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Journal articles on the topic 'Schwaden'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Göpfert, Eberhard, and Lutz Röhrich. "Rezension von: Röhrich, Lutz, Die schwarzen Führer: Schwaben, Bodensee ..." Württembergisch Franken 73 (October 11, 2023): 315. http://dx.doi.org/10.53458/wfr.v73i.7942.

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2

Aurnhammer, Achim. "Neues vom alten Ernst Schwabe von der Heyde." Daphnis 31, no. 1-2 (November 23, 2002): 279–98. http://dx.doi.org/10.1163/18796583-0310102011.

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Martin Opitz zählte Ernst Schwabe von der Heyde zu seinen wichtigsten Vorbildern. Gleichwohl machte er mit nur wenigen Dichtungen Schwabes bekannt. Der glückliche Fund von drei unbemerkt gebliebenen Alexandrinersonetten, die anläßlich der Krönung von Kaiser Matthias im Jahre 1612 entstanden sind, erweitert unsere Kenntnisse über Schwabes dichterisches Werk und eröffnet neue Einblicke in die voropitzische Modernisierung der deutschen Literatur.

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3

Tillmanns, Wolfgang, Alois Koci, and Karl Brunnacker. "Die Brunhes/Matuyama-Grenze in Roßhaupten (Bayerisch Schwaben)." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 68 (April 1, 1986): 241–47. http://dx.doi.org/10.1127/jmogv/68/1986/241.

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4

Zehnder, Adalbert. "Fitte Schwaben." kma - Klinik Management aktuell 12, no. 01 (January 2007): 13. http://dx.doi.org/10.1055/s-0036-1574049.

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5

Aktas, Ali. "Petrography of Gravel, Stratigraphy and Paleogeography of the Zusam-Platte (Bayerisch Schwaben)." Zeitschrift der Deutschen Geologischen Gesellschaft 141, no. 1 (January 1, 1990): 99–108. http://dx.doi.org/10.1127/zdgg/141/1990/99.

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6

Aktas, Ali. "Sedimentpetrographisch-stratigraphische Untersuchungen in der Zusam-Platte, Bayerisch Schwaben." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 71 (March 28, 1989): 247–74. http://dx.doi.org/10.1127/jmogv/71/1989/247.

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7

Ellwanger, Dietrich. "Paläogeographische Kartenskizzen zur Flußgeschichte des Aitrach-Iller-Gebiets (Schwaben)." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 71 (March 28, 1989): 445–66. http://dx.doi.org/10.1127/jmogv/71/1989/445.

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8

Münzing, Klaus, and Ali Aktas. "Weitere Funde molluskenführender Mergellagen im Unteren Deckenschotter von Bayerisch Schwaben." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 69 (April 21, 1987): 181–93. http://dx.doi.org/10.1127/jmogv/69/1987/181.

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9

Löslein, Barbara, and Peter Fassl. "Rezension von: Fassl, Peter (Hrsg.), Wissenschaftliche Tagung der Heimatpflege des Bezirks Schwaben in Zusammenarbeit mit der Schwabenakademie Irsee am 14./15. Oktober 1989." Württembergisch Franken 83 (June 9, 2023): 433–34. http://dx.doi.org/10.53458/wfr.v83i.6541.

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Peter Fassl (Hrsg.), Geschichte und Kultur der Juden in Schwaben. Wissenschaftliche Tagung der Heimatpflege des Bezirks Schwaben in Zusammenarbeit mit der Schwabenakademie Irsee am 14./15. Oktober 1989 (Irseer Schriften, Bd. 2) Sigmaringen (Thorbecke) 1994. 186 S„ 8 Abb.

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10

Mollenhauer, Dieter, and Barbara Hickel. "Gerhard Helmut Schwabe 1910-1987." Archiv für Hydrobiologie 115, no. 4 (June 27, 1989): 613–19. http://dx.doi.org/10.1127/archiv-hydrobiol/115/1989/613.

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11

Senn, Ernst, and Reichsverband für Deutsche Jugendherbergen. Gau Schwaben. "Rezension von: DJH-Wanderführer, Bd. 1." Zollerheimat 5, no. 3 (February 15, 2024): 12. http://dx.doi.org/10.53458/zh.v5i3.9657.

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Von Jugendherberge zu Jugendherberge durch das schöne Schwabenland. Wanderungen, Jugendherbergen u. Ortsgruppen in Württemberg u. Hohenzollern u. in den Nachbargauen, hg vom Gau Schwaben e.V. im Reichsverband für Deutsche Jugendherbergen, Bd. 1, 11., neu bearb. Auflage, Stuttgart : Gau Schwaben im Reichsverband für Deutsche Jugendherbergen, 1934. 255 Seiten : Ill., Kt.

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12

Stern, Sara. "Porträt Thomas Greiner." kma - Klinik Management aktuell 12, no. 10 (October 2007): 86–89. http://dx.doi.org/10.1055/s-0036-1574406.

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Nach gescheiterten Versuchen mit Kandidaten von außerhalb hat Peter Dussmann seinen neuen Vorstandsvorsitzenden jetzt im eigenen Haus gefunden: Thomas Greiner kommt – wie Dussmann selbst – aus Rottweil in Schwaben. Schwaben sind gewöhnlich sehr selbstbewusste Leute. Greiner ist zudem im Sternzeichen des Widders geboren. Denen wird besonderer Siegeswille nachgesagt. Was soll da noch schiefgehen?

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13

Sathyanarayanan, Ramanujam, Raghu Kumaravelu, and Nithin J. Jude. "An Uncommon and Rare Soft Tissue Tumor of the Cheek (Schwannoma): A Case Report." Journal of Scientific Dentistry 10, no. 2 (2020): 38–40. http://dx.doi.org/10.5005/jp-journals-10083-0936.

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ABSTRACT Schwannoma is usually an uncommon, benign, encapsulated, very slow-growing, usually solitary tumor that originates from Schwann cells of the nerve sheath derived from the neuroectoderm. Only 1% of schwannomas was intraoral of which the most common site is always the tongue after which the palate, floor of the mouth, buccal mucosa, lips, and jaws can be affected. Schwannoma is an uncommon benign tumor that originates from the Schwan cell of the peripheral nerves. It is difficult to diagnose clinically. In our case, the patient reported a solitary swelling present on the left cheek. The swelling was warmth, tender, and consistency is soft. Inflamed buccal mucosa was also noted and the patient had restricted mouth opening. Then, surgical excision was done under general anesthesia. How to cite this article: Kumaravelu R, Sathyanarayanan R, Jude NJ. An Uncommon and Rare Soft Tissue Tumor of the Cheek (Schwannoma): A Case Report. J Sci Dent 2020;10(2):38–40.

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14

Schick, Hermann. "Zwei Schwaben – ein Text." Schwäbische Heimat 63, no. 4 (May 24, 2022): 468–76. http://dx.doi.org/10.53458/sh.v63i4.2808.

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15

Murmann, Christoph. "MW Schwaben sind zuversichtlich." Lebensmittel Zeitung 74, no. 18 (2022): 20. http://dx.doi.org/10.51202/0947-7527-2022-18-020-1.

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16

Quarthal, Franz. "Warum wir «Schwaben» sind." Schwäbische Heimat 68, no. 2 (January 27, 2022): 150–60. http://dx.doi.org/10.53458/sh.v68i2.1635.

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17

Bannier, Hans-Joachim. "Sauerland, Saarland oder Schwaben?" Schwäbische Heimat 72, no. 3 (December 7, 2021): 65–68. http://dx.doi.org/10.53458/sh.v72i3.1131.

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18

Alber, Wolfgang. "Alles Schwaben oder was?" Literaturblatt für Baden-Württemberg, no. 1 (June 20, 2024): 12–14. http://dx.doi.org/10.53458/litbw.vi1.12376.

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19

Scheuenpflug, Lorenz. "Die altpleistozäne Hauptabflußrichtung der Gewässer in der Iller-Lech-Platte (Bayerisch Schwaben)." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 68 (April 1, 1986): 189–95. http://dx.doi.org/10.1127/jmogv/68/1986/189.

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20

Abd Razak, Nurul Husna, Jalilah Idris, Nur Hidayah Hassan, Fazlin Zaini, Noorzaid Muhamad, and Muhammad Fauzi Daud. "Schwann Cells Reprogram Into Repair Phenotype Instead of Dedifferentiating to Immature Phenotype in in Vitro Culture." ICMST 19, s9 (August 10, 2023): 107–12. http://dx.doi.org/10.47836/mjmhs.19.s9.16.

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Introduction: In vitro cultured Schwann cell has been suggested to adopt a phenotype of undifferentiated immature Schwann cells found in vivo during development. However, recent studies indicate that Schwann cells undergo cellular reprogramming into the phenotype of repair Schwann cells instead of reverting to an immature phenotype after peripheral nerve injury. The study hypothesized that in in vitro culture, Schwann cells assume the repair phenotype instead of de-differentiating to immature Schwann cells, similar to in vivo nerve injury response. Therefore, this study aimed to characterize the phenotype of cultured Schwann cells by examining the expression of classic Schwann markers and transcription factors c-Jun and Krox-20. Methods: Schwann cells, isolated from Wistar rat sciatic nerve, were grown in a standard Schwann cell growth medium for seven days. Then, cultured Schwann cells were analyzed using immunofluorescence analysis for classic Schwann cell markers (neurotrophin receptor p75 (p75NTR) and myelin basic protein (MBP)) and the expression profile of transcription factor c-Jun and Krox-20. Results: Immunofluorescence analysis revealed that cultured Schwann cells expressed a significantly high level of repair phenotype biomarkers (p75NTR and c-Jun) compared to the level of myelinating phenotype biomarkers (MBP and Krox-20). Conclusion: Schwann cells reprogram into repair Schwann cells instead of de-differentiating to immature Schwann cells in vitro.

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21

Fischer, Cornelius, and Andreas Koch. "Die Porenraumentwicklung eines schwarzen Dachschiefers bei oxidativer Verwitterung." Zeitschrift der Deutschen Gesellschaft für Geowissenschaften 156, no. 1 (January 1, 2005): 75–79. http://dx.doi.org/10.1127/1860-1804/2005/0156-0075.

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22

Scheuenpflug, Lorenz. "Zur Herkunft altpleistozäner Schotter in der östlichen Iller-Lech-Platte (Zusamplatte, Bayerisch Schwaben)." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 72 (April 17, 1990): 323–27. http://dx.doi.org/10.1127/jmogv/72/1990/323.

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23

Tolzmann, Don Heinrich, and Jacob Steigerwald. "Banat Topola's Schwaben: 1791-1945." German Quarterly 68, no. 1 (1995): 80. http://dx.doi.org/10.2307/408032.

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24

Yue, Young-Sang, and Jae-Dam Lee. "Vital Freezing of Human Schwann Cells from Acoustic Tumor for Storage and Reculture." Journal of Clinical Otolaryngology Head and Neck Surgery 4, no. 1 (May 1993): 64–67. http://dx.doi.org/10.35420/jcohns.1993.4.1.64.

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25

Graef, Hans, and Otto Heuschele. "Rezension von: Heuschele, Otto (Hrsg.), Geisteserbe aus Schwaben." Württembergisch Franken 66 (February 20, 2024): 282–83. http://dx.doi.org/10.53458/wfr.v66i.10493.

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26

Einheber, S., M. J. Hannocks, C. N. Metz, D. B. Rifkin, and J. L. Salzer. "Transforming growth factor-beta 1 regulates axon/Schwann cell interactions." Journal of Cell Biology 129, no. 2 (April 15, 1995): 443–58. http://dx.doi.org/10.1083/jcb.129.2.443.

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We have investigated the potential regulatory role of TGF-beta in the interactions of neurons and Schwann cells using an in vitro myelinating system. Purified populations of neurons and Schwann cells, grown alone or in coculture, secrete readily detectable levels of the three mammalian isoforms of TGF-beta; in each case, virtually all of the TGF-beta activity detected is latent. Expression of TGF-beta 1, a major isoform produced by Schwann cells, is specifically and significantly downregulated as a result of axon/Schwann cell interactions. Treatment of Schwann cells or Schwann cell/neuron cocultures with TGF-beta 1, in turn, has dramatic effects on proliferation and differentiation. In the case of purified Schwann cells, treatment with TGF-beta 1 increases their proliferation, and it promotes a pre- or nonmyelinating Schwann cell phenotype characterized by increased NCAM expression, decreased NGF receptor expression, inhibition of the forskolin-mediated induction of the myelin protein P0, and induction of the Schwann cell transcription factor suppressed cAMP-inducible POU protein. Addition of TGF-beta 1 to the cocultures inhibits many of the effects of the axon on Schwann cells, antagonizing the proliferation induced by contact with neurons, and, strikingly, blocking myelination. Ultrastructural analysis of the treated cultures confirmed the complete inhibition of myelination and revealed only rudimentary ensheathment of axons. Associated defects of the Schwann cell basal lamina and reduced expression of laminin were also detected. These effects of TGF-beta 1 on Schwann cell differentiation are likely to be direct effects on the Schwann cells themselves which express high levels of TGF-beta 1 receptors when cocultured with neurons. The regulated expression of TGF-beta 1 and its effects on Schwann cells suggest that it may be an important autocrine and paracrine mediator of neuron/Schwann cell interactions. During development, TGF-beta 1 could serve as an inhibitor of Schwann cell proliferation and myelination, whereas after peripheral nerve injury, it may promote the transition of Schwann cells to a proliferating, nonmyelinating phenotype, and thereby enhance the regenerative response.

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27

Hirbodian, Sigrid. "Schwäbische Reichsstädte im Spätmittelalter." Zeitschrift für Württembergische Landesgeschichte 77 (June 30, 2018): 11–14. http://dx.doi.org/10.53458/zwlg.v77i.23.

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Die Reichsstädte sind neben den großen Territorien Württemberg, Vorderöster-reich und Kurpfalz die bestimmenden politischen Kräfte in Schwaben über die gesamte Vormoderne hinweg – Kräfte zumal, die in anderen Regionen des Reiches (vom Mittelrhein, dem Elsass und Thüringen vielleicht einmal abgesehen) in dieser Form nicht vorhanden sind. Insofern sind die Reichsstädte in dieser Zahl und Bedeutung tatsächlich etwas Typisches und zugleich Besonderes für unsere Regi-on. Typisch, weil sie in ihrer Ausprägung, aber auch in ihren Zusammenschlüssen Schwaben nach außen hin repräsentierten, besonders, weil eine solch starke Städte-landschaft im spätmittelalterlichen Reich ihresgleichen suchte.

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28

Doppler, Gerhard. "Tertiär-Molasse und Quartär-Ablagerungen im nördlichen Schwaben (Exkursion F am 28. April 2011)." Jahresberichte und Mitteilungen des Oberrheinischen Geologischen Vereins 93 (April 26, 2011): 303–30. http://dx.doi.org/10.1127/jmogv/93/2011/303.

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29

Mason, P. W., J. W. Bigbee, and G. H. DeVries. "Cerebellar granule cells contain a membrane mitogen for cultured Schwann cells." Journal of Cell Biology 108, no. 2 (February 1, 1989): 607–11. http://dx.doi.org/10.1083/jcb.108.2.607.

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Proliferation of Schwann cells is one of the first events that occurs after contact with a growing axon. To further define the distribution and properties of this axonal mitogen, we have (a) cocultured cerebellar granule cells, which lack glial ensheathment in vivo with Schwann cells; and (b) exposed Schwann cell cultures to isolated granule cell membranes. Schwann cells cocultured with granule cells had a 30-fold increase in the labeling index over Schwann cells cultured alone, suggesting that the mitogen is located on the granule cell surface. Inhibition of granule cell proteoglycan synthesis caused a decrease in the granule cells' ability to stimulate Schwann cell proliferation. Membranes isolated from cerebellar granule cells when added to Schwann cell cultures caused a 45-fold stimulation in [3H]thymidine incorporation. The granule cell mitogenic signal was heat and trypsin sensitive and did not require lysosomal processing by Schwann cells to elicit its proliferative effect. The ability of granule cells and their isolated membranes to stimulate Schwann cell proliferation suggests that the mitogenic signal for Schwann cells is a ubiquitous factor present on all axons regardless of their ultimate state of glial ensheathment.

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30

Li, Jun-Qin, Hui-Jie Jiang, Xiu-Yun Su, Li Feng, Na-Zhi Zhan, Shan-Shan Li, Zi-Jie Chen, et al. "Schwann Cells Accelerate Osteogenesis via the Mif/CD74/FOXO1 Signaling Pathway In Vitro." Stem Cells International 2022 (January 13, 2022): 1–13. http://dx.doi.org/10.1155/2022/4363632.

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Schwann cells have been found to promote osteogenesis by an unclear molecular mechanism. To better understand how Schwann cells accelerate osteogenesis, RNA-Seq and LC-MS/MS were utilized to explore the transcriptomic and metabolic response of MC3T3-E1 to Schwann cells. Osteogenic differentiation was determined by ALP staining. Lentiviruses were constructed to alter the expression of Mif (macrophage migration inhibitory factor) in Schwann cells. Western blot (WB) analysis was employed to detect the protein expression. The results of this study show that Mif is essential for Schwann cells to promote osteogenesis, and its downstream CD74/FOXO1 is also involved in the promotion of Schwann cells on osteogenesis. Further, Schwann cells regulate amino acid metabolism and lipid metabolism in preosteoblasts. These findings unveil the mechanism for Schwann cells to promote osteogenesis where Mif is a key factor.

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31

Muir, D., S. Varon, and M. Manthorpe. "Schwann cell proliferation in vitro is under negative autocrine control." Journal of Cell Biology 111, no. 6 (December 1, 1990): 2663–71. http://dx.doi.org/10.1083/jcb.111.6.2663.

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In healthy adult peripheral nerve, Schwann cells are believed to be generally quiescent. Similarly, cultures of isolated rat sciatic nerve Schwann cells hardly proliferate in serum-supplemented medium. The possibility that Schwann cells negatively regulate their own proliferation was supported by the demonstration that conditioned media from Schwann cell cultures inhibited the proliferation of mitogen-stimulated test cultures. The inhibition could be complete, was dose dependent, and was exhibited when the test Schwann cells were under the influence of different types of mitogens such as cholera toxin, laminin, and living neurons. The inhibition of proliferation was completely reversible and a rapid doubling of cell number resulted when treatment with conditioned medium was withdrawn from mitogen-stimulated Schwann cells. Conditioned medium from cholera toxin-stimulated and immortalized Schwann cell cultures contained less antiproliferative activity than that found in medium from quiescent Schwann cell cultures. However, media conditioned by two actively proliferating rat Schwannoma cell lines were rich sources of antiproliferative activity for Schwann cells. Unlike the mitogen-stimulated Schwann cells, whose proliferation could be inhibited completely, the immortalized and transformed Schwann cell types were nearly unresponsive to the antiproliferative activity. The antiproliferative activity in Schwann and Schwannoma cell conditioned media was submitted to gel filtration and SDS-PAGE. The activity exists in at least two distinct forms: (a) a high molecular weight complex with an apparent molecular mass greater than 1,000 kD, and (b) a lower molecular weight form having a molecular mass of 55 kD. The active 55-kD form could be derived from the high molecular weight form by gel filtration performed under dissociating conditions. The 55-kD form was further purified to electrophoretic homogeneity. These results suggest that Schwann cells produce an autocrine factor, which we designate as a "neural antiproliferative protein," which completely inhibits the in vitro proliferation of Schwann cells but not that of immortalized Schwann cells or Schwannoma lines.

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32

Mendonça, Caroline Faria Leal. "RIAL, Carmen e SCHWADE, Elisete (orgs.), 2016.Diálogos antropológicos contemporâneos." Revista EntreRios do Programa de Pós-Graduação em Antropologia 1, no. 1 (June 3, 2018): 118. http://dx.doi.org/10.26694/rer.v1i1.7245.

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33

Wunder, Gerd, and Robert Uhland. "Rezension von: Uhland, Robert (Hrsg.), Lebensbilder aus Schwaben und Franken, 13." Württembergisch Franken 63 (March 13, 2024): 227. http://dx.doi.org/10.53458/wfr.v63i.10895.

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34

Kim, Muwoong, Hyosun Kim, Dogyeong Kim, Dokyoung Kim, Youngbuhm Huh, Chan Park, Hyung-Joo Chung, Junyang Jung, and Na Young Jeong. "Heme Oxygenase 1 in Schwann Cells Regulates Peripheral Nerve Degeneration Against Oxidative Stress." ASN Neuro 11 (January 2019): 175909141983894. http://dx.doi.org/10.1177/1759091419838949.

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During Wallerian degeneration, Schwann cells lose their characteristic of myelinating axons and shift into the state of developmental promyelinating cells. This recharacterized Schwann cell guides newly regrowing axons to their destination and remyelinates reinnervated axons. This Schwann cell dynamics during Wallerian degeneration is associated with oxidative events. Heme oxygenases (HOs) are involved in the oxidative degradation of heme into biliverdin/bilirubin, ferrous iron, and carbon monoxide. Overproduction of ferrous iron by HOs increases reactive oxygen species, which have deleterious effects on living cells. Thus, the key molecule for understanding the exact mechanism of Wallerian degeneration in the peripheral nervous system is likely related to oxidative stress-mediated HOs in Schwann cells. In this study, we demonstrate that demyelinating Schwann cells during Wallerian degeneration highly express HO1, not HO2, and remyelinating Schwann cells during nerve regeneration decrease HO1 activation to levels similar to those in normal myelinating Schwann cells. In addition, HO1 activation during Wallerian degeneration regulates several critical phenotypes of recharacterized repair Schwann cells, such as demyelination, transdedifferentiation, and proliferation. Thus, these results suggest that oxidative stress in Schwann cells after peripheral nerve injury may be regulated by HO1 activation during Wallerian degeneration and oxidative-stress-related HO1 activation in Schwann cells may be helpful to study deeply molecular mechanism of Wallerian degeneration.

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35

Carey, D. J., M. S. Todd, and C. M. Rafferty. "Schwann cell myelination: induction by exogenous basement membrane-like extracellular matrix." Journal of Cell Biology 102, no. 6 (June 1, 1986): 2254–63. http://dx.doi.org/10.1083/jcb.102.6.2254.

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Exposing rat Schwann cells co-cultured with nerve cells to a reconstituted basement membrane induced the formation of myelin segments by Schwann cells. This occurred in a serum-free culture medium in which, in the absence of this matrix, Schwann cells proliferate but fail to differentiate. This reconstituted basement membrane was prepared from solubilized extracellular matrix proteins synthesized by a basement membrane-producing murine tumor. The major constituents of this reconstituted matrix are collagen type IV, laminin, heparan sulfate proteoglycan, entactin, and nidogen. The matrix also elicited striking morphological changes in Schwann cells, inducing them to spread longitudinally along the nerve fibers (a necessary early step in the process of ensheathment of nerve fibers). Several observations indicated that the effect of the matrix was exerted directly on Schwann cells and not indirectly through an effect on nerve cells. First, the matrix-induced cell spreading occurred only in areas in which Schwann cells directly contacted the matrix; Schwann cells that were associated with the same nerve fibers but that did not themselves directly contact the matrix did not exhibit spreading. Second, the matrix-induced alteration in Schwann cell morphology was observed in cultures in which the nerve cells were removed. These results provide direct evidence that basement membrane contact induces normal Schwann cell differentiation, and support the idea that Schwann cell differentiation in vivo may be regulated by the appearance of the basement membrane, which normally envelops terminally differentiating Schwann cells.

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36

Sheela, S., V. M. Riccardi, and N. Ratner. "Angiogenic and invasive properties of neurofibroma Schwann cells." Journal of Cell Biology 111, no. 2 (August 1, 1990): 645–53. http://dx.doi.org/10.1083/jcb.111.2.645.

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Neurofibromas are benign tumors from patients with von Recklinghausen Neurofibromatosis (NF1) that are comprised primarily of Schwann cells. These Schwann cells are found both in association with axons and in the extracellular matrix that is prevalent in neurofibromas, and in which fibroblasts are also abundant. An unresolved question has been whether cells in neurofibromas are normal cells or are intrinsically abnormal. We have tested the hypothesis that cells in neurofibromas are abnormal and have shown that neurofibroma Schwann cells, unlike normal Schwann cells, promote angiogenesis in the chick chorioallantoic membrane model system, and invade basement membranes in this system. In contrast, neurofibroma fibroblasts neither promote angiogenic reactions nor invade basement membranes. When injected into nude mice, neurofibroma Schwann cells do not form progressive tumors. These results suggest that NF1 Schwann cells differ from normal Schwann cells, that they are preneoplastic, and that genetic and/or epigenetic changes in Schwann cells may be required for development of peripheral nerve tumors in NF1.

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37

Oliveira, Rosane B., Maria T. Ochoa, Peter A. Sieling, Thomas H. Rea, Anura Rambukkana, Euzenir N. Sarno, and Robert L. Modlin. "Expression of Toll-Like Receptor 2 on Human Schwann Cells: a Mechanism of Nerve Damage in Leprosy." Infection and Immunity 71, no. 3 (March 2003): 1427–33. http://dx.doi.org/10.1128/iai.71.3.1427-1433.2003.

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ABSTRACT Nerve damage is a clinical hallmark of leprosy and a major source of patient morbidity. We investigated the possibility that human Schwann cells are susceptible to cell death through the activation of Toll-like receptor 2 (TLR2), a pattern recognition receptor of the innate immune system. TLR2 was detected on the surface of human Schwann cell line ST88-14 and on cultured primary human Schwann cells. Activation of the human Schwann cell line and primary human Schwann cell cultures with a TLR2 agonist, a synthetic lipopeptide comprising the N-terminal portion of the putative Mycobacterium leprae 19-kDa lipoprotein, triggered an increase in the number of apoptotic cells. The lipopeptide-induced apoptosis of Schwann cells could be blocked by an anti-TLR2 monoclonal antibody. Schwann cells in skin lesions from leprosy patients were found to express TLR2. It was possible to identify in the lesions Schwann cells that had undergone apoptosis in vivo. The ability of M. leprae ligands to induce the apoptosis of Schwann cells through TLR2 provides a mechanism by which activation of the innate immune response contributes to nerve injury in leprosy.

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38

Huang, Zhong, Rebecca Powell, Svenja Kankowski, James B. Phillips, and Kirsten Haastert-Talini. "Culture Conditions for Human Induced Pluripotent Stem Cell-Derived Schwann Cells: A Two-Centre Study." International Journal of Molecular Sciences 24, no. 6 (March 10, 2023): 5366. http://dx.doi.org/10.3390/ijms24065366.

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Adult human Schwann cells represent a relevant tool for studying peripheral neuropathies and developing regenerative therapies to treat nerve damage. Primary adult human Schwann cells are, however, difficult to obtain and challenging to propagate in culture. One potential solution is to generate Schwann cells from human induced pluripotent stem cells (hiPSCs). Previously published protocols, however, in our hands did not deliver sufficient viable cell numbers of hiPSC-derived Schwann cells (hiPSC-SCs). We present here, two modified protocols from two collaborating laboratories that overcome these challenges. With this, we also identified the relevant parameters to be specifically considered in any proposed differentiation protocol. Furthermore, we are, to our knowledge, the first to directly compare hiPSC-SCs to primary adult human Schwann cells using immunocytochemistry and RT-qPCR. We conclude the type of coating to be important during the differentiation process from Schwann cell precursor cells or immature Schwann cells to definitive Schwann cells, as well as the amounts of glucose in the specific differentiation medium to be crucial for increasing its efficiency and the final yield of viable hiPSC-SCs. Our hiPSC-SCs further displayed high similarity to primary adult human Schwann cells.

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Fritz, Gerhard, and Karl Bosl. "Rezension von: Bosl, Karl, Die bayerische Stadt in Mittelalter und Neuzeit." Württembergisch Franken 75 (September 20, 2023): 322. http://dx.doi.org/10.53458/wfr.v75i.7775.

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Wunder, Gerd, and Klaus von Andrian-Werburg. "Rezension von: von Andrian-Werburg, Klaus, Kronburg." Württembergisch Franken 56 (May 22, 2024): 149–50. http://dx.doi.org/10.53458/wfr.v56i.11728.

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41

Wang, Jiayi, Shunyi Lu, Ya Yuan, Lei Huang, Mengxuan Bian, Jieqin Yu, Jiapeng Zou, Libo Jiang, Dehua Meng, and Jian Zhang. "Inhibition of Schwann Cell Pyroptosis Promotes Nerve Regeneration in Peripheral Nerve Injury in Rats." Mediators of Inflammation 2023 (April 25, 2023): 1–12. http://dx.doi.org/10.1155/2023/9721375.

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Background. Peripheral nerve injury (PNI) is one of the most debilitating injuries, but therapies for PNI are still far from satisfactory. Pyroptosis, a recently identified form of cell death, has been demonstrated to participate in different diseases. However, the role of pyroptosis of Schwann cells in PNI remains unclear. Methods. We established a rat PNI model, and western blotting, transmission electron microscopy, and immunofluorescence staining were used to confirm pyroptosis of Schwann cells in PNI in vivo. In vitro, pyroptosis of Schwann cells was induced by lipopolysaccharides (LPS)+adenosine triphosphate disodium (ATP). An irreversible inhibitor of pyroptosis, acetyl (Ac)-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-cmk), was used to attenuate Schwann cell pyroptosis. Moreover, the influence of pyroptotic Schwann cells on the function of dorsal root ganglion neurons (DRGns) was analyzed by a coculture system. Finally, the rat PNI model was intraperitoneally treated with Ac-YVAD-cmk to observe the effect of pyroptosis on nerve regeneration and motor function. Results. Schwann cell pyroptosis was notably observed in the injured sciatic nerve. LPS+ATP treatment effectively induced Schwann cell pyroptosis, which was largely attenuated by Ac-YVAD-cmk. Additionally, pyroptotic Schwann cells inhibited the function of DRGns by secreting inflammatory factors. A decrease in pyroptosis in Schwann cells promoted regeneration of the sciatic nerve and recovery of motor function in rats. Conclusion. Given the role of Schwann cell pyroptosis in PNI progression, inhibition of Schwann cell pyroptosis might be a potential therapeutic strategy for PNI in the future.

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Grove, Matthew, Noboru H. Komiyama, Klaus-Armin Nave, Seth G. Grant, Diane L. Sherman, and Peter J. Brophy. "FAK is required for axonal sorting by Schwann cells." Journal of Cell Biology 176, no. 3 (January 22, 2007): 277–82. http://dx.doi.org/10.1083/jcb.200609021.

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Signaling by laminins and axonal neuregulin has been implicated in regulating axon sorting by myelin-forming Schwann cells. However, the signal transduction mechanisms are unknown. Focal adhesion kinase (FAK) has been linked to α6β1 integrin and ErbB receptor signaling, and we show that myelination by Schwann cells lacking FAK is severely impaired. Mutant Schwann cells could interdigitate between axon bundles, indicating that FAK signaling was not required for process extension. However, Schwann cell FAK was required to stimulate cell proliferation, suggesting that amyelination was caused by insufficient Schwann cells. ErbB2 receptor and AKT were robustly phosphorylated in mutant Schwann cells, indicating that neuregulin signaling from axons was unimpaired. These findings demonstrate the vital relationship between axon defasciculation and Schwann cell number and show the importance of FAK in regulating cell proliferation in the developing nervous system.

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Kim, H. A., B. Ling, and N. Ratner. "Nf1-deficient mouse Schwann cells are angiogenic and invasive and can be induced to hyperproliferate: reversion of some phenotypes by an inhibitor of farnesyl protein transferase." Molecular and Cellular Biology 17, no. 2 (February 1997): 862–72. http://dx.doi.org/10.1128/mcb.17.2.862.

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We have developed a potential model of Schwann cell tumor formation in neurofibromatosis type 1 (NF1). We show that mouse Schwann cells heterozygous or null at Nf1 display angiogenic and invasive properties, mimicking the behavior of Schwann cells from human neurofibromas. Mutations at Nf1 are insufficient to promote Schwann cell hyperplasia. Here we show that Schwann cell hyperplasia can be induced by protein kinase A activation in mutant cells. Removal of serum from the culture medium also stimulates hyperplasia, but only in some mutant cells. After serum removal, clones of hyperproliferating Schwann cells lose contact with axons in vitro, develop growth factor-independent proliferation, and exhibit decreased expression of the cell differentiation marker P0 protein; hyperproliferating cells develop after a 1-week lag in Schwann cells heterozygous at Nf1. The experiments suggest that events subsequent to Nf1 mutations are required for development of Schwann cell hyperplasia. Finally, an anti-Ras farnesyl protein transferase inhibitor greatly diminished both clone formation and hyperproliferation of null mutant cells, but not invasion; farnesyl transferase inhibitors could be useful in treating benign manifestations of NF1.

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Bolin, L. M., and E. M. Shooter. "Neurons regulate Schwann cell genes by diffusible molecules." Journal of Cell Biology 123, no. 1 (October 1, 1993): 237–43. http://dx.doi.org/10.1083/jcb.123.1.237.

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Successful peripheral nerve regeneration and functional recovery require the reestablishment of the neuron-Schwann cell relationship in the regenerating rat sciatic nerve, neurons differentially regulate Schwann cell genes. The message for the low-affinity NGF receptor, p75NGFR, is induced in Schwann cells distal to the injury and is repressed as regenerating axons make contact with these cells. The inverse is true for mRNA of the myelin gene P0; expression decreases distal to injury and increases as new axons contact Schwann cells and a program of myelination is initiated. Using an in vitro co-culture paradigm in which primary neurons and adult Schwann cells are separated by a microporous membrane, we show that axon contact is not an absolute requirement for neuronal regulation of Schwann cell genes. In this system neurons but not other cell types, repress the expression of Schwann cell p75NGFR while inducing the expression of the POU domain transcription factor, suppressed cAMP inducible POU, and myelin P0. These results demonstrate that regenerating axons can direct the Schwann cell genetic program from a distance through diffusible molecules.

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Ratner, N., R. P. Bunge, and L. Glaser. "A neuronal cell surface heparan sulfate proteoglycan is required for dorsal root ganglion neuron stimulation of Schwann cell proliferation." Journal of Cell Biology 101, no. 3 (September 1, 1985): 744–54. http://dx.doi.org/10.1083/jcb.101.3.744.

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Axons of dorsal root ganglion neurons express on their surfaces one or more proteins which are mitogenic for Schwann cells (Salzer, J., R. P. Bunge, and L. Glaser, 1980, J. Cell Biol., 84:767-778). Incubation of co-cultures of dorsal root ganglion neurons and Schwann cells with 4-methylumbelliferyl-beta-D-xyloside, an inhibitor of proteoglycan biosynthesis, decreases the mitogenic response of the Schwann cell by over 95%. The effect of the beta-D-xyloside has been localized to the neurons; pretreatment of neurons but not of Schwann cells with the inhibitor causes a marked reduction of the mitogenic response. In addition, Schwann cells treated with beta-D-xyloside are still mitogenically responsive to soluble Schwann cell mitogens (cholera toxin and glial growth factor). Neurons treated with heparitinase and membrane vesicles prepared from heparitinase-treated neurons show diminished mitogenicity for Schwann cells, while other proteoglycan lyases have no effect. We conclude that a cell surface heparan sulfate proteoglycan is a component of the Schwann cell mitogen present on the surface of dorsal root ganglion neurons.

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Bauer, Hermann, and Carl Alexander von Heideloff. "Mittelalterliche Kunst." Zeitschrift des Historischen Vereins für das Württembergische Franken 3, no. 3 (June 27, 2022): 80–81. http://dx.doi.org/10.53458/zhvwf.v3i3.3183.

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Hillemeyer, Judit. "Steigende Kosten belasten Molkerei." Lebensmittel Zeitung 74, no. 35 (2022): 46. http://dx.doi.org/10.51202/0947-7527-2022-35-046.

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48

Stihler, Daniel, and Klaus Kraft. "Rezension von: Kraft, Klaus, Landkreis Günzburg." Württembergisch Franken 80 (August 9, 2023): 335. http://dx.doi.org/10.53458/wfr.v80i.7268.

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Sherman, Larry S., Tilat A. Rizvi, Saikumar Karyala, and Nancy Ratner. "Cd44 Enhances Neuregulin Signaling by Schwann Cells." Journal of Cell Biology 150, no. 5 (September 4, 2000): 1071–84. http://dx.doi.org/10.1083/jcb.150.5.1071.

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We describe a key role for the CD44 transmembrane glycoprotein in Schwann cell–neuron interactions. CD44 proteins have been implicated in cell adhesion and in the presentation of growth factors to high affinity receptors. We observed high CD44 expression in early rat neonatal nerves at times when Schwann cells proliferate but low expression in adult nerves, where CD44 was found in some nonmyelinating Schwann cells and to varying extents in some myelinating fibers. CD44 constitutively associated with erbB2 and erbB3, receptor tyrosine kinases that heterodimerize and signal in Schwann cells in response to neuregulins. Moreover, CD44 significantly enhanced neuregulin-induced erbB2 phosphorylation and erbB2–erbB3 heterodimerization. Reduction of CD44 expression in vitro resulted in loss of Schwann cell–neurite adhesion and Schwann cell apoptosis. CD44 is therefore crucial for maintaining neuron–Schwann cell interactions at least partly by facilitating neuregulin-induced erbB2–erbB3 activation.

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Eccleston, P. A., P. G. Bannerman, D. E. Pleasure, J. Winter, R. Mirsky, and K. R. Jessen. "Control of peripheral glial cell proliferation: enteric neurons exert an inhibitory influence on Schwann cell and enteric glial cell DNA synthesis in culture." Development 107, no. 1 (September 1, 1989): 107–12. http://dx.doi.org/10.1242/dev.107.1.107.

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Neuronal membranes from rat dorsal root ganglia provide a mitogenic signal to cultured Schwann cells and it has been suggested this is an important factor in regulating Schwann cell numbers during development. In this study, the influence of enteric neurons on the DNA synthesis of both Schwann cells and enteric glia has been investigated as well as the effect of axonal membrane fractions (axolemma) on enteric glia. The proliferation rate of rat Schwann cells and enteric glia was assessed in culture using [3H]thymidine uptake and autoradiography in combination with immunolabelling to identify cell types. When purified rat Schwann cells were co-cultured with guinea pig enteric neurons, their DNA synthesis rate was reduced compared with control cultures of pure Schwann cells or Schwann cells not close to neurites or neuronal cell bodies. Nevertheless, in accordance with previous findings that sensory neurons stimulate Schwann cell division, these Schwann cells increased their DNA synthesis rate when in contact with neurites from purified guinea pig or adult rat dorsal root ganglion neurons and on exposure to bovine axolemmal fractions. The enteric neurons also suppressed the DNA synthesis of enteric glia in co-cultures of purified enteric neurons and enteric glia, while bovine axolemma stimulated their DNA synthesis. These results indicate that a mitotic inhibitory signal is associated with enteric neurons and can exert its effect on both Schwann cells and enteric glia, and that enteric glia, like Schwann cells, are stimulated to divide by axolemmal fractions. It thus seems possible that during development glial cell numbers in the peripheral nervous system may be controlled by both positive and negative regulators of cell growth.

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