ObjectiveTo investigate the mechanisms by which Renshentang treats atherosclerosis （AS） in mice， focusing on the regulation of endothelial inflammatory responses mediated by transient receptor potential vanilloid subtype 1 （TRPV1）. MethodsAn AS model was established in apolipoprotein E knockout （ApoE^-/-） mice fed a high-fat diet. The mice were randomly divided into a simvastatin group （0.02 g·kg^-1·d^-1） and low-， medium-， and high-dose Renshentang groups （1.77， 3.54， 7.08 g·kg^-1·d^-1）， with 12 mice in each group. ApoE^-/- mice were fed a high-fat diet and treated simultaneously. C57BL/6J mice fed a normal diet served as the normal group （n=9）. After continuous administration for 12 weeks， mice were anesthetized and the aortas were collected. Oil Red O staining was used to observe lipid plaque formation in the aorta. Hematoxylin-eosin （HE） staining was performed to examine pathological changes in the aortic root. Immunohistochemistry was used to analyze the levels of pro-inflammatory factors tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β）， as well as the expression of TRPV1， phosphorylated phosphoinositide 3-kinase （p-PI3K）， and phosphorylated protein kinase B （p-Akt） in the aortic root. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect endothelial nitric oxide synthase （eNOS） mRNA expression in the aorta， and Western blot was used to detect TRPV1 protein expression. ResultsCompared with the normal group， the model group showed a significant increase in aortic plaque formation （P<0.01） and significantly elevated levels of TNF-α and IL-1β in the aortic root （P<0.01）. The expression levels of TRPV1， p-PI3K， and p-Akt were decreased （P<0.05， P<0.01）， and eNOS mRNA expression was reduced （P<0.05， P<0.01）. Compared with the model group， all Renshentang groups significantly reduced aortic plaque formation （P<0.01）， significantly decreased TNF-α and IL-1β levels （P<0.01）， and markedly increased the expression levels of TRPV1， p-PI3K， p-Akt， and eNOS mRNA （P<0.05， P<0.01）. ConclusionRenshentang may inhibit endothelial inflammation and suppress the formation of AS by increasing TRPV1 protein expression and up-regulating the PI3K/Akt/eNOS signaling pathway， which may be one of the molecular mechanisms underlying its therapeutic effect against AS.

Metabolic associated fatty liver disease （MAFLD） is the main type of chronic liver disease in the world， with an increasingly higher incidence rate and a younger age of onset. At present， the treatment of MAFLD mainly depends on lifestyle intervention and comorbidity management， and there is still a lack of effective drugs for MAFLD itself. As a classic nonsteroidal anti-inflammatory drug of the salicylic acid family， aspirin can intervene in the pathological process of MAFLD by regulating lipid metabolism， relieving insulin resistance， reducing liver inflammation and oxidative stress response， exerting an anti-liver fibrosis effect， and inhibiting hepatocellular carcinoma， and therefore， it has the value of preventing disease onset， delaying disease progression， and reversing disease condition. This article systematically reviews the mechanism of action and safety of aspirin in the treatment of MAFLD， in order to provide more drug treatment options for MAFLD patients.

Uveal melanoma(UM)is the most common primary intraocular malignancy in adults and arises predominantly from the choroid. Mitochondria, as essential organelles, not only fuel energy metabolism, but also orchestrate signal transduction and apoptosis. Recent studies have progressively uncovered the multifaceted roles of mitochondria in UM, including mitochondrial DNA copy-number alterations, reprogramming of mitochondria-related metabolic genes, and mitochondria-dependent autophagy. Moreover, mitochondria modulate UM progression partly through the PI3K/AKT axis. Natural compounds and small-molecule drugs that impair mitochondrial function have also shown promising activity in inducing UM cell dysfunction. These findings provide new insights into UM pathogenesis and highlight mitochondria as potential therapeutic targets.

Informed consent constitutes a fundamental ethical principle in medical practice. With the in-depth integration of generative artificial intelligence （AI） represented by Chat Generative Pre-trained Transformer （ChatGPT） with medicine， it has brought revolutionary development to traditional informed consent while also introducing new ethical challenges. ChatGPT offers features such as improving the readability of informed consent content， enhancing its comprehensiveness and accuracy， and increasing the convenience of obtaining informed consent. However， as the application of ChatGPT in informed consent is still in the exploratory stage， it is imperative to proactively and fully consider the accompanying ethical issues， such as information security， liability determination， transparency， and fairness. This paper conducted an ethical analysis on the challenges faced by generative AI， represented by ChatGPT， in the application of informed consent and proposed countermeasures， such as upholding free and fully informed consent， strengthening the balance of rights and obligations in informed consent， and establishing a transparent and fair supervision mechanism. The aim was to promote the ethically compliant， orderly， and controllable development of generative AI in the field of medical informed consent.

Objective To systematically evaluate the differences in clinicopathologic features and prog-nosis of colorectal cancer(CRC)between youth and middle-aged and elderly people.Methods The relevant literatures in Chinese and English databases before June 2024 were retrieved.The Stata 18 and RevMan5.3 softwares were used to perform the heterogeneity and sensitivity analyses as well as publication bias tests for the relevant outcome indicators.Results A total of 17 case-control studies were included,including a total of 6 817 patients with pathologically diagnosed CRC,among them 1 939 cases in the young group and 4 878 cases in the middle-aged and elderly group.The results of meta analysis showed that the proportion of family histo-ry in the young adult group(OR=3.09,95%CI:2.33-4.09),misdiagnosis rate(OR=4.40,95%CI:3.30-5.86),proportion of poorly differentiated carcinomas(OR=3.57,95%CI:2.73-4.67),proportion of mucin-ous adenocarcinomas and imprinted cell carcinomas(OR=3.41,95%CI:2.79-4.18),and proportion of TNM stage at diagnosis(stage Ⅲ-Ⅳ,OR=1.71,95%CI:1.44-2.02),incidence rate of lymph node metas-tasis(OR=1.92,95%CI:1.61-2.28),incidence rate of distant metastasis(OR=2.09,95%CI:1.53-2.86)were higher than those in the middle-aged and elderly group(all P<0.05);the CEA-positive rate at diagnosis(OR=0.68,95%CI:0.57-0.80)and 5-year survival rate(OR=0.24,95%CI:0.16-0.36)in the young group were lower than those in the middle-aged and elderly group(all P<0.05).The difference in the tumor diameter size(OR=1.32,95%CI:0.98-1.77)between the two groups was not statistically significant(P=0.07).Conclusion Compared with middle-aged and elderly CRC,young patients with CRC has a closer famil-ial correlation,may be more easily misdiagnosed clinically,its malignant degree would be higher,and the TNM stage in diagnosis is relatively late;in clinic the young population with CRC high risk could be appropriately relaxed in the age limit for screening.

ObjectiveTo explore the potential mechanism of action of the combination of Sanguisorbae Radix-Sophorae Flos （DH） in the treatment of ulcerative colitis （UC） using network pharmacology methods and molecular docking technology. MethodsNetwork pharmacology analysis was utilized to predict the potential targets of DH for the treatment of UC. The therapeutic effects were experimentally validated by inducing a UC model in mice with 3% dextran sulfate sodium （DSS）. The experimental groups were the normal group， the model group， the salazosulfapyridine group （100 mg·kg^-1）， and the low， medium， and high dose groups of DH （1.2， 2.4， and 4.8 g·kg^-1）. The efficacy of the treatment was assessed through the general condition of the mice， histopathological examination， and the expression levels of inflammatory markers in the colon. The effect of DH on angiogenesis was explored by messenger RNA （mRNA） detection of colonic angiogenesis-related mediators， vascular endothelial growth factor （VEGF） immunohistochemistry， microvessel density （MVD） detection， and transmission electron microscopy. The phosphatidylinositol-3-kinase （PI3K）-protein kinase B （Akt） signaling pathway proteins were quantitatively analyzed through Western blot to assess whether the suppression of pathological angiogenesis by DH is associated with this pathway. ResultsNetwork pharmacological analysis yielded 112 potential core therapeutic targets for the treatment of UC with DH， of which the core targets were tumor protein 53 （TP53）， JUN， interleukin （IL）-6， Akt1， and tumor necrosis factor （TNF）. Compared with the normal group， mice in the model group showed significant weight loss， colon shortening， and high DAI score， increased expression of inflammatory factors IL-6， IL-1β， and TNF-α， as well as increased mRNA expression levels of angiogenesis-related mediators VEGF， vascular cell adhesion molecule 1 （VCAM1）， angiotensin 1 （Ang1）， matrix metalloproteinase （MMP）-1， MMP-2， and MMP-9. The positive expression of CD31 and VEGF in colonic tissue increased， and the protein expression of the PI3K/Akt pathway was increased （P<0.05）. The endothelial cells of the colonic mucosa and the colonic vasculature were severely damaged. Compared with the model group， mice in the DH groups had significantly reduced weight loss and colon shortening， lower DAI scores， and a significant decrease in mRNA expression of inflammatory factors and angiogenesis-related mediators. In addition， there was decreased positive expression of CD31 and VEGF in colonic tissue and decreased protein expression of the PI3K/Akt pathway （P<0.05）. ConclusionNetwork pharmacology， molecular docking， and experimental validation are applied to explore the mechanism of action of DH in the treatment of UC， and it is found that DH is able to improve the symptoms of colitis and inhibit the pathological angiogenesis in UC mice. Its action might be related to affecting the PI3K/Akt pathway.

ObjectiveTo explore the potential mechanism of action of the combination of Sanguisorbae Radix-Sophorae Flos （DH） in the treatment of ulcerative colitis （UC） using network pharmacology methods and molecular docking technology. MethodsNetwork pharmacology analysis was utilized to predict the potential targets of DH for the treatment of UC. The therapeutic effects were experimentally validated by inducing a UC model in mice with 3% dextran sulfate sodium （DSS）. The experimental groups were the normal group， the model group， the salazosulfapyridine group （100 mg·kg^-1）， and the low， medium， and high dose groups of DH （1.2， 2.4， and 4.8 g·kg^-1）. The efficacy of the treatment was assessed through the general condition of the mice， histopathological examination， and the expression levels of inflammatory markers in the colon. The effect of DH on angiogenesis was explored by messenger RNA （mRNA） detection of colonic angiogenesis-related mediators， vascular endothelial growth factor （VEGF） immunohistochemistry， microvessel density （MVD） detection， and transmission electron microscopy. The phosphatidylinositol-3-kinase （PI3K）-protein kinase B （Akt） signaling pathway proteins were quantitatively analyzed through Western blot to assess whether the suppression of pathological angiogenesis by DH is associated with this pathway. ResultsNetwork pharmacological analysis yielded 112 potential core therapeutic targets for the treatment of UC with DH， of which the core targets were tumor protein 53 （TP53）， JUN， interleukin （IL）-6， Akt1， and tumor necrosis factor （TNF）. Compared with the normal group， mice in the model group showed significant weight loss， colon shortening， and high DAI score， increased expression of inflammatory factors IL-6， IL-1β， and TNF-α， as well as increased mRNA expression levels of angiogenesis-related mediators VEGF， vascular cell adhesion molecule 1 （VCAM1）， angiotensin 1 （Ang1）， matrix metalloproteinase （MMP）-1， MMP-2， and MMP-9. The positive expression of CD31 and VEGF in colonic tissue increased， and the protein expression of the PI3K/Akt pathway was increased （P<0.05）. The endothelial cells of the colonic mucosa and the colonic vasculature were severely damaged. Compared with the model group， mice in the DH groups had significantly reduced weight loss and colon shortening， lower DAI scores， and a significant decrease in mRNA expression of inflammatory factors and angiogenesis-related mediators. In addition， there was decreased positive expression of CD31 and VEGF in colonic tissue and decreased protein expression of the PI3K/Akt pathway （P<0.05）. ConclusionNetwork pharmacology， molecular docking， and experimental validation are applied to explore the mechanism of action of DH in the treatment of UC， and it is found that DH is able to improve the symptoms of colitis and inhibit the pathological angiogenesis in UC mice. Its action might be related to affecting the PI3K/Akt pathway.

Objective:To explore the correlation between serum nidogen-2 (NID-2) and thoracic aortic calcification in patients with chronic kidney disease (CKD), and construct a risk prediction model based on NID-2 to evaluate its value in predicting the risk of the severe thoracic aortic calcification and cardiovascular and cerebrovascular events in CKD patients.Methods:It was a prospective cohort study. Patients with CKD at stage 3 to 5D in the Zhongda Hospital Affiliated to Southeast University from January 2022 to January 2023 were enrolled. Syngo.via software was used to evaluate the volume of thoracic aortic calcification, and enzyme-linked immunosorbent assay was employed to determine the level of serum NID-2. According to the volume of thoracic aortic calcification, the patients were divided into three groups: no calcification group, mild calcification group and severe calcification group. The top 25% of the patients were defined as no or mild calcification group, and the latter 75% were defined as severe calcification group. The follow-up period was one year. During the follow-up period, cardiovascular and cerebrovascular events, as well as all-cause death among the enrolled patients were recorded. Logistic regression analysis was used to screen the influencing factors of thoracic aortic calcification. Based on the results of logistic regression analysis, a nomogram prediction model was constructed. The receiver operating characteristic curve (ROC curve), calibration curve, and decision curve were employed to evaluate the discrimination, calibration and clinical practicality of the nomogram model.Results:A total of 132 patients were included, with 91 males (68.94%) and age of (56.51±16.37) years. There were 60 CKD 3-5 stage patients (non-dialysis, 45.45%) and 72 CKD 5D patients (dialysis, 54.55%). Serum ND-2 levels differed significantly among healthy individuals, dialysis patients and non-dialysis patients ( H=70.651, P<0.001). There was no statistically significant difference in serum NID-2 level between the no or mild calcification group and the severe calcification group in dialysis patients ( Z=350.00, P=0.426). The serum NID-2 level in the severe calcification group was significantly higher than that in the no or mild calcification group in non-dialysis patients ( Z=242.00, P=0.019). In non-dialysis patients, there was a statistically significant correlation between serum NID-2 level and volume of thoracic aortic calcification ( r=0.40, P<0.001). In dialysis patients, there was no statistically significant correlation between serum NID-2 level and volume of each segment of thoracic aortic calcification (all P>0.05). The univariate logistic regression analysis showed that, age, hemoglobin, serum albumin, estimated glomerular filtration rate, NID-2, hypertension, type 2 diabetes mellitus and cerebral infarction were correlated factors of thoracic aortic calcification in non-dialysis patients (all P<0.05). Multivariate logistic regression analysis showed that age ( OR=1.22, 95% CI 1.08-1.50, P=0.010) was an independent correlated factor of thoracic aortic calcification in non-dialysis patients. The above related variables of univariate logistic regression analysis were incorporated into a nomogram to construct a predictive model for severe vascular calcification in non-dialysis patients, yielding an AUC of 0.94 (95% CI 0.89-0.99) in ROC curve, with a sensitivity of 83% and a specificity of 95%. A nomogram model based on above variables for predicting cardiovascular and cerebrovascular events in non-dialysis patients demonstrated an AUC of 0.95 (95% CI 0.90-1.00) in ROC curve, with a sensitivity of 95% and a specificity of 87%. Conclusions:In non-dialysis patients, serum NID-2 level in the severe calcification group is significantly higher than that in the no or mild calcification group. The serum NID-2 is a related factor of thoracic aortic calcification and cardiovascular and cerebrovascular events in non-dialysis patients. The nomogram prediction model constructed by combining NID-2 with age, hemoglobin, serum albumin, estimated glomerular filtration rate, hypertension, type 2 diabetes mellitus and cerebral infarction has a high predictive value for the risk of thoracic aortic calcification as well as cardiovascular and cerebrovascular events in non-dialysis patients.

Objective:To construct the supportive care intervention scheme for breast cancer radiotherapy patients based on the empowerment theory and discuss its application effect, so as to provide the reference for the clinical nursing intervention.Methods:According to the investigation results of the current situation of supportive care needs of patients with breast cancer radiotherapy and the results of literature review, a supportive care intervention scheme for breast cancer radiotherapy patients based on the empowerment theory was constructed by Delphi expert consultation method.Adopting experimental research, breast cancer radiotherapy patients in General Hospital of Ningxia Medical University were selected by convenient sampling method. They were divided into the control group from April to May 2023 (40 cases) for routine nursing care, and the experimental group from August to September 2023 (40 cases) for the supportive care intervention scheme for breast cancer radiotherapy patients based on the empowerment theory on the basis of routine nursing care according to the admission time. The 34-item Short-Form Supportive Cancer Needs Survey (SCNS-SF34), Strategies Used by People to Promte Health (SUPPH), Cancer Fatigue Scale(CFS) and Function Assessment of Cancer Therapy-Breast (FACT-B) were collected on the day of admission, the end of radiotherapy and 3 months after radiotherapy to evaluate the effects before and after intervention.Results:After 1, 2 rounds of expert correspondence, the positivity of experts were 95.24%(20/21) and 100.00%(20/20), the expert authority coefficient was 0.804 and 0.825, and the Kendall harmony coefficient was 0.129 and 0.138 (both P<0.05). Finally, a supportive care intervention scheme for breast cancer radiotherapy patients based on the enabling theory was formed, which included 5 primary items, 11 secondary items and 32 tertiary items.The application results showed that there were 37 cases in the control group with an age of (48.16 ± 10.21) years, and 38 cases in the experimental group with an age of (44.50 ± 9.81) years. All patients were female. There was no statistically significant difference in the scores of SCNS-SF34, SUPPH, CFS, and FACT-B between the two groups on the day of admission(all P>0.05). Three months after the end of radiotherapy, the score of SCNS-SF34 in the experimental group was (73.24 ± 11.99) points, which was lower than (79.91 ± 14.79) points in the control group, and the difference was statistically significant ( t=4.43, P<0.05). At the end of radiotherapy and 3 months after the end of radiotherapy, the scores of SUPPH in the experimental group were (80.39 ± 8.55) and (92.37 ± 8.14) points, respectively, which were higher than (73.95 ± 9.86) and (86.24 ± 7.10) points in the control group, and the difference was statistically significant ( t=-3.03, -3.47, both P<0.05). At the end of radiotherapy and 3 months after the end of radiotherapy, the scores of CFS in the experimental group were 30.00 (28.75, 33.00) and (25.29 ± 3.26) points, respectively, which were lower than 34.00 (31.50, 35.00) and (27.59 ± 3.43) points in the control group, and the difference was statistically significant ( Z=-3.51, t=2.98, both P<0.05). At the end of radiotherapy and 3 months after the end of radiotherapy, the scores of FACT-B in the experimental group were (85.08 ± 12.74) and (105.53 ± 6.53) points, respectively, which were higher than (79.03 ± 7.90) and (95.73 ± 7.61) points in the control group, and the difference was statistically significant ( t=-2.48, -5.99, both P<0.05). Conclusions:The supportive care intervention scheme for patients with breast cancer radiotherapy based on the empowerment theory established in this study is scientific and feasible, which can reduce patients' needs for supportive care, alleviate cancer-related fatigue, and improve self-management efficacy and quality of life.

Chinese medicine intestinal administration(CMIA)can avoid the degradation of drugs in gastric acid,bypass the first-pass effect of the liver,and deliver drugs directly to the lesion site.This approach increases local drug concentration,reduces drug dosage,and enhances bioavailability.This study systematically introduces the advantages,drug dosage forms,and whole-colon deliv-ery technologies of CMIA for treating UC,and reviews its mechanisms of action,including repairing intestinal epithelial layer and mu-cous layer,regulating the intestinal microbiota,improving immune function,and promoting local blood circulation.It also analyzes the current progress and limitations of research,aiming to provide a more solid theoretical basis for the treatment of UC with Chinese medi-cine and to offer references for the development of UC therapeutic drugs and administration methods.