Changes in biomechanical properties of tendons and ligaments from joint disuse

AbstractObjective: The purpose of this paper is to review changes in the biomechanical properties of tendons and ligaments from joint disuse.Method: We have reviewed 37 experimental studies on joint disuse, which have been carried out with various models of disuse and with various animals.Results: Immobilization of joints has most commonly been used as a model of disuse. Immobilization of the joint deteriorates the mechanical properties of tendons and ligaments, and reduces their cross-sectional area, although there are some differences in the speed of deterioration among tissues. Remobilization returns the mechanical properties once reduced by immobilization to nearly normal quickly, although the structural properties of the bone–ligament–bone complex continue to lag behind those of the controls. Stress deprivation has been regarded as an essential causative factor in joint disuse. Even if joint motion is allowed, stress deprivation rapidly reduces the mechanical properties of the tendon and ligament tissues, and increases the cross-sectional area of them. These effects appear time- and dose-dependent. Restressing increases the mechanical properties once reduced by stress deprivation, although it takes much time to completely recover them. The reduction of the ultimate stress may be explained by the reduction of the total area of collagen fibrils in tendon cross-section and the increase of thin and immature fibrils

Increases of Corporal Temperature as a Risk Factor of Atherosclerotic Plaque Instability

This work explores for the first time the effects of temperature increments on the development of high shear stresses between plaque and arterial wall due to their different dilatational properties. Data from the literature report febrile reactions prior to myocardial infarction in patients with normal coronary arteries and that coronary syndromes seem to be triggered by bacterial and viral infections, being fever the common symptom. Methods The thermo-mechanical behavior of thoracic aortas of New Zealand White rabbits with different degrees of atherosclerosis was measured by means of pressure–diameter tests at different temperatures. In addition, specific measurements of the thermal dilatation coefficient of atheroma plaques and of healthy arterial walls were performed by means of tensile tests at different temperatures. Results Results show a different thermo-mechanical behavior, the dilatation coefficient of atheroma plaque being at least twice that of the arterial wall. The calculation of temperature-induced mechanical stress at the plaque–vessel interface yielded shear stress levels enough to promote plaque rupture. Conclusions Increases of corporal temperature either local—produced by the inflammatory processes associated with atherosclerosis—or systemic—by febrile reactions—can play a role in increasing the risk of acute coronary syndromes, and they deserve a more comprehensive study

Inhibition of HSV-1 by chemoattracted neutrophils: supernatants of corneal epithelial cells (HCE) and macrophages (THP-1) treated with virus components chemoattract neutrophils (PMN), and supernatants of PMN treated with these conditioned media inhibit viral growth

The role of PMNs (neutrophils) in corneal herpes was studied using an in vitro system. Human corneal cells (HCE) and macrophages (THP-1) infected with HSV-1 or treated with virus components (DNA or virus immune complexes) released chemokines, which attracted PMNs. Highly reactive oxygen species were detected in PMNs. PMNs inhibited HSV when overlaid onto infected HCE cells (50:1). PMNs incubated with the supernatants of HCE cells treated with virus components released H2O2 and myeloperoxidase. These inhibited virus growth. PMNs released NO and MIG, which may differentiate CD4 T cells to Th1. PMNs participate in innate immune responses, limit virus growth, and initiate immunopathology

Xセンニヨルタケッショウキンゾクノコウシヒズミトヘンケイニカンスルケンキュウ

京都大学0048新制・課程博士工学博士甲第993号工博第206号新制||工||158(附属図書館)2606UT51-45-M203京都大学大学院工学研究科機械工学専攻(主査)教授 平 修二, 教授 河本 実, 教授 遠藤 吉郎学位規則第5条第1項該当Kyoto UniversityDA