Strain energy in human tibia during different exercises with adjustable leg weights: a subject-specific computational model analysis.

Physical exercise is recommended to improve tibia strength, a common site for stress injuries, while identifying optimal training regimens remains a significant challenge. This study investigated tibial responses to varied exercise regimens using a subject-specific computational modeling approach. A subject-specific neuro-musculoskeletal model was combined with a finite element model to assess the effects of various exercises (jumping, landing, squatting, and walking) on tibial strain energy density (SED), as well as the impact of adjustable leg weights placed at different sites (shank versus thigh).

Design and evaluation of a novel anti-reflux biliary stent with cone spiral valve.

Endoscopic placement of biliary stent is a well-established palliative treatment for biliary obstruction. However, duodenobiliary reflux after stent placement has been a common problem which may lead to dreadful complications. This paper designed a novel anti-reflux biliary stent with a cone spiral valve.

Haemin-enhanced expression of haem oxygenase-1 stabilizes erythrocyte-induced vulnerable atherosclerotic plaques.

Background And Purpose: Previous studies demonstrated that intraplaque haemorrhage increased the contents of cholesterol and oxidants in atherosclerotic plaques. The present study was aimed to test the hypothesis that enhanced expression of haem oxygenase-1 (HO-1) may stabilize vulnerable plaques.

Experimental Approach: Intravascular ultrasound (IVUS) was performed to identify three similar abdominal aortic plaques in each of 58 fat-fed New Zealand rabbits after aortic balloon injury.

Traditional Chinese medication Tongxinluo dose-dependently enhances stability of vulnerable plaques: a comparison with a high-dose simvastatin therapy.

This study was carried out to test the hypothesis that Tongxinluo (TXL) as a Chinese herbal medicine enhances stability of vulnerable plaque dose dependently via lipid-lowering and anti-inflammation effects, similar to a high-dose simvastatin therapy. After abdominal aortic balloon injury, 75 rabbits were fed a 1% cholesterol diet for 10 wk and were then divided into five groups for 8-wk treatment: control group, low-dose TXL group, moderate-dose TXL group, high-dose TXL group, and high-dose simvastatin group. At the end of week 16, an adenovirus containing p53 was injected into the abdominal aortic plaques.

Intraplaque injection of Ad5-CMV.p53 aggravates local inflammation and leads to plaque instability in rabbits.

This study aims to develop a new animal model of vulnerable plaques and investigate the potential mechanisms of exogenous p53-induced plaque instability. Forty rabbits underwent aortic balloon injury, were fed a 1% cholesterol diet for 10 weeks and then normal chow for 6 weeks. Rabbits were divided into Ad5-CMV.

Pathological mechanisms and dose dependency of erythrocyte-induced vulnerability of atherosclerotic plaques.

To test our hypothesis that erythrocytes may induce plaque vulnerability and investigate the mechanism involved, we established a novel model of intraplaque hemorrhage in 56 New Zealand white rabbits with established plaques. Three distinct abdominal aortic plaques with similar thickness were identified in each rabbit with use of intravascular ultrasound (IVUS) imaging. Rabbits were equally divided into 4 groups depending on dosage of treatment; with the guidance of IVUS, one of the three plaques from each rabbit was injected from adventitia with autologous erythrocytes (RBC) or cholesterol (CH) for the following groups: RBC, 50 microL or 100 microL, and CH, 50 microL or 100 microL.

Pathological mechanisms of erythrocyte-induced vulnerability of atherosclerotic plaques.

Erythrocytes are considered a new culprit contributing to atherosclerosis. Plaques with intraplaque hemorrhage are prone to new plaque hemorrhage, which may not only stimulate the progression of atherosclerosis but also promote the transition from a stable to an unstable lesion. However, the role of erythrocytes in inducing the vulnerability of plaque with intraplaque hemorrhage and the possible mechanism involved are not well understood.