PURCHASE BEHAVIOUR RELATED TO HEATING SYSTEMS IN GERMANY WITH SPECIAL CONSIDERATION OF CONSUMERS' ECOLOGICAL ATTITUDES

Paper prepared for presentation at the Energy Engineering, Economics and Policy (EEEP) Conference Orlando (USA), 13th July 2009Consumer behaviour, Germany, Heating systems, Demand and Price Analysis, Q41, R20, M39,

Syzygies of Abelian and Bielliptic Surfaces in P^4

So far only six families of smooth irregular surfaces are known to exist in P^4 (up to pullbacks by suitable finite covers of P^4). These are the elliptic quintic scrolls, the minimal abelian and bielliptic surfaces (of degree 10), two different families of non-minimal abelian surfaces of degree 15, and one family of non-minimal bielliptic surfaces of degree 15. The main purpose of the paper is to describe the structure of the Hartshorne-Rao modules and the syzygies for each of these smooth irregular surfaces in P^4, providing at the same time a unified construction method (via syzygies) for these families of surfaces.Comment: 64 pages, author-supplied DVI file available at http://oscar.math.brandeis.edu/~popescu/dvi/bielliptics2.dvi AmS-TeX v. 2.

Secrets Revealed in Container Images: An Internet-wide Study on Occurrence and Impact

Containerization allows bundling applications and their dependencies into a single image. The containerization framework Docker eases the use of this concept and enables sharing images publicly, gaining high momentum. However, it can lead to users creating and sharing images that include private keys or API secrets-either by mistake or out of negligence. This leakage impairs the creator's security and that of everyone using the image. Yet, the extent of this practice and how to counteract it remains unclear. In this paper, we analyze 337,171 images from Docker Hub and 8,076 other private registries unveiling that 8.5% of images indeed include secrets. Specifically, we find 52,107 private keys and 3,158 leaked API secrets, both opening a large attack surface, i.e., putting authentication and confidentiality of privacy-sensitive data at stake and even allow active attacks. We further document that those leaked keys are used in the wild: While we discovered 1,060 certificates relying on compromised keys being issued by public certificate authorities, based on further active Internet measurements, we find 275,269 TLS and SSH hosts using leaked private keys for authentication. To counteract this issue, we discuss how our methodology can be used to prevent secret leakage and reuse.Comment: 15 pages, 7 figure

Strigolactone biosynthesis is evolutionarily conserved, regulated by phosphate starvation and contributes to resistance against phytopathogenic fungi in a moss, Physcomitrella patens

In seed plants, strigolactones (SLs) regulate architecture and induce mycorrhizal symbiosis in response to environmental cues. SLs are formed by combined activity of the carotenoid cleavage dioxygenases (CCDs) 7 and 8 from 9-cis-β-carotene, leading to carlactone that is converted by cytochromes P450 (clade 711; MAX1 in Arabidopsis) into various SLs. As Physcomitrella patens possesses CCD7 and CCD8 homologs but lacks MAX1, we investigated if PpCCD7 together with PpCCD8 form carlactone and how deletion of these enzymes influences growth and interactions with the environment. We investigated the enzymatic activity of PpCCD7 and PpCCD8 in vitro, identified the formed products by high performance liquid chromatography (HPLC) and LC-MS, and generated and analysed ΔCCD7 and ΔCCD8 mutants. We defined enzymatic activity of PpCCD7 as a stereospecific 9-cis-CCD and PpCCD8 as a carlactone synthase. ΔCCD7 and ΔCCD8 lines showed enhanced caulonema growth, which was revertible by adding the SL analogue GR24 or carlactone. Wild-type (WT) exudates induced seed germination in Orobanche ramosa. This activity was increased upon phosphate starvation and abolished in exudates of both mutants. Furthermore, both mutants showed increased susceptibility to phytopathogenic fungi. Our study reveals the deep evolutionary conservation of SL biosynthesis, SL function, and its regulation by biotic and abiotic cues.Deutsche Forschungsgemeinschaft AL892/1-4Academy of Finland 125312

Magnetic resonance imaging of cerebrospinal fluid outflow after low-rate lateral ventricle infusion in mice.

The anatomical routes for the clearance of cerebrospinal fluid (CSF) remain incompletely understood. However, recent evidence has given strong support for routes leading to lymphatic vessels. A current debate centers upon the routes through which CSF can access lymphatics, with evidence emerging for either direct routes to meningeal lymphatics or along cranial nerves to reach lymphatics outside the skull. Here, a method was established to infuse contrast agent into the ventricles using indwelling cannulae during imaging of mice at 2 and 12 months of age by magnetic resonance imaging. As expected, a significant decline in overall CSF turnover was found with aging. Quantifications demonstrated that the bulk of the contrast agent flowed from the ventricles to the subarachnoid space in the basal cisterns. Comparatively little contrast agent signal was found at the dorsal aspect of the skull. The imaging dynamics from the two cohorts revealed that the contrast agent cleared from the cranium through the cribriform plate to the nasopharyngeal lymphatics. On decalcified sections, we confirmed that fluorescentlylabeled ovalbumin drains through the cribriform plate and can be found within lymphatics surrounding the nasopharynx. In conclusion, routes leading to nasopharyngeal lymphatics appear to be a major efflux pathway for cranial CSF

IKKbeta Deficiency in Myeloid Cells Ameliorates Alzheimer's Disease-Related Symptoms and Pathology

Alzheimer's disease (AD) is characterized by extracellular amyloid-beta (Abeta) deposits and microglia-dominated inflammatory activation. Innate immune signaling controls microglial inflammatory activities and Abeta clearance. However, studies examining innate immunity in Abeta pathology and neuronal degeneration have produced conflicting results. In this study, we investigated the pathogenic role of innate immunity in AD by ablating a key signaling molecule, IKKbeta, specifically in the myeloid cells of TgCRND8 APP-transgenic mice. Deficiency of IKKbeta in myeloid cells, especially microglia, simultaneously reduced inflammatory activation and Abeta load in the brain and these effects were associated with reduction of cognitive deficits and preservation of synaptic structure proteins. IKKbeta deficiency enhanced microglial recruitment to Abeta deposits and facilitated Abeta internalization, perhaps by inhibiting TGF-beta-SMAD2/3 signaling, but did not affect Abeta production and efflux. Therefore, inhibition of IKKbeta signaling in myeloid cells improves cognitive functions in AD mice by reducing inflammatory activation and enhancing Abeta clearance. These results contribute to a better understanding of AD pathogenesis and could offer a new therapeutic option for delaying AD progression

p38α-MAPK-deficient myeloid cells ameliorate symptoms and pathology of APP-transgenic Alzheimer's disease mice

Alzheimer's disease (AD), the most common cause of dementia in the elderly, is pathologically characterized by extracellular deposition of amyloid-β peptides (Aβ) and microglia-dominated inflammatory activation in the brain. p38α-MAPK is activated in both neurons and microglia. How p38α-MAPK in microglia contributes to AD pathogenesis remains unclear. In this study, we conditionally knocked out p38α-MAPK in all myeloid cells or specifically in microglia of APP-transgenic mice, and examined animals for AD-associated pathologies (i.e., cognitive deficits, Aβ pathology, and neuroinflammation) and individual microglia for their inflammatory activation and Aβ internalization at different disease stages (e.g., at 4 and 9 months of age). Our experiments showed that p38α-MAPK-deficient myeloid cells were more effective than p38α-MAPK-deficient microglia in reducing cerebral Aβ and neuronal impairment in APP-transgenic mice. Deficiency of p38α-MAPK in myeloid cells inhibited inflammatory activation of individual microglia at 4 months but enhanced it at 9 months. Inflammatory activation promoted microglial internalization of Aβ. Interestingly, p38α-MAPK-deficient myeloid cells reduced IL-17a-expressing CD4-positive lymphocytes in 9 but not 4-month-old APP-transgenic mice. By cross-breeding APP-transgenic mice with Il-17a-knockout mice, we observed that IL-17a deficiency potentially activated microglia and reduced Aβ deposition in the brain as shown in 9-month-old myeloid p38α-MAPK-deficient AD mice. Thus, p38α-MAPK deficiency in all myeloid cells, but not only in microglia, prevents AD progression. IL-17a-expressing lymphocytes may partially mediate the pathogenic role of p38α-MAPK in peripheral myeloid cells. Our study supports p38α-MAPK as a therapeutic target for AD patients