929 resultados para motor unit potential


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The cation\[Si,C,O](+) has been generated by 1) the electron ionisation (EI) of tetramethoxysilane and 2) chemical ionisation (CI) of a mixture of silane and carbon monoxide. Collisional activation (CA) experiments performed for mass-selected \[Si,C,O](+), generated by using both methods, indicate that the structure is not inserted OSiC+; however, a definitive structural assignment as Si+-CO, Si+-OC or some cyclic variant is impossible based on these results alone. Neutralisation-reionisation (+NR+) experiments for EI-generated \[Si,C,O](+) reveal a small peak corresponding to SiC+, but no detectable SiO+ signal, and thus establishes the existence of the Si+-CO isomer. CCSD(T)//B3LYP calculations employing a triple-zeta basis set have been used to explore the doublet and quartet potential-energy surfaces of the cation, as well as some important neutral states The results suggest that both Si+-CO and Si+ - OC isomers are feasible; however, the global minimum is (2)Pi SiCO+. Isomeric (2)Pi SiOC+ is 12.1 kcal mol(-1) less stable than (2)Pi SiCO+, and all quartet isomers are much higher in energy. The corresponding neutrals Si-CO and Si-OC are also feasible, but the lowest energy Si - OC isomer ((3)A") is bound by only 1.5 kcal mol(-1). We attribute most, if nor all, of the recovery signal in the +NR' experiment to SiCO+ survivor ions. The nature of the bonding in the lowest energy isomers of Si+ -(CO,OC) is interpreted with the aid of natural bond order analyses, and the ground stale bonding of SiCO+ is discussed in relation to classical analogues such as metal carbonyls and ketenes.

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Background Wearable monitors are increasingly being used to objectively monitor physical activity in research studies within the field of exercise science. Calibration and validation of these devices are vital to obtaining accurate data. This article is aimed primarily at the physical activity measurement specialist, although the end user who is conducting studies with these devices also may benefit from knowing about this topic. Best Practices Initially, wearable physical activity monitors should undergo unit calibration to ensure interinstrument reliability. The next step is to simultaneously collect both raw signal data (e.g., acceleration) from the wearable monitors and rates of energy expenditure, so that algorithms can be developed to convert the direct signals into energy expenditure. This process should use multiple wearable monitors and a large and diverse subject group and should include a wide range of physical activities commonly performed in daily life (from sedentary to vigorous). Future Directions New methods of calibration now use "pattern recognition" approaches to train the algorithms on various activities, and they provide estimates of energy expenditure that are much better than those previously available with the single-regression approach. Once a method of predicting energy expenditure has been established, the next step is to examine its predictive accuracy by cross-validating it in other populations. In this article, we attempt to summarize the best practices for calibration and validation of wearable physical activity monitors. Finally, we conclude with some ideas for future research ideas that will move the field of physical activity measurement forward.

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Interior permanent-magnet synchronous motors (IPMSMs) become attractive candidates in modern hybrid electric vehicles and industrial applications. Usually, to obtain good control performance, the electric drives of this kind of motor require one position, one dc link, and at least two current sensors. Failure of any of these sensors might lead to degraded system performance or even instability. As such, sensor fault resilient control becomes a very important issue in modern drive systems. This paper proposes a novel sensor fault detection and isolation algorithm based on an extended Kalman filter. It is robust to system random noise and efficient in real-time implementation. Moreover, the proposed algorithm is compact and can detect and isolate all the sensor faults for IPMSM drives. Thorough theoretical analysis is provided, and the effectiveness of the proposed approach is proven by extensive experimental results.

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The extraction of coal seam gas (CSG) produces large volumes of potentially contaminated water. It has raised concerns about the environmental health impacts of the co-produced CSG water. In this paper, we review CSG water contaminants and their potential health effects in the context of exposure pathways in Queensland’s CSG basins. The hazardous substances associated with CSG water in Queensland include fluoride, boron, lead and benzene. The exposure pathways for CSG water are: (1) water used for municipal purposes, (2) recreational water activities in rivers, (3) occupational exposures, (4) water extracted from contaminated aquifers, and; (5) indirect exposure through the food chain. We recommend mapping of exposure pathways into communities in CSG regions to determine the potentially exposed populations in Queensland. Future efforts to monitor chemicals of concern and consolidate them into a central database will build the necessary capability to undertake a much needed environmental health impact assessment.

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In the present study, we examined a panel of human breast cancer cell lines with regard to their expression of CD44 and ability to bind and degrade hyaluronan. The cell lines expressed varying amounts of different molecular weight forms of CD44 (85-200 kDa) and, in general, those that expressed the greatest amounts of CD44 were the most invasive as judged by in vitro assays. In addition, the ability to bind and degrade hyaluronan was restricted to the cell lines expressing high levels of CD44, and both these functions were blocked by an antibody to CD44 (Hermes-1). Moreover, the rate of [3H]hyaluronan degradation was highly correlated with the amount of CD44 (r = 0.951, P < 0.0001), as well as with the invasive potential of the cells. Scatchard analysis of the [3H]hyaluronan binding of these cells revealed the existence of significant differences in both their binding capacity and their dissociation constant. To determine the source of this deviation, the different molecular weight forms of CD44 were partially separated by gel filtration chromatography. In all cell lines, the 85 kDa form was able to bind hyaluronan, although with different affinities. In contrast, not all of the high molecular weight forms of CD44 had this ability. These results illustrate the diversity of CD44 molecules in invasive tumor cells, and suggest that one of their major functions is to degrade hyaluronan.

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The majority of individuals appear to have insight into their own sleepiness, but there is some evidence that this does not hold true for all, for example treated patients with obstructive sleep apnoea. Identification of sleep-related symptoms may help drivers determine their sleepiness, eye symptoms in particular show promise. Sixteen participants completed four motorway drives on two separate occasions. Drives were completed during daytime and night-time in both a driving simulator and on the real road. Ten eye symptoms were rated at the end of each drive, and compared with driving performance and subjective and objective sleep metrics recorded during driving. ‘Eye strain’, ‘difficulty focusing’, ‘heavy eyelids’ and ‘difficulty keeping the eyes open’ were identified as the four key sleep-related eye symptoms. Drives resulting in these eye symptoms were more likely to have high subjective sleepiness and more line crossings than drives where similar eye discomfort was not reported. Furthermore, drivers having unintentional line crossings were likely to have ‘heavy eyelids’ and ‘difficulty keeping the eyes open’. Results suggest that drivers struggling to identify sleepiness could be assisted with the advice ‘stop driving if you feel sleepy and/or have heavy eyelids or difficulty keeping your eyes open’.

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Metastasis, the passage of primary tumour cells throughout the body via the vascular system and their subsequent proliferation into secondary lesions in distant organs, represents a poor prognosis and therefore an understandably feared event for cancer patients. Despite considerable advances in cancer diagnosis and treatment, most deaths are the result of metastases resistant to conventional treatment [1]. Rather than being a random process, metastasis involves a series of organised steps leading to the growth of a secondary tumour. Malignant tumours stimulate the production of new vessels by the host, and this process is a prerequisite for the increase in size of a new tumour [2]. Angiogenesis, not only permits tumour expansion but also allows the entry of tumour cells into the circulation and is probably the most vital event for the metastatic process [3]. Metastasis and angiogenesis [4] have received much attention in recent years. A biological understanding of both phenomena seems to be an urgent priority towards the search for an effective prevention and treatment of tumour progression. Studies in vitro and in vivo have shown that one of the most important barriers to the passage of malignant cells is the basement membrane. The crossing of such barriers is a vital step in the formation of a metastasis [5].

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In Suncorp Metway Insurance Limited v Brown [2004] QCA 325 the Queensland Court of Appeal considered the extent of the duty of cooperation imposed on a claimant under s45 of the Motor Accident Insurance Act 1994 (Qld). The issue is an important one because it affects virtually all claims made under the Act.

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In Windon v Edwards [2005] QDC 029 Robin QC DCJ considered the cost consequence of mandatory final offers under the Motor Accident Insurance Act 1994 (Qld)

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In Bermingham v Priest [2002] QSC 057 jones J considered the position of persons seeking to claim damages where the Motor Accident Insurance Act 1994 applies prior to its amendment by the Motor Accident Insurance Amendment Act 2000, and where proceedings are brought close to expiration of the statutory limitation period.

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In Turpin v Allianz Australia Insurance Ltd (unreported, Supreme Court of Queensland, S5216 of 2001), Mullins J, 17.10.2001) the plaintiff applied for a declaration that the respondent disclose pursuant to s47 of the Motor Accident Insurance Act 1994 copies of three statements referred to in a loss assessor's investigation report as "attached". The issue involved determination of whether the statements must be disclosed under s48(2) even though protected by legal professional privilege. The Court applied the decision of the Queensland Court of Appeal in James v Workcover Queensland.

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In Hooper v Robinson [2002] QDC 080 (District Court of Queensland, D 4841 of 2001, McGill DCJ, 19.4.2002) McGill DCJ considered the application of the decision in John Pfeiffer Pty Ltd v Rogerson [2000] 203 CLR 503 to notice requirements such as in s42 of NSW Motor Accident Insurance Act 1988 and concluded such provisions are now substantive.

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Vimentin is an intermediate filament protein normally expressed in mesenchymal cells, but evidence is accumulating in the literature which suggests that the aberrant expression of vimentin in epithelial cancer cells might be related to local invasiveness and metastatic potential. Vimentin expression has previously been associated with invasive properties in an in vitro model consisting of a set of HPV-33-transformed cervical keratinocyte cell lines. In the present study, in order to emphasize those in vitro findings, the expression of vimentin has been investigated in cervical neoplasms of different grades, using immunohistochemistry. A clear association is reported between vimentin expression and metastatic progression, since vimentin was detected in all invasive carcinomas and lymph node metastases, but not in CIN III lesions. These in vivo results are compared with present and previous data obtained in vitro on cervical keratinocyte cell lines, where vimentin expression also correlated with in vitro invasiveness.

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Background: Expression of matrix metalloproteinase-2 (MMP-2), the 72-kd type IV collagenase/gelatinase, by cancer cells has been implicated in metastasis through cancer cell invasion of basement membranes mediated by degradation of collagen IV. However, the abundance of this latent proenzyme in normal tissues and fluids suggests that MMP-2 proenzyme utilization is limited by its physiological activation rather than expression alone. We previously reported activation of this proenzyme by normal and malignant fibroblastoid cells cultured on collagen I (vitrogen) gels. Purpose: Our purposes in this study were 1) to determine whether MMP-2 activation is restricted to the more invasive human breast cancer cell lines and 2) to localize the activating mechanism. Methods: Zymography was used to monitor MMP-2 activation through detection of latent MMP-2 (72 kd) and mature species of smaller molecular weight (59 or 62 kd). Human breast cancer cell lines cultured on plastic, vitrogen, and other matrices were thus screened for MMP- 2 activation. Collagen I-cultured cells were exposed to cycloheximide, a protein synthesis inhibitor, or to protease inhibitors to determine the nature of the MMP-2-activating mechanism. Triton X-114 (TX-114) detergent extracts from cells cultured on collagen I or plastic were incubated with latent MMP-2 and analyzed by zymography to localize the MMP-2 activator. Results: MMP-2 activation was only induced by collagen I culture in the more aggressive, highly invasive estrogen receptor-negative, vimentin-positive human breast cancer cell lines (Hs578T, MDA-MB-436, BT549, MDA-MB-231, MDA- MB-435, MCF-7(ADR)) and was independent of MMP-2 production. MMP-2 activation was detected in cells cultured on collagen I gels but not in those cultured on gelatin gels, Matrigel, or thin layers of collagen I or IV, gelatin, or fibronectin. Collagen-induced activation was specific for the enzyme species MMP-2, since MMP-9, the 92-kd type IV collagenase/gelatinase, was not activatable under similar conditions. MMP-2 activation was inhibited by cycloheximide and was sensitive to a metalloproteinase inhibitor but not to aspartyl, serine, or cysteinyl protease inhibitors. MMP-2 activation was detected in the hydrophobic, plasma membrane-enriched, TX-114 extracts from invasive collagen I-cultured cells. Conclusion: Collagen I-induced MMP-2 activation is restricted to highly invasive estrogen receptor-negative, vimentin-positive human breast cancer cell lines, is independent of MMP-2 production, and is associated with metastatic potential. Our findings are consistent with plasma membrane localization of the activator. Implications: The MMP-2 activation mechanism may represent a new target for diagnosis, prognosis, and treatment of human breast cancer.

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In Gideona v Nominal Defendant [2005] QCA 261, the Queensland Court of Appeal reconsidered the question of what is the material time for determining whether registration of a motor vehicle is required. The Court declined to follow the decision in Kelly v Alford [1988] 1 Qd R 404; deciding that the material time was the time when the accident occurred.