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AIM:To investigate the effects of total flavonoids of Pterocarya hupehensis Skan(PHSTF)on dex-tran sulfate sodium(DSS)-induced ulcerative colitis(UC)mouse model and lipopolysaccharide(LPS)-stimulated RAW264.7 macrophages.METHODS:Thirty-six male C57BL/6J mice(6 to 8 weeks old,SPF grade)were randomly di-vided into 6 groups:negative control(NC)group,3%DSS-induced model group,mesalazine(300 mg·kg-1·d-1)group,and low-dose(62.5 mg·kg-1·d-1),medium-dose(125 mg·kg-1·d-1)and high-dose(250 mg·kg-1·d-1)PHSTF treatment groups,with 6 mice in each group.The mice in NC group received distilled water,while those in other groups were treated with a 3%DSS solution for 7 d to induce the UC model.On the 1st day of DSS administration,the mice in treatment groups received the corresponding agents via oral gavage for 10 d,while those in NC and model groups were gavaged with distilled water.Throughout the study,the effects of PHSTF on body weight,fecal blood,and colon length were measured and recorded daily.Histopathological changes in colon tissues were assessed using hematoxylin-eosin staining.The levels of the pro-inflammatory cytokine interleukin-1β(IL-1β)and the anti-inflammatory cytokine IL-10 in colon tissues were quantified using ELISA.The LPS-induced RAW264.7 macrophage model was employed to evaluate the cellular effects of PHSTF.Cell viability was assessed by CCK-8 assay,and cell morphology was observed under a microscope.The mRNA expression of inflammatory markers[IL-1β,inducible nitric oxide synthase(iNOS),IL-10 and arginase-1(Arg-1)]was measured by RT-qPCR.Western blot and immunofluorescence double labeling were used to detect the protein expression of macrophage polarization markers(iNOS,CD206 and Arg-1).Finally,immunohistochemistry(IHC)was utilized to as-sess protein expression of iNOS in colon tissues.RESULTS:Compared to the DSS-induced UC model group,PHSTF sig-nificantly improved several parameters,including weight loss(P<0.05),rectal bleeding,and colon shortening in DSS-treated mice.PHSTF also reduced histopathological damage and inflammatory cell infiltration in the colon.It decreased IL-1β levels(P<0.05)and increased IL-10 levels(P<0.05)in colon tissues.In LPS-induced RAW264.7 cells,PHSTF reduced the mRNA expression of IL-1β and iNOS(P<0.01),while upregulating the mRNA expression of IL-10 and Arg-1(P<0.01).Additionally,PHSTF decreased iNOS protein expression(P<0.01)and elevated the expression of Arg-1 and CD206 proteins(P<0.01).IHC analysis further confirmed that PHSTF downregulated iNOS protein expression in colon tissues.CONCLUSION:Treatment with PHSTF promotes the polarization of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype,thereby alleviating inflammation in colon tissue and ameliorating ulcer-ative colitis in mice.

Paraplegia caused by spinal cord injury is a serious neurological complication, for which surgery is currently the main treatment method. Due to different surgical approaches, patients are usually expected to maintain a passive prone position for a long time or switch between the supine and prone positions. Affected by multiple factors such as neurogenic sensory disorders, pathological changes in muscle tone and operative duration, the risk of intraoperative acquired pressure injury (IAPI) is significantly increased. Current clinical prevention strategies for IAPI in these patients predominantly focus on localized pressure relief during positioning, lacking systematic, standardized comprehensive prevention protocols or evidence-based guidelines. To address it, Department of Nursing, Orthopedics Branch, China International Exchange and Promotive Association for Medical and Health Care, Spinal Trauma Professional Committee, Orthopedics Branch, Chinese Medical Doctor Association, Nursing Group of Spine and Spinal Cord Professional Committee of Chinese Association of Rehabilitation Medicine organized experts in relevant fields to formulate Guideline for the prevention of intraoperative acquired pressure injury in paraplegic patients with spinal cord injury ( version 2025), based on evidence-based medical evidence and latest research results and clinical practice at home and abroad. Eleven recommendations were put forward from the aspects of preoperative risk assessment, intraoperative prevention strategies, postoperative handover and monitoring, and supportive mechanisms for IAPI prevention, aiming to standardize the prevention measures and management strategies of IAPI in paraplegic patients with spinal cord injury and accelerate the recovery of patients and improve the therapeutic effect.

Objective: To explore effects and maintenance of school based sexual abuse prevention programs for minors, so as to provide scientific evidences for optimizing intervention design and policy making. Methods: Six Chinese and English databases were searched, including CNKI, Wanfang Database, Medline (via PubMed), Embase, Cochrane Library and Web of Science, with the time frame set from database inception to December 31, 2024. Studies on school based sexual abuse prevention programs for minors were selected, and data on knowledge, attitudes and skills related to sexual abuse prevention were extracted. Meta analysis was performed using Stata 17. Results: A total of 26 studies were included. The Meta analysis results showed that school based sexual abuse prevention programs improved participants knowledge ( SMD=1.24, 95%CI =0.96-1.52), attitudes ( SMD=0.62, 95%CI =0.19-1.04) and skills ( SMD=0.66, 95%CI =0.50-0.83) (all P <0.01). During the overall follow up, the maintenance rates for knowledge, attitudes, and skills were 0.97(95% CI =0.95-1.00), 0.99(95% CI =0.95-1.04) and 1.01(95% CI =0.99-1.04), respectively, with no statistically significant differences (all P >0.05). However, knowledge retention declined significantly when follow up exceeded three months ( R=0.91, 95%CI=0.83-0.99, P <0.01), while skills retention ( R=0.94, 95%CI=0.87-1.02, P = 0.23) remained higher than knowledge and attitudes ( R=0.98, 95%CI=0.96-1.00, P =0.13), demonstrating stronger long term effects. Conclusion School based sexual abuse prevention programs are effective in enhancing participants knowledge, attitudes and skills, but the intervention effects diminish over time, particularly in knowledge retention.

Osteoporosis is a systemic metabolic disease characterized by decreased bone mass, leading to an increased risk of fractures. Although osteoporosis in children and adolescents is rare, its incidence in younger populations is showing an increasingly notable trend. The diagnostic criteria for osteoporosis in children and adolescents include a bone mineral density(BMD) Z-score of≤-2.0 accompanied by a significant fracture history, defined as two or more long bone fractures before the age of 10, three or more long bone fractures before the age of 19, or the presence of low-energy vertebral compression fractures even in the absence of low BMD. The genetic causes and underlying mechanisms of pediatric osteoporosis remain largely unknown, requiring further research to elucidate the molecular pathways involved. Such advances could help reduce the disease′s impact on growth and development and improve the quality of life in affected children and adolescents.

Objective:To investigate the therapeutic effects of adeno-associated virus vector 5 (AAV5)-mediated hepatic lipoprotein lipase (LPL) expression on serum triglyceride (TG) metabolism and hypertriglyceridemic acute pancreatitis (HTG-AP) in mice.Methods:Ten male C57BL/6 Lpl+/- mice were randomly divided into two groups by a random number table: the Lpl+/- control group and the Lpl+/- gene therapy group, with five mice in each group. The Lpl+/- control group received a tail vein injection of AAV5 vector carrying the enhanced green fluorescent protein (EGFP) gene (AAV5-EGFP), while the Lpl+/- gene therapy group received a tail vein injection of AAV5 vector carrying the human LPLS447X gene (AAV5-LPLS447X). Oral fat tolerance tests were performed at 14, 28, and 56 days post-injection. Twenty wild-type ICR mice were randomly divided into a control group and a gene therapy group, with ten mice in each group. The ICR control group was injected with AAV5-EGFP, and the ICR gene therapy group was injected with AAV5-LPLS447X. Fourteen days after injection, the mice underwent intraperitoneal injection of P407 solution (0.5 g/kg) and caerulein (200 μg/kg) to induce HTG-AP. Serum TG, total cholesterol (TC), amylase, lipase levels, and plasma LPL activity after heparin injection were measured by microplate reader. Plasma LPL concentration was measured using an enzyme-linked immunosorbent assay (ELISA). LPL mRNA expression levels in the liver, heart, and adipose tissue of Lpl+/- mice were determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). LPL protein expression in the liver tissue of ICR mice was detected by immunohistochemistry at 28 days after gene therapy. Histopathological changes in the pancreas were observed using hematoxylin-eosin staining. Results:Compared to the Lpl+/- control group, the Lpl+/- gene therapy group showed a significant decrease in serum TG levels starting from day 21. After oral administration of olive oil, the increase and peak of serum TG levels were significantly lower than those in the control group. Furthermore, hepatic LPL mRNA expression levels were significantly higher (1.96±0.11 vs 1.02±0.12) with statistical significance ( P<0.05). Compared to the ICR control group, the ICR gene therapy group showed a significant decrease in serum TG and TC levels, and plasma LPL activity (0.17±0.05 mEq/L·h -1vs 0.06±0.02 mEq/L·h -1) was significantly higher at 28 days after heparin injection with statistical significance (all P value <0.05). Immunohistochemical results showed high expression of LPL protein on the hepatocyte membrane in the liver of ICR gene therapy group mice. Moreover, pancreatic edema, inflammatory infiltration, and acinar cell necrosis were significantly alleviated compared to the control group. Conclusions:LPLS447X treatment can promote LPL expression in the liver of mice, significantly reduce TG levels, and alleviate the severity of HTG-AP.

AIM:To investigate the effects of total flavonoids of Pterocarya hupehensis Skan(PHSTF)on dex-tran sulfate sodium(DSS)-induced ulcerative colitis(UC)mouse model and lipopolysaccharide(LPS)-stimulated RAW264.7 macrophages.METHODS:Thirty-six male C57BL/6J mice(6 to 8 weeks old,SPF grade)were randomly di-vided into 6 groups:negative control(NC)group,3%DSS-induced model group,mesalazine(300 mg·kg-1·d-1)group,and low-dose(62.5 mg·kg-1·d-1),medium-dose(125 mg·kg-1·d-1)and high-dose(250 mg·kg-1·d-1)PHSTF treatment groups,with 6 mice in each group.The mice in NC group received distilled water,while those in other groups were treated with a 3%DSS solution for 7 d to induce the UC model.On the 1st day of DSS administration,the mice in treatment groups received the corresponding agents via oral gavage for 10 d,while those in NC and model groups were gavaged with distilled water.Throughout the study,the effects of PHSTF on body weight,fecal blood,and colon length were measured and recorded daily.Histopathological changes in colon tissues were assessed using hematoxylin-eosin staining.The levels of the pro-inflammatory cytokine interleukin-1β(IL-1β)and the anti-inflammatory cytokine IL-10 in colon tissues were quantified using ELISA.The LPS-induced RAW264.7 macrophage model was employed to evaluate the cellular effects of PHSTF.Cell viability was assessed by CCK-8 assay,and cell morphology was observed under a microscope.The mRNA expression of inflammatory markers[IL-1β,inducible nitric oxide synthase(iNOS),IL-10 and arginase-1(Arg-1)]was measured by RT-qPCR.Western blot and immunofluorescence double labeling were used to detect the protein expression of macrophage polarization markers(iNOS,CD206 and Arg-1).Finally,immunohistochemistry(IHC)was utilized to as-sess protein expression of iNOS in colon tissues.RESULTS:Compared to the DSS-induced UC model group,PHSTF sig-nificantly improved several parameters,including weight loss(P<0.05),rectal bleeding,and colon shortening in DSS-treated mice.PHSTF also reduced histopathological damage and inflammatory cell infiltration in the colon.It decreased IL-1β levels(P<0.05)and increased IL-10 levels(P<0.05)in colon tissues.In LPS-induced RAW264.7 cells,PHSTF reduced the mRNA expression of IL-1β and iNOS(P<0.01),while upregulating the mRNA expression of IL-10 and Arg-1(P<0.01).Additionally,PHSTF decreased iNOS protein expression(P<0.01)and elevated the expression of Arg-1 and CD206 proteins(P<0.01).IHC analysis further confirmed that PHSTF downregulated iNOS protein expression in colon tissues.CONCLUSION:Treatment with PHSTF promotes the polarization of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype,thereby alleviating inflammation in colon tissue and ameliorating ulcer-ative colitis in mice.

Objective:To investigate the therapeutic effects of adeno-associated virus vector 5 (AAV5)-mediated hepatic lipoprotein lipase (LPL) expression on serum triglyceride (TG) metabolism and hypertriglyceridemic acute pancreatitis (HTG-AP) in mice.Methods:Ten male C57BL/6 Lpl+/- mice were randomly divided into two groups by a random number table: the Lpl+/- control group and the Lpl+/- gene therapy group, with five mice in each group. The Lpl+/- control group received a tail vein injection of AAV5 vector carrying the enhanced green fluorescent protein (EGFP) gene (AAV5-EGFP), while the Lpl+/- gene therapy group received a tail vein injection of AAV5 vector carrying the human LPLS447X gene (AAV5-LPLS447X). Oral fat tolerance tests were performed at 14, 28, and 56 days post-injection. Twenty wild-type ICR mice were randomly divided into a control group and a gene therapy group, with ten mice in each group. The ICR control group was injected with AAV5-EGFP, and the ICR gene therapy group was injected with AAV5-LPLS447X. Fourteen days after injection, the mice underwent intraperitoneal injection of P407 solution (0.5 g/kg) and caerulein (200 μg/kg) to induce HTG-AP. Serum TG, total cholesterol (TC), amylase, lipase levels, and plasma LPL activity after heparin injection were measured by microplate reader. Plasma LPL concentration was measured using an enzyme-linked immunosorbent assay (ELISA). LPL mRNA expression levels in the liver, heart, and adipose tissue of Lpl+/- mice were determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). LPL protein expression in the liver tissue of ICR mice was detected by immunohistochemistry at 28 days after gene therapy. Histopathological changes in the pancreas were observed using hematoxylin-eosin staining. Results:Compared to the Lpl+/- control group, the Lpl+/- gene therapy group showed a significant decrease in serum TG levels starting from day 21. After oral administration of olive oil, the increase and peak of serum TG levels were significantly lower than those in the control group. Furthermore, hepatic LPL mRNA expression levels were significantly higher (1.96±0.11 vs 1.02±0.12) with statistical significance ( P<0.05). Compared to the ICR control group, the ICR gene therapy group showed a significant decrease in serum TG and TC levels, and plasma LPL activity (0.17±0.05 mEq/L·h -1vs 0.06±0.02 mEq/L·h -1) was significantly higher at 28 days after heparin injection with statistical significance (all P value <0.05). Immunohistochemical results showed high expression of LPL protein on the hepatocyte membrane in the liver of ICR gene therapy group mice. Moreover, pancreatic edema, inflammatory infiltration, and acinar cell necrosis were significantly alleviated compared to the control group. Conclusions:LPLS447X treatment can promote LPL expression in the liver of mice, significantly reduce TG levels, and alleviate the severity of HTG-AP.

Paraplegia caused by spinal cord injury is a serious neurological complication, for which surgery is currently the main treatment method. Due to different surgical approaches, patients are usually expected to maintain a passive prone position for a long time or switch between the supine and prone positions. Affected by multiple factors such as neurogenic sensory disorders, pathological changes in muscle tone and operative duration, the risk of intraoperative acquired pressure injury (IAPI) is significantly increased. Current clinical prevention strategies for IAPI in these patients predominantly focus on localized pressure relief during positioning, lacking systematic, standardized comprehensive prevention protocols or evidence-based guidelines. To address it, Department of Nursing, Orthopedics Branch, China International Exchange and Promotive Association for Medical and Health Care, Spinal Trauma Professional Committee, Orthopedics Branch, Chinese Medical Doctor Association, Nursing Group of Spine and Spinal Cord Professional Committee of Chinese Association of Rehabilitation Medicine organized experts in relevant fields to formulate Guideline for the prevention of intraoperative acquired pressure injury in paraplegic patients with spinal cord injury ( version 2025), based on evidence-based medical evidence and latest research results and clinical practice at home and abroad. Eleven recommendations were put forward from the aspects of preoperative risk assessment, intraoperative prevention strategies, postoperative handover and monitoring, and supportive mechanisms for IAPI prevention, aiming to standardize the prevention measures and management strategies of IAPI in paraplegic patients with spinal cord injury and accelerate the recovery of patients and improve the therapeutic effect.

Osteoporosis is a systemic metabolic disease characterized by decreased bone mass, leading to an increased risk of fractures. Although osteoporosis in children and adolescents is rare, its incidence in younger populations is showing an increasingly notable trend. The diagnostic criteria for osteoporosis in children and adolescents include a bone mineral density(BMD) Z-score of≤-2.0 accompanied by a significant fracture history, defined as two or more long bone fractures before the age of 10, three or more long bone fractures before the age of 19, or the presence of low-energy vertebral compression fractures even in the absence of low BMD. The genetic causes and underlying mechanisms of pediatric osteoporosis remain largely unknown, requiring further research to elucidate the molecular pathways involved. Such advances could help reduce the disease′s impact on growth and development and improve the quality of life in affected children and adolescents.