| 1. |
- Steck, T., et al.
(author)
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Bias determination and precision validation of ozone profiles from MIPAS-Envisat retrieved with the IMK-IAA processor
- 2007
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In: Atmospheric Chemistry And Physics. - : Copernicus GmbH. - 1680-7316 .- 1680-7324. ; 7:13, s. 3639-3662
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Journal article (peer-reviewed)abstract
- This paper characterizes vertical ozone profiles retrieved with the IMK-IAA (Institute for Meteorology and Climate Research, Karlsruhe – Instituto de Astrofisica de Andalucia) science-oriented processor from high spectral resolution data (until March 2004) measured by the Michelson Interferometer for Passive Atmospheric Sounding (MIPAS) aboard the environmental satellite Envisat. Bias determination and precision validation is performed on the basis of correlative measurements by ground-based lidars, Fourier transform infrared spectrometers, and microwave radiometers as well as balloon-borne ozonesondes, the balloon-borne version of MIPAS, and two satellite instruments (Halogen Occultation Experiment and Polar Ozone and Aerosol Measurement III). Percentage mean differences between MIPAS and the comparison instruments for stratospheric ozone are generally within ±10%. The precision in this altitude region is estimated at values between 5 and 10% which gives an accuracy of 15 to 20%. Below 18 km, the spread of the percentage mean differences is larger and the precision degrades to values of more than 20% depending on altitude and latitude. The main reason for the degraded precision at low altitudes is attributed to undetected thin clouds which affect MIPAS retrievals, and to the influence of uncertainties in the water vapor concentration.
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| 2. |
- Tang, C A, et al.
(author)
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Fracture spacing in layered materials and pattern transition from parallel to polygonal fractures
- 2006
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In: Physical Review E. Statistical, Nonlinear, and Soft Matter Physics. - 1539-3755 .- 1550-2376. ; 73:5, s. 056120-28
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Journal article (peer-reviewed)abstract
- We perform three-dimensional simulations of fracture growth in a three-layered plate model with an embedded heterogeneous layer under horizontal biaxial stretch (representing stretch from directional to isotropic) by the finite element approach. The fractures develop under a quasistatical, slowly increasing biaxial strain. The material inhomogeneities are accounted for by assigning each element a failure threshold that is defined by a given statistical distribution. A universal scale law of fracture spacing to biaxial strain in terms of principal stress ratio is well demonstrated in a three-dimensional fashion. The numerically obtained fracture patterns show a continuous pattern transition from parallel fractures, laddering fracture to polygonal fractures, which depends strongly on the far-field loading conditions in terms of principal stress ratio ......
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| 3. |
- Young, D., et al.
(author)
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The A2b adenosine receptor protects against inflammation and excessive vascular adhesion
- 2006
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In: Journal of Clinical Investigation. - 0021-9738 .- 1558-8238. ; 116:7, s. 1913-1923
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Journal article (peer-reviewed)abstract
- Adenosine has been described as playing a role in the control of inflammation, but it has not been certain which of its receptors mediate this effect. Here, we generated an A2B adenosine receptor-knockout/reporter gene-knock-in (A2BAR-knockout/reporter gene-knock-in) mouse model and showed receptor gene expression in the vasculature and macrophages, the ablation of which causes low-grade inflammation compared with age-, sex-, and strain-matched control mice. Augmentation of proinflammatory cytokines, such as TNF-alpha, and a consequent downregulation of IkappaB-alpha are the underlying mechanisms for an observed upregulation of adhesion molecules in the vasculature of these A2BAR-null mice. Intriguingly, leukocyte adhesion to the vasculature is significantly increased in the A2BAR-knockout mice. Exposure to an endotoxin results in augmented proinflammatory cytokine levels in A2BAR-null mice compared with control mice. Bone marrow transplantations indicated that bone marrow (and to a lesser extent vascular) A2BARs regulate these processes. Hence, we identify the A2BAR as a new critical regulator of inflammation and vascular adhesion primarily via signals from hematopoietic cells to the vasculature, focusing attention on the receptor as a therapeutic target
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