2020 Proceedings of the 3rd International Conference on Trauma Surgery Technology in Giessen

The 3 rd event of the Giessen International Conference on Trauma Surgery Technology on October, the 17th 2020 was hosted on Zoom in accordance with the worldwide corona situation. Dr Mieczakowski, Dr Yu, and Wolfram drafted in 2018 from Jan’s apartment in Bremen the manuscript which was submitted to and approved for funding by the Deutsche Forschungsgemeinschaft (DFG). At that time, we had no idea what substantial changes the conferencing concept would require. This is why we would like to thank again Michele. She first planned this year’s event after the 2019 date and then in the spring of 2020 had to replan for the new situation

Synergy between TLR-2 and TLR-3 signaling in primary human nasal epithelial cells

Although we have a detailed understanding of how single microbial derived triggers activate specialized Toll-like receptors (TLR) on airway epithelial cells, we know little of how these receptors react in a more complex environment. In everyday life, nasal epithelial cells are exposed to multiple TLR agonists, therefore we explored whether exposure to one trigger could affect the responsiveness to another TLR trigger. Primary nasal epithelium from healthy individuals and the bronchial epithelium cell line NCI-H292 were exposed in vitro to different TLR specific agonists. The effect on the expression of different TLRs was determined using the q-PCR. We also evaluated the effect of TLR-3 stimulation on TLR-2, functionally using ELISA to determine levels of secreted mediators. Stimulation of airway epithelial cells with a specific TLR agonist affects gene expression of other TLRs. In primary nasal epithelium, poly(I:C) challenge results in an up-regulation of the TLR-1, TLR-2, and TLR-3 genes and reduction of expression of TLR-5. Poly(I:C) induced activation of TLR-2 contributes to stronger cell responses to a TLR-2 agonist and regulation of these synergistic responses may take place at the mRNA level of IL-6 and IL-8. The effect of TLR-3 stimulation on TLR-2 functionality and most of the effects on the expression of other TLRs could be replicated in NCI-H292. Poly(I:C) failed to up-regulate TLR-1 and showed an additional up-regulation of TLR-4. Our data suggest that to better understand TLR mediated innate responses we need to consider the impact of the presence of multiple trigger

Rating supplements and dispensing of food supplements / / in pregnant women in selected pharmacies in 2006 and 2007

The selective abstrakt: Rigorous work The classification supplementary and dispensation of feed supplement for gravid women from selected pharmacy in the years 2006 and 2007 treat of suitability for supplementary usage during gravidity. In this work I also evaluate individual supplement`s for gravidity period that are used in the years 2006 and 2007 in the Czech market. Result of my rigorous work is recommendation for give priority to healthy and mixed fare during gravidity before vitamin supplement. This kind of recommendation is valid just for normal physiological conditions for all kinds of vitamins and minerals except of folic acid that they shoud be used before planned pregnacy. The products Centrum materna, Calibrum mami or Calibrum babyplan I can recommend each time if they have incomplete nutritive-supply

EGR-1 and DUSP-1 are important negative regulators of pro-allergic responses in airway epithelium

Background: Primary nasal epithelium of house dust mite allergic individuals is in a permanently activated inflammatory transcriptional state. Objective: To investigate whether a deregulated expression of EGR-1 and/or DUSP-1, two potential negative regulators of pro-inflammatory responses, could contribute to the activation of the inflammatory state. Methods: We silenced the expression of EGR-1 or DUSP-1 in the airway epithelial cell line NCI-H292. The cell lines were stimulated in a 24-h time course with the house dust mite allergen or poly(I:C). RNA expression profiles of cytokines were established using q-PCR and protein levels were determined in supernatants with ELISA. Results: The shRNA-mediated gene silencing reduced expression levels of EGR-1 by 92% (p <0.0001) and of DUSP-1 by 76% (p <0.0001). Both mutant cells lines showed an increased and prolonged response to the HDM allergen. The mRNA induction of IL-6 was 4.6 fold (p = 0.02) and 2.4 fold higher (p = 0.01) in the EGR-1 and DUSP-1 knock-down, respectively when compared to the induced levels in the control cell line. For IL-8, the induction levels were 4.6 fold (p = 0.01) and 13.0 (p = 0.001) fold higher. The outcome was largely similar, yet not identical at the secreted protein levels. Furthermore, steroids were able to suppress the poly(I:C) induced cytokine levels by 70-95%. Conclusions: Deregulation of EGR-1 and/or DUSP-1 in nasal epithelium could be responsible for the prolonged activated transcriptional state observed in vivo in allergic disease. This could have clinical consequences as cytokine levels after the steroid treatment in EGR-1 or DUSP-1 knock-down remained higher than in the control cell line. (C) 2015 Elsevier Ltd. All rights reserve

High degree of overlap between responses to a virus and to the house dust mite allergen in airway epithelial cells

Airway epithelium is widely considered to play an active role in immune responses through its ability to detect changes in the environment and to generate a microenvironment for immune competent cells. Therefore, besides its role as a physical barrier, epithelium affects the outcome of the immune response by the production of various pro-inflammatory mediators. We stimulated airway epithelial cells with viral double stranded RNA analogue poly(I:C) or with house dust mite in a time course of 24 hours. In order to determine cytokines production by stimulated cells, we performed multiplex enzyme linked immunosorbant assay (ELISA). We demonstrate that the temporal pattern of the genes that respond to virus exposure in airway epithelium resembles to a significant degree their pattern of response to HDM. The gene expression pattern of EGR1, DUSP1, FOSL1, JUN, MYC, and IL6 is rather similar after viral (poly(I:C)) and HDM exposure. However, both triggers also induce a specific response (e.g. ATF3, FOS, and NFKB1). We confirmed these data by showing that epithelial cells produce a variety of similar mediators in response to both poly(I:C) and HDM challenge (IL1-RA, IL-17, IFN-α and MIP1-α), sometimes with a quantitative difference in response (IL2-R, IL-6, IL-8, MCP-1, MIG, and HGF). Interestingly, only four mediators (IL-12, IP-10, RANTES and VEGF) where up-regulated specifically by poly(I:C) and not by HDM. Additionally, we report that pre-exposure to HDM deregulates production of cytokines and mediators in response to poly(I:C). Epithelial cells responses to the HDM-allergen and a virus strongly resemble both in gene expression and in protein level explaining why these two responses may affect each othe

The endocrine function of adipose tissue and its importance for initiation and development of insulin resistance and diabetes

Endocrine production of adipose tissue is a very complex process affected by numerous endogenous and exogenous stimuli. Peroxisome proliferator-activated receptors-alpha (PPAR-) are important modulators of metabolic processes which can also affect endocrine function of adipose tissue. Recently, numerous novel factors produced by adipose tissue with important metabolic effects were identified. Some of them can directly bind PPAR receptors. One of the examples of these factors is fatty acid binding protein 4 (FABP4) which can directly bind PPAR receptors and indirectly modify its activation by changing availability of endogenous PPAR ligands -free fatty acids. We hypothesized that the mechanism of action of PPAR receptors to metabolic processes may partially lie in their complex interaction with adipose tissue-derived hormones. The unraveling of these interactions may have important consequences in finding approaches to treat patients with type 2 diabetes mellitus. (...) In summary, our data show an important role for the interplay of PPAR activation and endocrine function of adipose tissue in metabolic regulations which may have important clinical consequences