1.Status quo, influencing factors, and improving path of nursing undergraduates' humanistic concern
Can GU ; Wanting ZHANG ; Dan LIU ; Yao WANG ; Honghong WANG ; Jia CHEN
Chinese Journal of Medical Education Research 2025;24(6):802-808
Objective:To investigate the status quo and influencing factors of humanistic concern among nursing undergraduates, and to explore the educational path of improving humanistic concern.Methods:A total of 345 nursing undergraduates from Xiangya School of Nursing of Central South University were investigated using a questionnaire of general demographic data, the Caring Ability Inventory, and the Self-directed Learning Instrument. The SPSS 26.0 statistical software was used for data analysis. The humanistic caring ability scores of nursing undergraduates with different characteristics were compared by the independent sample t-test and analysis of variance, and the pairwise comparison was conducted by the least significant difference t-test. All dimensions and total scores of humanistic caring ability and self-directed learning ability failed to meet normal distribution, and the correlation between them was determined by Spearman correlation analysis. Results:The humanistic caring ability score of nursing undergraduates was (169.52±10.62). The correlation analysis showed that the humanistic caring ability of nursing undergraduates was positively correlated with their self-directed learning ability ( r=0.426, P<0.001). The stepwise regression analysis showed that interpersonal communication ability, learning motivation, grades, genders, and class leader experience were influencing factors of humanistic caring ability of nursing undergraduates. Conclusions:Nursing undergraduates should improve their humanistic caring ability, whose score is lower than that in the existing research (175.70±18.74). In humanistic education, nursing educators should pay attention to individualized development needs of nursing undergraduates with different grades and genders, set students with class leader experience as a good example, and effectively improve the humanistic caring ability of nursing undergraduates by stimulating learning motivation and strengthening interpersonal communication.
2.Exploring mechanism of action of hypericin in antidepressant effects based on single-cell sequencing
Hui-xin NI ; Hai-xin LIU ; Bing-can ZHOU ; Ming-heng CHEN ; Ping-yan LIN ; Zheng-tao GAO ; Xin-pei LIN ; Yao LIN ; Fang-zhen WU ; Qian XU
Chinese Pharmacological Bulletin 2025;41(5):837-843
Aim To investigate the antidepressant mechanism of hyperforin via the utilization of single-cell sequencing technology.Methods C57BL/6 mice were randomly divided into the control group,depres-sion model group,and hyperforin intervention group.The chronic unpredictable mild stress(CUMS)model was induced and drug interventions were administered for 28 d.Behavioral experiments were conducted to as-sess depressive symptoms,and hippocampal tissue was collected for single-cell RNA sequencing.Key cell populations and differentially expressed genes across groups were identified,followed by PPI network,GO,and KEGG enrichment analysis.Results Behavioral experiments indicated that CUMS successfully induced depressive symptoms in mice,while hyperforin im-proved depressive behavior.In the depression model group,the proportion of brain perivascular macrophages(PVM)increased,and this proportion decreased after hyperforin intervention,approaching the level seen in the control group.The top 20 common differentially ex-pressed genes in the PVM subpopulation were Saa3,Hbb-bs and Ccl24.PPI network analysis identified core targets,including Ccl2,Dhx9,C3,Msr1,Cxcl2 and Cx3cr1.KEGG enrichment analysis revealed pathways related to chemokines,phagosome formation,and inosi-tol phosphate metabolism.Conclusion The antide-pressant mechanism of hyperforin may be related to the regulation of Ccl24 and its related chemokine signaling pathway by PVM.
3.Exploring mechanism of action of hypericin in antidepressant effects based on single-cell sequencing
Hui-xin NI ; Hai-xin LIU ; Bing-can ZHOU ; Ming-heng CHEN ; Ping-yan LIN ; Zheng-tao GAO ; Xin-pei LIN ; Yao LIN ; Fang-zhen WU ; Qian XU
Chinese Pharmacological Bulletin 2025;41(5):837-843
Aim To investigate the antidepressant mechanism of hyperforin via the utilization of single-cell sequencing technology.Methods C57BL/6 mice were randomly divided into the control group,depres-sion model group,and hyperforin intervention group.The chronic unpredictable mild stress(CUMS)model was induced and drug interventions were administered for 28 d.Behavioral experiments were conducted to as-sess depressive symptoms,and hippocampal tissue was collected for single-cell RNA sequencing.Key cell populations and differentially expressed genes across groups were identified,followed by PPI network,GO,and KEGG enrichment analysis.Results Behavioral experiments indicated that CUMS successfully induced depressive symptoms in mice,while hyperforin im-proved depressive behavior.In the depression model group,the proportion of brain perivascular macrophages(PVM)increased,and this proportion decreased after hyperforin intervention,approaching the level seen in the control group.The top 20 common differentially ex-pressed genes in the PVM subpopulation were Saa3,Hbb-bs and Ccl24.PPI network analysis identified core targets,including Ccl2,Dhx9,C3,Msr1,Cxcl2 and Cx3cr1.KEGG enrichment analysis revealed pathways related to chemokines,phagosome formation,and inosi-tol phosphate metabolism.Conclusion The antide-pressant mechanism of hyperforin may be related to the regulation of Ccl24 and its related chemokine signaling pathway by PVM.
4.Regulation of ATF6 on ZEA-induced injury of murine luteinized granulosa cell
Xingyao XIAO ; Tao HUANG ; Li CHEN ; Xiaochuan LONG ; Yao WU ; Xiayu MIN ; Can LUO ; Jin OU ; Xin WEN
Chinese Journal of Veterinary Science 2025;45(10):2231-2238
This study examines the effects of zearalenone(ZEA)on the survival and function of lu-teinized granulosa cells,and studies the role of activating transcription factor 6(ATF6)in regula-ting apoptosis and functional abnormalities of luteinized granulosa cells induced by ZEA.An in vitro model of luteinized granulosa cells was utilized to examine the effects of ZEA treatment on apoptosis,hormone secretion,and the expression of relevant proteins.Furthermore,the expression of ATF6 was manipulated using siRNA to elucidate its regulatory function in the ZEA-induced damage of luteinized granulosa cells in mice.Our findings revealed that ZEA inhibited the activity of luteinized granulosa cells and reduced the secretion of estradiol(E2)and progesterone(P4)in a dose-dependent manner.The expression levels of p-IRE1,ATF6 and StAR in both low(20 pmol/L)and high(40 μmol/L)ZEA groups were significantly increased after 24 h(P<0.05).GRP78 had no significant change at low concentration treatment(P>0.05),but significantly increased at high concentration treatment(P<0.05).Similarly,ATF4 and p-EIF2α had no significant change at low concentration treatment(P>0.05),but significantly decreased at high concentration treat-ment(P<0.05).HSD3B2 and CYP19A1 were significantly decreased in both low and high concentration treatments(P<0.05).After 48 h of treatment,ATF6 and GRP78 were significantly increased in both low and high concentration treatments(P<0.05).p-IRE1 was significantly de-creased at low concentration treatment(P<0.05),but remained unchanged at high concentration treatment(P>0.05).ATF4,p-EIF2α,HSD3B2 and CYP19A1 were significantly decreased in both low and high concentration treatments(P<0.05).St AR was significantly increased in both low and high concentration treatments(P<0.05).Interference with the expression of ATF6 could sig-nificantly reduce the apoptosis induced by low concentration group(P<0.05),and enhanced the hormone secretion in both high and low concentration groups(P<0.05).In conclusion,ZEA can cause damage to luteinized granulosa cells and activate ATF6 signaling pathway.Interference with ATF6 can alleviate apoptosis and hormone secretion disturbance induced by low concentration ZEA,but has limited effect on damage caused by high concentration ZEA.
5.Temporomandibular joint capsule suspension for neocondyle stability in free fibular flap reconstruction of the mandibular condyle
Shuang BAI ; Yao YU ; Wen-Bo ZHANG ; Ya-Qing MAO ; Yang WANG ; Chi MAO ; Dian-Can WANG ; Xin PENG
Journal of the Korean Association of Oral and Maxillofacial Surgeons 2025;51(1):46-53
Objectives:
This study evaluates the efficacy of a new temporomandibular joint (TMJ) capsule suspension technique for stabilizing the TMJ after free fibular flap reconstruction of the mandibular condyle.
Patients and Methods:
Patients undergoing the TMJ capsule suspension technique during free fibular flap reconstruction after mandibulectomy with condylectomy (study group; n=9) were compared with a control group (n=9). Mandibular movement trajectory and surface electromyographic signals of bilateral masseters were recorded. The neocondyle–disc relationship was examined with magnetic resonance imaging (MRI) at 6 months after surgery.
Results:
Maximal mouth opening and bilateral marginal movement distances were comparable between the two groups (P>0.05). The asymmetry index of the condyle path length was significantly higher in controls (P=0.02). Bilateral mouth opening trajectories were symmetric in 7 patients and deviated to the affected side in 2 patients in the study group; they deviated to the affected side in all controls. The mean electromyographic values of the masseter on the affected side in resting, maximum bite, and chewing states were comparable between the two groups (P=0.13, P=0.65, and P=0.82, respectively). On MRI at 6 months, the thicknesses of the anterior, medial, and posterior bands and TMJ disc length were similar on the affected and normal sides in the study group (P=0.57, P=0.13, P=0.48, and P=0.87, respectively).
Conclusion
The proposed TMJ capsule suspension technique could improve postoperative TMJ structure and function after fibular free flap reconstruction following mandibulectomy with condylectomy.
6.Toxic Components, Toxicity Mechanisms, Toxicity Attenuation Measures, and Evaluation Methods of Renal Injury-inducing Chinese Medicine
Xin HUANG ; Lujin ZHANG ; Mingsan MIAO ; Can WANG
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(11):295-304
ObjectiveWe reviewed the existing experimental studies about renal injury-inducing Chinese medicine and systematically analyzed the toxicity mechanisms, toxic components, toxicity attenuation measures, and modern evaluation methods of renal injury-inducing Chinese medicine. The results are expected to provide new ideas for the modern research on kidney injury-inducing Chinese medicine, offer new breakthrough points for the toxicity attenuation of Chinese medicine by compatibility and processing, and give insights into the future research of Chinese medicine toxicology on the basis of ensuring the safety and scientific application of Chinese medicine. MethodsThe animal, cell, and clinical studies of kidney injury-inducing Chinese medicine were retrieved from CNKI, Wanfang Data, VIP, PubMed, and Web of Science. The names and toxic components of renal injury-inducing Chinese medicine, renal injury sites, toxicity mechanisms, toxicity attenuation measures, and related evaluation methods were summarized. ResultsThe toxicity mechanisms of kidney injury-inducing Chinese medicine mainly involved oxidative stress, endoplasmic reticulum stress, inflammatory cell infiltration, and organic anion transporters. Processing and compatibility were the main toxicity attenuation measures. The evaluation methods encompassed animal experiments, cell models, network pharmacology, metabolomics, toxicology genomics, and fluorescent probe technology. ConclusionAt present, the toxicological verification of kidney injury-inducing Chinese medicine starts from toxic components and combines various experimental methods, which is more comprehensive and systematic than the previous studies based on only animal experiments. According to the classical theories of traditional Chinese medicine, the toxicity of kidney injury-inducing Chinese medicine is mainly attenuated by decocting in water, steaming, and frying. With the progress of science and technology, new processing methods for toxicity attenuation are emerging, and structural transformation, fermentation, and microwave methods are the key research directions of toxicity attenuation of Chinese medicine in recent years.
7.Toxic Components, Toxicity Mechanisms, Toxicity Attenuation Measures, and Evaluation Methods of Renal Injury-inducing Chinese Medicine
Xin HUANG ; Lujin ZHANG ; Mingsan MIAO ; Can WANG
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(11):295-304
ObjectiveWe reviewed the existing experimental studies about renal injury-inducing Chinese medicine and systematically analyzed the toxicity mechanisms, toxic components, toxicity attenuation measures, and modern evaluation methods of renal injury-inducing Chinese medicine. The results are expected to provide new ideas for the modern research on kidney injury-inducing Chinese medicine, offer new breakthrough points for the toxicity attenuation of Chinese medicine by compatibility and processing, and give insights into the future research of Chinese medicine toxicology on the basis of ensuring the safety and scientific application of Chinese medicine. MethodsThe animal, cell, and clinical studies of kidney injury-inducing Chinese medicine were retrieved from CNKI, Wanfang Data, VIP, PubMed, and Web of Science. The names and toxic components of renal injury-inducing Chinese medicine, renal injury sites, toxicity mechanisms, toxicity attenuation measures, and related evaluation methods were summarized. ResultsThe toxicity mechanisms of kidney injury-inducing Chinese medicine mainly involved oxidative stress, endoplasmic reticulum stress, inflammatory cell infiltration, and organic anion transporters. Processing and compatibility were the main toxicity attenuation measures. The evaluation methods encompassed animal experiments, cell models, network pharmacology, metabolomics, toxicology genomics, and fluorescent probe technology. ConclusionAt present, the toxicological verification of kidney injury-inducing Chinese medicine starts from toxic components and combines various experimental methods, which is more comprehensive and systematic than the previous studies based on only animal experiments. According to the classical theories of traditional Chinese medicine, the toxicity of kidney injury-inducing Chinese medicine is mainly attenuated by decocting in water, steaming, and frying. With the progress of science and technology, new processing methods for toxicity attenuation are emerging, and structural transformation, fermentation, and microwave methods are the key research directions of toxicity attenuation of Chinese medicine in recent years.
8.Temporomandibular joint capsule suspension for neocondyle stability in free fibular flap reconstruction of the mandibular condyle
Shuang BAI ; Yao YU ; Wen-Bo ZHANG ; Ya-Qing MAO ; Yang WANG ; Chi MAO ; Dian-Can WANG ; Xin PENG
Journal of the Korean Association of Oral and Maxillofacial Surgeons 2025;51(1):46-53
Objectives:
This study evaluates the efficacy of a new temporomandibular joint (TMJ) capsule suspension technique for stabilizing the TMJ after free fibular flap reconstruction of the mandibular condyle.
Patients and Methods:
Patients undergoing the TMJ capsule suspension technique during free fibular flap reconstruction after mandibulectomy with condylectomy (study group; n=9) were compared with a control group (n=9). Mandibular movement trajectory and surface electromyographic signals of bilateral masseters were recorded. The neocondyle–disc relationship was examined with magnetic resonance imaging (MRI) at 6 months after surgery.
Results:
Maximal mouth opening and bilateral marginal movement distances were comparable between the two groups (P>0.05). The asymmetry index of the condyle path length was significantly higher in controls (P=0.02). Bilateral mouth opening trajectories were symmetric in 7 patients and deviated to the affected side in 2 patients in the study group; they deviated to the affected side in all controls. The mean electromyographic values of the masseter on the affected side in resting, maximum bite, and chewing states were comparable between the two groups (P=0.13, P=0.65, and P=0.82, respectively). On MRI at 6 months, the thicknesses of the anterior, medial, and posterior bands and TMJ disc length were similar on the affected and normal sides in the study group (P=0.57, P=0.13, P=0.48, and P=0.87, respectively).
Conclusion
The proposed TMJ capsule suspension technique could improve postoperative TMJ structure and function after fibular free flap reconstruction following mandibulectomy with condylectomy.
9.Temporomandibular joint capsule suspension for neocondyle stability in free fibular flap reconstruction of the mandibular condyle
Shuang BAI ; Yao YU ; Wen-Bo ZHANG ; Ya-Qing MAO ; Yang WANG ; Chi MAO ; Dian-Can WANG ; Xin PENG
Journal of the Korean Association of Oral and Maxillofacial Surgeons 2025;51(1):46-53
Objectives:
This study evaluates the efficacy of a new temporomandibular joint (TMJ) capsule suspension technique for stabilizing the TMJ after free fibular flap reconstruction of the mandibular condyle.
Patients and Methods:
Patients undergoing the TMJ capsule suspension technique during free fibular flap reconstruction after mandibulectomy with condylectomy (study group; n=9) were compared with a control group (n=9). Mandibular movement trajectory and surface electromyographic signals of bilateral masseters were recorded. The neocondyle–disc relationship was examined with magnetic resonance imaging (MRI) at 6 months after surgery.
Results:
Maximal mouth opening and bilateral marginal movement distances were comparable between the two groups (P>0.05). The asymmetry index of the condyle path length was significantly higher in controls (P=0.02). Bilateral mouth opening trajectories were symmetric in 7 patients and deviated to the affected side in 2 patients in the study group; they deviated to the affected side in all controls. The mean electromyographic values of the masseter on the affected side in resting, maximum bite, and chewing states were comparable between the two groups (P=0.13, P=0.65, and P=0.82, respectively). On MRI at 6 months, the thicknesses of the anterior, medial, and posterior bands and TMJ disc length were similar on the affected and normal sides in the study group (P=0.57, P=0.13, P=0.48, and P=0.87, respectively).
Conclusion
The proposed TMJ capsule suspension technique could improve postoperative TMJ structure and function after fibular free flap reconstruction following mandibulectomy with condylectomy.
10.CDK1-mediated phosphorylation of USP37 regulates SND1 stability and promotes oncogenesis in colorectal cancer.
Liang WU ; Can CHENG ; Ning ZHAO ; Liang ZHU ; Heng LI ; Jingwen LIU ; Yang WU ; Xi CHEN ; Hanhui YAO ; Lianxin LIU
Acta Pharmaceutica Sinica B 2025;15(4):1938-1955
Colorectal cancer (CRC) poses a severe global health challenge with high incidence and mortality rates. USP37 has been identified as the bona fide deubiquitinase of SND1, playing a critical role in stabilizing SND1, thereby augmenting its oncogenic potential. The interaction between USP37 and SND1 was confirmed through extensive proteomics, ubiquitinomics, and interactomics, underscoring their synergistic effects on CRC proliferation and metastasis. Additionally, CDK1 has emerged as a pivotal regulator of USP37, phosphorylating it at threonine 631 rather than serine 628, enhancing its deubiquitinase activity, and consequently stabilizing SND1 to drive CRC malignancy further. Histological analyses of human CRC samples linked the upregulation of CDK1 and USP37 with increased SND1 levels and poor patient prognosis. High-throughput virtual screening and subsequent experimental validation identified Dacarbazine as a pharmacological inhibitor of USP37, and its inhibition disrupted SND1 stability, hindering CRC cell proliferation and metastasis. This study reveals a novel and promising molecular mechanism driving CRC progression through the CDK1-USP37-SND1 axis, highlighting the clinical importance of targeting this pathway to improve patient outcomes.

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