A displacement based optimization method for geometrically nonlinear frame structures

An extension of the displacement based optimization method to frames with geometrically nonlinear response is presented. This method, when applied to small-scale trusses with linear and nonlinear response, appeared to be efficient providing the same solutions as the classical optimization method. The efficiency of the method is due to the elimination of numerous finite element analyses that are required in using the traditional optimization approach. However, as opposed to trusses, frame problems have typically a larger number of degrees of freedom than cross sectional area design variables. This leads to difficulties in the implementation of the method compared to the truss implementation. A scheme that relaxes the nodal equilibrium equations is introduced, and the method is validated using test examples. The optimal designs obtained by using the displacement based optimization and the classical approaches are compared to validate the application to frame structures. The characteristics and limitations of the optimization in the displacement space for sizing problems, based on the current formulation, are discussed.     

Analysis of dependent events and multiple unavailabilities with particular reference to common-cause failures

Historically the concern of reliability engineers in the aircraft, nuclear and chemical industries when dealing with dependent failures in high integrity systems has been with common mode or common cause failures. Starting from this perspective the paper considers dependent events, failure definition and classification schemes. Recently these schemes have explicitly distinguished different types of multi-unavailabilities and dependent events. The CSNI and EPRI sponsored data analyses are reviewed. CCF modelling and defenses are discussed and the limitations imposed by data are shown to lead to a possible requirement to consider a structured model that enables the engineer to consider various factors explicitly which could affect the specific system being assessed. This enables judgement to be used in an explicit way in evaluating common cause failures.     

The medial capsule of the human temporomandibular joint

PURPOSE: Attachments of the medial capsule of the temporomandibular joint (TMJ) to structures other than the medial fossa wall are thought to exist and to have functional significance. This study evaluated these relationships. MATERIALS AND METHODS: The anatomic relationships between the medial capsule and other medial structures, the sphenomandibular ligament, discomalleolar ligament, and auriculotemporal nerve, were examined in 14 cadaver heads. RESULTS: The results showed that the sphenomandibular ligament attaches separately from the medial capsule of the TMJ and therefore has no functional significance to the biomechanics of the joint. The discomalleolar ligament was found to be a continuation of the retrodiscal tissues and minimally associated with the medial capsule. The auriculotemporal nerve was not found to be in a relationship with the medial aspect of the condyle to the extent that mechanical irritation is possible during TMJ movement or disc displacement.     

Persistent or recurrent carpal tunnel syndrome following prior endoscopic carpal tunnel release

Immunohistochemistry was applied in the investigation of the possible existence of serotonin in human skin. It was found that epidermal melanocytes express a serotonin-like immunoreactivity. The immunoreactivity was associated with both the cytoplasm and the cellular membrane, though the latter was only found in certain cells. The serotonin anti-serum labeled the same cells as NKI-beteb, which is known as a reliable marker of melanocytes. Blocking experiments showed that both serotonin and NKI-beteb have different epitopes in the melanocytes. In in vitro studies, serotonin-like immunoreactivity appeared in approximately 90% of cultured human melanocytes, and was found both in the cytoplasm and also in the nuclei. Thus, we believe the melanocytes to be the origin of serotonin (or a serotonin-like molecule) in the skin.     

Sulindac enhances cell proliferation in DMH-treated mouse colonic mucosa

In a previous study we reported that the NSAID sulindac had a marked inhibitory effect on the development of colonic tumours in mice treated with the carcinogen 1,2-dimethylhydrazine (DMH). In this study we examined the effects of sulindac in respect of cell-kinetic changes in mouse colonic mucosa as determined by flash labelling with the thymidine analogue bromodeoxyuridine (BrdUrd) at varying intervals during the process of colonic carcinogenesis. We also investigated the possibility that these changes may be modulated by misoprostol a prostaglandin E1 analogue. Four groups of 36 mice each were treated for 18 weeks with the following drug/s respectively: (1) DMH; (2) DMH and sulindac; (3) DMH, sulindac and misoprostol; and (4) DMH and misoprostol. Three animals from each group were killed each week between the sixth week and the eighteenth week after the start of the experiment. A 1-h flash label technique was employed and paraffin sections of colonic mucosa were examined. For each animal a total of 50 perfect axially cut crypts were chosen and the following parameters determined: crypt length, labelling index and labelling index distribution: the data were analysed using the computer program GLIM. For each of the four groups, crypt lengths increased significantly with the duration of treatment with no significant difference between the groups. In sulindac-treated animals the labelling index for all positions increased with duration of treatment whereas for animals not treated with sulindac there was no significant difference in labelling index with respect to duration of treatment. The administration of misoprostol did not appear to significantly alter the effects of sulindac. It is postulated that the observed increase in cell proliferation could be a compensatory phenomenon occurring secondary to loss of crypt epithelial cells by apoptosis induced by sulindac. Also the finding of an increase in labelling index mediated by a chemopreventive agent indirectly questions the rationale behind the therapeutic manipulation of crypt cell proliferation in order to reduce the risk of colon cancer.