Geology, mineralogy, ore paragenesis, and molybdenite Re-Os geochronology of Sn-W (-Mo) mineralization in Padatgyaung and Dawei, Myanmar: Implications for timing of mineralization and tectonic setting

The Sn-W (-Mo) deposits of Myanmar are mostly located in the Western Granite Province that is well known for its world-class Sn-W (-Mo) deposits. Previous studies have constrained the age of the granitic intrusions of the province and the timing of mineralization for a few deposits, but most of the mineralization ages are not well established. In this study, new molybdenite Re-Os dating of two Sn-W-(Mo) regions, Padatgyaung and Dawei, together with their geological setting and mineral paragenesis are carried out to constrain the timing of ore formation and geodynamic setting. In the Padatgyaung region, two weighted average Re-Os model ages of 64.23 ± 0.29 Ma (MSWD = 0.49, 2σ) and of 60.54 ± 0.45 Ma (MSWD = 1.3, 2σ) from vein molybdenites are considerably younger than molybdenite from tin mineralized greisen which has a weighted Re-Os model age of 68.5 ± 2.7 Ma (MSWD = 0.14, 2σ). This demonstrates that the vein-type W-Mo mineralization formed after tin mineralized greisenization. Combining our new age data with previous geochronological data, the Re-Os model age of 63.09 ± 0.17 Ma from the Wagone quartz vein suggests that the Sn-W(-Mo) mineralization in the Dawei region took place at around 70–60 Ma (Late Cretaceous to Paleocene). This study indicates the presence of a significant and discrete granite-related Sn-W(-Mo) mineralization with an age of 75–60 Ma in the Western Granite Province, although the overall age range of Sn-W mineralization in the belt spans from 120 to around 40 Ma emplaced during normal subduction and roll-back of the Neo-Tethyan oceanic crust

Tumor-associated Endo180 requires stromal-derived LOX to promote metastatic prostate cancer cell migration on human ECM surfaces

The diverse composition and structure of extracellular matrix (ECM) interfaces encountered by tumor cells at secondary tissue sites can influence metastatic progression. Extensive in vitro and in vivo data has confirmed that metastasizing tumor cells can adopt different migratory modes in response to their microenvironment. Here we present a model that uses human stromal cell-derived matrices to demonstrate that plasticity in tumor cell movement is controlled by the tumor-associated collagen receptor Endo180 (CD280, CLEC13E, KIAA0709, MRC2, TEM9, uPARAP) and the crosslinking of collagen fibers by stromal-derived lysyl oxidase (LOX). Human osteoblast-derived and fibroblast-derived ECM supported a rounded ‘amoeboid-like’ mode of cell migration and enhanced Endo180 expression in three prostate cancer cell lines (PC3, VCaP, DU145). Genetic silencing of Endo180 reverted PC3 cells from their rounded mode of migration towards a bipolar ‘mesenchymal-like’ mode of migration and blocked their translocation on human fibroblast-derived and osteoblast-derived matrices. The concomitant decrease in PC3 cell migration and increase in Endo180 expression induced by stromal LOX inhibition indicates that the Endo180-dependent rounded mode of prostate cancer cell migration requires ECM crosslinking. In conclusion, this study introduces a realistic in vitro model for the study of metastatic prostate cancer cell plasticity and pinpoints the cooperation between tumor-associated Endo180 and the stiff microenvironment imposed by stromal-derived LOX as a potential target for limiting metastatic progression in prostate cancer

Sicherung von Dämmen, Deichen und Stauanlagen : Handbuch für Theorie und Praxis ; Vol. V - 2015

Die Universität Siegen beschäftigt sich seit über 15 Jahren wissenschaftlich und im Bereich der anwendungsorientierten Forschung mit diesem Thema und hat dazu mittlerweile fünf Symposien durchgeführt. Mit der Veröffentlichung soll die langjährige Tradition als etablierte wissenschaftliche Plattform mit einem Wissensaustausch auf europäischer Ebene fortgesetzt werden. Die Bearbeitung dieser Thematik erfolgt auf der Basis der bewährten Kooperation zwischen Geotechnik und Wasserbau an der Universität Siegen. Aktuelle Ereignisse, wie z.B. die aus England oder Australien im Februar des Jahres 2014, machen uns aber auch deutlich, dass ein absoluter Schutz gegen Extremereignisse nicht möglich ist. Sie zeigen aber auch, dass dort wo technischer Hochwasserschutz konsequent umgesetzt wurde Schäden vermieden werden konnten. Wir sind nach den Ereignissen in den vergangenen Jahren aufgefordert wissenschaftlich noch leistungsfähigere und duktilere Systeme zu entwickeln. Weiter ist die Wissenschaft in der Pflicht, die Zivile Sicherheit im Hochwasser-schutz permanent zu bewerten, zu bearbeiten und ganzheitliche-interdisziplinäre und länderübergreifende Lösungen für die Zivilgesellschaft einzufordern

Degradation models for the collapse analysis of composite aerospace structures

For the next generation of aircraft, the use of fibre-reinforced polymer composites and the design of "postbuckling" structures to withstand immense loads after buckling are key technologies for considerable weight and cost savings. However, the application of postbuckling composite structures has been limited, as today's analysis tools are not capable of accurately predicting the collapse of these structures under compression. The major objective of this PhD work was the development of an analysis methodology and complementary software package for composite postbuckling structures, which included the degrading effects of the critical damage mechanisms. From a comprehensive literature review and extensive benchmark study, a methodology was developed for analysing postbuckling composite structures that was capable of representing the critical damage mechanisms. One aspect of this was a degradation model to represent the growth of interlaminar damage such as delaminations and skin-stiffener debonds. In this degradation model, layers of shell elements were tied with user-defined multi-point constraints (MPCs), and fracture mechanics calculations using the Virtual Crack Closure Technique were applied to control the release of these MPCs to model crack growth. Another aspect of the methodology was an approach to predict the initiation of interlaminar damage in intact structures. This was implemented using strength-based criteria, and demonstrated on cross-section models of skin-stiffener interfaces, on which the input of deformations from a global postbuckling analysis of an entire panel was also shown. Separately, a degradation model was developed to capture pl y damage such as matrix cracking and fibre fracture, which was based on the Hashin criteria for damage prediction and the Chang-Chang approach for material softening. The analysis methodology was implemented into the finite element (FE) code MSC.Marc, using a combination of nine user subroutines and several external data files. The methodology was incorporated into a user-friendly software tool in MSC.Patran, which provided a suite of functions for including the damage representations into nonlinear FE analysis. Extensive validation was performed with experimental results from the European Union project COCOMAT, which included fracture mechanics characterisation coupons, single-stiffener flat panels, and large, multi-stiffener curved panels representative of composite fuselage designs. This demonstrated the applicability of the methodology for the design and analysis of both intact and pre-damaged postbuckling composite structures, and the capacity for accurate and detailed analysis of the critical damage mechanisms

Alcohol Consumption, Genetic Variants in Alcohol Deydrogenases, and Risk of Cardiovascular Diseases: A Prospective Study and Meta-Analysis

OBJECTIVE: First, to investigate and compare associations between alcohol consumption and variants in alcohol dehydrogenase (ADH) genes with incidence of cardiovascular diseases (CVD) in a large German cohort. Second, to quantitatively summarize available evidence of prospective studies on polymorphisms in ADH1B and ADH1C and CVD-risk. METHODS: We conducted a case-cohort study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort including a randomly drawn subcohort (n = 2175) and incident cases of myocardial infarction (MI; n = 230) or stroke (n = 208). Mean follow-up time was 8.2±2.2 years. The association between alcohol consumption, ADH1B or ADH1C genotypes, and CVD-risk was assessed using Cox proportional hazards regression. Additionally, we report results on associations of variants in ADH1B and ADH1C with ischemic heart disease and stroke in the context of a meta-analysis of previously published prospective studies published up to November 2011. RESULTS: Compared to individuals who drank >0 to 6 g alcohol/d, we observed a reduced risk of MI among females consuming >12 g alcohol/d (HR = 0.31; 95% CI: 0.10-0.97) and among males consuming >24 to 60 g/d (HR = 0.57; 95% CI: 0.33-0.98) or >60 g alcohol/d (HR = 0.30; 95% CI: 0.12-0.78). Stroke risk was not significantly related to alcohol consumption >6 g/d, but we observed an increased risk of stroke in men reporting no alcohol consumption. Individuals with the slow-coding ADH1B*1/1 genotype reported higher median alcohol consumption. Yet, polymorphisms in ADH1B or ADH1C were not significantly associated with risk of CVD in our data and after pooling results of eligible prospective studies [ADH1B*1/1: RR = 1.35 (95% CI: 0.98-1.88; p for heterogeneity: 0.364); ADH1C*2/2: RR = 1.07 (95% CI: 0.90-1.27; p for heterogeneity: 0.098)]. CONCLUSION: The well described association between alcohol consumption and CVD-risk is not reflected by ADH polymorphisms, which modify the rate of ethanol oxidation