25 resultados para Shift-and

em BORIS: Bern Open Repository and Information System - Berna - Suiça


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Southern Switzerland is a fire prone area where fire has to be considered as a natural environmental factor. In the past decades, fire frequency has tended to increase due to changes in landscape management. The most common type of fire is surface fire which normally breaks out during the vegetation resting period. Usually this type of fire shows short residence time (rapid spread), low to medium fire intensity and limited size. South-facing slopes are particularly fire-prone, so that very high fire frequency is possible: under these conditions passive resistant species and postfire resprouting species are favoured, usually leading to a reduction in the number of surviving species to a few fire adapted sprouters. Evergreen broadleaves are extremely sensitive to repeated fires. A simulation of the potential vegetation of southern Switzerland under climatic changed conditions evidenced the coincidence of the potential area of spreading forests rich in evergreen broad-leaved species with the most fire-prone area of the region. Therefore, in future, wildfires could play an important regulating role: most probably they will not stop the large-scale laurophyllisation of the thermophilous forests of southern Switzerland, but at sites with high fire frequency the vegetation shift could be slowed or even prevented by fire-disturbances.

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The prognostic relevance of quantitative an intracoronary occlusive electrocardiographic (ECG) ST-segment shift and its determinants have not been investigated in humans. In 765 patients with chronic stable coronary artery disease, the following simultaneous quantitative measurements were obtained during a 1-minute coronary balloon occlusion: intracoronary ECG ST-segment shift (recorded by angioplasty guidewire), mean aortic pressure, mean distal coronary pressure, and mean central venous pressure (CVP). Collateral flow index (CFI) was calculated as follows: (mean distal coronary pressure minus CVP)/(mean aortic pressure minus CVP). During an average follow-up duration of 50 ± 34 months, the cumulative mortality rate from all causes was significantly lower in the group with an ST-segment shift <0.1 mV (n = 89) than in the group with an ST-segment shift ≥0.1 mV (n = 676, p = 0.0211). Factors independently related to intracoronary occlusive ECG ST-segment shift <0.1 mV (r(2) = 0.189, p <0.0001) were high CFI (p <0.0001), intracoronary occlusive RR interval (p = 0.0467), right coronary artery as the ischemic region (p <0.0001), and absence of arterial hypertension (p = 0.0132). "High" CFI according to receiver operating characteristics analysis was ≥0.217 (area under receiver operating characteristics curve 0.647, p <0.0001). In conclusion, absence of ECG ST-segment shift during brief coronary occlusion in patients with chronic coronary artery disease conveys a decreased mortality and is directly influenced by a well-developed collateral supply to the right versus left coronary ischemic region and by the absence of systemic hypertension in a patient's history.

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Exposure to polycyclic aromatic hydrocarbons (PAH) and DNA damage were analyzed in coke oven (n = 37), refractory (n = 96), graphite electrode (n = 26), and converter workers (n = 12), whereas construction workers (n = 48) served as referents. PAH exposure was assessed by personal air sampling during shift and biological monitoring in urine post shift (1-hydroxypyrene, 1-OHP and 1-, 2 + 9-, 3-, 4-hydroxyphenanthrenes, SigmaOHPHE). DNA damage was measured by 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) and DNA strand breaks in blood post shift. Median 1-OHP and SigmaOHPHE were highest in converter workers (13.5 and 37.2 microg/g crea). The industrial setting contributed to the metabolite concentrations rather than the air-borne concentration alone. Other routes of uptake, probably dermal, influenced associations between air-borne concentrations and levels of PAH metabolites in urine making biomonitoring results preferred parameters to assess exposure to PAH. DNA damage in terms of 8-oxo-dGuo and DNA strand breaks was higher in exposed workers compared to referents ranking highest for graphite-electrode production. The type of industry contributed to genotoxic DNA damage and DNA damage was not unequivocally associated to PAH on the individual level most likely due to potential contributions of co-exposures.

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An inherited polyneuropathy (PN) observed in Leonberger dogs has clinical similarities to a genetically heterogeneous group of peripheral neuropathies termed Charcot-Marie-Tooth (CMT) disease in humans. The Leonberger disorder is a severe, juvenile-onset, chronic, progressive, and mixed PN, characterized by exercise intolerance, gait abnormalities and muscle atrophy of the pelvic limbs, as well as inspiratory stridor and dyspnea. We mapped a PN locus in Leonbergers to a 250 kb region on canine chromosome 16 (Praw = 1.16×10-10, Pgenome, corrected = 0.006) utilizing a high-density SNP array. Within this interval is the ARHGEF10 gene, a member of the rho family of GTPases known to be involved in neuronal growth and axonal migration, and implicated in human hypomyelination. ARHGEF10 sequencing identified a 10 bp deletion in affected dogs that removes four nucleotides from the 3'-end of exon 17 and six nucleotides from the 5'-end of intron 17 (c.1955_1958+6delCACGGTGAGC). This eliminates the 3'-splice junction of exon 17, creates an alternate splice site immediately downstream in which the processed mRNA contains a frame shift, and generates a premature stop codon predicted to truncate approximately 50% of the protein. Homozygosity for the deletion was highly associated with the severe juvenile-onset PN phenotype in both Leonberger and Saint Bernard dogs. The overall clinical picture of PN in these breeds, and the effects of sex and heterozygosity of the ARHGEF10 deletion, are less clear due to the likely presence of other forms of PN with variable ages of onset and severity of clinical signs. This is the first documented severe polyneuropathy associated with a mutation in ARHGEF10 in any species.

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Much of the recent interest in educational gender differences is based on differences in academic performance. Several studies have shown that young women now out-perform males in terms of school grades and university degrees. But while there is a lot of research into the reasons for this shift, and into gender gaps in reading and maths achievement, little research has been done on the consequences of these differences in educational and early occupational success. - See more at: https://cerp.aqa.org.uk/perspectives/male-and-female-routes-success#sthash.HR8fFTen.dpuf

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Theoretical models predict that parents should adjust the amount of care both to their own and their partner's body condition. In most biparental species, parental duties are switched repeatedly allowing for repeated mutual adjustment of the amount of care. In the mouthbrooding cichlid Eretmodus cyanostictus, terms are switched only once with females taking the first share. The timing of the shift of the clutch between mates strongly determines both partners' brooding period and thereby their parental investment. Females signal their readiness to transfer the young several days before the male finally takes them, suggesting sexual conflict over the timing of the shift. In a lab experiment, we reduced the body condition of either the female or the male of a pair to test whether energy reserves affect the timing of the shift and whether female signalling behaviour depends on energetic state. Males with a lowered condition took the young later and incubated for a shorter period, which prolonged the incubation time of their female partners. When female condition was lowered, female and male incubation durations remained unchanged, although females signalled their readiness to shift more intensely. Our results suggest that males adjust their parental investment to own energy reserves but are unresponsive to their mate's condition. Females appear to carry the entire costs for the male's adjustment of care. We propose that intrinsic asymmetries in the scope for mutual adjustment of parental investment and the costs of negotiation crucially influence solutions of the conflict between sexes over care.

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The enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) catalyzes the conversion of inactive to active glucocorticoids. 11beta-HSD1 plays a crucial role in the pathogenesis of obesity and controls glucocorticoid actions in inflammation. Several studies have demonstrated that TNF-alpha increases 11beta-HSD1 mRNA and activity in various cell models. Here, we demonstrate that mRNA and activity of 11beta-HSD1 is increased in liver tissue from transgenic mice overexpressing TNF-alpha, indicating that this effect also occurs in vivo. To dissect the molecular mechanism of this increase, we investigated basal and TNF-alpha-induced transcription of the 11beta-HSD1 gene (HSD11B1) in HepG2 cells. We found that TNF-alpha acts via p38 MAPK pathway. Transient transfections with variable lengths of human HSD11B1 promoter revealed highest activity with or without TNF-alpha in the proximal promoter region (-180 to +74). Cotransfection with human CCAAT/enhancer binding protein-alpha (C/EBPalpha) and C/EBPbeta-LAP expression vectors activated the HSD11B1 promoter with the strongest effect within the same region. Gel shift and RNA interference assays revealed the involvement of mainly C/EBPalpha, but also C/EBPbeta, in basal and only of C/EBPbeta in the TNF-alpha-induced HSD11B1 expression. Chromatin immunoprecipitation assay confirmed in vivo the increased abundance of C/EBPbeta on the proximal HSD11B1 promoter upon TNF-alpha treatment. In conclusion, C/EBPalpha and C/EBPbeta control basal transcription, and TNF-alpha upregulates 11beta-HSD1, most likely by p38 MAPK-mediated increased binding of C/EBPbeta to the human HSD11B1 promoter. To our knowledge, this is the first study showing involvement of p38 MAPK in the TNF-alpha-mediated 11beta-HSD1 regulation, and that TNF-alpha stimulates enzyme activity in vivo.

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In contrast-enhanced (CE) MR myelography, hyperintense signal outside the intrathecal space in T1-weighted sequences with spectral presaturation inversion recovery (SPIR) is usually considered to be due to CSF leakage. We retrospectively investigated a hyperintense signal at the apex of the lung appearing in this sequence in patients with SIH (n = 5), CSF rhinorrhoea (n = 2), lumbar spine surgery (n = 1) and in control subjects (n = 6). Intrathecal application of contrast agent was performed in all patients before MR examination, but not in the control group. The reproducible signal increase was investigated with other fat suppression techniques and MR spectroscopy. All patients and controls showed strongly hyperintense signal at the apex of the lungs imitating CSF leakage into paraspinal tissue. This signal increase was identified as an artefact, caused by spectroscopically proven shift and broadening of water and lipid resonances (1-2 ppm) in this anatomical region. Only patients with SIH showed additional focal enhancement along the spinal nerve roots and/or in the spinal epidural space. In conclusion CE MR myelography with spectral selective fat suppression shows a reproducible cervicothoracic artefact, imitating CSF leakage. Selective water excitation technique as well as periradicular and epidural contrast collections may be helpful to discriminate between real pathological findings and artefacts.

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In this paper, we present a novel technique for the removal of astigmatism in submillimeter-wave optical systems through employment of a specific combination of so-called astigmatic off-axis reflectors. This technique treats an orthogonally astigmatic beam using skew Gaussian beam analysis, from which an anastigmatic imaging network is derived. The resultant beam is considered truly stigmatic, with all Gaussian beam parameters in the orthogonal directions being matched. This is thus considered an improvement over previous techniques wherein a beam corrected for astigmatism has only the orthogonal beam amplitude radii matched, with phase shift and phase radius of curvature not considered. This technique is computationally efficient, negating the requirement for computationally intensive numerical analysis of shaped reflector surfaces. The required optical surfaces are also relatively simple to implement compared to such numerically optimized shaped surfaces. This technique is implemented in this work as part of the complete optics train for the STEAMR antenna. The STEAMR instrument is envisaged as a mutli-beam limb sounding instrument operating at submillimeter wavelengths. The antenna optics arrangement for this instrument uses multiple off-axis reflectors to control the incident radiation and couple them to their corresponding receiver feeds. An anastigmatic imaging network is successfully implemented into an optical model of this antenna, and the resultant design ensures optimal imaging of the beams to the corresponding feed horns. This example also addresses the challenges of imaging in multi-beam antenna systems.

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Postmodernism, deconstruction and subversion have been the buzzwords of the last few decades. But not any longer. Ever since the end of the millennium an increasingly perceptible desire to turn towards other concerns can be noted. Only, what comes after postmodernism? Where are we going now? Irmtraud Huber suggests some answers to these questions, focusing on novels by Michael Chabon, Mark Z. Danielewski, Jonathan Safran Foer and David Mitchell and highlighting the ways in which they go beyond postmodernism and turn from deconstruction to reconstruction. Approaching the question from an unusual direction by exploring the novelists' particular use of the fantastic mode, this book offers both further insights into the present aesthetic shift and a new perspective on the literary fantastic.

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BACKGROUND: Accurate projection of implanted subdural electrode contacts in presurgical evaluation of pharmacoresistant epilepsy cases by invasive EEG is highly relevant. Linear fusion of CT and MRI images may display the contacts in the wrong position due to brain shift effects. OBJECTIVE: A retrospective study in five patients with pharmacoresistant epilepsy was performed to evaluate whether an elastic image fusion algorithm can provide a more accurate projection of the electrode contacts on the pre-implantation MRI as compared to linear fusion. METHODS: An automated elastic image fusion algorithm (AEF), a guided elastic image fusion algorithm (GEF), and a standard linear fusion algorithm (LF) were used on preoperative MRI and post-implantation CT scans. Vertical correction of virtual contact positions, total virtual contact shift, corrections of midline shift and brain shifts due to pneumencephalus were measured. RESULTS: Both AEF and GEF worked well with all 5 cases. An average midline shift of 1.7mm (SD 1.25) was corrected to 0.4mm (SD 0.8) after AEF and to 0.0mm (SD 0) after GEF. Median virtual distances between contacts and cortical surface were corrected by a significant amount, from 2.3mm after LF to 0.0mm after AEF and GEF (p<.001). Mean total relative corrections of 3.1 mm (SD 1.85) after AEF and 3.0mm (SD 1.77) after GEF were achieved. The tested version of GEF did not achieve a satisfying virtual correction of pneumencephalus. CONCLUSION: The technique provided a clear improvement in fusion of pre- and post-implantation scans, although the accuracy is difficult to evaluate.

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RATIONALE Early reperfusion in patients experiencing acute ischemic stroke is critical, especially for patients with large vessel occlusion who have poor prognosis without revascularization. Solitaire™ stent retriever devices have been shown to immediately restore vascular perfusion safely, rapidly, and effectively in acute ischemic stroke patients with large vessel occlusions. AIM The aim of the study was to demonstrate that, among patients with large vessel, anterior circulation occlusion who have received intravenous tissue plasminogen activator, treatment with Solitaire revascularization devices reduces degree of disability 3 months post stroke. DESIGN The study is a global multicenter, two-arm, prospective, randomized, open, blinded end-point trial comparing functional outcomes in acute ischemic stroke patients who are treated with either intravenous tissue plasminogen activator alone or intravenous tissue plasminogen activator in combination with the Solitaire device. Up to 833 patients will be enrolled. PROCEDURES Patients who have received intravenous tissue plasminogen activator are randomized to either continue with intravenous tissue plasminogen activator alone or additionally proceed to neurothrombectomy using the Solitaire device within six-hours of symptom onset. STUDY OUTCOMES The primary end-point is 90-day global disability, assessed with the modified Rankin Scale (mRS). Secondary outcomes include mortality at 90 days, functional independence (mRS ≤ 2) at 90 days, change in National Institutes of Health Stroke Scale at 27 h, reperfusion at 27 h, and thrombolysis in cerebral infarction 2b/3 flow at the end of the procedure. ANALYSIS Statistical analysis will be conducted using simultaneous success criteria on the overall distribution of modified Rankin Scale (Rankin shift) and proportions of subjects achieving functional independence (mRS 0-2).

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Osteogenesis imperfecta (OI) is a heritable connective tissue disease characterized by bone fragility and increased risk of fractures. Up to now, mutations in at least 18 genes have been associated with dominant and recessive forms of OI that affect the production or post-translational processing of procollagen or alter bone homeostasis. Among those, SERPINH1 encoding heat shock protein 47 (HSP47), a chaperone exclusive for collagen folding in the ER, was identified to cause a severe form of OI in dachshunds (L326P) as well as in humans (one single case with a L78P mutation). To elucidate the disease mechanism underlying OI in the dog model, we applied a range of biochemical assays to mutant and control skin fibroblasts as well as on bone samples. These experiments revealed that type I collagen synthesized by mutant cells had decreased electrophoretic mobility. Procollagen was retained intracellularly with concomitant dilation of ER cisternae and activation of the ER stress response markers GRP78 and phospho-eIF2α, thus suggesting a defect in procollagen processing. In line with the migration shift detected on SDS-PAGE of cell culture collagen, extracts of bone collagen from the OI dog showed a similar mobility shift, and on tandem mass spectrometry, the chains were post-translationally overmodified. The bone collagen had a higher content of pyridinoline than control dog bone. We conclude that the SERPINH1 mutation in this naturally occurring model of OI impairs how HSP47 acts as a chaperone in the ER. This results in abnormal post-translational modification and cross-linking of the bone collagen.

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We report on the structural characterization of junctions between atomically well-defined graphene nanoribbons (GNRs) by means of low-temperature, noncontact scanning probe microscopy. We show that the combination of simultaneously acquired frequency shift and tunneling current maps with tight binding (TB) simulations allows a comprehensive characterization of the atomic connectivity in the GNR junctions. The proposed approach can be generally applied to the investigation of graphene nanomaterials and their interconnections and is thus expected to become an important tool in the development of graphene-based circuitry.