The hemodynamics within the aortic lumen is highly complex,and the mechanical stimuli generated by blood flow play a crucial role in the occurrence and progression of aortic dilation disease.Endothelial cells,as key components of the vascular endothelium,respond precisely to microenvironmental changes caused by blood flow through mechanoreceptors,including ion channels,receptor tyrosine kinases,and membrane structures.These mechanoreceptors convert mechanical stresses into biochemical signals,thereby affecting the physiological functions and pathological changes of blood vessels.In recent years,significant advances have been made in understanding the mechanisms by which endothelial mechanoreceptors are involved in aortic dilation diseases.This review summarizes the research progress of mechanoreceptor-mediated endothelial cell function in regulating aortic dilation diseases and provides a perspective on future research directions,with the aim of offering new insights and potential targets for the development of clinical treatment strategies.

Endoleak is a major cause of poor long-term outcomes and reintervention after endovascular aneurysm repair(EVAR)for abdominal aortic aneurysms.The prevention and management of endoleaks are critical to improving the safety and efficacy of EVAR procedures.This article aims to summarize the key challenges and strategies in managing various types of endoleaks during EVAR,providing guidance to reduce the incidence of postoperative endoleaks.

The hemodynamics within the aortic lumen is highly complex,and the mechanical stimuli generated by blood flow play a crucial role in the occurrence and progression of aortic dilation disease.Endothelial cells,as key components of the vascular endothelium,respond precisely to microenvironmental changes caused by blood flow through mechanoreceptors,including ion channels,receptor tyrosine kinases,and membrane structures.These mechanoreceptors convert mechanical stresses into biochemical signals,thereby affecting the physiological functions and pathological changes of blood vessels.In recent years,significant advances have been made in understanding the mechanisms by which endothelial mechanoreceptors are involved in aortic dilation diseases.This review summarizes the research progress of mechanoreceptor-mediated endothelial cell function in regulating aortic dilation diseases and provides a perspective on future research directions,with the aim of offering new insights and potential targets for the development of clinical treatment strategies.

Objective To establish a pose estimation model for recognizing instruments in intraluminal aortic intervention and to evaluate its efficiency as well as clinical applicability.Methods Forty-eight digital subtraction angiography(DSA)video clips of 45 patients who underwent intraluminal aortic intervention by physician or robot-assisted physician were collected and preprocessed into one video with totally 10 220 frames.The frames were categorized into 5 levels of background complexity.A key dataset of 5 110 frames was selected from 10 220 frames after intermittent frame extraction and divided into training set(n=4 599)and validation set(n=511).The accumulative numbers of guidewires,catheters,guidewire tips and catheter tips with manual labels in training set were recorded.Feature extraction was performed via a backbone network of this model,and an optical flow tracking algorithm was combined to achieve key point tracking between consecutive frames.After frame-by-frame inference across all 10 220 frames,the confusion results in training set were calculated,while the accuracy was calculated in validation set,the inference speeds were record in all sets,and the results were compared with those of U-Net.Results In validation set,the mean accuracy of the model for recognizing guidewires and catheters was 0.832 and 0.808,respectively,better than those of U-Net(0.767 and 0.793).For physician-operated procedures,the average accuracy of this model for recognizing guidewires and catheters within chest aorta was 0.787 and 0.756,which within abdominal aortic was 0.826 and 0.806,respectively.For robot-assisted procedures,the average accuracy of this model for recognizing guidewires and catheters in validation set was 0.855 and 0.834,respectively.Under 5 descending levels of background complexity,the model achieved recognizing accuracies of 0.594,0.865,0.817,0.793 and 0.764 for guidewires,and of 0.626,0.847,0.795,0.739 and 0.694 for catheters.In training set,this model accumulatively correctly classified guidewires,catheters,guidewire tips and catheter tips in 7 971,7 026,7 551 and 7 533 ones,accumulatively missed classified guidewires,catheters,guidewire tips and catheter tips in 1 271,1 357,812 and 863 ones,respectively.For all 10 220 frames,the inference frame rate of this model was 20.66 frames per second.Conclusion The obtained pose estimation model demonstrated excellent accuracies for recognizing instruments in intraluminal aortic intervention with real-time processing capability,which was able for clinical application.

The automation technology of surgical robots(SR)integrates key techniques such as force feedback,visual feedback,medical image alignment,and surgical navigation.This integration not only effectively reduces the workload of surgeons,enabling them to focus more on the overall execution of the surgical procedure,but also decreases reliance on surgical experience,contributing to the standardization and homogenization of surgical outcomes.Although most current SR systems are primarily used for assisting operations,some robots have demonstrated conditional automation capabilities,showcasing significant potential in automated surgery research.However,the development of automated surgery still faces numerous challenges,including limited perception capabilities,constraints of artificial intelligence algorithms,and technical bottlenecks in surgical navigation.This paper summarizes the key technologies of commonly used SR systems globally,analyzes the progress in automation research,and discusses the challenges and trends in future development.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

ObjectiveTo investigate the clinical features and outcomes of recompensation in patients with autoimmune hepatitis （AIH）-related decompensated cirrhosis， to identify independent predictive factors， and to construct a nomogram prediction model for the probability of recompensation. MethodsA retrospective cohort study was conducted among the adult patients with AIH-related decompensated cirrhosis who were admitted to The Fifth Medical Center of PLA General Hospital from January 2015 to August 2023 （n=211）. The primary endpoint was achievement of recompensation， and the secondary endpoint was liver-related death or liver transplantation. According to the outcome of the patients at the end of the follow-up， the patients were divided into the recompensation group （n=16） and the persistent decompensation group（n=150）.The independent-samples t test was used for comparison of normally distributed continuous data with homogeneity of variance， and the Mann-Whitney U rank sum test was used for comparison of non-normally distributed continuous data with heterogeneity of variance； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups； the Kaplan-Meier method was used for survival analysis； the Cox proportional-hazards regression model was used to identify independent predictive factors， and a nomogram model was constructed and validated. ResultsA total of 211 patients were enrolled， with a median age of 55.0 years and a median follow-up time of 44.0 months， and female patients accounted for 87.2%. Among the 211 patients， 61 （with a cumulative proportion of 35.5%） achieved recompensation. Compared with the persistent decompensation group， the recompensation group had significantly higher white blood cell count， platelet count （PLT）， total bilirubin （TBil）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， total bile acid， prothrombin time， international normalized ratio （INR）， SMA positive rate， Model for End-Stage Liver Disease （MELD） score， Child-Pugh score， and rate of use of glucocorticoids （all P0.05）， as well as significantly lower age at baseline， number of complications， and death/liver transplantation rate （all P0.05）. At 3 and 12 months after treatment， the recompensation group had continuous improvements in AST， TBil， INR， IgG， MELD score， and Child-Pugh score， which were significantly lower than the values in the persistent decompensation group （all P0.05）， alongside with continuous increases in PLT and albumin， which were significantly higher than the values in the persistent decompensation group （P0.05）. The multivariate Cox regression analysis showed that baseline ALT （hazard ratio ［HR］=1.067， 95% confidence interval ［CI］： 1.010 — 1.127， P=0.021）， IgG （HR=0.463，95%CI：0.258 — 0.833， P=0.010）， SMA positivity （HR=3.122，95%CI：1.768 — 5.515， P0.001）， and glucocorticoid therapy （HR=20.651，95%CI：8.744 — 48.770， P0.001） were independent predictive factors for recompensation， and the nomogram model based on these predictive factors showed excellent predictive performance （C-index=0.87，95%CI：0.84 — 0.90）. ConclusionAchieving recompensation significantly improves clinical outcomes in patients with AIH-related decompensated cirrhosis. Baseline SMA positivity， a high level of ALT， a low level of IgG， and corticosteroid therapy are independent predictive factors for recompensation. The predictive model constructed based on these factors can provide a basis for decision-making in individualized clinical management.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.

Geraniin, a polyphenol derived from the fruit peel of Nephelium lappaceum L., has been shown to possess anti-inflammatory and antioxidant properties in the cardiovascular system. The present study explored whether geraniin could protect against an isoproterenol (ISO)-induced cardiac hypertrophy model. Mice in the ISO group received an intraperitoneal injection of ISO (5 mg/kg) once daily for 9 days, and the administration group were injected with ISO after 5 days of treatment with geraniin or spironolactone. Potential therapeutic effects and related mechanisms analysed by anatomical coefficients, histopathology, blood biochemical indices, reverse transcription-PCR and immunoblotting. Geraniin decreased the cardiac pathologic remodeling and myocardial fibrosis induced by ISO, as evidenced by the modifications to anatomical coefficients, as well as the reduction in collagen I/III á1mRNA and protein expression and cross-sectional area in hypertrophic cardiac tissue. In addition, geraniin treatment reduced ISO-induced increase in the mRNA and protein expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor-α, whereas ISO-induced IL-10 showed the opposite behaviour in hypertrophic cardiac tissue.Further analysis showed that geraniin partially reversed the ISO-induced increase in malondialdehyde and nitric oxide, and the ISO-induced decrease in glutathione, superoxide dismutase and glutathione. Furthermore, it suppressed the ISO-induced cellular apoptosis of hypertrophic cardiac tissue, as evidenced by the decrease in Bcell lymphoma-2 (Bcl-2)-associated X/caspase-3/caspase-9 expression, increase in Bcl-2 expression, and decrease in TdT-mediated dUTP nick-end labeling-positive cells.These findings suggest that geraniin can attenuate ISO-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.