@misc{18887, author = {{Peckhaus, Volker}}, booktitle = {{Mathematical Reviews, MR2840103}}, title = {{{Mancosu, Paolo, The Adventure of Reason. Interplay between Philosophy of Mathematics and Mathematical Logic, 1900–1940, Oxford University Press: Oxford 2010}}}, year = {{2012}}, } @misc{18702, author = {{Peckhaus, Volker}}, booktitle = {{zbMATH Open, Zbl. 1244.01006}}, title = {{{Chareix, Fabien, “Geometrization or Mathematization. Christiaan Huygens’s Critiques of Infinitesimal Analysis in his Correspondence with Leibniz”, in: The Practice of Reason. Leibniz and his Controversies, hg. v. Marcelo Dascal, John Benjamins Publishing: Philadelphia 2010, 33–49}}}, year = {{2012}}, } @misc{18885, author = {{Peckhaus, Volker}}, booktitle = {{Mathematical Reviews, MR2766474 (2012g:01020)}}, title = {{{Math.ch/100 – Schweizerische Mathematische Gesellschaft/Société Mathématique Suisse/Swiss Mathematical Society 1910–2010, hg. v. Bruno Colbois/Christine Riedtmann/Victor Schroeder, European Mathematical Society: Zürich 2010}}}, year = {{2012}}, } @misc{18703, author = {{Peckhaus, Volker}}, booktitle = {{zbMATH Open, Zbl. 1244.01034}}, title = {{{Pollard, Stephen (Hg.), Essays on the Foundations of Mathematics by Moritz Pasch, Springer: Dordrecht u.a. 2010 (Western Ontario Series in Philosophy of Science; 83)}}}, year = {{2012}}, } @misc{18700, author = {{Peckhaus, Volker}}, booktitle = {{zbMATH Open, Zbl. 1238.01119}}, title = {{{Hersh, Reuben/Verena John-Steiner, Loving + Hating Mathematics. Challenging three Myths of Mathematical Life, Princeton University Press: Princeton/Oxford 2011}}}, year = {{2012}}, } @misc{18884, author = {{Peckhaus, Volker}}, booktitle = {{Mathematical Reviews, MR2732670 (2012d:03012)}}, title = {{{McCarty, David, “Constructivism in Mathematics”, in: Handbook of the Philosophy of Science. Philosophy of Mathematics, hg. v. Andrew D. Irvine, Elesevier: Amsterdam 2009, 311–343}}}, year = {{2012}}, } @misc{18886, author = {{Peckhaus, Volker}}, booktitle = {{Mathematical Reviews, MR2895608 (2012m:03010)}}, title = {{{Vilkko, Risto, “The Logic Question During the First Half of the Nineteenth Century”, in: The Development of Modern Logic, Oxford University Press: Oxford 2009, 203–221}}}, year = {{2012}}, } @misc{18705, author = {{Peckhaus, Volker}}, booktitle = {{zbMATH Open, Zbl. 1245.00016}}, title = {{{Schottenkirk, Dena, Nominalism and Its Aftermath. The Philosophy of Nelson Goodman, Springer: Dordrecht u.a. 2009 (Synthese Library; 343)}}}, year = {{2012}}, } @misc{18888, author = {{Peckhaus, Volker}}, booktitle = {{Mathematical Reviews, MR2952222 }}, title = {{{Glaschick, Rainer, “Alan Turings Wirkung in Münster”, Mitteilungen der Deutschen Mathematiker-Vereinigung 20 (2012), 42–48}}}, year = {{2012}}, } @article{54937, abstract = {{Purpose: The epithelial sodium channel (ENaC) is typically expressed in sodium-absorbing epithelia. Several reports suggest that ENaC is also expressed in ocular tissues and may play a role in aqueous humor secretion and glaucoma. However, the precise localization of ENaC in the human eye is still unclear. Here, the authors studied ENaC expression in 12 normal human donor eyes and in six eyes of patients with glaucoma. Methods: Quantitative real-time PCR was used to investigate the expression of $\alpha$-, $\beta$-, $\gamma$-, and $\delta$-ENaC transcripts in ocular tissues. In addition, the authors performed immunohistochemical studies using recently generated antibodies against human $\beta$- and $\gamma$-ENaC. Results: At the mRNA level, all four ENaC subunits were found to be expressed in a wide range of ocular tissues from normal and glaucomatous human eyes, with the cornea, ciliary body, iris, and retina showing the highest expression levels. At the protein level, $\beta$- and $\gamma$-ENaC subunits showed distinct distribution patterns and could be immunolocalized primarily to the cell membranes of epithelial cells of the cornea and to the conjunctiva, iris, ciliary body, lens, and retinal pigment epithelium but also to vascular endothelial cells, smooth muscle cells, stromal cells, and retinal neurons. The authors found no altered mRNA level of any subunit in glaucomatous eyes. Conclusions: All four ENaC subunits ($\alpha$$\beta$$\gamma$$\delta$) are expressed in the normal human eye, with distinct localization of subunits possibly reflecting different functional states of the channel. The (patho-)physiological roles of ENaC in the various localizations in the eye remain to be determined.}}, author = {{Krueger, Bettina and Schlötzer-Schrehardt, Ursula and Haerteis, Silke and Zenkel, Matthias and Chankiewitz, Verena E. and Amann, Kerstin U. and Kruse, Friedrich E. and Korbmacher, Christoph}}, journal = {{Investigative Opthalmology & Visual Science}}, number = {{2}}, pages = {{596–604}}, publisher = {{Association for Research in Vision and Ophthalmology (ARVO)}}, title = {{{Four Subunits ($\alpha$$\beta$$\gamma$$\delta$) of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations}}}, doi = {{10.1167/iovs.11-8581}}, volume = {{53}}, year = {{2012}}, } @article{54930, abstract = {{Background: Increased expression of the pro-fibrotic protein connective tissue growth factor (CTGF) has been detected in injured kidneys and elevated urinary levels of CTGF are discussed as prognostic marker of chronic kidney disease. There is evidence that epithelial cells lining the renal tubular system contribute to uptake and secretion of CTGF. However, the role of different types of tubular epithelial cells in these processes so far has not been addressed in primary cultures of human cells. Results: Tubular epithelial cells of proximal and distal origin were isolated from human kidneys and cultured as polarized cells in insert wells. The pro-fibrotic stimuli lysophosphatidic acid (LPA) and transforming growth factor $\beta$ (TGF-$\beta$) were used to induce CTGF secretion.LPA activated CTGF secretion in proximal tubular cells when applied from either the apical or the basolateral side as shown by immunocytochemistry. CTGF was secreted exclusively to the apical side. Signaling pathways activated by LPA included MAP kinase and Rho kinase signaling. TGF-$\beta$ applied from either side also stimulated CTGF secretion primarily to the apical side with little basolateral release.Interestingly, TGF-$\beta$ activation induced different signaling pathways depending on the side of TGF-$\beta$ application. Smad signaling was almost exclusively activated from the basolateral side most prominently in cells of distal origin. Only part of these cells also synthesized CTGF indicating that Smad activation alone was not sufficient for CTGF induction. MAP kinases were involved in apical TGF-$\beta$-mediated activation of CTGF synthesis in proximal cells and a subset of epithelial cells of distal origin. This subpopulation of distal tubular cells was also able to internalize recombinant apical CTGF, in addition to proximal cells which were the main cells to take up exogenous CTGF. Conclusions: Analysis of polarized human primary renal epithelial cells in a transwell system shows that vectorial secretion of the pro-fibrotic protein CTGF depends on the cell type, the stimulus and the signaling pathway activated. In all conditions, CTGF was secreted mainly to the apical side upon TGF-$\beta$ and LPA treatment and therefore, likely contributes to increased urinary CTGF levels in vivo. Moreover, CTGF secreted basolaterally may be active as paracrine pro-fibrotic mediator.}}, author = {{Zuehlke, Jonathan and Ebenau, Astrid and Krueger, Bettina and Goppelt-Struebe, Margarete}}, journal = {{Cell Communication and Signaling}}, number = {{1}}, publisher = {{Springer}}, title = {{{Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\beta$ in human tubular epithelial cells}}}, doi = {{10.1186/1478-811x-10-25}}, volume = {{10}}, year = {{2012}}, } @article{54934, abstract = {{Aldosterone is thought to be the main hormone to stimulate the epithelial sodium channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT) and the entire collecting duct (CD). There is immunohistochemical evidence for an axial gradient of ENaC expression along the ASDN with highest expression in the DCT2 and CNT. However, most of our knowledge about renal ENaC function stems from studies in the cortical collecting duct (CCD). Here we investigated ENaC function in the transition zone of DCT2/CNT or CNT/CCD microdissected from mice maintained on different sodium diets to vary plasma aldosterone levels. Single-channel recordings demonstrated amiloride-sensitive Na(+) channels in DCT2/CNT with biophysical properties typical for ENaC previously described in CNT/CCD. In animals maintained on a standard salt diet, the average ENaC-mediated whole cell current ($\Delta$I(ami)) was higher in DCT2/CNT than in CNT/CCD. A low salt diet increased $\Delta$I(ami) in CNT/CCD but had little effect on $\Delta$I(ami) in DCT2/CNT. To investigate whether aldosterone is necessary for ENaC activity in the DCT2/CNT, we used aldosterone synthase knockout (AS(-/-)) mice that lack aldosterone. In CNT/CCD of AS(-/-) mice, $\Delta$I(ami) was lower than that in wild-type (WT) animals and was not stimulated by a low salt diet. In contrast, in DCT2/CNT of AS(-/-) mice, $\Delta$I(ami) was similar to that in DCT2/CNT of WT animals both on a standard and on a low salt diet. We conclude that ENaC function in the DCT2/CNT is largely independent of aldosterone which is in contrast to its known aldosterone sensitivity in CNT/CCD.}}, author = {{Nesterov, Viatcheslav and Dahlmann, Anke and Krueger, Bettina and Bertog, Marko and Loffing, Johannes and Korbmacher, Christoph}}, journal = {{American Journal of Physiology-Renal Physiology}}, number = {{9}}, pages = {{F1289–F1299}}, publisher = {{American Physiological Society}}, title = {{{Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron}}}, doi = {{10.1152/ajprenal.00247.2012}}, volume = {{303}}, year = {{2012}}, } @article{54939, abstract = {{Background: Renal tubular epithelial cells of proximal and distal origin differ markedly in their physiological functions. Therefore, we hypothesized that they also differ in their capacity to undergo epithelial to mesenchymal alterations. Results: We used cultures of freshly isolated primary human tubular cells. To distinguish cells of different tubular origin we took advantage of the fact that human proximal epithelial cells uniquely express N-cadherin instead of E-cadherin as major cell-cell adhesion molecule. To provoke mesenchymal alteration we treated these cocultures with TGF-$\beta$ for up to 6 days. Within this time period, the morphology of distal tubular cells was barely altered. In contrast to tubular cell lines, E-cadherin was not down-regulated by TGF-$\beta$, even though TGF-$\beta$ signal transduction was initiated as demonstrated by nuclear localization of Smad2/3. Analysis of transcription factors and miRNAs possibly involved in E-cadherin regulation revealed high levels of miRNAs of the miR200-family, which may contribute to the stability of E-cadherin expression in human distal tubular epithelial cells. By contrast, proximal tubular epithelial cells altered their phenotype when treated with TGF-$\beta$. They became elongated and formed three-dimensional structures. Rho-kinases were identified as modulators of TGF-$\beta$-induced morphological alterations. Non-specific inhibition of Rho-kinases resulted in stabilization of the epithelial phenotype, while partial effects were observed upon downregulation of Rho-kinase isoforms ROCK1 and ROCK2. The distinct reactivity of proximal and distal cells was retained when the cells were cultured as polarized cells. Conclusions: Interference with Rho-kinase signaling provides a target to counteract TGF-$\beta$-mediated mesenchymal alterations of epithelial cells, particularly in proximal tubular epithelial cells. Furthermore, primary distal tubular cells differed from cell lines by their high phenotypic stability which included constant expression of E-cadherin. Our cell culture system of primary epithelial cells is thus suitable to understand and modulate cellular remodeling processes of distinct tubular cells relevant for human renal disease.}}, author = {{Keller, Christof and Kroening, Sven and Zuehlke, Jonathan and Kunath, Frank and Krueger, Bettina and Goppelt-Struebe, Margarete}}, issn = {{1932-6203}}, journal = {{PLOS ONE}}, number = {{8}}, pages = {{e43584}}, publisher = {{Public Library of Science}}, title = {{{Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial Cells}}}, doi = {{10.1371/journal.pone.0043584}}, volume = {{7}}, year = {{2012}}, } @inproceedings{54994, author = {{Wagner, Thorsten and Tiemann, Michael and Kohl, Claus-Dieter and Morandi, Sara and Malagù, Cesare and Donato, Nicola and Latino, Mariangela and Neri, Giovanni}}, booktitle = {{Proceedings IMCS 2012}}, publisher = {{AMA Service GmbH, Von-Münchhausen-Str. 49, 31515 Wunstorf, Germany}}, title = {{{Mechanistic Model for UV light-enhanced NO2 Sensing utilizing Ordered Mesoporous In2O3}}}, doi = {{10.5162/imcs2012/p1.3.17}}, year = {{2012}}, } @inproceedings{54995, author = {{Klaus, Dominik and Tiemann, Michael and Wagner, Thorsten}}, booktitle = {{Proceedings IMCS 2012}}, publisher = {{AMA Service GmbH, Von-Münchhausen-Str. 49, 31515 Wunstorf, Germany}}, title = {{{Nanostructured Metal Oxides for High-Temperature Gas Sensing: Structural Stabilization in Porous Metal Oxides}}}, doi = {{10.5162/imcs2012/p2.0.3}}, year = {{2012}}, } @article{9214, author = {{Mildorf, Jarmila}}, journal = {{Storyworlds}}, pages = {{75--98}}, title = {{{Second-Person Narration in Literary and Conversational Storytelling}}}, volume = {{4}}, year = {{2012}}, } @book{9198, editor = {{Kinzel, Till and Mildorf, Jarmila}}, isbn = {{978-3-8253-5989-8}}, pages = {{266}}, publisher = {{Universitätsverlag Winter}}, title = {{{Imaginary Dialogues in English: Explorations of a Literary Form}}}, volume = {{46}}, year = {{2012}}, } @inbook{9239, author = {{Kinzel, Till and Mildorf, Jarmila}}, booktitle = {{Imaginary Dialogues in English: Explorations of a Literary Form}}, editor = {{Kinzel, Till and Mildorf, Jarmila}}, pages = {{9--28}}, publisher = {{Universitätsverlag Winter}}, title = {{{New Perspectives on Imaginary Dialogues: An Interdisciplinary Dialogue}}}, year = {{2012}}, } @inbook{9240, author = {{Mildorf, Jarmila}}, booktitle = {{Imaginary Dialogues in English: Explorations of a Literary Form}}, editor = {{Kinzel, Till and Mildorf, Jarmila}}, pages = {{89--109}}, publisher = {{Universitätsverlag Winter}}, title = {{{Polite Conversation, Implicatures, and Comical Effect: Jonathan Swift and P. G. Wodehouse}}}, year = {{2012}}, } @article{55227, author = {{Milkov, Nikolay}}, journal = {{Grazer philosophische Studien }}, pages = {{137--156}}, title = {{{Karl Popper’s Debt to Leonard Nelson}}}, volume = {{86}}, year = {{2012}}, }