1.Current situation and influencing factors of family resilience of children with cancer
Funa YANG ; Rui YANG ; Yan QIN ; Junhan CHEN ; Lanwei GUO ; Yongqi WANG ; Kayan HO ; Qi LIU ; Ting MAO ; Xiaoxiao MEI ; Wenying WANG ; Xiaoxia XU ; Hongying SHI
Chinese Journal of Nursing 2025;60(4):446-453
Objective To investigate the current status of family resilience of children with cancer and analyze its influencing factors,to provide a basis for medical staff to formulate intervention plans.Methods Using a convenient sampling method,children with cancer who were hospitalized in 2 tertiary hospitals in Henan Province from January to April 2024 were selected for the survey.A general information questionnaire,family resilience assessment scale,quality of life family version,ZBI caregiver burden interview,and social support rating scale were used to understand the current status of family resilience of children with cancer and to explore the related influencing factors by univariate analysis and multiple stepwise linear regression analysis.Results A total of 280 questionnaires were distributed and 265 valid questionnaires were recovered,with a valid questionnaire recovery rate of 94.64%.The total score of family resilience for primary caregivers of children with cancer was(185.63±30.66).The multiple stepwise linear regression analysis results showed that the children's self-care ability,caregiver's work status,family care burden,and social support level were the influencing factors for family resilience of children with cancer(P<0.05),and the explanatory variance was 51.3%.Conclusion The family resilience of children with cancer is at a medium level.The worse the children's self-care ability and the heavier the family care burden,the worse the family resilience;the caregiver's work status and good social support are helpful for the family resilience of children with cancer.Healthcare workers should develop intervention programs to address these factors to enhance the family resilience of children with cancer.
2.Role and mechanism of PRMT1 and its inhibitors in the occurrence and development of corneal neovascularization in mice
Yuelan GAO ; Qian DENG ; Jiewen MAO ; Rui ZHANG ; Xiaoshuo SHI ; Shanshan WAN ; Yanning YANG
Chinese Journal of Experimental Ophthalmology 2025;43(8):688-703
Objective:To investigate the role and underlying mechanism of protein arginine methyltransferase 1 (PRMT1) and its inhibitor in alkali burn-induced corneal neovascularization (CNV).Methods:Seventy-two SPF-grade C57BL/6 mice were randomly divided into a normal group and 1 day post-modeling, 4 days post-modeling, and 7 days post-modeling groups to establish an alkali burn-induced CNV model and determine the optimal time point for analysis.Another 90 mice were randomly assigned to five groups: alkali burn group, dimethyl sulfoxide (DMSO) group, PRMT1 inhibitor group, fibroblast growth factor 2 (FGF2) inhibitor group, and PRMT1 inhibitor combined with FGF2 group to evaluate the role of PRMT1 in CNV.Human umbilical vein endothelial cells (HUVECs) and murine macrophage-like RAW264.7 cells were used to establish a hypoxia/reoxygenation (H/R)-induced in vitro model to mimic the ischemic microenvironment.Cells were assigned to the following groups: control group, H/R group, H/R+ DMSO group, H/R+ si-NC group, H/R+ si-PRMT1 group, H/R+ si-FGF2 group, H/R+ PRMT1 inhibitor group, and H/R+ PRMT1 inhibitor+ FGF2 group.Corneal opacity and CNV areas were assessed by slit-lamp microscopy.Corneal structural changes and inflammatory cell count were determined by hematoxylin and eosin staining.PRMT1-positive cell count was determined by immunohistochemistry and the expression of PRMT1, CD31, vascular endothelial growth factor (VEGF), F4/80, CD206, and inducible nitric oxide synthase (iNOS) was assessed by immunofluorescence staining.The expression levels of macrophage markers, including F4/80, iNOS, CD206, interleukin-10 (IL-10), and arginase-1 (Arg-1), were quantified by real-time quantitative PCR and Western blot.Cell proliferation, migration, and angiogenic capacity were evaluated by functional assays including the CCK-8 assay, wound healing assay, Transwell migration assay, and tube formation assay.The research process followed the relevant regulations of the Visual and Ophthalmology Association, and the research plan was approved by the Laboratory Animal Committee of Wuhan University (No.20220504A). Results:Compared with the normal group, the 7 days post-modeling group showed significantly increased corneal opacity scores and CNV area, upregulated VEGF expression, and increased inflammatory cells (all P<0.05).The number of PRMT1-positive cells in the alkali burn group was (39.67±3.51) cells/visual field, which was significantly higher than (3.33±0.58) cells/visual field in the normal group ( t=17.68, P<0.01).Both mRNA and protein expression levels of PRMT1 and FGF2 were significantly elevated in the alkali burn group compared with the normal group (all P<0.01).Compared with the alkali burn group, the PRMT1 inhibitor group showed reduced corneal opacity scores, decreased CNV area, fewer inflammatory cells, and lower expression levels of PRMT1, FGF2, VEGF, Arg-1, IL-10 proteins, as well as CD206 mRNA (all P<0.05).Cell viability, migration distance, migration number, and tubes formed were significantly increased in the H/R group compared with the control group, significantly reduced in the H/R+ si-PRMT1 and H/R+ PRMT1 inhibitor groups compared with the H/R group and significantly increased in H/R+ PRMT1 inhibitor+ FGF2 group than in H/R+ PRMT1 inhibitor group (all P<0.05).Compared with the H/R group, the H/R+ PRMT1 inhibitor group exhibited reduced expression of FGF2, VEGFA, p-PI3K, and p-Akt, while those were upregulated in the H/R+ PRMT1 inhibitor+ FGF2 group compared with the H/R+ PRMT1 inhibitor group (all P<0.05).The proportions of CD206-positive cells in the H/R, H/R+ DMSO, H/R+ PRMT1 inhibitor, and H/R+ PRMT1 inhibitor+ FGF2 groups were all significantly higher than those in the control group, and significantly higher in the H/R, H/R+ DMSO, and H/R+ PRMT1 inhibitor+ FGF2 groups compared with the H/R+ PRMT1 inhibitor group (all P<0.05).Compared with the alkali burn group, the FGF2 inhibitor group, PRMT1 inhibitor group, and PRMT1 inhibitor+ FGF2 group all showed reduced corneal opacity scores, CNV area, and decreased number of VEGFA-, CD206-, and F4/80-positive cells, with the above indicators being lower in the PRMT1 inhibitor group compared with the FGF2 inhibitor and PRMT1 inhibitor+ FGF2 groups and higher in PRMT1 inhibitor+ FGF2 group than in the FGF2 inhibitor group (all P<0.05).Compared with the alkali burn group, the PRMT1 inhibitor group had decreased protein expression levels of FGF2, p-PI3K, p-Akt, CD31, VEGFA and Arg-1, with higher protein expression levels in the PRMT1 inhibitor+ FGF2 group than in the PRMT1 inhibitor group (all P<0.05). Conclusions:PRMT1 may regulate macrophage activation and anti-inflammatory polarization via the FGF2/PI3K/Akt signaling pathway, thereby promoting the occurrence and development of CNV.Targeted inhibition of PRMT1 may serve as an effective therapeutic strategy for CNV.
3.Role and mechanism of PRMT1 and its inhibitors in the occurrence and development of corneal neovascularization in mice
Yuelan GAO ; Qian DENG ; Jiewen MAO ; Rui ZHANG ; Xiaoshuo SHI ; Shanshan WAN ; Yanning YANG
Chinese Journal of Experimental Ophthalmology 2025;43(8):688-703
Objective:To investigate the role and underlying mechanism of protein arginine methyltransferase 1 (PRMT1) and its inhibitor in alkali burn-induced corneal neovascularization (CNV).Methods:Seventy-two SPF-grade C57BL/6 mice were randomly divided into a normal group and 1 day post-modeling, 4 days post-modeling, and 7 days post-modeling groups to establish an alkali burn-induced CNV model and determine the optimal time point for analysis.Another 90 mice were randomly assigned to five groups: alkali burn group, dimethyl sulfoxide (DMSO) group, PRMT1 inhibitor group, fibroblast growth factor 2 (FGF2) inhibitor group, and PRMT1 inhibitor combined with FGF2 group to evaluate the role of PRMT1 in CNV.Human umbilical vein endothelial cells (HUVECs) and murine macrophage-like RAW264.7 cells were used to establish a hypoxia/reoxygenation (H/R)-induced in vitro model to mimic the ischemic microenvironment.Cells were assigned to the following groups: control group, H/R group, H/R+ DMSO group, H/R+ si-NC group, H/R+ si-PRMT1 group, H/R+ si-FGF2 group, H/R+ PRMT1 inhibitor group, and H/R+ PRMT1 inhibitor+ FGF2 group.Corneal opacity and CNV areas were assessed by slit-lamp microscopy.Corneal structural changes and inflammatory cell count were determined by hematoxylin and eosin staining.PRMT1-positive cell count was determined by immunohistochemistry and the expression of PRMT1, CD31, vascular endothelial growth factor (VEGF), F4/80, CD206, and inducible nitric oxide synthase (iNOS) was assessed by immunofluorescence staining.The expression levels of macrophage markers, including F4/80, iNOS, CD206, interleukin-10 (IL-10), and arginase-1 (Arg-1), were quantified by real-time quantitative PCR and Western blot.Cell proliferation, migration, and angiogenic capacity were evaluated by functional assays including the CCK-8 assay, wound healing assay, Transwell migration assay, and tube formation assay.The research process followed the relevant regulations of the Visual and Ophthalmology Association, and the research plan was approved by the Laboratory Animal Committee of Wuhan University (No.20220504A). Results:Compared with the normal group, the 7 days post-modeling group showed significantly increased corneal opacity scores and CNV area, upregulated VEGF expression, and increased inflammatory cells (all P<0.05).The number of PRMT1-positive cells in the alkali burn group was (39.67±3.51) cells/visual field, which was significantly higher than (3.33±0.58) cells/visual field in the normal group ( t=17.68, P<0.01).Both mRNA and protein expression levels of PRMT1 and FGF2 were significantly elevated in the alkali burn group compared with the normal group (all P<0.01).Compared with the alkali burn group, the PRMT1 inhibitor group showed reduced corneal opacity scores, decreased CNV area, fewer inflammatory cells, and lower expression levels of PRMT1, FGF2, VEGF, Arg-1, IL-10 proteins, as well as CD206 mRNA (all P<0.05).Cell viability, migration distance, migration number, and tubes formed were significantly increased in the H/R group compared with the control group, significantly reduced in the H/R+ si-PRMT1 and H/R+ PRMT1 inhibitor groups compared with the H/R group and significantly increased in H/R+ PRMT1 inhibitor+ FGF2 group than in H/R+ PRMT1 inhibitor group (all P<0.05).Compared with the H/R group, the H/R+ PRMT1 inhibitor group exhibited reduced expression of FGF2, VEGFA, p-PI3K, and p-Akt, while those were upregulated in the H/R+ PRMT1 inhibitor+ FGF2 group compared with the H/R+ PRMT1 inhibitor group (all P<0.05).The proportions of CD206-positive cells in the H/R, H/R+ DMSO, H/R+ PRMT1 inhibitor, and H/R+ PRMT1 inhibitor+ FGF2 groups were all significantly higher than those in the control group, and significantly higher in the H/R, H/R+ DMSO, and H/R+ PRMT1 inhibitor+ FGF2 groups compared with the H/R+ PRMT1 inhibitor group (all P<0.05).Compared with the alkali burn group, the FGF2 inhibitor group, PRMT1 inhibitor group, and PRMT1 inhibitor+ FGF2 group all showed reduced corneal opacity scores, CNV area, and decreased number of VEGFA-, CD206-, and F4/80-positive cells, with the above indicators being lower in the PRMT1 inhibitor group compared with the FGF2 inhibitor and PRMT1 inhibitor+ FGF2 groups and higher in PRMT1 inhibitor+ FGF2 group than in the FGF2 inhibitor group (all P<0.05).Compared with the alkali burn group, the PRMT1 inhibitor group had decreased protein expression levels of FGF2, p-PI3K, p-Akt, CD31, VEGFA and Arg-1, with higher protein expression levels in the PRMT1 inhibitor+ FGF2 group than in the PRMT1 inhibitor group (all P<0.05). Conclusions:PRMT1 may regulate macrophage activation and anti-inflammatory polarization via the FGF2/PI3K/Akt signaling pathway, thereby promoting the occurrence and development of CNV.Targeted inhibition of PRMT1 may serve as an effective therapeutic strategy for CNV.
4.Current situation and influencing factors of family resilience of children with cancer
Funa YANG ; Rui YANG ; Yan QIN ; Junhan CHEN ; Lanwei GUO ; Yongqi WANG ; Kayan HO ; Qi LIU ; Ting MAO ; Xiaoxiao MEI ; Wenying WANG ; Xiaoxia XU ; Hongying SHI
Chinese Journal of Nursing 2025;60(4):446-453
Objective To investigate the current status of family resilience of children with cancer and analyze its influencing factors,to provide a basis for medical staff to formulate intervention plans.Methods Using a convenient sampling method,children with cancer who were hospitalized in 2 tertiary hospitals in Henan Province from January to April 2024 were selected for the survey.A general information questionnaire,family resilience assessment scale,quality of life family version,ZBI caregiver burden interview,and social support rating scale were used to understand the current status of family resilience of children with cancer and to explore the related influencing factors by univariate analysis and multiple stepwise linear regression analysis.Results A total of 280 questionnaires were distributed and 265 valid questionnaires were recovered,with a valid questionnaire recovery rate of 94.64%.The total score of family resilience for primary caregivers of children with cancer was(185.63±30.66).The multiple stepwise linear regression analysis results showed that the children's self-care ability,caregiver's work status,family care burden,and social support level were the influencing factors for family resilience of children with cancer(P<0.05),and the explanatory variance was 51.3%.Conclusion The family resilience of children with cancer is at a medium level.The worse the children's self-care ability and the heavier the family care burden,the worse the family resilience;the caregiver's work status and good social support are helpful for the family resilience of children with cancer.Healthcare workers should develop intervention programs to address these factors to enhance the family resilience of children with cancer.
5.Dual activation of GCGR/GLP1R signaling ameliorates intestinal fibrosis via metabolic regulation of histone H3K9 lactylation in epithelial cells.
Han LIU ; Yujie HONG ; Hui CHEN ; Xianggui WANG ; Jiale DONG ; Xiaoqian LI ; Zihan SHI ; Qian ZHAO ; Longyuan ZHOU ; JiaXin WANG ; Qiuling ZENG ; Qinglin TANG ; Qi LIU ; Florian RIEDER ; Baili CHEN ; Minhu CHEN ; Rui WANG ; Yao ZHANG ; Ren MAO ; Xianxing JIANG
Acta Pharmaceutica Sinica B 2025;15(1):278-295
Intestinal fibrosis is a significant clinical challenge in inflammatory bowel diseases, but no effective anti-fibrotic therapy is currently available. Glucagon receptor (GCGR) and glucagon-like peptide 1 receptor (GLP1R) are both peptide hormone receptors involved in energy metabolism of epithelial cells. However, their role in intestinal fibrosis and the underlying mechanisms remain largely unexplored. Herein GCGR and GLP1R were found to be reduced in the stenotic ileum of patients with Crohn's disease as well as in the fibrotic colon of mice with chronic colitis. The downregulation of GCGR and GLP1R led to the accumulation of the metabolic byproduct lactate, resulting in histone H3K9 lactylation and exacerbated intestinal fibrosis through epithelial-to-mesenchymal transition (EMT). Dual activating GCGR and GLP1R by peptide 1907B reduced the H3K9 lactylation in epithelial cells and ameliorated intestinal fibrosis in vivo. We uncovered the role of GCGR/GLP1R in regulating EMT involved in intestinal fibrosis via histone lactylation. Simultaneously activating GCGR/GLP1R with the novel dual agonist peptide 1907B holds promise as a treatment strategy for alleviating intestinal fibrosis.
6.Application of OpenSim musculoskeletal model in biomechanics research of orthopedics and traumatology.
Rui LI ; Yang LIU ; Zhao-Jie ZHANG ; Xin-Wei ZHANG ; Yan-Zhen ZHANG ; Yan-Qi HU ; Can YANG ; Shu-Shi MAO ; Jia-Ming QIU
China Journal of Orthopaedics and Traumatology 2025;38(3):319-324
OpenSim is an open source, free motion simulation and gait analysis software, which can be used to dynamically simulate and analyze the complex motion of the human body, and is widely used in human biomechanical research. Since OpenSim can analyze multi-dimensional motion data such as muscle strength, joint torque, and muscle synergistic activation during human movement, it can be used to study the biomechanical mechanism of musculoskeletal imbalance diseases and various treatment methods in TCM orthopedics, and has a broad application prospect in the field of TCM orthopedics. By the analysis of the basic characteristics, elements, analysis process, and application prospects of OpenSim, it is concluded that OpenSim musculoskeletal model has a large application space in the field of traditional Chinese medicine orthopedic, which is helpful to explain the pathogenesis and mechanism of diseases, and promote the precision diagnosis and treatment of orthopedics diseases;the application of OpenSim musculoskeletal model can solve the problem that the previous research paid attention to the bone malalignment and not enough attention to the tendon, and provide a new method for the research of orthopedic diseases. At present, there are still problems in the promotion and application of OpenSim, such as large equipment requirements and high operation threshold. Therefore, multidisciplinary cooperation, clinical research, and data sharing are the basic research strategies in this field.
Humans
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Biomechanical Phenomena
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Orthopedics
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Traumatology
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Software
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Medicine, Chinese Traditional
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Musculoskeletal System
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Models, Biological
7.A Health Economic Evaluation of an Artificial Intelligence-assisted Prescription Review System in a Real-world Setting in China.
Di WU ; Ying Peng QIU ; Li Wei SHI ; Ke Jun LIU ; Xue Qing TIAN ; Ping REN ; Mao YOU ; Jun Rui PEI ; Wen Qi FU ; Yue XIAO
Biomedical and Environmental Sciences 2025;38(3):385-388
8.Identification, expression and protein interaction analysis of Aux/IAA and ARF gene family in Senna tora L.
Zhao FENG ; Shi-peng LIU ; Rui-hua LÜ ; Rui-hua LÜ ; Xiao-chen HU ; Ming-ying ZHANG ; Ren-jun MAO ; Gang ZHANG
Acta Pharmaceutica Sinica 2024;59(3):751-763
The early response of plant auxin gene family
9.A quantitative research on China's basic medical insurance policy text for Traditional Chinese Medicine from the perspective of policy instrument
Sheng-Hui SHI ; Mao YOU ; Rui-Feng LI ; Xue-Qing TIAN ; Ping REN ; Lan-Tao WU ; Qiu-Ying ZHENG
Chinese Journal of Health Policy 2024;17(4):16-22
Objective:To summarize and analyze the composition characteristics and problems of basic medical insurance policies for traditional Chinese medicine in various provinces of China,providing reference for optimizing and improving subsequent basic medical insurance policies for traditional Chinese medicine.Methods:Based on the perspective of policy instrument,combined with two dimensions of policy instrument types and policy development process,the content analysis method is used to quantitatively analyze the content of the basic medical insurance policies for traditional Chinese medicine released at the provincial level from 2011 to 2023.Results:The 93 included policy documents were coded and sorted,with a cumulative total of 487 codes.From the perspective of policy instrument dimensions,subcategories of policy instruments involve diverse themes,but there are differences in the level of attention paid to each policy tool.From the perspective of policy development process,each link also presents a discrete trend,indicating a dominant feature of policy planning and implementation.Conclusion:To improve the basic medical insurance policy system of traditional Chinese medicine in China,it is necessary to optimize the combination of policy instrument and construct a coordinated and balanced policy instrument framework;Overall planning of the development process of traditional Chinese medicine medical insurance policies,highlighting the unique advantages of traditional Chinese medicine;Emphasize policy synergy between dimensions and strengthen the implementation of traditional Chinese medicine medical insurance policies.
10.Guillain-Barre syndrome after allogeneic hematopoietic stem cell transplantation: a case report and literature review
Yajun SHI ; Ying HAN ; Ying WANG ; Rui ZHOU ; Rui SONG ; Dongfeng MAO ; Rui XI ; Hai BAI ; Tao WU
Chinese Journal of Hematology 2024;45(5):509-511
Guillain-Barre syndrome rarely develops after allogeneic hematopoietic stem cell transplantation (allo-HSCT), and only a few reports exist in China. Guillain-Barre syndrome is an acute and life-threatening condition that requires early diagnosis and treatment. A patient with acute myeloid leukemia underwent allogeneic HSCT for >5 months and gradually developed limb muscle weakness and limited eye movement after coexisting with delayed acute intestinal graft-versus-host disease. After the examination of cerebrospinal fluid and electromyography, the diagnosis of Guillain–Barre syndrome was confirmed. After a high-dose intravenous immunoglobulin (IVIg) treatment, muscle strength gradually recovered, and the prognosis was good.

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