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November 01 - November 30

9 entries found

Start date: November 06
End date:  - November 08
09:30 am 12:00 pm



Additive Manufacturing

Drug Delivery-Systeme

Calciumphosphate und SFB/TR 79

In vivo-Testung

In vitro-Testung/Tissue Engineering

International Session with the Polish BiomaterialSociety and SFB/TR67

Metallische Biomaterialien

Polymere Biomaterialien I /Scaffolds

Polymere Biomaterialien II

Workshop Biomaterialien in der chirurgischen Anwendung

Young Scientists Forum

Start date: November 07
11:00 am 12:00 pm


Scientific discoveries for improvement of human health must be translated into practical applications. Such discoveries typically begin at “the bench” with basic research, then progress to the clinical level. For this reason animal models should reproduce the clinical manifestation of the disease, standardize the injury, so that effects can be detected in a  shorter time with a smaller number of cases. A useful animal model of a human condition not only has to reproduce some aspect of that condition but also has to offer advantages over direct clinical observation and experiment. These advantages usually include the ability to obtain proof-of-principle experience with less concern for the safety of the patient, the ability to use more invasive measures to investigate the effects of treatment, and the ability to standardize the injury, so that effects can be detected in a shorter time with a smaller number of cases. The advances made so far with the benefit of animal models have been primarily in understanding the cell biology of the injured nervous system. The central nervous system (CNS) is characterized by an intrigated response repertoire named “neuroinflammation”, which enables it to cope with pathogens, toxins, traumata and degeneration. This inflammatory response is characterized by increased glial activation, proinflammatory cytokine concentration, blood-brain-barrier permeability and leukocyte invasion. The inflammatory reactions in the CNS that are based on response to neuronal activity are called with the term of “neurogenic neuroinflammation”. This state regulates homeostasis to  enable the CNS to cope with enhanced metabolic demands and increases the computational power and plasticity of CNS neuronal networks.
In this context animal models have been employed to study the pathophysiology of neurological diseases such as Major Depressive Disorders (MDD), Traumatic Brain Injury (TBI) and Spinal Cord Injury (SCI). Animal models of depression aim to reproduce specific cardinal symptoms of MDD and are used to study the biological mechanisms that engender the human pathology. The main limitation of these animal models is that they may not accurately reflect the mechanisms underlying MDD and, as a result, may not accurately model the biological bases of MDD in humans. Spinal cord injury is a highly debilitating pathology. Although innovative medical care has improved patient outcome, advances in pharmacotherapy for the purpose of limiting neuronal injury and promoting regeneration have been limited. The primary traumatic mechanical injury to the spinal cord causes the death of a number of neurons that cannot be recovered and regenerated. The events that characterize this successive phase to mechanical injury are called “secondary damage.”
The secondary damage is determined by a large number of cellular, molecular, and biochemical cascades. Traumatic brain injury is a leading cause of death and disability worldwide, especially in the industrialized countries. The diagnosis of TBI includes a broad range of short- and long-term physical, cognitive, and emotional impairments, depending on the severity of the injury. TBI are used to elucidate primary and secondary sequelae underlying human head injury in an effort to identify potential neuroprotective therapies for developing and adult brains. The choice of experimental model depends upon both the research goal and underlying objectives. The intrinsic ability to study injury-induced changes in behavior, physiology, metabolism, the blood/tissue interface, the blood brain barrier, and/or inflammatory- and immune-mediated responses, makes in vivo TBI models essential for neurotrauma research. Whereas human TBI is a highly complex multifactorial disorder, animal trauma models tend to replicate only single factors involved in the
pathobiology of head injury using genetically well-defined inbred animals of a single sex.

A nonpeptidyl mimic of superoxide dismutase with therapeutic activity in rats. Salvemini D, Wang ZQ, Zweier JL, Samouilov A, Macarthur H, Misko TP, Currie MG, Cuzzocrea S, Sikorski JA, Riley DP. Science. 1999; 286(5438):304-6. I.F. 28,103

SOD mimetics are coming of age. Salvemini D, Riley DP, Cuzzocrea S. Nat Rev Drug Discov. 2002; 1(5):367-74. Review. I.F. 28,690

A nonpeptidyl mimic of superoxide dismutase, m40403, inhibits dose-limiting hypotension associated with interleukin-2 and increases its antitumor effects Samlowski WE, Petersen R, Cuzzocrea S, Macarthur H, Burton D, McGregor JR, Salvemini D. Nat Med. 2003 Jun;9(6):750-5. I.F. 27,553

Selective N-acylethanolamine-hydrolyzing acid amidase inhibition reveals a key role for endogenous palmitoylethanolamide in inflammation. Solorzano C, Zhu C, Battista N, Astarita G, Lodola A, Rivara S, Mor M, Russo R, Maccarrone M, Antonietti F, Duranti A, Tontini A, Cuzzocrea S, Tarzia G, Piomelli D. Proc Natl Acad Sci U S A. 2009 Dec 8;106(49):20966-71. I.F. 9.681

Traumatic brain injury: oxidative stress and neuroprotection.Cornelius C, Crupi R, Calabrese V, Graziano A, Milone P, Pennisi G, Radak Z, Calabrese EJ, Cuzzocrea S. Antioxid Redox Signal. 2013 Sep 10;19(8):836-53. doi: 10.1089/ars.2012.4981. I.F. 7.667

Start date: November 10
04:00 pm 05:00 pm


If you want to talk to the speaker, please contact Andrea Meinhardt (Andrea.Meinhardt@crt-dresden.de). Everybody is welcome! Abstract

My laboratory is interested in the mechanisms which govern homeostasis and prevent inflammation in host organs such as the liver and the intestine. Of particular interest to our studies is the role of parenchymal cells as non-professional antigen-presenting cells in the regulation of innate and adaptive immunity. As such, we could demonstrate that hepatocytes and intestinal epithelial cells can present lipid antigens via the non-classical MHC class I molecule CD1d to natural killer T cells thus providing the basis for protection from infectious hepatitis as well as intestinal inflammation (Zeissig et al., Nat. Med. 2012; Olszak et al., Nature 2014). Furthermore, this work revealed an essential role of the commensal microbiota and microbiota-derived lipid antigens in the control of homeostasis at mucosal surfaces and demonstrated that primary defects in lipid antigen presentation are associated with immunodeficiency in humans (An et al., Cell 2014; Olszak et al., Science 2012; Zeissig et al., J. Clin. Invest.; Zeissig et al., Nat. Immunol. 2014). Current work in the laboratory is focused on the identification of lipid antigens which link metabolism and immunity in the liver and the intestine. Further, we are investigating the role of inflammation-associated pathways in the intestinal epithelium and their contribution to microbiota-dependent intestinal stem cell function and the control of inflammation, regeneration, and carcinogenesis.



An D, Oh SF, Olszak T, Neves JF, Erturk-Hasdemir D, Lu X, Zeissig S, Blumberg RS, Kasper DL. Sphingolipids from a symbiotic microbe regulate homeostasis of host intestinal natural killer T cells. Cell. 2014 Jan 16;156(1-2): 123-33.

Olszak T, Neves JF, Dowds CM, Baker K, Glickman J, Davidson NO, Lin CS, Jobin C, Brand S, Sotlar K, Wada K, Katayama K, Nakajima A, Mizuguchi H, Kawasaki K, Nagata K, Müller W, Snapper SB, Schreiber S, Kaser A, Zeissig S*, Blumberg RS*.  Protective mucosal immunity mediated by epithelial CD1d and IL-10. Nature. 2014 May 22;509(7501):497-502.  (*co-senior authors)

Olszak T, An D, Zeissig S, Vera MP, Richter J, Franke A, Glickman JN, Siebert R, Baron RM, Kasper DL, Blumberg RS. Microbial exposure during early life has persistent effects on tissue-associated iNKT cells and their function. Science. 2012 Apr 27;336(6080):489-93.

Zeissig S, Dougan SK, Barral D, Junker Y, Chen Z, Kaser A, Ho M, Mandel H, McIntyre A, Kennedy SM, Painter, GF, Veerapen N, Besra GS, Cerundolo V, Yue S, Beladi S, Behar SM, Chen X, Gumpertz JE, Breckpot K, Raper A, Baer A, Exley MA, Hegele RA, Cuchel M, Rader DJ, Davidson NO, Blumberg RS, Primary deficiency of microsomal triglyceride transfer protein in human abetalipoproteinemia is associated with loss of CD1 function. J Clin Invest. 2010 Aug 2;120(8):2889-99.

Zeissig S, Blumberg RS. Life at the beginning: perturbation of the microbiota by antibiotics in early life and its role in health and disease. Nat. Immunol. 2014 Mar 19; 15(4): 307-10.

Zeissig S, Murata M, Sweet L, Publicover J, Hu Z, Kaser A, Bosse E, Iqbal J, Hussain MM, Balschun K, Röcken C, Arlt A, Günther R, Hampe J, Schreiber S, Baron JL, Moody DB, Liang JT, Blumberg RS. Hepatitis B virus-induced alterations in hepatocyte CD1d lipid antigens activate natural killer T cells and contribute to protective immunity. Nat. Med. 2012. Jul;18(7):1060-8. 

Neue Therap..
Start date: November 12
10:00 am 11:30 am


Osteoporose ist eine Knochenkrankheit, die 40% aller Frauen, aber auch jeden  5. Mann trifft. Deutschlandweit leiden mehr als sieben Millionen Menschen an dieser Krankheit - Tendenz steigend. Die Knochen der Osteoporose-Patienten sind weniger dicht und instabiler, wodurch sie leichter brechen können. Vor allem ältere Mitbürger leiden zusätzlich an häufigen Stürzen als Folge der nachlassenden Muskelkraft, eines eingeschränkten Gleichgewichtssinns oder Sehvermögens. Knochenbrüche der Unter- und Oberarmknochen oder der Hüfte können die Folge sein.
In diesem Vortrag stellt Ihnen Professor Lorenz Hofbauer, Bereichsleiter für Endokrinologie, Diabetes und Knochenerkrankungen an der Medizinischen Klinik III des Universitätsklinikum Carl-Gustav-Carus Dresden, sowohl neue Behandlungsmöglichkeiten für Osteoporose als auch vorbeugende Maßnahmen  vor.

Start date: November 13
09:20 am 10:20 am

Start date: November 14
11:00 am 12:00 pm


Dr. Nishikawa about his research and talk: A large gap has existed in our understanding of the course of differentiation from mesoderm to definitive hematopoietic stem cells (HSCs). Through 10 year research in CDB, now we are able to explain all details of this process in which a round of decision makings, migrations, and tissue organizations take place. I will show that this process proceed through four distinct intermediate stages that we named ETV2-primed mesoderm, hemoangiogenic mesoderm, hemogenic angioblasts, and hemogenic endothelial cells. Our results contradict to a previous notion that hematopoiesis in the yolk sac and embryo proper are derived from distinct subset, but I hope that the results are enough to convince the new scenario.

Publications related to his talk:

1) Tanaka Y, Sanchez V, Takata N, Yokomizo T, Yamanaka Y, Kataoka H, Hoppe PS, Schroeder T, Nishikawa S. (2014), Circularion-independent differentiation pathway from extraembryonic mesoderm toward hematopoietic stem cells via hemogenic angioblasts. Cell Rep. 10: 31-39.

2) Jakt L.M. Moriwaki S, Nishikawa S. (2013). A continuum of transcriptional identities visualized by combinatorial fluorescent in situ hybridization. Development 140:216-25.

3) Tanaka Y, Hayashi M, Kubota Y, Nagai H, Sheng G, Nishikawa S, Samokhvalov M. I. 2012. Early ontogenic origin of the hematopoietic stem cell lineage. Proc Natl Acad Sci USA 109:4515-20.

4) Kataoka Hiroshi, Hayashi Misato, Nakagawa Reiko, Tanaka Yosuke, Izumi Naoki, Nishikawa Satomi, Jakt Lars Martin, Tarui Hiroshi, Nishikawa Shinichi, (2011). Etv2/ER71 induces vascular mesoderm from Flk1+PDGFR{alpha}+ primitive mesoderm. Blood. 118: 6975-6986.

5) Samokhvalov, I.M., N.I. Samokhvalova, and S.I. Nishikawa. 2007. Cell tracing shows the contribution of the yolk sac to adult haematopoiesis. Nature 446: 1056-1061.

Molecular P..
Start date: November 20
04:30 pm 05:30 pm

Mechanical ..
Start date: November 21
11:00 am 12:00 pm


For the analysis, diagnosis and medical treatment of cardiovascular diseases there exists a large interest in information regarding the patient-specific distributions of mechanical fields such as stress and strain even at the microscale. In this context computational simulations can help to provide this data on the basis of numerical calculations. In this presentation different aspects are discussed which play an important role in describing the complex mechanical behavior of arterial walls under physiological and supra-physiological loading conditions. These include the analysis of convexity conditions to arrive at a mathematically sound description of the incompressible anisotropic and highly nonlinear material behavior. In particular for supra-physiological loading situations, e.g. when an artery is massively overstretched during balloon-angioplasty, a model taking into account microscopic damage is presented which is based on statistical distributions of microscopic properties.
For the prediction of an eventual rupture of arterial tissues, which may particularly be important in e.g. aneurysms, a framework for the optimal quantification of uncertainties is proposed. Finally, large-scale calculations of patient-specific arterial geometries will be presented.

T. Schmidt, D. Balzani, and G.A. Holzapfel. Statistical approach for a micromechanically based continuum description of damage evolution in soft collagenous tissues. Computer Methods in Applied Mechanics and Engineering, 278:41–61, 2014.

D. Kardas, U. Nackenhorst, and D. Balzani. Computational model for the cell-mechanical response of the osteocyte-cytoskeleton based on self-stabilizing tensegrity structures. Biomechanics and Modeling in Mechanobiology, 12:167–183, 2013.

D. Balzani, D. Böse, D. Brands, R. Erbel, A. Klawonn, O. Rheinbach, and J. Schröder. Parallel simulation of patient-specific atherosclerotic arteries for the enhancement of intravascular ultrasound diagnostics. Engineering Computations, 29(8), 2012.

D. Balzani, S. Brinkhues, and G.A. Holzapfel. Constitutive framework for the modeling of damage in collagenous soft tissues with application to arterial walls. Computer Methods in Applied Mechanics and Engineering, 213–216:139–151, 2012.

D. Balzani and M. Ortiz. Relaxed incremental variational formulation for damage at large strains with application to fiber-reinforced materials and materials with truss-like microstructures. Computer Methods in Applied Mechanics and Engineering, 92:551–570, 2012.

Start date: November 28
04:00 pm 05:00 pm


Many patterns during development result from the function of morphogens, which based on their concentration gradient, provide qualitative information to cells, leading to activation of different cellular programs. Fibroblast Growth Factor 8 (Fgf8) is one such morphogen which mediates patterning during early embryonic development. Formation of the gradient involves transport of Fgf8 through the extracellular matrix by free diffusion but additional mechanisms regulating transport and distribution are not very clear. Using the single molecule method of Fluorescence Correlation Spectroscopy, we studied the interaction of Fgf8 with components of the extracellular matrix, namely Heparan Sulfate Proteoglycans (HSPGs) in different compartments of a zebrafish embryo. We first identified specific HSPGs which affect Fgf signaling by directly binding to it in the extracellular matrix. This interaction resulted in a reduced extracellular diffusion of Fgf8 and also affected its gradient distribution. Additionally we could show that Fgf8 – Fgf-receptor interaction is not influenced by extracellular binding, but requires HSPGs which are attached on the cell membrane. Together we propose a mechanism of spatial regulation of Fgf8 transport by transient extracellular binding, which is essential for its gradient formation and distribution.

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