62 resultados para Old Bridge


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Cases of high-sided vehicles striking low bridges is a large problem in many countries, especially the UK. This paper describes an experiment to evaluate a new design of markings for low bridges. A full size bridge was constructed which was capable of having its overhead clearance adjusted. Subjects sat in a truck cab as. it drove towards the bridge and were asked to judge whether the vehicle could pass safely under the bridge. The main objective of the research, was to determine whether marking the bridge with a newly devised experimental marking would result in more cautious decisions from subjects regarding whether or not the experimental bridge structure could be passed under safely compared with the currently used UK bridge marking standard. The results show that the type of bridge marking influenced the level of caution associated with decisions regarding bridge navigation, with the new marking design producing the most cautious decisions for the two different bridge heights used, at all distances away from the bridge structure. Additionally, the distance before the bridge at which decisions were given had an effect on the level of caution associated with decisions regarding bridge navigation (the closer to the bridge, the more cautious the decisions became, irrespective of the marking design). The implications of these results for reducing the number of bridge strikes are discussed. (C) 2002 Elsevier Science Ltd. All rights reserved.

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Purpose: The aims of this study are two-fold: first, to analyze intraindividual allometric development of aerobic power of 73 boys followed at annual intervals from 8 to 16 yr, and second, to relate scaled aerobic power with level of habitual physical activity and biological maturity status. Methods: Peak (V) over dot O-2 (treadmill), height, and body mass were measured. Biological maturity was based on age at peak height velocity (PHV) and level of physical activity was based on five assessments between 11 and 15 yr and at 17 yr. Interindividual and intraindividual allometric coefficients were calculated. Multilevel modeling was applied to verify if maturity status and activity explain a significant proportion of peak (V) over dot O-2 after controlling for other explanatory characteristics. Results: At most age levels, interindividual allometry coefficients for body mass exceed k = 0.750. Intraindividual coefficients of peak (V) over dot O-2 by body mass vary widely and range from k' = 0,555 to k' = 1,178. Late maturing boys have smaller k' coefficients than early maturing boys. Conclusion: Peak (V) over dot O-2 is largely explained by body mass, but activity level and its interaction with maturity status contribute independently to peak (V) over dot O-2 even after adjusting for body mass.

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Evoked otoacoustic emissions have demonstrated potential for application in the community-based hearing screening of paediatric populations. Distortion-product otoacoustic emissions (DPOAEs), as opposed to transient evoked otoacoustic emissions (TEOAEs), have not been extensively researched in this regard. The current study aimed to describe the range of DPOAE values obtained in a large cohort (1576 ears) of 6-year-old children in school settings and to examine possible ear asymmetry, gender and history of ear infection effects on the data. Results indicated a variety of significant effects, particularly in the high frequencies, for DPOAE signal-to-noise ratio. The measurement parameter, DPOAE amplitude (DP-amp), was found to display potentially less clinical applicability due to large standard deviation values. Use of descriptive normative data, as derived in the present investigation, may contribute toward future improvements in the hearing screening of 6-year-old schoolchildren

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We report a 12-month-old infant who presented with a 4-month history of isosexual precocious puberty secondary to an estrogenizing Sertoli-Leydig cell tumor of the ovary. Total serum immunoreactive inhibin and subunits A and B were markedly elevated before surgical resection and subsequently decreased 7 wk later into the normal prepubertal range. Twenty weeks following surgical removal, the patient presented again with central precocious puberty; inhibin B levels were raised on this occasion, a luteinizing releasing hormone stimulation test confirmed central precocious puberty. This is the youngest reported occurrence of this rare sex cord stromal neoplasm. The prognosis of this extremely rare tumor presenting at this early juvenile stage is uncertain. This report illustrates the usefulness of serum inhibin as a tumor marker during therapeutic suppression with leuprorelin acetate for central precocious puberty. Analysis of genomic and tumor DNA revealed a normal nucleotide sequence for the LH receptor and the G{alpha}s gene. To understand the molecular pathogenesis of this tumor we analyzed mRNA levels for the inhibin A and B subunits, FSH receptor, LH receptor aromatase, steroidogenic factor-1 and the ER ß genes. Molecular characterization reveals the presence of genes specific for granulosa and Leydig cells; the relative expression of these genes, in addition to its histologic characteristics, suggests that this tumor may result from a dysdifferentiation of a primordial follicle.

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Passive avoidance learning is with advantage studied in day-old chicks trained to distinguish between beads of two different colors, of which one at training was associated with aversive taste. During the first 30-min post-training, two periods of glutamate release occur in the forebrain. One period is immediately after the aversive experience, when glutamate release is confined to the left hemisphere. A second release, 30 min later, may be bilateral, perhaps with preponderance of the right hemisphere. The present study showed increased pool sizes of glutamate and glutamine, specifically in the left hemisphere, at the time when the first glutamate release occurs, indicating de novo synthesis of glutamate/glutamine from glucose or glycogen, which are the only possible substrates. Behavioral evidence that memory is extinguished by intracranial administration at this time of iodoacetate, an inhibitor of glycolysis and glycogenolysis, and that the extinction of memory is counteracted by injection of glutamine, supports this concept. A decrease in forebrain glycogen of similar magnitude and coinciding with the increase in glutamate and glutamine suggests that glycogen rather than glucose is the main source of newly synthesized glutamate/glutamine. The second activation of glutamatergic activity 30 min after training, when memory is consolidated into stable, long-term memory, is associated with a bilateral increase in pool size of glutamate/glutamine. No glycogenolysis was observed at this time, but again there is a temporal correlation with sensitivity to inhibition by iodoacetate and rescue by glutamine, indicating the importance of de novo synthesis of glutamate/glutamine from glucose or glycogen. (C) 2003 Elsevier B.V All rights reserved.

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One of the major regulators of mitosis in somatic cells is cdc25B. cdc25B is tightly regulated at multiple levels. The final activation step involves the regulated binding of 14-3-3 proteins. Previous studies have demonstrated that Ser-323 is a primary 14-3-3 binding site in cdc25B, which influences its activity and cellular localization. 14-3-3 binding to this site appeared to interact with the N-terminal domain of cdc25B to regulate its activity. The presence of consensus 14-3-3 binding sites in the N-terminal domain suggested that the interaction is through direct binding of the 14-3-3 dimer to sites in the N-terminal domain. We have identified Ser-151 and Ser-230 in the N-terminal domain as functional 14-3-3 binding sites utilized by cdc25B in vivo. These low affinity sites cooperate to bind the 14-3-3 dimer bound to the high affinity Ser-323 site, thus forming an intramolecular bridge that constrains cdc25B structure to prevent access of the catalytic site. Loss of 14-3-3 binding to either N-terminal site relaxes cdc25B structure sufficiently to permit access to the catalytic site, and the nuclear export sequence located in the N-terminal domain. Mutation of the Ser-323 site was functionally equivalent to the mutation of all three sites, resulting in the complete loss of 14-3-3 binding, increased access of the catalytic site, and access to nuclear localization sequence.