RepoMed (Medizinische Hochschule Hannover)
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Identifikation und Charakterisierung von IL-17 und IL-22 produzierenden Lymphozyten in Lungengewebe und bronchialen Lymphknoten bei CF-Patienten im Vergleich zu anderen terminalen Lungenerkrankungen
No full textSphingosine-1 Phosphate Lyase Regulates Sensitivity of Pancreatic Beta-Cells to Lipotoxicity.
No full textElevated levels of free fatty acids (FFAs) have been related to pancreatic beta-cell failure in type 2 diabetes (T2DM), though the underlying mechanisms are not yet fully understood. FFAs have been shown to dysregulate formation of bioactive sphingolipids, such as ceramides and sphingosine-1 phosphate (S1P) in beta-cells. The aim of this study was to analyze the role of sphingosine-1 phosphate lyase (SPL), a key enzyme of the sphingolipid pathway that catalyzes an irreversible degradation of S1P, in the sensitivity of beta-cells to lipotoxicity. To validate the role of SPL in lipotoxicity, we modulated SPL expression in rat INS1E cells and in human EndoC-βH1 beta-cells. SPL overexpression in INS1E cells (INS1E-SPL), which are characterized by a moderate basal expression level of SPL, resulted in an acceleration of palmitate-mediated cell viability loss, proliferation inhibition and induction of oxidative stress. SPL overexpression affected the mRNA expression of ER stress markers and mitochondrial chaperones. In contrast to control cells, in INS1E-SPL cells no protective effect of oleate was detected. Moreover, Plin2 expression and lipid droplet formation were strongly reduced in OA-treated INS1E-SPL cells. Silencing of SPL in human EndoC-βH1 beta-cells, which are characterized by a significantly higher SPL expression as compared to rodent beta-cells, resulted in prevention of FFA-mediated caspase-3/7 activation. Our findings indicate that an adequate control of S1P degradation by SPL might be crucially involved in the susceptibility of pancreatic beta-cells to lipotoxicity
Detailed Revision Risk Analysis after Single- vs. Two-Stage Revision Total Knee Arthroplasty in Periprosthetic Joint Infection: a Retrospective Tertiary Center Analysis
No full textPeriprosthetic joint infection (PJI) remains one of the most common causes of revision knee arthroplasty. Controversy continues to surround the proper operative technique of PJI in knee arthroplasty with single- or two-stage replacement. Significant variations are seen in the eradication rates of PJI and in implant survival rates. This detailed retrospective analysis of a single tertiary center is intended to provide further data and insight comparing single- and two-stage revision surgery. A retrospective analysis of all revision total knee arthroplasty (TKA) surgeries from 2013 to 2019 was performed and screened with respect to single- or two-stage TKA revisions. Single- and two-stage revisions were analyzed with regard to implant survival, revision rate, microbiological spectrum, and other typical demographic characteristics. A total of 63 patients were included, with 15 patients undergoing single-stage revision and 48 patients undergoing two-stage revision. The mean follow-up time was 40.7 to 43.7 months. Statistically, no difference was found between both groups in overall survival (54.4% vs. 70.1%, p = 0.68) and implant survival with respect to reinfection (71.4% vs. 82.4%, p = 0.48). Further, high reinfection rates were found for patients with difficult-to-treat organisms and low- to semi-constrained implant types, in comparison to constrained implant types. A statistically comparable revision rate for recurrence of infection could be shown for both groups, although a tendency to higher reinfection rate for single-stage change was evident. The revision rate in this single-center study was comparably high, which could be caused by the high comorbidity and high proportion of difficult-to-treat bacteria in patients at a tertiary center. In this patient population, the expectation of implant survival should be critically discussed with patients
Neue PET Tracer für das Fibroblasten-Aktivierungs-Protein α und Evaluierung neuer PET Tracer für die Identifikation bakterieller Infektion
No full textDie osteosynthetische Stabilisierung periprothetischer Humerusfrakturen des Typs Worland C: eine biomechanische Analyse
No full textWeb-based survey among animal researchers on publication practices and incentives for increasing publication rates
No full textObjectives Publication bias, non-publication, and selective reporting of animal studies limit progress toward the 3Rs (Replacement, Reduction, and Refinement) that guide ethical animal testing, waste public resources, and result in redundant research, which collectively undermine the public's trust in scientific reliability. In this study, we aimed to 1) validate findings from a previous follow-up study by our team that examined the publication rates of animal studies from protocol to publication and 2) identify incentives for improving publication rates in animal research. Methods The researchers responsible for the animal proposals (n = 210) from our previous study were contacted as participants for a Web-based survey between October 2019 and April 2020. Question types varied between free text questions, answer options based on a 5-point Likert scale and closed yes/no questions. Results In total, 78 researchers responsible for 101 of 210 animal study proposals participated, yielding a response rate of 48.1%. Results showed that the publication rate increased from 67% in our follow-up study to 70%. According to a 5-point Likert scale (from 1 = "not relevant" to 5 = "extremely relevant"), the most widely accepted suggestions for increasing publication rates were "Publication costs for open access journals are fully covered by funders or universities" (mean 4.02, SD 1.01), "Performance-based allocation of intramural funds for results reporting of animal research not supporting the initial hypothesis (including preprints and repositories)" (mean 3.37, SD 1.05), and "Researchers receive more information from scientific journals that also publish non-significant results" (mean 3.30, SD 1.02). Conclusion While the extent of publication and publication practices have been thoroughly investigated for clinical trials, less data is available for animal research to date. Therefore, the study contributes in complementing the picture of publication practice in animal research. Suggestions from our survey may help improve the publication rates of animal studies
CO2 permeability of the rat erythrocyte membrane and its inhibition.
No full textWe have studied the CO2 permeability of the erythrocyte membrane of the rat using a mass spectrometric method that employs 18 O-labelled CO2. The method yields, in addition, the intraerythrocytic carbonic anhydrase activity and the membrane HCO3- permeability. For normal rat erythrocytes, we find at 37 °C a CO2 permeability of 0.078 ± 0.015 cm/s, an intracellular carbonic anhydrase activity of 64,100, and a bicarbonate permeability of 2.1 × 10-3 cm/s. We studied whether the rat erythrocyte membrane possesses protein CO2 channels similar to the human red cell membrane by applying the potential CO2 channel inhibitors pCMBS, Dibac, phloretin, and DIDS. Phloretin and DIDS were able to reduce the CO2 permeability by up to 50%. Since these effects cannot be attributed to the lipid part of the membrane, we conclude that the rat erythrocyte membrane is equipped with protein CO2 channels that are responsible for at least 50% of its CO2 permeability
