The long term success of total joint replacement can be limited by fatigue failure of the acrylic cement and the resulting disruption of the bone-cement interface. The incidence of such problems may be diminished by reduction of the fatigue notch factor in the cement, so that stress concentrations are avoided and the fatigue crack initiation time maximized. This study describes a method for numerical shape optimization whereby the finite element method is used to determine an optimal shape for the femoral stem of a hip prosthesis in order to minimize the fatigue notch factor in the cement layer and at interfaces with the bone and stem.
A two-dimensional model of the proximal end of a femur fitted with a total hip prosthesis was used which was equivalent to a simplified three-dimensional axisymmetric model. Software was developed to calculate the fatigue notch factor in the cement along the cement/stem and cement/bone interfaces and in the proximal bone. The fatigue notch factor in the cement at the cement/stem interface was then minimized using the ANSYS finite element program while constraining the fatigue notch factor at the cement/bone interface at or below its initial level and maintaining levels of stress in the proximal bone to prevent stress shielding. The results were compared with those from other optimization studies. 相似文献
In order to investigate the role of monocyte/macrophages and their relationship to the expression of macrophage colony-stimulating factor (MCSF) in pulmonary atherosclerosis, lungs were excised from rabbits that had been fed for 60 and 90 days on a diet containing 0.5% cholesterol. In the lungs, fatty streaks and elevated foam cell lesions predominated in the large or medium-sized elastic pulmonary arteries, while massive accumulation of foam cells in the intima of muscular arteries produced marked luminal narrowing and nearly complete occlusion. In these lesions, most of the foam cells were reactive with RbM2, a monoclonal antibody (mAb) against rabbit macrophages, while smooth muscle cell-derived foam cells were detected by mAb against smooth muscle actin in the deeper area of elevated foam cell lesions of elastic arteries. Ultrastructural observation confirmed the presence of monocytes in the intima, their differentiation into macrophages, and their transformation into foam cells in the atherosclerotic lesions. lmmunohistochemical expression of MCSF was demonstrated in the endothelial cells, smooth muscle cells and foam cells. A minor macrophagederived foam cell population was demonstrated to possess a prolif-erative capacity. These data suggest that MCSF is involved in the differentiation of monocytes into macrophages, their transformation into foam cells, and their proliferation during pulmonary atherogenesis. 相似文献
Basophil leukocytes obtained from AIDS patients, allergic patients and healthy controls were stimulated in vitro with interleukin 4, lymphotoxin, tumour necrosis factor alpha and interferon gamma to examine the histamine releasing effect. The cytokines caused histamine release from the basophils of approximately half the AIDS patients and from 8-17% of the allergic patients. No response was obtained in the control group. Removal of cell surface immunoglobulins abolished the response to cytokines, indicating an Ig-dependent mechanism. Passive sensitization with cell-derived Ig, with Ig deprived of IgE, or with IgG, indicated that cell-bound IgE was responsible for the cytokine-induced histamine release in AIDS patients. This response may be mediated by cytokine-selective IgE antibodies. 相似文献
The structure of hard tissue areas (with osteoid and calcified matrix) in 10 osteoblastic, chondroblastic, and fibroblastic osteogenic sarcomas was studied in the electron microscope. Neoplastic cells commonly associated with these areas and presumably actively involved in the production of hard tissue were osteo-blastlike cells types 1 and 3, chondroblastlike cells type 1, and fibroblastlike cells, as defined and characterized in previous studies. The cells differed from those in soft tissue areas of osteogenic sarcomas in but one respect: they usually showed presence of irregular extrusions at their surfaces. Other types of osteoblastlike and chondroblastlike cells occurred rarely or not at all. Two types of multinucleated giant cells were recognized in these areas, one showing a fine structure reminiscent of that in osteoclasts, the other probably being of a neoplastic nature and engaged in the production of the calcifying matrix. The evidence suggested that neoplastic osteoblastlike, chondroblastlike, and fibrolastlike cells as well as certain multincleated giant cells might all be involved in the mineralization process and/or the formation of osteoid in osteogenic sarcomas. Although phenotypically of highly variable appearance, all these different cells may thus functionally (and probably histogenetically) be closely related.
The mineralization process in the tumor tissue appeared to be a modification of what occurs in normal ossification, possibly with an alternative or complementary pathway involving the production of spherical bodies with layered contents. 相似文献
Amyloid enhancing factor (AEF), which has recently been shown to have identity with ubiquitin (Ub), is believed to play a causative role in experimentally induced AA amyloidosis in mice. We have examined the profile of Ub in activated leukocytes and splenic reticulo-endothelial (RE) cells and its relationship with serum amyloid A protein (SAA) and AA amyloid deposits in an alveolar hydatid cyst (AHC)-infected mouse model of AA amyloidosis. Two monospecific antibodies, anti-ubiquitin (RABU) and anti-mouse AA amyloid, were used as immunological probes to localize Ub, SAA, and AA amyloid. In response to AHC infection, the dull and diffuse Ub immunoreactivity in normal mouse leukocytes and RE cells promptly changed to a discrete granular pattern suggesting an increase in the intracellular concentration of Ub and the formation of Ub-protein conjugates. This corresponded to an elevation in SAA levels, SAA uptake by RABU-positive phagocytic cells, co-localization of Ub-SAA immunoreactive splenocytes in the perifollicular areas, and deposition of Ub-bound AA amyloid in the splenic and hepatic tissues. These results suggest that Ub-loaded monocytoid cells may play an important role in the physiological processing of the sequestered SAA into AA amyloid. Aspects of AA amyloidogenesis are discussed in relation to other experimental models in which stress-induced Ub-protein conjugate formation and its transport to lysosomal vesicles have been studied. 相似文献
Summary The presence of decay-accelerating factor (DAF) was clearly demonstrated on the surface of normal cardiomyocytes. In patients who had died of myocardial infarction (MI) cardiomyocytes displayed different appearances: outside the ischaemically damaged region the myocytes showed no significant variations in DAF expression when compared with controls without MI. Within myocardial zones damaged by ischaemia, however, apparently normal myocytes showed large gaps in surface staining of DAF or formed clusters which were entirely devoid of reactivity with anti-DAF antibodies. The number of DAF-deficient myocytes increased with the extent of necrosis and also with the number of days between onset of MI and death. Even though injury to myocytes is to a large extent related to anoxia and to the presence of free oxygen radicals, the complement system also appears to be involved; DAF may have protective functions against complement-mediated injury. We speculate that phospholipase may be involved in the removal of DAF from the cardiomyocyte surface.This work was supported in part by grant no. 3.157.88 from the Swiss National Foundation for Scientific Research and a contribution from Sandoz Ltd. Pharma Division, Basel 相似文献