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Patients in high dose groups had significantly lower rates for surgical or percutaneous intervention, recurrence of angina, and rehospitalization. K-M curve analysis also showed cumulative incidence freedom time of overall MACE in high dose groups was significantly longer. No significant differences were found among different drugs with the same doses. CONCLUSION Patients with higher doses had lower level of CK-MB, BNP, ALT, and TnI and lower occurrence of MACE after PCI. © 2020 Wiley Periodicals, Inc.OBJECTIVES/HYPOTHESIS To assess the ability of specific positron emission tomography/computed tomography (PET/CT) and magnetic resonance imaging (MRI) features to detect extracapsular extension (ECE) in head and neck squamous cell carcinoma (HNSCC) patients. STUDY DESIGN Retrospective study in a tertiary certified university cancer institute. METHODS We performed a review of patients with advanced HNSCC at Bern University Hospital between 2014 and 2018. Patients with pretherapeutic PET/CT and/or MRI who underwent neck dissection were included, with 212 patients fulfilling inclusion criteria. Blinded evaluation of specific PET/CT and MRI features with respect to presence of ECE was performed. Histopathological examination of neck dissection specimens was used as the gold standard to determine ECE status. RESULTS Out of the 212 included patients, 184 had PET/CT, 186 MRI, and 158 both modalities. Overall clinical stage IV (odds ratio [OR] 2.26, 95% confidence interval [CI] 2.25-11.74), ill-defined margins in both PET/CT and MRI (OR 3.48, 95% CI 1.21-9.98 and OR 2.14, 95% CI 0.94-4.89, respectively), and a maximum standardized uptake value ≥ 10 (OR 5.44, 95% CI 1.21-9.98) were all significant independent predictors of ECE. When combined, these four features led to a cumulative score able to predict ECE status with an accuracy of 91.43%. CONCLUSIONS The current findings indicate specific features in PET/CT and MRI are potential predictors of ECE status and may help in pretherapeutic stratification in HNSCC. LEVEL OF EVIDENCE 4 Laryngoscope, 2020. find more © 2020 The American Laryngological, Rhinological and Otological Society, Inc.Plasma exchange (PE) is performed for patients with autoimmune blistering diseases by using multiple vascular access routes. We retrospectively examined the safety and the efficacy of PE using direct femoral vein puncture (FVP) technique, by comparing with that using double-lumen catheter (DLC). The troubles related to vascular route, such as catheter occlusion, insufficient blood flow and hematoma, were not different between the FVP group (4.6%) and the DLC group (6.7%), whereas access-related infections occurred more frequently in the DLC group (6.7%) than the FVP group (0.4%). Regarding the efficacy, the removal rate of autoantibodies in PE using the FVP technique was similar or lower, as compared with that using the DLC. These results suggest that PE with the FVP technique is able to be performed safely in patients with autoimmune blistering diseases, although the removal of autoantibodies is not superior to that using the DLC. © 2020 Wiley Periodicals, Inc.Antibody-dependent complement activity is associated with autoimmune morbidity, but also anti-tumor efficacy. In infectious disease, both recombinant monoclonal antibodies and polyclonal antibodies generated in natural adaptive responses can mediate complement activity to protective, therapeutic, or disease-enhancing effect. Recent advances have contributed to the structural resolution of molecular complexes involved in antibody-mediated complement activation, defining the avid nature of participating interactions, and pointing to how antibody isotype, subclass, hinge flexibility, glycosylation state, amino acid sequence, and the contextual nature of the cognate antigen/epitope are all factors that can determine complement activity through impact on antibody multimerization and subsequent recruitment of C1q. Beyond the efficiency of activation, complement activation products interact with various cell types that mediate immune adherence, trafficking, immune education, and innate functions. Similarly, depending on the anatomical location and extent of activation, complement can support homeostatic restoration or be leveraged by pathogens or neoplasms to enhance infection or promote tumorigenic microenvironments, respectively. Advances in means to suppress complement activation by intravenous immunoglobulin (IVIG), IVIG mimetics, and complement-intervening antibodies represent proven and promising exploratory therapeutic strategies, while antibody engineering has likewise offered frameworks to enhance, eliminate, or isolate complement activation to interrogate in vivo mechanisms of action. Such strategies promise to support the optimization of antibody-based drugs that are able to tackle emerging and difficult-to-treat diseases by improving our understanding of the synergistic and antagonistic relationships between antibody mechanisms mediated by Fc receptors, direct binding, and the products of complement activation. This article is protected by copyright. All rights reserved.Chronic inflammation plays an important role in primary liver cancer (PLC) etiology and can be influenced by dietary habits. No prospective study has investigated the association of dietary inflammatory index (DII) with PLC incidence and mortality. Therefore, we used prospective data from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial to fill this gap. The DII was calculated from a validated 137-item food frequency questionnaire in a cohort of 103,902 individuals. Cox regression was used to estimate hazard ratios (HRs) for PLC incidence, and competing risk regression was used to estimate subdistribution HRs (SHRs) for PLC mortality. Restricted cubic spline regression was employed to identify the potential dose-response pattern. A total of 120 PLC cases and 102 PLC deaths were observed during follow-up. Higher DII scores from food and supplement were found to be associated with higher risks of developing PLC (HRTertile 3 vs. 1 2.05; 95% confidence interval [CI] 1.23-3.41) and death from this disease (SHRTertile 3 vs.