OBJECTIVE To investigate the ameliorative effects and mechanisms of Miao medicine Euphorbia humifusa on hepatic fibrosis （HF） model rats. METHODS Thirty-eight rats were randomly assigned according to a random number table into control group （normal saline， n＝7）， model group （normal saline， n＝7）， E. humifusa low-， medium- and high-dose groups （0.675， 1.35， 2.70 g/kg， n＝6）， and silybin group （positive control， 18.9 mg/kg， n＝6）. All groups except the control group were subjected to HF induction via intraperitoneal injection of carbon tetrachloride. After modeling， rats were administered their respective drugs/normal saline by gavage， once a day， for 30 days. At the last medication， the liver index was calculated， and serum levels of tumor necrosis factor-α （TNF-α）， interleukin-17 （IL-17）， IL-1β， IL-6， alanine transaminase （ALT）， aspartate transaminase （AST）， and hydroxyproline （HYP） were measured. Liver morphology and HF changes were observed. Levels of transforming growth factor- β1 （TGF- β1） and α-smooth muscle actin （α-SMA）， as well as the expressions of α -SMA， proteins related to TNF- α/NF- κB signaling pathway， mRNA expressions of TNF-α and NF-κB p65 in liver tissue were determined. RESULTS Compared with model group， liver index， serum levels of TNF-α， IL-17， IL-1β， IL-6， ALT， AST and HYP， relative expression of NF-κB p65 mRNA， and the levels of TNF-α and α-SMA proteins and phosphorylated NF-κB p65 in liver tissues of rats from administration groups， the expressions of α-SMA and TGF-β1 in liver tissue of rats from E. humifusa medium-dose and high-dose groups， as well as positive staining percentage and mRNA expression of TNF- α in liver tissue of rats from E. humifusa high-dose group were all decreased significantly （P＜0.05 or P＜0.01）； IκBα protein expression from administration groups was significantly increased （P＜0.05 or P＜0.01）. Pathological changes and the degree of HF in the liver tissues of rats from administration groups were ameliorated to various extents. CONCLUSIONS E. humifusa may alleviate HF in rats by inhibiting the activation of the TNF-α/NF-κB signaling pathway.

Objective: To evaluate the intervention effectiveness of co-occurrence and prevention for myopia and obesity among primary and secondary school students, so as to provide a scientific basis for the development of comprehensive intervention measures in myopia and obesity. Methods: From September 2022 to September 2023, a cluster random sampling method was used to select 6 primary schools and 6 junior high schools from Tongzhou District, Beijing. Participants were randomly assigned to an intervention group (914 before intervention and 754 after intervention) and a control group (868 before intervention and 652 after intervention), with an expected duration of one academic year. Based on the RE-AIM framework, integrate resources from families, schools, communities, and medical institutions to develop a school-based intervention technology packagefor the co-occurrence and prevention of myopia and obesity in children. The intervention group received intervention according to the comprehensive intervention technology package, while the control group did not receive any intervention measures. Relevant health indicators during the baseline period and after intervention were measured and collected, and groups were compared by Chi quest test, t-test and Wilcoxon rank sum test. Results: After intervention, the uncorrected visual acuity of primary and secondary school students in the intervention group (4.79±0.30) and the control group (4.77±0.33) both decreased compared to those before intervention (4.80±0.30, 4.90±0.32) ( t =-7.00,-5.24); the decrease in uncorrected visual acuity in the intervention group was smaller than that in the control group( t =5.33)( P <0.01). After intervention, body mass index, waist circumference, hip circumference, and body fat percentage of primary and secondary school students in the intervention group decreased compared to those before intervention. However, the changes in these indicators were not statistically significant ( t/Z =-0.03, - 0.36，- 0.30，- 0.01, P >0.05); the above indicators in the control group increased compared to those before intervention, but only hip circumference and body fat percentage showed statistically significant changes ( t/Z =2.17, 2.62, P <0.05). After intervention, both the intervention group and the control group showed increases in systolic and diastolic blood pressure compared to those before intervention(intervention group: t =2.16,5.29; control group: t =6.84,5.07); the intervention group had lower systolic and diastolic blood pressure than the control group( t = -5.27 , -2.08)( P <0.05). After intervention, the intervention and the control groups had statistically significant differences in cognitive accuracy(92.48%, 69.33%) in terms of "outdoor exercise can prevent myopia" and "having 5 servings of adult fist sized vegetables and fruits every day" ( χ 2=6.30, 7.86, P <0.05). There was a statistically significant difference in the proportion of primary and secondary school students in the intervention group (40.98%) and the control group (35.43%) for "who did not drink sugary drinks for every day in the past 7 days" ( χ 2=4.32, P <0.05). After intervention, the intervention group and the control group showed increases in "school outdoor activity duration on school days" and "outdoor activity duration on rest days" compared to those before intervention ( t/Z =-13.32,-9.71;- 2.59，-2.69）；the behavior rate of "visual acuity measurement frequency at least once every 3 months" in the intervention group (46.68%) and the control group (52.76%) increased compared to those before intervention (36.43%, 44.01%), and the increases in the intervention group were greater than that in the control group ( χ 2=17.52,11.08) ( P <0.05). Conclusions Comprehensive intervention measures have significant intervention effects on controlling the occurrence and development of comorbidity of myopia and obesity in children. It could actively promote collaboration and cooperation among families, schools, communities and medical institutions to reduce the occurrence of myopia and obesity among primary and secondary school students.

BACKGROUND:Flap transplantation technique is a commonly used surgical procedure for the treatment of severe tissue defects,but postoperative flap necrosis is easily triggered by ischemia-reperfusion injury.Therefore,it is still an important research topic to improve the survival rate of transplanted flaps. OBJECTIVE:To review the pathogenesis and latest treatment progress of flap ischemia-reperfusion injury. METHODS:CNKI,WanFang Database and PubMed database were searched for relevant literature published from 2014 to 2024.The search terms used were"flap,ischemia-reperfusion injury,inflammatory response,oxidative stress,Ca2+overload,apoptosis,mesenchymal stem cells,platelet-rich plasma,signaling pathways,shock wave,pretreatment"in Chinese and English.After elimination of irrelevant literature,poor quality and obsolete literature,77 documents were finally included for review. RESULTS AND CONCLUSION:Flap ischemia/reperfusion injury may be related to pathological factors such as inflammatory response,oxidative stress response,Ca2+overload,and apoptosis,which can cause apoptosis of vascular endothelial cells,vascular damage and microcirculation disorders in the flap,and eventually lead to flap necrosis.Studies have found that mesenchymal stem cell transplantation,platelet-rich plasma,signaling pathway modulators,shock waves,and pretreatment can alleviate flap ischemia/reperfusion injuries from different aspects and to varying degrees,and reduce the necrosis rate and necrosis area of the grafted flap.Although there are many therapeutic methods for skin flap ischemia/reperfusion injury,a unified and effective therapeutic method has not yet been developed in the clinic,and the advantages and disadvantages of various therapeutic methods have not yet been compared.Most of the studies remain in the stage of animal experiments,rarely involving clinical observations.Therefore,a lot of research is required in the future to gradually move from animal experiments to the clinic in order to better serve the clinic.

The accumulation of uremic toxins such as urea nitrogen, blood creatinine, and uric acid of patients with renal failure in vivo would lead to aggravated kidney damage. In this study, coated aldehyde oxy-starch (CAO) was used as an adsorbent to investigate its in vitro adsorption performance on renal failure indexes for urea, indoxyl sulfate (INS), monomethylamine (MMA), dimethylamine (DMA), uric acid (UA), and creatinine (Cr). The effects of variables such as pH, temperature, concentration, dosage, and time on the adsorption capacity of CAO were systematically investigated, employing analytical techniques of high-performance liquid chromatography (HPLC) and gas chromatography (GC). The results revealed that CAO exhibited a strong adsorption capacity for urea, INS, and MMA, alongside a moderate adsorption capacity for DMA, UA, and Cr. The adsorption kinetics and thermodynamic studies indicated that the adsorption of urea and UA by CAO were fitted in pseudo-first-order kinetics, and the adsorption isotherm aligned with the Freundlich adsorption model. The enthalpy change ΔH of urea in adsorption was in the range of 40 to 60 kJ·mol^-1, which demonstrated the presence of strong adsorption force due to the interactions of coordinating groups. The ΔH of UA was greater than 80 kJ·mol^-1, indicating the generation of chemical bonds during the adsorption. Both of them, Gibbs free energy ΔG was less than 0, within the range of -20 to 0 kJ·mol^-1, suggested that the adsorption of urea and UA by CAO occurred spontaneously as physical adsorption process. The adsorption entropy ΔS of urea and UA was > 0, which indicated an increase in entropy throughout the adsorption. The infrared spectroscopygram showed the formation of a chemical bond, specifically the imine bond, following the adsorption of urea by CAO, thereby indicating a chemical reaction during the adsorption. This study elucidates the adsorption mechanism of CAO on various indexes of renal failure, providing a scientific basis for its clinical usage.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.