66 research outputs found
Development and evolution of detachment faulting along 50 km of the Mid-Atlantic Ridge near 16.5N
This is the accepted manuscript. An edited version of this paper was published by AGU. Copyright 2014 American Geophysical Union.A multifaceted study of the slow-spreading Mid-Atlantic Ridge (MAR) at 16.5ÂșN provides
new insights into detachment faulting and its evolution through time. The survey included
regional multibeam bathymetry mapping, high-resolution mapping using AUV Sentry, seafloor imaging using the TowCam system, and an extensive rock-dredging program. At different times, detachment faulting was active along ~50 km of the western flank of the study area, and may have dominated spreading on that flank for the last 5 Ma. Detachment morphologies vary and include a classic corrugated massif, non-corrugated massifs, and back-tilted ridges marking detachment breakaways. High-resolution Sentry data reveal one other detachment morphology; a low-angle, irregular surface in the regional bathymetry is shown to be a finely corrugated detachment surface (corrugation wavelength of only tens of meters and relief of just a few meters). Multi-scale corrugations are observed 2-3 km from the detachment breakaway suggesting that they formed in the brittle layer, perhaps by anastomosing faults. The thin wedge of hanging wall lavas that covers a low-angle (6Âș) detachment footwall near its termination are intensely faulted and fissured; this deformation may be enhanced by the low-angle of the emerging footwall. Active detachment faulting currently is limited to the western side of the rift valley. Nonetheless, detachment fault morphologies also are present over a large portion of the eastern flank on crust > 2 Ma indicating that within the last 5 Ma parts of the ridge axis have experienced periods of two-sided detachment faulting.This work was supported by the National Science Foundation grant number OCE-1155650
Understanding the dynamics of Toll-like Receptor 5 response to flagellin and its regulation by estradiol
© 2017 The Author(s). Toll-like receptors (TLRs) are major players of the innate immune system. Once activated, they trigger a signalling cascade that leads to NF-Ă° B translocation from the cytoplasm to the nucleus. Single cell analysis shows that NF-Ă° B signalling dynamics are a critical determinant of transcriptional regulation. Moreover, the outcome of innate immune response is also affected by the cross-talk between TLRs and estrogen signalling. Here, we characterized the dynamics of TLR5 signalling, responsible for the recognition of flagellated bacteria, and those changes induced by estradiol in its signalling at the single cell level. TLR5 activation in MCF7 cells induced a single and sustained NF-k B translocation into the nucleus that resulted in high NF-k B transcription activity. The overall magnitude of NF-k B transcription activity was not influenced by the duration of the stimulus. No significant changes are observed in the dynamics of NF-k B translocation to the nucleus when MCF7 cells are incubated with estradiol. However, estradiol significantly decreased NF-k B transcriptional activity while increasing TLR5-mediated AP-1 transcription. The effect of estradiol on transcriptional activity was dependent on the estrogen receptor activated. This fine tuning seems to occur mainly in the nucleus at the transcription level rather than affecting the translocation of the NF-k B transcription factor
Improving diaper design to address incontinence associated dermatitis
<p>Abstract</p> <p>Background</p> <p>Incontinence associated dermatitis (IAD) is an inflammatory skin disease mainly triggered by prolonged skin contact with urine, feces but also liberal detergent use when cleansing the skin. To minimize the epidermal barrier challenge we optimized the design of adult incontinence briefs. In the fluid absorption area we interposed a special type of acidic, curled-type of cellulose between the top sheet in contact with the skin and the absorption core beneath containing the polyacrylate superabsorber. The intention was to minimize disturbance of the already weak acid mantle of aged skin. We also employed air-permeable side panels to minimize skin occlusion and swelling of the stratum corneum.</p> <p>Methods</p> <p>The surface pH of diapers was measured after repeated wetting with a urine substitute fluid at the level of the top sheet. Occlusive effects and hydration of the stratum corneum were measured after a 4 hour application of different side panel materials by corneometry on human volunteers. Finally, we evaluated skin symptoms in 12 patients with preexisting IAD for 21 days following the institutional switch to the optimized diaper design. Local skin care protocols remained in place unchanged.</p> <p>Results</p> <p>The improved design created a surface pH of 4.6 which was stable even after repeated wetting throughout a 5 hour period. The "standard design" briefs had values of 7.1, which is alkaline compared to the acidic surface of normal skin. Side panels made from non-woven material with an air-permeability of more than 1200 l/m<sup>2</sup>/s avoided excessive hydration of the stratum corneum when compared to the commonly employed air-impermeable plastic films. Resolution of pre-existing IAD skin lesions was noted in 8 out of 12 patients after the switch to the optimized brief design.</p> <p>Conclusions</p> <p>An improved design of adult-type briefs can create an acidic pH on the surface and breathable side panels avoid over-hydration of the stratum corneum and occlusion. This may support the epidermal barrier function and may help to reduce the occurrence of IAD.</p
Lipopolysaccharide-induced NF-ÎșB nuclear translocation is primarily dependent on MyD88, but TNF expression requires TRIF and MyD88
TLR4 signalling through the MyD88 and TRIF-dependent pathways initiates translocation of the transcription factor NF-ÎșB into the nucleus. In cell population studies using mathematical modeling and functional analyses, Cheng et al. suggested that LPS-driven activation of MyD88, in the absence of TRIF, impairs NF-ÎșB translocation. We tested the model proposed by Cheng et al. using real-time single cell analysis in macrophages expressing EGFP-tagged p65 and a TNF promoter-driven mCherry. Following LPS stimulation, cells lacking TRIF show a pattern of NF-ÎșB dynamics that is unaltered from wild-type cells, but activation of the TNF promoter is impaired. In macrophages lacking MyD88, there is minimal NF-ÎșB translocation to the nucleus in response to LPS stimulation, and there is no activation of the TNF promoter. These findings confirm that signalling through MyD88 is the primary driver for LPS-dependent NF-ÎșB translocation to the nucleus. The pattern of NF-ÎșB dynamics in TRIF-deficient cells does not, however, directly reflect the kinetics of TNF promoter activation, supporting the concept that TRIF-dependent signalling plays an important role in the transcription of this cytokine.J.S. is supported by the Cambridge Commonwealth, European and International Trust. CEB was supported by a BBSRC fellowship (BB/H021930/1) and a Wellcome Trust Investigator award (WT108045AIA). E.C. and P.C. acknowledge EU-ITN Transpol and EU-ERC Hydrosync. I.D.C.F. is supported by the intramural Research Program of the National Institute of Allergy and Infectious Diseases
El rol de los sistemas cacaoteros en los medios de vida de los hogares productores en el Municipio de Waslala, Nicaragua
3 ilustraciones, 20 tabulaciones, 72 p?gina
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