Saying Hello World with Henshin - A Solution to the TTC 2011 Instructive Case

This paper gives an overview of the Henshin solution to the Hello World case study of the Transformation Tool Contest 2011, intended to show basic language concepts and constructs.Comment: In Proceedings TTC 2011, arXiv:1111.440

Solving the TTC 2011 Reengineering Case with Henshin

This paper presents the Henshin solution to the Model Transformations for Program Understanding case study as part of the Transformation Tool Contest 2011.Comment: In Proceedings TTC 2011, arXiv:1111.440

Precision measurements of the 60^{60}Co β\beta-asymmetry parameter in search for tensor currents in weak interactions

The $\beta$-asymmetry parameter $\widetilde{A}$ for the Gamow-Teller decay of $^{60}$Co was measured by polarizing the radioactive nuclei with the brute force low-temperature nuclear-orientation method. The $^{60}$Co activity was cooled down to milliKelvin temperatures in a $^3$He-$^4$He dilution refrigerator in an external 13 T magnetic field. The $\beta$ particles were observed by a 500 ${\mu}m$ thick Si PIN diode operating at a temperature of about 10 K in a magnetic field of 0.6 T. Extensive GEANT4 Monte-Carlo simulations were performed to gain control over the systematic effects. Our result, $\widetilde{A} = -1.014(12)_{stat}(16)_{syst}$, is in agreement with the Standard-Model value of $-0.987(9)$, which includes recoil-order corrections that were addressed for the first time for this isotope. Further, it enables limits to be placed on possible tensor-type charged weak currents as well as other physics beyond the Standard Model

Calcifying fibrous tumor and inflammatory myofibroblastic tumor are epigenetically related: A comparative genome-wide methylation study

Item does not contain fulltextBased on histological findings, calcifying fibrous tumor (CFT) may be a late (burned out) stage of inflammatory myofibroblastic tumor (IMT). This concept, however, has not been proven by molecular means. Five CFTs were analyzed for IMT-related rearrangements in ALK, ROS1 and RET using fluorescence in situ hybridization (FISH). Additionally, genome-wide methylation patterns were investigated and compared with IMT (n=7), leiomyoma (n=7), angioleiomyoma (n=9), myopericytoma (n=7) and reactive soft tissue lesions (n=10) using unsupervised hierarchical cluster analysis and t distributed stochastic neighbor embedding. CFT patients, 4 females and 1 male, had a median age of 20years ranging from 7 to 43years. Two patients were younger than 18years old. The tumors originated in the abdomen (n=4) and axilla (n=1). Histologically, all lesions were (multi) nodular and hypocellular consisting of bland looking (myo)fibroblasts embedded in a collagenous matrix with calcifications. FISH analysis brought up negative results for ALK, RET and ROS1 rearrangements. However, genome-wide methylation analysis revealed overlapping methylation patterns of CFT and IMT forming a distinct homogeneous methylation cluster with exception of one case clustering with myopericytoma/angioleiomyoma. In conclusion, DNA methylation profiling supports the concept that CFT and IMT represent both ends of a spectrum of one entity with CFT being the burn out stage of IMT

Influenza infection and risk of acute pulmonary embolism

<p>Abstract</p> <p>Background</p> <p>Influenza infections have been associated with procoagulant changes. Whether influenza infections lead to an increased risk of pulmonary embolism remains to be established.</p> <p>Methods</p> <p>We conducted a nested case control study in a large cohort of patients with a clinical suspicion of having pulmonary embolism. Blood samples were collected to investigate the presence of influenza A and B by complement fixation assay (CFA). We compared case patients, in whom pulmonary embolism was proven (n = 102), to controls, in whom pulmonary embolism was excluded (n = 395). Furthermore, we compared symptoms of influenza-like illness in both patient groups 2 weeks prior to inclusion in the study, using the influenza-like illness (ILI) score, which is based on a questionnaire. We calculated the risk of pulmonary embolism associated with influenza infection.</p> <p>Results</p> <p>The percentage of patients with influenza A was higher in the control group compared to the case group (4.3% versus 1.0%, respectively, odds ratio 0.22; 95% CI: 0.03–1.72). Influenza B was not detectable in any of the cases and was found in 3 of the 395 controls (0.8%). The ILI score was positive in 24% of the cases and 25% in the control persons (odds ratio 1.16, 95% CI: 0.67–2.01). We did not observe an association between the ILI score and proven influenza infection.</p> <p>Conclusion</p> <p>In this clinical study, influenza infection was not associated with an increased risk of acute pulmonary embolism. The ILI score is non-specific in this clinical setting.</p

Probing sporadic and familial Alzheimer's disease using induced pluripotent stem cells.

Our understanding of Alzheimer's disease pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model the sporadic form of the disease. It may be possible to overcome these challenges by reprogramming primary cells from patients into induced pluripotent stem cells (iPSCs). Here we reprogrammed primary fibroblasts from two patients with familial Alzheimer's disease, both caused by a duplication of the amyloid-β precursor protein gene (APP; termed APP(Dp)), two with sporadic Alzheimer's disease (termed sAD1, sAD2) and two non-demented control individuals into iPSC lines. Neurons from differentiated cultures were purified with fluorescence-activated cell sorting and characterized. Purified cultures contained more than 90% neurons, clustered with fetal brain messenger RNA samples by microarray criteria, and could form functional synaptic contacts. Virtually all cells exhibited normal electrophysiological activity. Relative to controls, iPSC-derived, purified neurons from the two APP(Dp) patients and patient sAD2 exhibited significantly higher levels of the pathological markers amyloid-β(1-40), phospho-tau(Thr 231) and active glycogen synthase kinase-3β (aGSK-3β). Neurons from APP(Dp) and sAD2 patients also accumulated large RAB5-positive early endosomes compared to controls. Treatment of purified neurons with β-secretase inhibitors, but not γ-secretase inhibitors, caused significant reductions in phospho-Tau(Thr 231) and aGSK-3β levels. These results suggest a direct relationship between APP proteolytic processing, but not amyloid-β, in GSK-3β activation and tau phosphorylation in human neurons. Additionally, we observed that neurons with the genome of one sAD patient exhibited the phenotypes seen in familial Alzheimer's disease samples. More generally, we demonstrate that iPSC technology can be used to observe phenotypes relevant to Alzheimer's disease, even though it can take decades for overt disease to manifest in patients