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1

Nguyen, Thanh Phong, et Carsten Cuhls. « The effect of turning frequency on methane generation during composting of anaerobic digestion material ». Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-227893.

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Methane (CH4) is included in the direct greenhouse gases listed in the Kyoto protocol. The composting of anaerobic digestion (henceforth AD) material is a source of CH4. CH4 is the major contributor to overall CO2 emissions. Therefore, it is important to know the formation of this gas from different stages and substrates of the composting process. This study investigated CH4, CO2 and O2 profiles in two open-windrows in composting plants treating AD material. One composting windrow was turned one a week; whereas another was turned twice a week using a special windrow turner. To assess the gaseous formation in the composting windrows, CH4, CO2 and O2 volume concentrations were measured at different depths. Active aeration has been considered as a method to reduce CH4 generation during composting. However, our results showed that frequent turned windrow generated more CH4 than less turned windrow. The highest CH4 concentrations were found at a depth of 1 m, and were 45% and 37% for 2 times a week turned windrow and 1 time a week turned windrow respectively. Gas concentrations of CH4, O2 and CO2 in both windrows differed. Concentrations of CO2 and CH4 increased with depth, whereas concentration of O2 decreased from the surface to the lowest point. The O2 and CO2 are important factors in determining whether the windrows are anaerobic or aerobic
Khí mê tan (CH4) là một trong những khí nhà kính được liệt kê trong nghị định thư Kyoto. Quá trình ủ phân compost từ các chất thải của hầm ủ biogas là nguồn phát sinh loại khí này. Khí mê tan đóng góp chủ yếu trong tổng lượng khí nhà kính phát thải vào khí quyển. Do đó, những hiểu biết về quá trình hình thành loại khí này trong các giai đoạn khác nhau của quá trình ủ phân compost từ chất thải hầm ủ biogas là rất quan trọng. Nghiên cứu này tìm hiểu sự phát thải khí CH4, CO2 và O2 trong 2 luống ủ ngoài trời tại các nhà máy xử lý rác thải hữu cơ bằng phương pháp kỵ khí. Luống ủ 1 được đảo trộn một lần một tuần trong khi luống ủ số 2 được đảo trộn 2 lần 1 tuần. Để đo đạc lượng khí phát thải từ các luống ủ phân compost, nồng độ các khí CH4, CO2 và O2 được đo ở các độ sâu khác nhau. Việc cung cấp khí oxy được coi như là một biện pháp để làm giảm sự hình thành khí mê tan. Tuy nhiên, kết quả đo đạc của chúng tôi chứng minh rằng việc đảo trộn thường xuyên phát thải nhiều khí mê tan hơn ít đảo trộn. Nồng độ khí mê tan cao nhất 45% và 37% đo được ở khoảng cách 1m từ bề mặt đối với luống ủ đảo trộn hai lần và một lần. Nồng độ các khí CH4, CO2 và O2 khác nhau ở hai luống trong thí nghiệm. Nồng độ khí CH4 và CO2 tăng theo độ sâu, trong khi O2 giảm theo độ sâu. Nồng độ khí CO2 và O2 đóng vai trò quyết định luống ủ được cung cấp đủ oxy cho quá trình phân hủy hiếu khí hay không
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2

Nguyen, Thanh Phong, et Carsten Cuhls. « Methane removal using materials from biofilters at composting plants ». Technische Universität Dresden, 2018. https://tud.qucosa.de/id/qucosa%3A33315.

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Methane (CH4) source of Greenhouse Gases should be considered; CH4 is formed by composting under anaerobic conditions. Using microbial Methane oxidation is a solution with low cost and effective. In this study, 27 bio-filters and 18 laboratory-scale bioreactors were used to investigate the potential for CH4 removal in biogas. The CH4, Dinitrogen monoxide (N2O) and Carbon dioxide (CO2) concentrations at the inlet and outlet of the air purifier were measured by gas chromatography. The results showed that the CH4 concentration decreased in experiments while the CO2 and N2O content increased in all experiments. An experiment was conducted with 1 kg of biofilter material with the input of 800 ppm CH4 contained in a 5-liter flask for 49 hours containing. The results also showed that the CH4 concentration decreased by 71% after 20 hours and N2O was formed in the reactor.
Mê-tan (CH4) là nguồn khí gây nên hiệu ứng nhà kính cần được quan tâm, khí CH4 được sinh ra trong quá trình ủ vi sinh trong điều kiện kị khí. Một giải pháp với chi phí thấp là sử dụng vi sinh vật oxy hóa khí CH4 cố định trên giá thể là vật liệu sử dụng trong thiết bị lọc sinh học. Trong nghiên cứu này, 27 thiết bị lọc sinh học trên thực tế và 19 bình lọc tại phòng thí nghiệm đã được sử dụng nhằm mục đích khảo sát khả năng loại bỏ CH4 có trong khí sinh học. Nồng độ khí CH4, N2O và CO2 ở đầu vào và đầu ra bể lọc khí được đo đạc bằng phương pháp sắc ký khí. Kết quả cho thấy nồng độ khí CH4 giảm sau khi qua hệ thống lọc sinh học ở một số bình, trong khi nồng độ khí CO2 và N2O lại tăng lên ở tất cả các bình. Khi khảo sát khả năng oxi hóa CH4 ở nồng độ 800 ppm của 1kg vật liệu thiết bị lọc sinh học chứa trong bình phản ứng thể tích 5L với thời gian 49 giờ. Kết quả cho thấy nồng nồng độ CH4 giảm 71% sau 20 giờ. Tuy nhiên, N2O đã được ghi nhận có hình thành trong bình phản ứng đó.
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3

König, Werner Zeisberger Andrea Funk Edith Renn Manfred Schwarz Brigitte. « Sprachatlas von Bayerisch-Schwaben ». Heidelberg : C. Winter, 2003. http://catalogue.bnf.fr/ark:/12148/cb38905935c.

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4

Birk, Hella. « Das Gesetz zur Verhütung erbkranken Nachwuchses : eine Untersuchung zum Erbgesundheitswesen im bayerischen Schwaben in der Zeit des Nationalsozialismus / ». Augsburg : Wißner, 2005. http://www.gbv.de/dms/spk/sbb/recht/toc/479459053.pdf.

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5

Жукова, Світлана Вячеславівна, Светлана Вячеславовна Жукова, Svitlana Viacheslavivna Zhukova et Ahmed Heblo. « Theodor Schwann ». Thesis, Видавництво СумДУ, 2010. http://essuir.sumdu.edu.ua/handle/123456789/6659.

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6

Wecker-Kleiner, Bernadette. « Sprechen nach der Schrift : die Vorleseaussprache von DialektsprecherInnen in Bayerisch-Schwaben im Spannungsfeld zwischen Dialekt und Orthoepie / ». Berlin : Dissertation.de - Verl. im Internet, 2009. http://www.dissertation.de/buch.php3?buch=5822.

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7

Ammann, Martin. « Schutzwirkung abgestorbener Bäume gegen Naturgefahren / ». Birmensdorf : Eidg. Forschungsanstalt für Wald, Schnee und Landschaft WSL, 2006. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=16638.

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8

Weiß, Peter. « Frühe Siegelurkunden in Schwaben (10. - 12. Jahrhundert) ». [S.l.] : Universität Konstanz , Philosophische Fakultät, Fachgruppe Geschichte, 1995. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB8500761.

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9

Schütte, Bernd. « König Philipp von Schwaben : Itinerar, Urkundenvergabe, Hof / ». Hannover : Hansche Buchhandlung, 2002. http://catalogue.bnf.fr/ark:/12148/cb390488206.

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10

Lengger, Werner. « Leben und Sterben in Schwaben : Studien zur Bevölkerungsentwicklung und Migration zwischen Lech und Iller, Ries und Alpen im 17. Jahrhundert / ». Augsburg : Wissner, 2002. http://opac.nebis.ch/cgi-bin/showAbstract.pl?u20=3896393480.

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11

Brenner, Bernhard. « Ludwig der Bayer - ein Motor für die Urbanisierung Ostschwabens ? zu den Auswirkungen herrscherlicher Städtepolitik auf die Entwicklung der schwäbischen Städtelandschaft im ausgehenden Mittelalter ». Augsburg Wissner, 2003. http://deposit.ddb.de/cgi-bin/dokserv?id=2670666&prov=M&dok_var=1&dok_ext=htm.

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12

Schöning, Brigitte. « "Friedrich von Schwaben" : Aspekte des Erzählens im spätmittelalterlichen Versroman / ». Erlangen : Palm & ; Enke, 1991. http://catalogue.bnf.fr/ark:/12148/cb36151844g.

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13

Köllermann, Antje-Fee. « Conrad Laib : ein spätgotischer Maler aus Schwaben in Salzburg / ». Berlin : Deutscher Verlag für Kunstwissenschaft, 2007. http://catalogue.bnf.fr/ark:/12148/cb41293019z.

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14

Bosch, Anton. « Stalins Bauernopfer am Schwarzen Meer / ». Nürnberg : Histor. Forschungsverein der Deutschen aus Russland, 2009. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=018949181&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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15

Mohr, Lutz. « Die Nixe vom Schwarzen Teich ». Lutz Mohr, 2017. https://slub.qucosa.de/id/qucosa%3A7964.

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16

Ehlers, Tim [Verfasser], Robert [Akademischer Betreuer] [Gutachter] Schwager et Gerhard [Gutachter] Rübel. « Modeling Approaches in Educational Research / Tim Ehlers ; Gutachter : Robert Schwager, Gerhard Rübel ; Betreuer : Robert Schwager ». Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/1125105798/34.

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17

Schüller, Stephan Olaf. « Für Glaube, Führer, Volk, Vater- oder Mutterland ? : die Kämpfe um die deutsche Jugend im rumänischen Banat (1918-1944) / ». Münster : LIT, 2009. http://deposit.d-nb.de/cgi-bin/dokserv?id=3330481&prov=M&dokv̲ar=1&doke̲xt=htm.

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18

Schüller, Stephan Olaf. « Für Glaube, Führer, Volk, Vater- oder Mutterland ? die Kämpfe um die deutsche Jugend im rumänischen Banat (1918 - 1944) ». Berlin Münster Lit, 2006. http://d-nb.info/995196788/04.

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19

Gruber, Michael. « Schulische Werteerziehung unter Pluralitätsbedingungen Bestandsaufnahme und Empfehlungen auf der Basis einer Lehrerbefragung ». Würzburg Ergon-Verl, 2009. http://d-nb.info/997133716/04.

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20

Kirchner, Michael. « Kokristallisation mit schwachen und starken Wasserstoffbrücken ». [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96957441X.

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21

Kruse, Guido. « Statistische Untersuchungen zum schwachen kosmologischen Gravitationslinseneffekt ». Diss., lmu, 2000. http://nbn-resolving.de/urn:nbn:de:bvb:19-3379.

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22

Vieregge, André. « Nachtseiten die Literatur der Schwarzen Romantik ». Frankfurt, M. Berlin Bern Bruxelles New York, NY Oxford Wien Lang, 2007. http://d-nb.info/987274651/04.

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Lobsiger, Christian S. Lobsiger Christian S. « Early Schwann cell lineage development / ». [S.l.] : [s.n.], 2001. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=14079.

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Meya, Johannes [Verfasser], Robert [Akademischer Betreuer] Schwager et Panu [Akademischer Betreuer] Poutvaara. « Microanalyses of Voting, Regulation and Higher Education / Johannes Meya. Gutachter : Robert Schwager ; Panu Poutvaara. Betreuer : Robert Schwager ». Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1072820366/34.

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Mocek, Claudia. « Kommunale Repräsentation auf den Landtagen Schwäbisch-Österreichs eine Prosopographie der Abgeordneten aus der Grafschaft Hohenberg und der Landvogtei Schwaben ». Ostfildern Thorbecke, 2007. http://d-nb.info/988786028/04.

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Danilowicz-Gösele, Kamila Verfasser], Robert [Akademischer Betreuer] [Gutachter] Schwager et Thushyanthan [Gutachter] [Baskaran. « Everyday Decision Making : A Theoretical and Empirical Study / Kamila Danilowicz-Gösele ; Gutachter : Robert Schwager, Thushyanthan Baskaran ; Betreuer : Robert Schwager ». Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2017. http://d-nb.info/113086832X/34.

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Mocek, Claudia. « Kommunale Repräsentation auf den Landtagen Schwäbisch-Österreichs : eine Prosopographie der Abgeordneten aus der Grafschaft Hohenberg und der Landvogtei Schwaben / ». Ostfildern : J. Thorbecke, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?u20=9783799552615.

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Wecker-Kleiner, Bernadette. « Sprechen nach der Schrift die Vorleseaussprache von DialektsprecherInnen in Bayerisch-Schwaben im Spannungsfeld zwischen Dialekt und Orthoepie ». Berlin dissertation.de, 2005. http://d-nb.info/99398682X/04.

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Cotter, Laurent. « Rôle des gènes de polarité Dlg1 et Crb3 dans la géométrie de la myéline du nerf périphérique ». Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT113/document.

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Chez les vertébrés, la vitesse de la conduction nerveuse dépend du processus de myélinisation. Dans le système nerveux périphérique, ce sont les cellules de Schwann (CS) qui en s’enroulant autour de l’axone, constituent les gaines de myéline, séparés par des nœuds de Ranvier. La succession de ces gaines augmente la vitesse de conduction nerveuse car les potentiels d’action sont forcés de « sauter » d’un nœud de Ranvier à un autre, ce qui accélère leur vitesse de propagation. La géométrie (l’épaisseur et la longueur) de la gaine de myéline est donc un paramètre essentiel de la conduction de l’influx. Une publication à laquelle j’ai participé, a mis en évidence la polarisation cellulaire de la cellule de Schwann myélinisante. Notre hypothèse est que ce processus est capital pour la formation d’une gaine de myéline fonctionnelle. Comme trois complexes protéiques, conservés au cours de l’évolution, établissent et maintiennent la polarisation cellulaire (ces complexes sont: aPKC/Par3/Par6, Pals1/Patj/Crb3 et Dlg1/Lgl/Scrib chez les mammifères), mon travail consiste à étudier le rôle fonctionnel des protéines de la polarité Dlg1 et Crb3 lors de la myélinisation. Comme l’altération de la géométrie de la myéline est la cause d’un grand nombre de pathologies du système nerveux périphérique mais aussi central. Mon travail sur la mise en lumière des mécanismes qui préside à ce phénomène permet d’envisager de nouvelles voies thérapeutiques
In the mammalian nervous system, the nerve conduction velocity depends on the myelin sheath. Myelin is produced by Schwann cells in the peripheral nervous system. The myelin sheath, together with the highly specialized nodes of Ranvier that are regulary arrayed along the myelinated fibers, is responsible for efficient and rapid propagation of action potentials along the nerve. Optimal conduction is obtained by adjusting the geometry (length and thickness) of the myelin sheath When I arrived in the laboratory, the team just showed the polarization of the myelinating Schwann cell ( mSC). We hypothesized then that cell polarity proteins are key players for the formation of the myelin sheath. Three complexes, well conserved among species, organize polarized cellular processes. In mammals, these complexes are aPKC/Par3/Par6, Pals1/Patj/Crb3 et Dlg1/Lgl/Scrib. Using an approch allowing the in vivo transduction of mSC, I investigate the relevance of Dlg1 and Crb3 in myelin formation. Changes in the myelin geometry is linked to several human neuropathies in the central and peripheral nervous system. This work highlights mechanisms which control correct myelin formation and allow designing strategies for their treatment
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Fücker, Michael. « Korrekturen der schwachen Wechselwirkung zur hadronischen Topquark-Paarproduktion ». [S.l.] : [s.n.], 2007. http://deposit.ddb.de/cgi-bin/dokserv?idn=984657207.

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Heide, Jesper. « Koexistenz vom klassischen und schwachen Chaos im Pottsmodell ». [S.l. : s.n.], 2000. http://e-diss.uni-kiel.de/diss/d382.pdf.

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Schwerdt, Judith. « Morphosemantik der schwachen Verben im Ostgermanischen und Kontinentalwestgermanischen ». Frankfurt, M. Berlin Bern Bruxelles New York, NY Oxford Wien Lang, 2005. http://d-nb.info/987537245/04.

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Schwander, Timo [Verfasser]. « Extraterritoriale Wirkungen von Grundrechten im Mehrebenensystem. / Timo Schwander ». Berlin : Duncker & ; Humblot, 2018. http://d-nb.info/1238444784/34.

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Schwahn, Anne [Verfasser]. « Cut Trees : Bases and Games / Anne Schwahn ». München : Verlag Dr. Hut, 2010. http://d-nb.info/1004342845/34.

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Wingfield, Digby K. P. M. « Schwann cell/axonal interactions in peripheral nerve ». Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1419154/.

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Schwann cells are found in close proximity with axons from an early developmental stage, where, in adult nerve, they exist as either myelinating or non-myelinating Schwann cells. Reciprocal, contact-dependent signalling, between Schwann cells and axons, is central to the regulation of Schwann cell proliferation, survival and differentiation, as well as axonal survival. Cell adhesion molecules (CAMs) mediate homotypic and heterotypic interactions. They are required during development, in homeostatic nerve and in nerve repair following injury. Dysregulation of signal pathways and resulting aberrant CAM expression, can lead to irreversible Schwann cell/axonal dissociation, which is a hallmark of various peripheral neuropathies and nerve sheath tumours, e.g. neurofibromas in NF1 patients. In this thesis, I conducted a microarray screen to identify early mediators of Schwann cell/axonal interaction, using a Large-T (LT)-expressing Schwann cell that had spontaneously lost the ability to interact with axons, termed LT-derived (LTD) cells. This analysis revealed that multiple cell adhesion genes had become dysregulated including N-cadherin, Semaphorin-4F, Necl-4, NCAM and L1-CAM. This shift in adhesion profile suggested that a transcription factor, for example Sox2, might be the genetic lesion responsible; however, Sox2 was found not to be responsible for the LTD phenotype, although over-expression of Sox2 altered N-cadherin localisation at Schwann cell-cell junctions. Further study showed that N-cadherin was required for homotypic interactions and was an important mediator of heterotypic interactions, where heterologous N-cadherin expression in fibroblasts was sufficient to induce fibroblasts to recognise and partially associate with axons. In addition, N-cadherin was implicated in the regulation of the cell cycle; while N-cadherin silencing, in Schwann cells prior to axonal contact, was found to impede myelination in vitro. Finally, this work showed that N-cadherin and Semaphorin-4F operate at distinct stages of the interaction process, with N-cadherin mediating axonal recognition and Semaphorin-4F involved in stabilising the Schwann cell/axonal association.
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RANGWALA, RESHMA. « ERBIN MEDIATES SCHWANN CELL GROWTH AND DIFFERENTIATION ». University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1108938909.

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Stückemann, Frank. « Johann Moritz Schwager (1738 - 1804) ein westfälischer Landpfarrer und Aufklärer ohne Misere ». Bielefeld Aisthesis, 2008. http://d-nb.info/996693300/04.

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Greig, Alan Hudson. « 'Warum geht es in Schwaben schlechter' : the Nazi Party in Württemberg 1920-1933 ». Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247220.

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Hamacher, Michael. « Molekularbiologische Untersuchungen am Tetraspan-Molekül Plasmolipin ». [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=966440781.

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40

Wosch, Susanne S. « Konstruktion und Etablierung von AAV-Tet-Vektorsystemen für den Gentransfer in humane Schwannzellen ». [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962854794.

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41

Fontenas, Laura. « Analyse fonctionnelle des gènes ndrg4 et elmo1 dans le développement du système nerveux périphérique chez le poisson zèbre ». Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS060.

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Les cellules gliales qui forment les segments de myéline du système nerveux périphérique (SNP) sont appelées cellules de Schwann. Elles assurent aux nerfs un soutien fonctionnel et permettent une conduction rapide et efficace de l'influx nerveux. Cette fonction requiert une communication réciproque entre les neurones et les cellules gliales qui les entourent. Une perturbation de cette interaction entraine le plus souvent une situation pathologique comme les neuropathies périphériques dont la plus connue est la maladie de Charcot-Marie-Tooth. Cependant, les mécanismes qui conduisent à ces pathologies sont encore peu connus et leur compréhension demande au préalable l'élucidation des mécanismes physiologiques qui contrôlent le développement du SNP. Ce travail a consisté en l'analyse de nouvelles fonctions des gènes ndrg4 et elmo1, dans le développement du système nerveux périphérique, chez le poisson zèbre. Nous avons montré que ndrg4 (n-myc downstream regulated gene) est un facteur neuronal qui régule le développement de la myéline périphérique en contrôlant le regroupement des canaux sodiques aux nœuds de Ranvier et l'expression de la mbp. Ndrg4 semble moduler l'échange vésiculaire entre les axones et les cellules de Schwann, en contrôlant l'expression de certaines protéines de relargage vésiculaire comme SNAP25, membre du complexe SNARE.Ce travail décrit par ailleurs une nouvelle fonction de elmo1 (engulfment and cell motility 1) dans le développement du SNP du poisson zèbre, où il favorise la survie des neurones dans lesquels il est exprimé. Nous avons montré qu'elmo1 protège les neurones de l'apoptose et que cette fonction est contrôlée par la voie nétrine1/unc5b en amont de Rac1. De ce fait, elmo1 est requis pour le développement du ganglion de la ligne latérale postérieure et des axones qui en émergent pour donner un système nerveux fonctionnel. Ainsi, ces travaux contribuent à une meilleure connaissance du développement du SNP et élucident pour la première fois une nouvelle voie de signalisation requise pour la survie des neurones dans le SNP
The glial cells that form myelin segments in the peripheral nervous system (PNS) are called Schwann cells (SCs). They provide functional support for nerves and allow a fast and efficient conduction of the action potentials. This requires a bilateral communication between axons and the associated glial cells. Disruption of this interaction often leads to peripheral neuropathies e.g. Charcot-Marie-Tooth disease. However, the mechanisms underlying these diseases remain poorly known and their understanding requires, at first, the elucidation of the physiological mechanisms responsible for PNS development. This work consists of a functional analysis of two genes, ndrg4 and elmo1, in the PNS development, using the zebrafish model. We showed that the neuronal factor ndrg4 (n-myc downstream regulated gene 4) regulates nodes of Ranvier organization and mbp expression along the Posterior Lateral Line nerve (PLLn). This is achieved, most likely, by the ability of ndrg4 to modulate vesicular exchange between axons and SCs. Indeed, the expression of some key proteins involved in vesicle docking and release such as SNAP25, a member of the SNARE complex, are significantly dependent on ndrg4.Moreover, this work describes a novel role for neuronal elmo1 (engulfment and cell motility 1) in PNS development by promoting neuronal survival within the PLL ganglion. We showed that elmo1 has protective role against apoptosis and that its function is controlled by the netrin1/unc5b signalling upstream of Rac1 and independently of macrophages role in apoptotic clearance. Therefore, elmo1 is required for the proper development of the PLL ganglion and the axonal development of the PLLn. Thus, this study further contributes to our understanding of PNS development and unravels a novel molecular pathway required for neuronal survival in the PNS
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42

Aghamaleky, Sarvestany Arwin. « Schwann cell pathology in spinal muscular atrophy (SMA) ». Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15908.

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The childhood neuromuscular disease spinal muscular atrophy (SMA) is caused by low levels of survival motor neuron (SMN) protein. Historically, SMA has been characterised as a disease primarily affecting lower motor neurons. However, recent breakthroughs have revealed defects in other non-neuronal cells and tissues. In vivo analysis of peripheral nerve showed defects in Schwann cells, manifesting as abnormal myelination and delayed maturation of axo-glia interactions. The experiments in this thesis were designed to build on these observations and examine whether Schwann cell defects are intrinsic and occur as a primary result of low levels of SMN in that cell type, or rather represent a secondary consequence of pathology in neighbouring motor neurons. I initially developed a protocol to allow isolation of high-yields of purified, myelination-competent Schwann cells from ‘Taiwanese’ SMA mice. SMA-derived Schwann cells had significantly reduced SMN levels and failed to respond normally to differentiation cues. Increasing SMN levels restored myelin protein expression in Schwann cells from SMA mice. Perturbations in expression of key myelin proteins were likely due to failure of protein translation and/or stability rather than transcriptional defects. Co-cultures of healthy neurons with SMA Schwann cells revealed a significant reduction in myelination compared to cultures where wild-type Schwann cells were used. The presence of SMA Schwann cells also disrupted neurite stability. Perturbations in the expression of key extracellular matrix proteins, such as laminin α2, in SMA-derived Schwann cells suggests that Schwann cells were influencing neurite stability by modulating the composition of the extracellular matrix. Previous studies have demonstrated that low levels of SMN lead to disruption of ubiquitin homeostasis and decreased expression of ubiquitin-like modifier activating enzyme (UBA1) in the neuromuscular system, driving neuromuscular pathology via a beta-catenin dependent pathway. Label-free proteomics analysis of SMA and control Schwann cells identified 195 proteins with modified expression profiles. Bioinformatic analysis of these proteins using Ingenuity Pathway Analysis (IPA) software confirmed that major disruption of protein ubiquitination pathways was also present in Schwann cells from SMA mice. Immunolabeling and proteomics data both revealed that UBA1 levels were significantly reduced in SMA-derived Schwann cells. However, loss of UBA1 in Schwann cells did not lead to downstream modifications in beta-catenin pathways. Pharmacological inhibition of UBA1 in healthy Schwann cells was sufficient to induce defects in myelin protein expression, suggesting that UBA1 defects contribute directly to Schwann cell disruption in SMA. I conclude that low levels of SMN induce intrinsic defects in Schwann cells, mediated at least in part through disruption to ubiquitination pathways.
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43

Davis, Catherine Monica. « Signalling pathways regulating Schwann cell survival and differentiation ». Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17978/.

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The generation of mature Schwann cells from the neural crest occurs by a transition through two intermediate cell types, namely the Schwann cell precursor and the immature Schwann cell. Immature Schwann cells mature into the myelinating and non-myelinaling Schwann cells present in the adult nerve. These cell types are well characterised and can be readily distinguished from one another by their distinct antigenic profile, survival responses, and morphological changes. In this study I investigated the effects of BMP in the Schwann cell lineage in vitro. I found that BMP2/4 acts to maintain the immature Schwann cell type by promoting its differentiation from the Schwann cell precursor and inhibiting the upregulation of myelin proteins. I also found that survival responses to BMP2/4 differ between embryonic and postnatal Schwann cell. I examined the role of STAT3 in Schwann cells both in vitro and in vivo using mice with a conditional mutation of STAT3 specifically in Schwann cells. I found that STAT3 is activated by, and supports survival following stimulation by autocrine factors secreted by Schwann cells both in vitro and following nerve injury in vivo. I also discovered that STAT3 promotes the expression of myelin proteins in vitro and that it is involved in the timing of demyelination following sciatic nerve injury. I also investigated the repression of the transcription factor c-Jun, by itself and by Krox-20, in immature Schwann cells and found that this occurs mainly at the protein, rather than the transcriptional level.
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Gumy, Laura Fernanda. « Investigations into Schwann cell dysfunction under hyperglycaemic conditions ». Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614047.

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Rosenberg, L. H. « Ras/Raf/ERK signalling and Schwann cell dedifferentiation ». Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19504/.

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Schwann cells are a highly specialized cell type whose function is to ensheathe and myelinate axons of the peripheral nervous system (PNS). Remarkably, Schwann cells retain the capacity to regenerate throughout the lifespan of an animal, responding to peripheral nervous system damage by dedifferentiating and reverting to a proliferating, progenitor like state. Following successful axon outgrowth, dedifferentiated Schwann cells re-differentiate, thereby reconstituting a repaired and functional nerve. Previously, we have shown that the Ras/Raf/ERK pathway is sufficient to drive Schwann cell dedifferentiation and that damage to peripheral nerves results in strong and sustained activation of ERK in Schwann cells. This data suggests an important physiological role of Ras/Raf/ERK signalling in controlling Schwann cell plasticity. The molecular mechanism by which this occurs is unknown. The transcription factor Krox-20 is required for both the initiation and the maintenance of the myelinated state. Loss of Krox-20 is sufficient to drive mature, differentiated Schwann cells towards the less differentiated, progenitor like state and decreased levels of Krox-20 are associated with damaged peripheral nerves. In this thesis I show that activation of Raf/ERK signalling in differentiated Schwann cells induces the rapid downregulation of Krox-20 and myelin associated mRNA expression. At the protein level however, Krox-20 persists past the point of myelin gene down-regulation both in vitro following activation of Raf, and in vivo in response to peripheral nerve damage. Moreover, constitutive expression of Krox-20 does not abolish the ability of Raf/ERK signalling to downregulate myelinassociated genes. Schwann cell dedifferentiation therefore occurs independently of Krox-20 protein loss. Further work shows that Raf/ERK signalling acts to block Krox- 20 dependent activation of myelin-associated genes and that this occurs via negative regulation of myelin gene promoters. To address the mechanism by which Raf/ERK signalling blocks Krox-20 dependent activity, I have studied the role of a number of candidate transcription factors, including the immature-Schwann cell associated factors cJun and Sox-2. Interestingly, activation of Raf is sufficient to drive the expression of these factors in differentiated Schwann cells. Nevertheless, further studies showed that neither cJun nor Sox-2 are required for Raf driven dedifferentiation. To further study the mechanism I have used microarray analysis to identify candidates whose expression changed following Raf activation. I have identified and examined the role of a number of transcription factors in this process.
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46

Zorick, Todd S. « The transcriptional control of myelination in Schwann cells / ». Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9840049.

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Robertson, Andrea Marie. « The mechanism of neuropathy in peripheral myelin protein 22 mice ». Thesis, University College London (University of London), 1999. http://discovery.ucl.ac.uk/1348752/.

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Mutations in the gene for peripheral myelin protein 22 (PMP22) are associated with peripheral neuropathy in mice and humans. PMP22 is produced mainly in Schwann cells in the peripheral nervous system where it is localised to compact myelin. The function of PMP22 is unclear but its low abundance makes it unlikely to be a structural myelin protein. I have studied the peripheral nerves of two different mouse models with alterations in the pmp22 gene. (1) The Trembler-J (Tr^J) mouse which has a point mutation [L16P] in the first transmembrane domain of PMP22. (2) PMPP22 overexpressing transgenic mice which have 7 (C22), 4 (C61) and 2 (C2) copies of the human PMP22 gene in addition to the mouse pmp22 gene. In the nerves of adult Tr^J mice there was considerable evidence of abnormal Schwann cell-axon interactions. Abnormal features were reproduced in the early stages of regeneration following crush injury. This demonstrates that the abnormalities are a result of an intrinsic abnormality of Tr^J Schwann cells and not secondary changes related to demyelination. In the initial stages of postnatal development the number of axons that were singly ensheathed was the same in all the mutants examined, indicating that PMP22 does not function in the initial enclosure of groups of axons and subsequent separation of single axons. All strains examined had an increased proportion of fibres that were incompletely surrounded by Schwann cell cytoplasm indicating that this step is disrupted in PMP22 mutants. Increasing the number of copies of PMP22 resulted in an increasing severity of phenotype. In C22 (7 copy) animals myelin formation was delayed or non-existent in many fibres whereas in C61 animals myelination initially appeared normal with abnormality appearing later in a small population of fibres. The C2 strain appeared relatively unaffected. It is concluded that PMP22 functions in the initiation of myelination and most probably involves the ensheathment of the axon by the Schwann cell, and the extension of this cell along the axon. Abnormalities are most likely to result from defective interactions between the axon and the Schwann cell.
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Wang, Xiang. « Die Eindeutigkeit der schwachen Lösung eines Systems mit zwei Erhaltungssätzen / ». [S.l.] : [s.n.], 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10468.

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49

Bend, Jutta. « Extra- und intrazelluläre Laccasen der acidophilen schwarzen Hefe Hortaea acidophilai ». [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=980715504.

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50

Seehuber, Ulrich. « Litho- und biostratigraphische Untersuchungen in der Oberen Süßwassermolasse in der Umgebung von Kirchheim in Schwaben ». Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-99934.

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