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121.
Madeleine P 《Journal of applied biomechanics》2012,28(3):297-303
This laboratory study investigated seated computer work before and after prolonged constrained sitting. Discomfort ratings and kinetic and kinematics data were recorded in nine healthy males performing computer work for 5 min before and after 96 min of sitting. The displacement of the center of pressure (CoP) in anterior-posterior and medial-lateral directions and lumbar curvature (LC) were calculated. The root mean square, standard deviation, and sample entropy values were computed from the CoPs and LC signals to assess the magnitude, amount of variability, and regularity of sitting dynamics, respectively. The discomfort increased for the buttocks (p = .02).The standard deviation and sample entropy values of the CoPs and LC signals, respectively, increased (p < .04) and decreased (p < .004) whereas the root mean square remained unchanged (p > .15) after prolonged constrained sitting compared with before. This present study showed that during seated computer work, prolonged constrained sitting affected the amount of variability and the regularity of sitting postural control, whereas the magnitude was not affected. The importance of the dynamics of sitting control may challenge the idea of a static and ideal seated posture at work. 相似文献
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Diviney S Tuplin A Struthers M Armstrong V Elliott RM Simmonds P Evans DJ 《Journal of virology》2008,82(18):9008-9022
The genome of hepatitis C virus (HCV) contains cis-acting replication elements (CREs) comprised of RNA stem-loop structures located in both the 5' and 3' noncoding regions (5' and 3' NCRs) and in the NS5B coding sequence. Through the application of several algorithmically independent bioinformatic methods to detect phylogenetically conserved, thermodynamically favored RNA secondary structures, we demonstrate a long-range interaction between sequences in the previously described CRE (5BSL3.2, now SL9266) with a previously predicted unpaired sequence located 3' to SL9033, approximately 200 nucleotides upstream. Extensive reverse genetic analysis both supports this prediction and demonstrates a functional requirement in genome replication. By mutagenesis of the Con-1 replicon, we show that disruption of this alternative pairing inhibited replication, a phenotype that could be restored to wild-type levels through the introduction of compensating mutations in the upstream region. Substitution of the CRE with the analogous region of different genotypes of HCV produced replicons with phenotypes consistent with the hypothesis that both local and long-range interactions are critical for a fundamental aspect of genome replication. This report further extends the known interactions of the SL9266 CRE, which has also been shown to form a "kissing loop" interaction with the 3' NCR (P. Friebe, J. Boudet, J. P. Simorre, and R. Bartenschlager, J. Virol. 79:380-392, 2005), and suggests that cooperative long-range binding with both 5' and 3' sequences stabilizes the CRE at the core of a complex pseudoknot. Alternatively, if the long-range interactions were mutually exclusive, the SL9266 CRE may function as a molecular switch controlling a critical aspect of HCV genome replication. 相似文献
124.
Bottrill MC Joseph LN Carwardine J Bode M Cook C Game ET Grantham H Kark S Linke S McDonald-Madden E Pressey RL Walker S Wilson KA Possingham HP 《Trends in ecology & evolution》2008,23(12):649-654
Conservation efforts and emergency medicine face comparable problems: how to use scarce resources wisely to conserve valuable assets. In both fields, the process of prioritising actions is known as triage. Although often used implicitly by conservation managers, scientists and policymakers, triage has been misinterpreted as the process of simply deciding which assets (e.g. species, habitats) will not receive investment. As a consequence, triage is sometimes associated with a defeatist conservation ethic. However, triage is no more than the efficient allocation of conservation resources and we risk wasting scarce resources if we do not follow its basic principles. 相似文献
125.
Obestatin is purported to be a peptide hormone encoded in preproghrelin. We studied the metabolic effects of continuous infusion of obestatin via subcutaneously implanted osmotic mini-pumps. Administration of up to 500nmol/kg body weight/day obestatin did not change 24h cumulative food intake or body weight in rats. Similarly, no effects were observed when obestatin was infused at 1000nmol/kg body weight/day for seven days. This dose of obestatin infused during a 24h fast did not alter weight loss, suggesting that obestatin has no effect on energy expenditure, and this dose did not alter glucose or insulin responses during an IPGTT. Obestatin was originally proposed to interact with GPR39 and subsequently the receptor for GLP-1. While both receptors are expressed in pancreatic islets, incubation with obestatin did not alter insulin release from islets in vitro. Moreover, obestatin did not bind to INS-1 beta-cells or HEK cells overexpressing GLP-1 receptors or displace GLP-1 binding to these cells. Our findings do not support the concept that obestatin is a hormone with metabolic actions. 相似文献
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Hammer GP Fehringer F Seitz G Zeeb H Dulon M Langner I Blettner M 《Radiation and environmental biophysics》2008,47(1):95-99
A historical cohort study of German nuclear power workers was set up to investigate the overall and cancer mortality risk
related to a long-term low-level exposure to ionising radiation. The cohort was part of an international collaborative study
whose pooled analyses were carried out at the International Agency for Research on Cancer (IARC), Lyon, and published recently.
Due to delays in data collection, data from the German cohort were not included in these analyses. This cohort includes 4,844
employees who worked in any of 10 nuclear power plants, between 1 January 1991 and 31 December 1997. Sixty-eight deaths among
men were observed in 31,000 person years, and none among women. Standardized mortality ratios (SMRs) were computed for all
causes of death, all cancers, cardiovascular diseases, external causes, and all other causes. Overall, a strong healthy worker
effect was observed (all-cause SMR = 0.54, 95% CI 0.42–0.67), and no increase in total cancer mortality was seen (SMR = 0.66,
95% CI 0.43–0.95). These results are in line with and complement IARC results. Figures are yet too small for stable risk estimates
and further work is therefore under way to include more power plants, and to extend the follow-up until the year 2005. 相似文献
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Laura L Koth Madeleine W Rodriguez Xin Liu Bernstein Salina Chan Xiaozhu Huang Israel F Charo Barrett J Rollins David J Erle 《Respiratory research》2004,5(1):12
BackgroundAsthma is characterized by type 2 T-helper cell (Th2) inflammation, goblet cell hyperplasia, airway hyperreactivity, and airway fibrosis. Monocyte chemoattractant protein-1 (MCP-1 or CCL2) and its receptor, CCR2, have been shown to play important roles in the development of Th2 inflammation. CCR2-deficient mice have been found to have altered inflammatory and physiologic responses in some models of experimental allergic asthma, but the role of CCR2 in contributing to inflammation and airway hyperreactivity appears to vary considerably between models. Furthermore, MCP-1-deficient mice have not previously been studied in models of experimental allergic asthma.MethodsTo test whether MCP-1 and CCR2 are each required for the development of experimental allergic asthma, we applied an Aspergillus antigen-induced model of Th2 cytokine-driven allergic asthma associated with airway fibrosis to mice deficient in either MCP-1 or CCR2. Previous studies with live Aspergillus conidia instilled into the lung revealed that MCP-1 and CCR2 play a role in anti-fungal responses; in contrast, we used a non-viable Aspergillus antigen preparation known to induce a robust eosinophilic inflammatory response.ResultsWe found that wild-type C57BL/6 mice developed eosinophilic airway inflammation, goblet cell hyperplasia, airway hyperreactivity, elevations in serum IgE, and airway fibrosis in response to airway challenge with Aspergillus antigen. Surprisingly, mice deficient in either MCP-1 or CCR2 had responses to Aspergillus antigen similar to those seen in wild-type mice, including production of Th2 cytokines.ConclusionWe conclude that robust Th2-mediated lung pathology can occur even in the complete absence of MCP-1 or CCR2. 相似文献