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    Die Auswirkungen der ersten COVID-19-Welle auf die medizinische Versorgung in dermatologischen Praxen

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    Serum levels of C-terminal peptides of alpha-1 antitrypsin as potential biomarkers in non-small cell lung cancer

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    Background: Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related mortality worldwide. Alpha-1 antitrypsin (AAT) has been identified as a prognostic factor for lung cancer survival. Proteolytic cleavage of AAT by specific enzymes generates C-terminal peptides with varying lengths and biological activities. So far, the role of these peptides in NSCLC progression and prognosis remains unexplored. In this study, we aim to investigate the prognostic potential of AAT peptides in patients with NSCLC. Methods: Serum levels of the 9 peptides (C22, C36, C37, C39, C40, C42, C43, C44 and C45) were simultaneously quantified using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Correlations between peptide levels and full-length AAT protein, clinical parameters, and patient outcomes were analyzed. Additionally, the potential of these peptides as prognostic markers was evaluated, and changes in the AAT-to-peptide ratio were assessed in relation to tumor progression. Results: Peptides C36, C37, and C42 showed the highest levels and strong correlations with each other, AAT, a precursor of these peptides, and a trend-level association with C-reactive protein (CRP) levels. Notably, peptide levels were significantly associated with smoking status. In a multivariate Cox hazard model, C42 emerged as an independent prognostic factor for overall survival when combined with clinical parameters. Following surgical tumor resection, the concentrations of these peptides increased, along with their ratio to AAT, suggesting a tumor-related impact on AAT levels and its peptide generation. Conclusions: Our study highlights the potential prognostic value of AAT-derived peptides in NSCLC. Among the analyzed peptides, C36, C37, and C42 showed the strongest correlations with full-length AAT, and their levels were affected by smoking status. Notably, C42 emerged as an independent prognostic marker for overall survival

    Factors Affecting the Efficacy of Airflowing in Cleaning Implant Surfaces in a Surgical Peri‐Implantitis Treatment Simulation—A Laboratory Study

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    Objective To evaluate, in a simulation of surgical peri-implantitis treatment, the impact of type of handpiece, device settings, and instrumentation time on the efficacy of airflowing in cleaning the implant surface, depending on the type of bone defect and implant surface. Methods Turned and modified surface implants (54 each) were coated with biofilm imitation and mounted on resin models replicating purely horizontal or circumferential intraosseous peri-implant defects (both 5 mm deep). Implants were instrumented with an airflowing device using a supra- or submucosal handpiece, with three settings: (a) power 5, 5 s (b) power 10, 5 s, and (c) power 5, 15 s per implant/defect sextant. Results The amount of residual biofilm imitation was associated with defect configuration, type of handpiece, and device settings (p  5% residual biofilm imitation and 23 of 54 implants were completely clean; with the submucosal handpiece, 12 of 18 implants showed ≤ 5% residual biofilm imitation when used for 15 s/sextant, yet none were completely clean. In intraosseous defects, all implants presented ≤ 5% residual biofilm imitation and 10 of 18 implants were completely clean with the submucosal handpiece used for 15 s/sextant; the supramucosal handpiece was largely inefficacious. Conclusion Within the limitations of this laboratory study, peri-implant bone defect configuration should dictate the choice of airflowing handpiece (i.e., for horizontal defects, the supramucosal handpiece; for intraosseous defects, the submucosal handpiece) and intrasurgical airflowing requires a prolonged instrumentation time, but not increased power

    CCC-News: Newsletter des CCC Niedersachsen, Ausgabe 1/2025

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    Replication genotyping and functional follow-up of OSGIN1 in cervical cancer

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    Effekte von Histamin und IL-4 auf humane T-Zellen und Makrophagen

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    Interplay between noise-induced sensorineural hearing loss and hypertension: pathophysiological mechanisms and therapeutic prospects

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    More than 5% of the global population suffers from disabling hearing loss, primarily sensorineural hearing loss (SNHL). SNHL is often caused by factors such as vascular disorders, viral infections, ototoxic drugs, systemic inflammation, age-related labyrinthine membrane degeneration, and noise-induced hearing loss (NIHL). NIHL, in particular, leads to changes in blood-labyrinth-barrier (BLB) physiology, increased permeability, and various health issues, including cardiovascular disease, hypertension, diabetes, neurological disorders, and adverse reproductive outcomes. Recent advances in neuromodulation and vector-based approaches offer hope for overcoming biological barriers such as the BLB in the development of innovative treatments. Computational methods, including molecular docking, molecular dynamics simulations, QSAR/QSPR analysis with machine/deep learning algorithms, and network pharmacology, hold potential for identifying drug candidates and optimizing their interactions with BLB transporters, such as the glutamate transporter. This paper provides an overview of NIHL, focusing on its pathophysiology; its impact on membrane transporters, ion channels, and BLB structures; and associated symptoms, comorbidities, and emerging therapeutic approaches. Recent advancements in neuromodulation and vector-based strategies show great promise in overcoming biological barriers such as BLB, facilitating the development of innovative treatment options. The primary aim of this review is to examine NIHL in detail and explore its underlying mechanisms, physiological effects, and cutting-edge therapeutic strategies for its effective management and prevention

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