of GERD.

Objective To explore the mechanism of Huoxin pill(HXP)in the prevention and treatment of heart failure(HF)based on transcriptomics and network pharmacology.Methods The mice were randomly divided into the normal control group,model control group,positive control group treated with sacubitril/valsartan(60 mg·kg-1),low-dose group treated with HXP(31.2 mg·kg-1),and high-dose group treated with HXP(62.4 mg·kg-1).The model control group and each drug treat-ment group were subcutaneously injected with an equal volume of ISO(5 mg·kg-1)for modeling,while the normal control group was given an equal volume of sterile saline.Six hours later,each drug administration group was gavaged with the corresponding drug for intervention,and the normal control and model control groups were gavaged with an equal volume of sterile water.The modeling and drug administration were continued for 21 days.The cardiac function parameters of the mice were measured using color Doppler ultrasound imaging;ELISA was used to detect the levels of mouse serum cAMP,NT-proBNP,and BNP;HE staining and Masson's trichrome staining were used to evaluate the pathological morphology of cardiac tissue,and the CVF was calculated.Network pharmacology combined with transcriptomics was used to predict potential targets and signaling pathways of HXP in the prevention and treatment of HF,and molecular biology methods were used for validation.Results Compared with the normal control group,the model control group showed an increase in LVESd and LVEDd(P＜0.01),and a decrease in LVEF and LVFS(P＜0.01);BNP,NT-proBNP,and cAMP levels were increased(P＜0.01);myocardial collagen fibers increased and CVF in-creased(P＜0.01).Compared with the model control group,the HXP low-dose group,HXP high-dose group,and positive control groups showed a decrease in LVESd and LVEDd(P＜0.01),and an increase in LVEF and LVFS(P＜0.01);serum levels of BNP,NT-proBNP,and cAMP decreased(P＜0.05);the degree of myocardial fibrosis decreased and CVF decreased(P＜0.01).Network pharmacology combined with transcriptomics predicted 10 key targets for HXP in the prevention and treatment of HF:CACNA1H,SCN10A,FGF12,PVALB,ACAN,LGALS3,SERPINE1,MMP3,GSTM1,VDR.Western blot results showed that the protein activation levels of PKA and CREB in myocardial tissue were increased in the model control group compared with the nor-mal control group(P＜0.01).Compared with the model control group,HXP low-dose group、HXP high-dose group,and positive control groups showed a decrease in the protein activation levels of PKA and CREB in myocardial tissue(P＜0.05).Conclusion HXP has an improvement effect on ISO-induced HF in mice,which may involve numerous targets and the cAMP/PKA signaling pathway.

Objective To explore the mechanism of Huoxin pill(HXP)in the prevention and treatment of heart failure(HF)based on transcriptomics and network pharmacology.Methods The mice were randomly divided into the normal control group,model control group,positive control group treated with sacubitril/valsartan(60 mg·kg-1),low-dose group treated with HXP(31.2 mg·kg-1),and high-dose group treated with HXP(62.4 mg·kg-1).The model control group and each drug treat-ment group were subcutaneously injected with an equal volume of ISO(5 mg·kg-1)for modeling,while the normal control group was given an equal volume of sterile saline.Six hours later,each drug administration group was gavaged with the corresponding drug for intervention,and the normal control and model control groups were gavaged with an equal volume of sterile water.The modeling and drug administration were continued for 21 days.The cardiac function parameters of the mice were measured using color Doppler ultrasound imaging;ELISA was used to detect the levels of mouse serum cAMP,NT-proBNP,and BNP;HE staining and Masson's trichrome staining were used to evaluate the pathological morphology of cardiac tissue,and the CVF was calculated.Network pharmacology combined with transcriptomics was used to predict potential targets and signaling pathways of HXP in the prevention and treatment of HF,and molecular biology methods were used for validation.Results Compared with the normal control group,the model control group showed an increase in LVESd and LVEDd(P＜0.01),and a decrease in LVEF and LVFS(P＜0.01);BNP,NT-proBNP,and cAMP levels were increased(P＜0.01);myocardial collagen fibers increased and CVF in-creased(P＜0.01).Compared with the model control group,the HXP low-dose group,HXP high-dose group,and positive control groups showed a decrease in LVESd and LVEDd(P＜0.01),and an increase in LVEF and LVFS(P＜0.01);serum levels of BNP,NT-proBNP,and cAMP decreased(P＜0.05);the degree of myocardial fibrosis decreased and CVF decreased(P＜0.01).Network pharmacology combined with transcriptomics predicted 10 key targets for HXP in the prevention and treatment of HF:CACNA1H,SCN10A,FGF12,PVALB,ACAN,LGALS3,SERPINE1,MMP3,GSTM1,VDR.Western blot results showed that the protein activation levels of PKA and CREB in myocardial tissue were increased in the model control group compared with the nor-mal control group(P＜0.01).Compared with the model control group,HXP low-dose group、HXP high-dose group,and positive control groups showed a decrease in the protein activation levels of PKA and CREB in myocardial tissue(P＜0.05).Conclusion HXP has an improvement effect on ISO-induced HF in mice,which may involve numerous targets and the cAMP/PKA signaling pathway.

Gastroesophageal reflux disease(GERD)is a chronic recurrent disorder characterized by typical symptoms such as acid regurgitation and heartburn.Its high recurrence rate and long-term complications not only significantly impact patients' quality of life but also impose a heavy healthcare burden.Traditional proton pump inhibitors(PPIs),as first-line therapeutic agents,are often inadequate for long-term maintenance therapy of GERD due to shortcomings such as short half-life,susceptible to genetic polymorphisms,and nocturnal acid breakthrough.Recently,the potassium-competitive acid blocker(P-CAB)vonoprazan has demonstrated advantages increasingly in the maintenance therapy of GERD.This article reviewed the research progress on vonoprazan in the maintenance therapy of GERD,aiming to provide a reference for optimizing the long-term management of GERD.

Objective To investigate the mechanism of Bixie Fenqing Pills in improving renal injury caused by hyperuricemia (HUA). Methods The HUA model rats were induced by gavaging with oxonic acid potassium salt, adenine combined with 10% yeast powder feed for 2 weeks. The model was evaluated based on serum uric acid (SUA) level. The successfully modeled rats were randomly divided into model group, low-dose Bixie Fenqing Pills group, medium-dose Bixie Fenqing Pills group, high-dose Bixie Fenqing Pills group, and febuxostat group, with 8 rats in each group. The drug administration groups were gavaged with the corresponding drugs, while the control group and the model group were gavaged with an equal volume of 0.5% carboxymethyl cellulose sodium (CMC-Na). After 4 weeks of continuous drug administration, the rats were sacrificed for sampling. Biochemical method was used to detect the serum levels of SUA, adenosine deaminase (ADA), xanthine oxidase (XOD), blood urea nitrogen (BUN), and serum creatinine (SCr) in the rats in each group; hematoxylin-eosin (HE) staining was used to observe the pathological changes of renal tissues; the Western blot was used to detect the expression levels of ATP-binding cassette subfamily G member 2 (ABCG2), glucose transporter 9 (GLUT9), and multi-drug resistance-associated protein 4 (MRP4) in renal tissues; immunohistochemistry was used to detect the protein expression levels of phosphatidylinositol-3-kinase (PI3K), protein kinase B (AKT), and nuclear factor-κB (NF-κB) in renal tissues. Results HE staining showed that the renal unitstructure in the model group was incomplete, with multiple edema in the renal interstitium, a small number of glomeruli showing atrophy, and incomplete epithelial cells on the glomerular capsule wall; the serum levels of SUA, ADA, XOD, SCr and BUN in the model group were significantly increased (P < 0.01); the expression of GLUT9 protein in renal tissue was upregulated, while the expression levels of ABCG2 and MRP4 proteins were significantly decreased (P < 0.05); immunohistochemical results showed that the expression levels of PI3K, AKT and NF-κB proteins in renal tissues in the model group were increased significantly (P < 0.05). Compared with the model group, Bixie Fenqing Pills could significantly effectively improve renal injuryin HUA rats, reduce serum levels of SUA, ADA, XOD, SCr and BUN, downregulate the expression of GLUT9 protein in renal tissues, and increase the expression levels of ABCG2, MRP4, PI3K, AKT and NF-κB proteins (P < 0.05). Conclusion Bixie Fenqing Pills may affect the production and metabolism of uric acid by regulating the PI3K/AKT/NF-κB pathway and the expression of uric acid transporter proteins, thereby improving renal injury in HUA rats.

Objective:To construct a new nurse pre-job training program based on transformative learning and explore its preliminary application effect.Methods:A quasi-experimental study was conducted, and 52 new nurses enrolled in 2019 in a three-A hospital of Hangzhou were randomly divided into experimental group ( n=26) and control group ( n=26). The experimental group adopted transformative learning based pre-job training program for new nurses, while the control group adopted traditional pre-job training program for new nurses. SPSS 20.0 and Microsoft Excel 2010 were performed for data processing, and t test and Fisher's exact probability test were used for statistical analysis. Results:After the training, the comparison of two groups of new nurses showed that, the total score of clinical core competence of the experimental group (226.62±32.84) was higher than that of the control group (197.00±29.54), the total score of self-efficacy of the experimental group (28.46±4.94) was higher than that of the control group (24.31±4.76), the total score of the transition shock of the experimental group (77.23±14.13) was lower than that of the control group (91.27±17.98), and the mean value of clinical assessment of the experimental group (73.16±17.05) was higher than that of the control group (61.58±14.24), all with statistical significance ( P<0.05). Conclusion:The pre-job training program for new nurses based on transformative learning can improve the clinical ability and self-efficacy of new nurses, reduce the transition shock of new nurses, and have a profound impact on their career.

Objective:To study the clinical efficacy of modified open elbow arthrolysis in the treatment of traumatic elbow stiffness.Methods:A retrospective analysis was performed on 120 patients who underwent modified open elbow arthrolysis in Beijing Jishuitan Hospital from January 2018 to December 2020. The age of the included patients was (37.7±12.4) years (ranged 18-64 years), including 54 males and 66 females. The medical records were reviewed, the range of motion (ROM) and functional status of the patients before operation and at the last follow-up were compared including visual analogue scale (VAS), Mayo elbow performance score (MEPS), Disabilities of the arm, shoulder and hand (DASH) score. Complications and secondary operations were also recorded. Measurement data with normal distribution were presented as mean ± standard deviation( ± s) and comparison between groups was conducted using the t-test; Measurement data of skewed distribution were expressed as M ( Q1, Q3), and Rank-sum test was used for inter-group comparison. Results:The preoperative extension of 120 patients was 43.6° (33.8°, 60.1°), the flexion was 78.7° (59.8°, 98.1°), and the flexion-extension ROM was 25.6° (0.0°, 54.5°); the preoperative pronation was 51.8° (33.0°, 67.0°), the supination was 85.1° (65.7°, 90.0°), and the rotation ROM was 136.9° (99.1°, 157.5°). Postoperative extension was 14.2° (7.0°, 24.8°), flexion was 129.5° (120.0°, 138.1°), flexion-extension ROM was 115.5° (94.4°, 127.3°); postoperative pronation was 65.0° (47.1°, 75.0°), the supination was 88.3° (78.6°, 90.0°), and the rotation ROM was 151.9° (131.7°, 163.4°). Postoperative extension, flexion, flexion-extension ROM, pronation, supination, and rotation ROM were all higher than those before operation, and the differences were statistically significant ( P<0.001). The VAS of 120 patients was 1.0 (0.0, 3.0) scores before operation and 0.0 (0.0, 1.0) scores after operation. The MEPS was 60.0 (50.0, 75.0) scores before operation and 100.0 (85.0, 100.0) scores after operation. The preoperative DASH was 37.5 (20.1, 51.3) scores, and the postoperative DASH was 7.9 (3.3, 13.3) scores. The postoperative VAS, MEPS, and DASH were significantly improved compared with those before operation, and the differences were statistically significant ( P<0.001). Residual ulnar nerve symptoms occurred in 18 cases, recurrence of heterotopic ossification in 42 cases, and hematoma in 3 cases. Conclusions:Modified open elbow arthrolysis is a safe and effective surgical method for the treatment of traumatic elbow stiffness. It can significantly improve the function of the patient, reduce the occurrence of elbow instability, avoid the use of external fixators, and reduce the cost of the patient.