The design of a closed-loop voltage regulator for a D-C generator

The methods of obtaining voltage regulation for a d-c generator are many, and they vary in complexity according to the requirements of the loads being supplied. A need for zero voltage regulation is not uncommon in power supplies that are used in laboratory work. It is frequently not enough, however, to have a supply whose steady state regulation is zero; the need may also exist for fast transient response to changes in load. In general, then, the criteria for excellent voltage-versus-load characteristics of a d-c power supply might be stated as follows: It has zero steady state error. It has no transient variations as load is varied in any manner. Of course a power supply which exhibits such excellence of voltage regulation is non-existant, but these criteria do establish a goal for the regulator designer. There are many approaches to the solution of the voltage regulation problem, but in general all regulators can be classified as closed-loop or open-loop systems. It is with the former type of system that this paper is concerned. More specifically this paper will present mathematical and experimental design studies of two closed-loop voltage regulators for use with a 125V 4 Kw d-c generator --Introduction, page 1

Lies es zwischen den Pixeln: Prototypische Textualität in Computerspielen

Sind Computerspiele ‚Text’? Um diese Frage zu beantworten, entwickelt der vorliegende Beitrag zunächst eine Text-Definition, die dem Medium ‚Computerspiel’ gerecht wird. Auf dieser Basis werden die Kriterien prototypischer Textualität diskutiert und Überschneidungen der Merkmale beim klassischen Text und bei den Spielelementen von Computerspielen aufgezeigt. Ausblickend auf die Konsequenzen eines Transfers des Textbegriffes werden daneben die Konzepte ‚Intertextualität’ sowie ‚Isotopie’ an Computerspielen beleuchtet

The very 5′ end and the constant region of Ig genes are spared from somatic mutation because AID does not access these regions

Somatic hypermutation (SHM) is restricted to VDJ regions and their adjacent flanks in immunoglobulin (Ig) genes, whereas constant regions are spared. Mutations occur after about 100 nucleotides downstream of the promoter and extend to 1–2 kb. We have asked why the very 5′ and most of the 3′ region of Ig genes are unmutated. Does the activation-induced cytosine deaminase (AID) that initiates SHM not gain access to these regions, or does AID gain access, but the resulting uracils are repaired error-free because error-prone repair does not gain access? The distribution of mutations was compared between uracil DNA glycosylase (Ung)-deficient and wild-type mice in endogenous Ig genes and in an Ig transgene. If AID gains access to the 5′ and 3′ regions that are unmutated in wild-type mice, one would expect an “AID footprint,” namely transition mutations from C and G in Ung-deficient mice in the regions normally devoid of SHM. We find that the distribution of total mutations and transitions from C and G is indistinguishable in wild-type and Ung-deficient mice. Thus, AID does not gain access to the 5′ and constant regions of Ig genes. The implications for the role of transcription and Ung in SHM are discussed

Epithelial-to-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma and Pancreatic Tumor Cell Lines: The Role of Neutrophils and Neutrophil-Derived Elastase

Pancreatic ductal adenocarcinoma (PDAC) is frequently associated with fibrosis and a prominent inflammatory infiltrate in the desmoplastic stroma. Moreover, in PDAC, an epithelial-to-mesenchymal transition (EMT) is observed. To explore a possible connection between the infiltrating cells, particularly the polymorphonuclear neutrophils (PMN) and the tumor cell transition, biopsies of patients with PDAC (n=115) were analysed with regard to PMN infiltration and nuclear expression of β-catenin and of ZEB1, well-established indicators of EMT. In biopsies with a dense PMN infiltrate, a nuclear accumulation of β-catenin and of ZEB1 was observed. To address the question whether PMN could induce EMT, they were isolated from healthy donors and were cocultivated with pancreatic tumor cells grown as monolayers. Rapid dyshesion of the tumor cells was seen, most likely due to an elastase-mediated degradation of E-cadherin. In parallel, the transcription factor TWIST was upregulated, β-catenin translocated into the nucleus, ZEB1 appeared in the nucleus, and keratins were downregulated. EMT was also induced when the tumor cells were grown under conditions preventing attachment to the culture plates. Here, also in the absence of elastase, E-cadherin was downmodulated. PMN as well as prevention of adhesion induced EMT also in liver cancer cell line. In conclusion, PMN via elastase induce EMT in vitro, most likely due to the loss of cell-to-cell contact. Because in pancreatic cancers the transition to a mesenchymal phenotype coincides with the PMN infiltrate, a contribution of the inflammatory response to the induction of EMT and—by implication—to tumor progression is possible

Imaging features of fibrolamellar hepatocellular carcinoma in gadoxetic acid-enhanced MRI

Background: Fibrolamellar hepatocellular carcinoma (FLC) is a rare malignancy occurring in young patients without cirrhosis. Objectives of our study were to analyze contrast material uptake in hepatobiliary phase imaging (HBP) in gadoxetic acid-enhanced liver MRI in patients with FLC and to characterize imaging features in sequence techniques other than HBP. Methods: In this retrospective study on histology-proven FLC, contrast material uptake in HBP was quantitatively assessed by calculating the corrected FLC enhancement index (CEI) using mean signal intensities of FLC and lumbar muscle on pre-contrast imaging and HBP, respectively. Moreover, enhancement patterns in dynamic contrast-enhanced MRI and relative signal intensities compared with background liver parenchyma were determined by two radiologists in consensus for HBP, diffusion-weighted imaging using high b-values (DWI), and T2 and T1 weighted pre-contrast imaging. Results: In 6 of 13 patients with FLC gadoxetic acid-enhanced liver MRI was available. The CEI suggested presence of HBP contrast material uptake in all FLCs. A mean CEI of 1.35 indicated FLC signal increase of 35% in HBP compared with pre-contrast imaging. All FLCs were hypointense in HBP compared with background liver parenchyma. Three of 6 FLCs had arterial hyperenhancement and venous wash-out. In DWI and T2 weighted imaging, 5 of 6 FLCs were hyperintense. In T1 weighted imaging, 5 of 6 FLCs were hypointense. Conclusion: Hepatobiliary uptake of gadoxetic acid was quantitatively measurable in all FLCs investigated in our study. The observation of hypointensity of FLCs in HBP compared with background liver parenchyma emphasizes the role of gadoxetic acid-enhanced liver MRI for non-invasive diagnosis of FLC and its importance in the diagnostic work-up of indeterminate liver lesions