ObjectiveTo explore the effects of Yimei Baijiang formula （YMBJF） on colitis-associated colorectal cancer （CAC） and the nuclear factor kappaB （NF-κB） signaling pathway in mice. MethodsSixty male Balb/c mice of 4-6 weeks old were randomized into 6 groups： Normal， model， capecitabine （0.83 g·kg^-1）， and low-， medium-， and high-dose （4.63， 9.25， 18.50 g·kg^-1， respectively） YMBJF. The mouse model of CAC was established by combining azoxymethane （AOM， 10 mg·kg^-1） and dextran sulfate sodium （DSS， 2%）. At the 5^th week after the start of modeling， the capecitabine group and the YMBJF groups were respectively administrated with the corresponding doses of drugs by gavage once a day for a total of 6 weeks. The body weights and general conditions of mice were measured and observed， and the disease activity index （DAI） was scored. The tumors in the colorectal tissue were counted， and the colorectal length was measured. The histological features of the colorectal tissue in each group of mice were observed by hematoxylin-eosin （HE） staining. The levels of inflammatory cytokines including interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the serum were determined by enzyme-linked immunosorbent assay （ELISA）. The expression and localization of proliferating cell nuclear antigen-67 （Ki67）， proliferating cell nuclear antigen （PCNA）， and phosphorylated nuclear transcription factor-κB p65 （p-NF-κB p65） proteins were observed by immunohistochemistry （IHC）. The apoptosis of tumor cells was observed by the TUNEL assay. The mRNA levels of IL-6，IL-1β， TNF-α， nuclear transcription factor-κB p65 （NF-κB p65）， NF-κB inhibitor alpha （IκBα）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the colorectal tissue were quantified by Real-time polymerase chain reaction（Real-time PCR）. The protein levels of NF-κB p65， phosphorylated （p）-NF-κB p65， IκBα， p-IκBα， Bcl-2， and Bax in the colorectal tissue were determined by Western blot. ResultsCompared with the model group， each YMBJF group showed decreases in DAI and tumor number （P0.01）， and the medium-dose and high-dose YMBJF groups showed increases in colorectal length （P0.05）. In addition， each YMBJF group showed alleviated colorectal mucosal pathological injury， declined levels of IL-6， IL-1β， and TNF-α in the serum （P0.05）， reduced expression of Ki67 and PCNA （P0.01）， and down-regulated expression of p-NF-κB p65 （P0.05）. The apoptosis in the medium-dose and high-dose YMBJF groups increased （P0.01）. Each YMBJF group and the capecitabine group showed down-regulated mRNA levels of IL-1β， TNF-α， IL-6， NF-κB p65， and Bcl-2 （P0.05） and up-regulated mRNA levels of IκBα and Bax （P0.05）. The mRNA level of IκBα was up-regulated， and that of Bcl-2 was down-regulated （P0.05） in the high-dose YMBJF group. The protein levels of p-IκBα and Bcl-2 were down-regulated （P0.05） in each YMBJF group. The protein levels of IκBα and Bax were up-regulated in the medium-dose and high-dose YMBJF groups （P0.01）， while those of NF-κB p65 and p-NF-κB p65 were down-regulated （P0.05）. ConclusionYMBJF can reduce the number of tumors， reduce the levels of inflammatory factors， promote tumor cell apoptosis， and inhibit tumor cell proliferation by regulating the direct effector molecules of the NF-κB signaling pathway in the mouse model of CRC.

ObjectiveTo explore the effects of Yimei Baijiang formula （YMBJF） on colitis-associated colorectal cancer （CAC） and the nuclear factor kappaB （NF-κB） signaling pathway in mice. MethodsSixty male Balb/c mice of 4-6 weeks old were randomized into 6 groups： Normal， model， capecitabine （0.83 g·kg^-1）， and low-， medium-， and high-dose （4.63， 9.25， 18.50 g·kg^-1， respectively） YMBJF. The mouse model of CAC was established by combining azoxymethane （AOM， 10 mg·kg^-1） and dextran sulfate sodium （DSS， 2%）. At the 5^th week after the start of modeling， the capecitabine group and the YMBJF groups were respectively administrated with the corresponding doses of drugs by gavage once a day for a total of 6 weeks. The body weights and general conditions of mice were measured and observed， and the disease activity index （DAI） was scored. The tumors in the colorectal tissue were counted， and the colorectal length was measured. The histological features of the colorectal tissue in each group of mice were observed by hematoxylin-eosin （HE） staining. The levels of inflammatory cytokines including interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the serum were determined by enzyme-linked immunosorbent assay （ELISA）. The expression and localization of proliferating cell nuclear antigen-67 （Ki67）， proliferating cell nuclear antigen （PCNA）， and phosphorylated nuclear transcription factor-κB p65 （p-NF-κB p65） proteins were observed by immunohistochemistry （IHC）. The apoptosis of tumor cells was observed by the TUNEL assay. The mRNA levels of IL-6，IL-1β， TNF-α， nuclear transcription factor-κB p65 （NF-κB p65）， NF-κB inhibitor alpha （IκBα）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the colorectal tissue were quantified by Real-time polymerase chain reaction（Real-time PCR）. The protein levels of NF-κB p65， phosphorylated （p）-NF-κB p65， IκBα， p-IκBα， Bcl-2， and Bax in the colorectal tissue were determined by Western blot. ResultsCompared with the model group， each YMBJF group showed decreases in DAI and tumor number （P0.01）， and the medium-dose and high-dose YMBJF groups showed increases in colorectal length （P0.05）. In addition， each YMBJF group showed alleviated colorectal mucosal pathological injury， declined levels of IL-6， IL-1β， and TNF-α in the serum （P0.05）， reduced expression of Ki67 and PCNA （P0.01）， and down-regulated expression of p-NF-κB p65 （P0.05）. The apoptosis in the medium-dose and high-dose YMBJF groups increased （P0.01）. Each YMBJF group and the capecitabine group showed down-regulated mRNA levels of IL-1β， TNF-α， IL-6， NF-κB p65， and Bcl-2 （P0.05） and up-regulated mRNA levels of IκBα and Bax （P0.05）. The mRNA level of IκBα was up-regulated， and that of Bcl-2 was down-regulated （P0.05） in the high-dose YMBJF group. The protein levels of p-IκBα and Bcl-2 were down-regulated （P0.05） in each YMBJF group. The protein levels of IκBα and Bax were up-regulated in the medium-dose and high-dose YMBJF groups （P0.01）， while those of NF-κB p65 and p-NF-κB p65 were down-regulated （P0.05）. ConclusionYMBJF can reduce the number of tumors， reduce the levels of inflammatory factors， promote tumor cell apoptosis， and inhibit tumor cell proliferation by regulating the direct effector molecules of the NF-κB signaling pathway in the mouse model of CRC.

Diabetic tendinopathy is a common and disabling musculoskeletal complication of diabetes, clinically characterized by tendon thickening, pain, impaired healing capacity and compromised biomechanical performance, collectively undermining joint function and quality of life. Its pathogenesis is multifactorial. On the one hand, chronic hyperglycaemia promotes the abnormal accumulation of advanced glycation end products (AGEs) within tendon collagen, leading to non-enzymatic crosslinking and engagement of the receptor for AGEs (RAGE), which in turn triggers inflammasome activation and sustains inflammatory responses. On the other hand, the diabetic milieu disrupts collagen metabolic homeostasis, impairs microvascular function and induces peripheral neuropathy; together, these alterations drive extracellular matrix degeneration and weaken the mechanical properties of tendon. Exercise, as a non-pharmacological intervention, can ameliorate these pathological changes through multiple integrated mechanisms. First, exercise attenuates tendon inflammation and restores microenvironmental homeostasis. Regular physical activity reduces AGE-RAGE signalling, thereby suppressing downstream expression of tumour necrosis factor (TNF) and interleukin-1β (IL-1β), while upregulating the anti-inflammatory cytokine interleukin-10 (IL-10). This shift from a pro-inflammatory to a pro-resolving milieu not only restrains chronic inflammation but may also limit excessive inflammasome activation in tenocytes and tissue-resident immune cells. Second, exercise enhances local expression of insulin-like growth factor 1 (IGF-1), thereby activating the phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt) signalling pathway. This axis stimulates tenocyte proliferation, augments synthesis of type I collagen —— the principal load-bearing component of tendon —— and thereby promotes tissue repair, preserves tensile strength and supports matrix synthesis and structural integrity. In addition, exercise improves blood supply and nutrient delivery to tendon by increasing the expression of vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF) and the small leucine-rich proteoglycan decorin (DCN), thereby enhancing capillary growth, coordinating collagen fibrillogenesis and actively suppressing pathological vascular calcification. Exercise also increases the expression of angiopoietin-like 4 (ANGPTL4), fibroblast growth factor 2 (FGF-2) and CD34. Through the concerted actions of these factors, exercise promotes angiogenesis, restores the microvascular network and ensures adequate oxygen and nutrient supply to relatively ischaemic tendon tissue. Finally, exercise elevates levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), supporting neuronal survival, axonal growth and the function of sensory and sympathetic nerve endings within tendon, thereby exerting neurotrophic and neuromodulatory effects and improving tendon innervation and neuromuscular control. Moreover, exercise upregulates collapsin response mediator protein 2 (CRMP-2), a molecule involved in axonal guidance and regeneration, and moderately increases the activity of substance P (SP), thereby helping to regulate neurogenic inflammation, pain perception and trophic support for tenocytes. Drawing together current evidence, this review systematically summarizes the mechanisms underlying diabetic tendinopathy and examines the mechanistic basis of exercise intervention, with the aim of providing a theoretical framework for the development of precise exercise strategies for affected individuals. However, several key issues remain unresolved: the therapeutic efficacy and mechanistic specificity of different exercise modalities in diabetic tendinopathy have yet to be defined, and early diagnostic biomarkers remain insufficiently characterized. Future studies should apply multi-omics approaches to profile AGE subtypes, miRNA signatures and collagen metabolic products, and should also clarify the adverse effects and underlying mechanisms of excessive exercise or mechanical overloading in diabetic tendinopathy. Such efforts will further elucidate the therapeutic effects and mechanisms of exercise in diabetic tendinopathy and provide a stronger basis for precision exercise prescription and fitness guidance in patients with diabetes.

ObjectiveTo investigate the inhibitory effects and mechanisms of Yupingfeng San （YPFS） on high-mobility group box protein 1 （HMGB1）-induced angiogenesis in liver cancer. MethodsAn orthotopic liver cancer model was established in 30 C57BL/6 mice. The mice were randomly divided into a model group， YPFS low-， medium-， and high-dose groups （20， 30， 40 g·kg^-1， respectively）， a positive control group （sorafenib， 10 mg·kg^-1）， and a normal control group. After 14 days of medication， tumor and adjacent tissues were harvested. Tumor inhibition rates were calculated based on tumor weight. Microvascular density was determined via immunohistochemistry. HMGB1 and vascular endothelial growth factor （VEGF） expression levels were determined using immunofluorescence. An HMGB1-induced human umbilical vein endothelial cell （HUVEC） proliferation model was established， and cell proliferation was evaluated by a methylthiazolyldiphenyl-tetrazolium bromide （MTT） assay. HUVECs were randomly divided into a blank group， a model group （HMGB1 800 μg·L^-1）， along with YPFS low-， medium-， and high-dose groups （HMGB1 800 μg·L^-1 + YPFS 10， 30， 50 g·L^-1， respectively）. HUVEC migration ability was evaluated via a scratch assay and a Trans well chamber assay. Tube formation ability was detected by a tube formation assay. Microvascular sprouting ability was evaluated by an aortic ring assay. Furthermore， RAGE/MEK1/2/ERK1/2 pathway-related protein expression in HUVECs was measured using Western blot （WB）. ResultsCompared with the model group， all three doses of YPFS significantly reduced tumor weight in mice with orthotopic liver cancer （P<0.01）， with inhibition rates of 31.49% ± 8.27%， 49.60% ± 3.77%， and 56.81% ± 9.70%， respectively. Also， YPFS significantly decreased microvascular density in tumor and adjacent tissues （P<0.05）， as well as VEGF and HMGB1 expression levels （P<0.01）. Compared with the blank group， HMGB1 promoted HUVEC proliferation， migration， tube formation， and microvascular sprouting in aortic rings （P<0.05）. After YPFS administration， the HMGB1-induced proliferation rate， migration rate， number of tube formations， and microvascular sprouting in aortic rings were significantly reduced compared with the model group （P<0.01）. Additionally， YPFS downregulated receptor for advanced glycation end products （RAGE）， mitogen-activated protein kinase kinase 1/2 （MEK1/2）， phosphorylated MEK1/2 （p-MEK1/2）， extracellular signal-regulated kinase 1/2 （ERK1/2）， and phosphorylated ERK1/2 （p-ERK1/2） protein expression in HMGB1-induced HUVECs （P<0.01）. ConclusionYPFS exerts anti-angiogenic effects against HMGB1 induction by suppressing the RAGE/MEK/ERK signaling pathway， thereby inhibiting liver cancer tumor growth.

The morphological characteristics of hepatocellular carcinoma(HCC)tumor margins are pivotal in influencing patient's prognosis and the selection of therapeutic strategies.This paper re-viewed the classification methods of HCC tumor margins,ranging from traditional macroscopic classifi-cations to refined classification systems based on multi-omics analysis,and analyzed the role of these classification methods in guiding the formulation of personalized treatment plans.Additionally,this paper emphasized the crucial role of three-dimensional imaging techniques in assessing tumor margin morphology and outlined future research directions,including validating the effectiveness of multi-omics classification systems and developing new imaging and molecular biomarkers to achieve more precise treatment plans and prolong patient survival.

[Purpose]To analyze the cost-effectiveness and cost-utility conducted on the lung can-cer screening project in urban areas of Anhui Province,and to provide suggestions for the formu-lation of lung cancer screening policies in Anhui Province.[Methods]A Markov decision model for low-dose computed tomography(LDCT)lung cancer screening intervention was established based on on-site survey data and literature data.The development of the population under different interventions was simulated,using saved life years(LYS)and quality-adjusted life years(QALY)as effectiveness indicators,to conduct cost-effectiveness and cost-utility analyses of different screening strategies.Cost data were discounted at a 3％discount rate.[Results]The screening schemes of once a year,once every two years,once every three years,and once every five years all meet the cost-effectiveness principle for saving one LYS or QALY.Among them,the best screening strategy in terms of cost-effectiveness and cost-utility was the LDCT lung cancer screening strategy once every two years,with costs of 72 441.54 CNY and 71 050.24 CNY,respectively.[Conclusion]The LDCT lung cancer screening program demonstrates good cost-effectiveness,with strategies of dif-ferent screening frequencies being viable options.The optimal screening strategy is screening once every two years.

AIM To investigate the repair effects of tauroursodeoxycholic acid(TUDCA)combined with bone marrow mesenchymal stem cells(BMSCs)transplantation on spinal cord injury(SCI)in rats.METHODS The rats were randomly divided into the sham operation group,the model group,the TUDCA group,the BMSCs transplantation group and the combination therapy of TUDCA and BMSCs transplantation group,with the SCI rat model established by Allen's method.The next day after modeling,the rats of TUDCA and combination therapy groups were given 200 mg/kg TUDCA by gavage.On the 3rd day after modeling,rats in BMSCs transplantation group and combination therapy group were injected with 1 mL tuned bone marrow BMSCs(the 3rd generation,1× 106/mL)via tail vein.Rats in the sham operation group and the model group were given gastric perfusion of normal saline and injection of 1 mL PBS through tail vein.On the 3rd,7th and 14th day after modeling,the rats had their motor function of hind limbs observed and BBB score determined.After the corresponding drug administration,the rats had their movement track of hind limbs recorded by footprint experiment;their the protein expressions of IL-6,IL-10,Arg-1,PI3K and Akt in spinal cord tissue detected by Western blot;their pathological changes of spinal cord tissue observed by HE staining and Nissl staining;and their expressions of MAP2,GAP43 and GFAP detected by immunofluorescence staining.RESULTS Compared with the model group,the groups intervened with TUDCA,or BMSCs transplantation,or combination therapy shared improved hind limb function and spinal cord histomorphology(P＜0.05);increased fluorescence intensity of MAP2 and GAP43,and protein expressions of IL-10,Arg-1,p-PI3K and p-Akt(P＜0.05);decreased fluorescence intensity of GFAP and IL-6 protein expressions(P＜0.05);among which the combination therapy group took the lead(P＜0.05).CONCLUSION The combination therapy of TUDCA and BMSCs transplantation may restore the function of the rat model of SCI by reducing inflammatory reaction,alleviating secondary injury,and promoting axon and myelin regeneration via PI3K/Akt signaling pathway.

AIM To study the chemical constituents from the stems and barks of Maytenus variabilis(Hemsl.)C.Y.Cheng.METHODS The 95％ethanol extract from the stems and barks of M.variabilis was isolated and purified by silica gel,Sephadex LH-20 and semi preparative HPLC,then the structures of obtained compounds were identified by physicochemical properties and spectral data.RESULTS Twenty-three compounds were isolated and identified as β-amyrin(1),3β-acetoxyolean-12-en-11-one(2),ursa-12-ene-11-one-3-ol octocosate(3),friedelin(4),canophyllol(5),pinoresinol(6),medioresinol(7),isolariciresinol(8),dihydrodehydrodiconiferyl alcohol(9),vanillic acid(10),7R,8S-5-methoxydihydrodehydroconiferyl alcohol(11),β-hydroxypropiovanillone(12),triptregeline B(13),triptregeline E(14),(+)-evofolin B(15),2,5-dimethoxybenzoquinone(16),olean-12-ene-3,11-dione(17),β-sitosterol(18),(-)-(7R,7'R,7"S,8S,8'S,8"S)-4',4"-dihydroxy-3,3',3",5-tetramethoxy-7,9',7',9-diepoxy-4,8"-oxy-8,8'-sesquineolignan-7",9"-diol(19),phyllostadimer B(20),rayalinol(21),lyoniresinol(22),dihydrobuddlenol B(23).CONCLUSION Compounds 3,9-11,13-14,16,19-21,23 are isolated from genus Maytenus for the first time,and compounds 2,4-5,7-8,12,15,17,22 are first found from this plant.

Middle aortic syndrome(MAS)is a rare aortic disease characterized by primary or secondary factors leading to localized or diffuse narrowing of the middle segment of the aorta,which often involves the primary branches of the middle segment of the aorta,resulting in clinical manifestations such as severe hypertension and intermittent claudication.This article reviewed the current research status and advances in the diagnosis and treatment of MAS.

Objective:To evaluate the efficacy of lamb′s tripe extract and vitamin B 12 capsule (LTEVB 12C) on chronic atrophic gastritis (CAG) at different locations (antrum lesser curvature, antrum greater curvature, gastric angle, corpus lesser curvature, and corpus greater curvature). Methods:From August 2011 to January 2013, 715 patients with CAG in a multicenter, randomized, double-blind, placebo-controlled trial were enrolled from 16 tertiary first-class hospitals across the country, including the First Affiliated Hospital of Air Force Medical University, Nanfang Hospital of Southern Medical University, the First Hospital of Jilin University, West China Hospital of Sichuan University, etc., there were 476 cases in the LTEVB 12C group and 239 cases in the placebo group. The patients of the LTEVB 12C group received LTEVB 12C, and the patients of placebo group received LTEVB 12C mimetic, all the medications were taken 3 capsules each time and 3 times a day after meals, and the treatment course of 2 groups were both 6 months. The efficacy evaluation criteria included the effective rate (a decrease of ≥1 in histopathological score compared with baseline after 6 months of treatment) and the reversal rate (a decrease of ≥ 2 in histopathological score compared with baseline after 6 months of treatment in the patients with moderate to severe CAG). The impact of lesion sites on the therapeutic effects of LTEVB 12C was analyzed by logistic regression analysis. The two-way unordered Cochran-Mantel-Haenszel chi-square test considering the center effect and Pearson chi-square test were used for statistical analysis. Results:The effective rates of chronic inflammation at the antrum greater curvature and corpus greater curvature (23.3%, 110/473 vs. 13.0%, 31/239; 20.3%, 96/472 vs. 12.6%, 30/239), the effective rates of atrophy at the antrum lesser curvature, antrum greater curvature, gastric angle, corpus lesser curvature, and the corpus greater curvature (27.0%, 118/437 vs. 15.7%, 34/216; 29.2%, 126/432 vs. 18.5%, 38/205; 27.8%, 121/435 vs. 16.7%, 36/216; 32.5%, 127/391 vs. 19.8%, 37/187; 33.0%, 119/361 vs. 21.8%, 39/179), and the effective rates of intestinal metaplasia at the antrum lesser curvature, antrum greater curvature, gastric angle, and the corpus lesser curvature (45.0%, 112/249 vs. 29.8%, 31/104; 53.8%, 86/160 vs. 33.9%, 21/62; 45.8%, 103/225 vs. 24.0%, 25/104; 51.9%, 83/160 vs. 28.3%, 17/60) of the LTEVB 12C group were all higher than those of the placebo group, and the differences were statistically significant ( χ2=10.76, 6.39, 9.69, 7.91, 11.05, 9.62, 8.57, 5.20, 7.11, 12.45, and 6.73; all P<0.05). The reversal rates of chronic inflammation at the corpus lesser curvature and corpus greater curvature (5.2%, 12/231 vs. 0, 0/123; 4.7%, 8/170 vs. 0, 0/88), the reversal rates of atrophy at the antrum lesser curvature, antrum greater curvature, corpus lesser curvature, and the corpus greater curvature (6.8%, 22/323 vs. 1.3%, 2/151; 9.2%, 29/315 vs. 1.4%, 2/144; 14.2%, 38/267 vs. 2.5%, 3/121; 20.8%, 35/168 vs. 5.8%, 4/69), and the reversal rates of intestinal metaplasia at the antrum lesser curvature, antrum greater curvature, gastric angle, and the corpus lesser curvature (29.8%, 39/131 vs. 9.1%, 4/44; 41.0%, 32/78 vs. 12.5%, 3/24; 33.3%, 44/132 vs. 4.8%, 3/63; 50.0%, 37/74 vs. 8.7%, 2/23) of the LTEVB 12C group were all higher than those of the placebo group, and the differences were statistically significant ( χ2=6.58, 5.12, 5.60, 8.61, 11.43, 6.59, 7.30, 4.95, 15.92, 7.62; all P<0.05). There were no statistically significant differences in the effective rates and reversal rates of active inflammation at different locations between the LTEVB 12C group and the placebo group (all P>0.05). The results of logistic regression analysis (taking the antrum lesser curvature as the reference) further confirmed that the reversal rates of chronic inflammation ( OR=0.22, 95% confidence interval (95% CI): 0.07 to 0.67; OR=0.24, 95% CI: 0.07 to 0.80), atrophy ( OR=0.28, 95% CI: 0.16 to 0.49; OR=0.28, 95% CI: 0.16 to 0.49), and intestinal metaplasia ( OR=0.42, 95% CI: 0.24 to 0.77; OR=0.20, 95% CI: 0.08 to 0.52) at the corpus lesser curvature and corpus greater curvature were all higher than those at the antrum lesser curvature, and the differences were statistically significant (all P<0.05). There were no statistically siginificant differences in the reversal rates of the aforementioned pathological features between the antrum greater curvature, gastric angle, and the antrum lesser curvature (all P>0.05). Conclusion:LTEVB 12C can achieve good efficacy in the treatment of CAG, and the chronic inflammation, atrophy, and intestinal metaplasia at multiple locations are improved, especially at the corpus lesser curvature and the corpus greater curvature.