The impact of anatomy variation on temperature based time of death estimation.

Temperature-based time of death estimation using simulation methods such as the finite element method promise higher accuracy and broader applicability in nonstandard cooling scenarios than established phenomenological methods. Their accuracy depends crucially on the simulation model to capture the actual situation, which in turn hinges on the representation of the corpse's anatomy in form of computational meshes as well as on the thermodynamic parameters. While inaccuracies in anatomy representation due to coarse mesh resolution are known to have a minor impact on the estimated time of death, the sensitivity with respect to larger differences in the anatomy has so far not been studied. We assess this sensitivity by comparing four independently generated and vastly different anatomical models in terms of the estimated time of death in an identical cooling scenario. In order to isolate the impact of shape variation, the models are scaled to a reference size, and the possible impact of measurement location variation is excluded explicitly by finding measurement locations leading to minimum deviations. The thus obtained lower bound on the impact of anatomy on the estimated time of death shows, that anatomy variations lead to deviations of at least 5-10%.

Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis.

Sprouty-related proteins with EVH1 (enabled/vasodilator-stimulated phosphoprotein homology 1) domain (SPREDs) are inhibitors of MAPK signaling. To elucidate SPRED2 in vivo function, we characterized body homeostasis in SPRED2(-/-) mice. They showed a doubled daily water uptake, induced by elevated serum osmolality, originating from increased blood salt load. Accordingly, serum aldosterone was doubled, accompanied by augmented adrenal aldosterone synthase (AS) expression. Surprisingly, serum vasopressin (AVP) was unaltered, and, as evidenced by halved angiotensin II (Ang II) levels, the renin angiotensin system (RAS) was down-regulated. Adrenocorticotropic hormone (ACTH) was significantly elevated in SPRED2(-/-) mice, together with its secretagogue corticotropin-releasing hormone (CRH) and its downstream target corticosterone. ERK phosphorylation in brains was augmented, and hypothalamic CRH mRNA levels were elevated, both contributing to the increased CRH release. Our data were supported by CRH promoter reporter assays in hypothalamic mHypoE-44 cells, revealing a SPRED-dependent inhibition of Ets (ERK/E-twenty-six)-dependent transcription. Furthermore, SPRED suppressed CRH production in these cells. In conclusion, our study suggests that SPRED2 deficiency leads to an increased MAPK signaling, which results in an augmented CRH promoter activity. The subsequent CRH overproduction causes an up-regulation of downstream hypothalamic-pituitary-adrenal (HPA) hormone secretion. This constitutes a possible trigger for the observed compulsive grooming in SPRED2(-/-) mice and may, together with hyperplasia of aldosterone-producing cells, contribute to the hyperaldosteronism and homeostatic imbalances.

Piezo-Sensitive Fabrics from Carbon Black Containing Conductive Cellulose Fibres for Flexible Pressure Sensors.

The design of flexible sensors which can be incorporated in textile structures is of decisive importance for the future development of wearables. In addition to their technical functionality, the materials chosen to construct the sensor should be nontoxic, affordable, and compatible with future recycling. Conductive fibres were produced by incorporation of carbon black into regenerated cellulose fibres. By incorporation of 23 wt.% and 27 wt.% carbon black, the surface resistance of the fibres reduced from 1.3 × 1010 Ω·cm for standard viscose fibres to 2.7 × 103 and 475 Ω·cm, respectively. Fibre tenacity reduced to 30-50% of a standard viscose; however, it was sufficient to allow processing of the material in standard textile operations. A fibre blend of the conductive viscose fibres with polyester fibres was used to produce a needle-punched nonwoven material with piezo-electric properties, which was used as a pressure sensor in the very low pressure range of 400-1000 Pa. The durability of the sensor was demonstrated in repetitive load/relaxation cycles. As a regenerated cellulose fibre, the carbon-black-incorporated cellulose fibre is compatible with standard textile processing operations and, thus, will be of high interest as a functional element in future wearables.

Overexpression of ABCG1 protein attenuates arteriosclerosis and endothelial dysfunction in atherosclerotic rabbits.

The ABCG1 protein is centrally involved in reverse cholesterol transport from the vessel wall. Investigation of the effects of ABCG1 overexpression or knockdown in vivo has produced controversial results and strongly depended on the gene intervention model in which it was studied. Therefore, we investigated the effect of local overexpression of human ABCG1 in a novel model of vessel wall-directed adenoviral gene transfer in atherosclerotic rabbits. We conducted local, vascular-specific gene transfer by adenoviral delivery of human ABCG1 (Ad-ABCG1-GFP) in cholesterol-fed atherosclerotic rabbits in vivo. Endothelial overexpression of ABCG1 markedly reduced atheroprogression (plaque size) and almost blunted vascular inflammation, as shown by markedly reduced macrophage and smooth muscle cell invasion into the vascular wall. Also endothelial function, as determined by vascular ultrasound in vivo, was improved in rabbits after gene transfer with Ad-ABCG1-GFP. Therefore, both earlier and later stages of atherosclerosis were improved in this model of somatic gene transfer into the vessel wall. In contrast to results in transgenic mice, over-expression of ABCG1 by somatic gene transfer to the atherosclerotic vessel wall results in a significant improvement of plaque morphology and composition, and of vascular function in vivo.