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Copyright of Spektrum der Augenheilkunde is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Die Dermatologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Zeitschrift für Rheumatologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Gynäkologische Endokrinologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Gliomas represent the most frequent malignant primary brain tumors in adults. Despite multimodal treatment concepts involving surgery, irradiation and chemotherapy, the prognosis remains poor and they are incurable. Recent insights into the interactions between the immune system and the central nervous system as well as breakthroughs in the results of other cancer types have led to the fact that various immunotherapeutic approaches against gliomas have also been investigated and in some cases specifically developed. Objective: This article provides an overview of the current status of different immunotherapeutic concepts against gliomas, highlighting the advantages, disadvantages, and challenges. Additionally, it provides an overview of currently ongoing immunotherapeutic clinical trials in Germany and neighboring countries. Results: Previous randomized studies on antibodies against programmed cell death protein 1 (anti-PD1) immune checkpoint inhibition, viral treatment and peptide vaccination targeting the variant III of the epidermal growth factor receptor (EGFRvIII) in glioblastomas were negative with respect to survival benefits. Conversely, other immunotherapeutic approaches, such as multivalent or driver mutation-based vaccinations, cytokine-based therapy and cell therapy, demonstrated a robust scientific foundation, with at least early studies showing promising safety and pharmacodynamic effects on the tumors. Discussion: Currently, immunotherapies against gliomas should only be applied within the framework of well-designed clinical studies. There are still many knowledge gaps regarding the mechanisms of action and resistance of various immunotherapies. Accompanying translational research is essential to address these gaps and develop more effective therapies. [ABSTRACT FROM AUTHOR]

Copyright of Wiener Klinisches Magazin is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Innere Medizin (2731-7080) is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Wiener Medizinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Zeitschrift für Gerontologie und Geriatrie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Der Granulozyten‐Kolonie‐stimulierende Faktor (G‐CSF) ist ein Zytokin, das zur Behandlung von Neutropenie eingesetzt wird. Unterschiedlich glykosylierte und nicht glykosylierte Varianten von G‐CSF werden für therapeutische Anwendungen derzeit durch rekombinante Expression hergestellt. Im Folgenden beschreiben wir unsere Herangehensweise zur Etablierung einer ersten Semisynthesestrategie für die Synthese des Aglykons und verschiedener O‐Glykoformen von G‐CSF, um die Herstellung von selektiv und homogen posttranslational modifizierten Varianten dieses wichtigen Zytokins zu ermöglichen. Letztendlich erreichten wir dies, durch die Selenoesterligation eines rekombinant hergestellten N‐terminalen Segments mit einem synthetisch hergestellten C‐terminalen Segment, welches vorübergehend mit einer lichtabspaltbaren Polyethylenglykol‐ (PEG) Gruppe an einer Seitenkette versehen wurde, bei niedrigen Konzentrationen. Die transiente PEGylierung ermöglichte dabei die quantitative enzymatische Verlängerung des Kohlenhydrates an Thr133. Insgesamt ist es uns gelungen, die Syntheseherausforderungen auf Grund der niedrigen Löslichkeit und der Aggregationstendenz der zwei Proteinsegmente, signifikant zu reduzieren. Dies ermöglichte uns die Herstellung von vier G‐CSF Varianten, die erfolgreich gefaltet wurden und in Zellproliferationsexperimenten biologische Aktivität zeigten. [ABSTRACT FROM AUTHOR]

Copyright of Der Schmerz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Interactions of the immune system and the nociceptive system play an important role in the generation and maintenance of pain in musculoskeletal diseases and in disease development. In inflamed tissue peripheral nociceptive neurons are rendered hyperexcitable by proinflammatory cytokines, antigen/antibody complexes and other immune mediators. Spinal nociceptive neurons are rendered hyperexcitable with the support of microglial cells, the immune cells of the central nervous system. The so-elicited sensitization of pain pathways has a strong impact on pain processing in the brain. On the other hand, immune processes are regulated by the nervous system. Sensory neurons, by releasing neuropeptides, and efferent neurons of the sympathetic nervous system support immune processes which promote disease development. [ABSTRACT FROM AUTHOR]

Copyright of Zeitschrift für Rheumatologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Best Practice Onkologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The immune system is an effective defense against invading pathogens and is accompanied by recruitment of immune cells and initiation of an inflammatory reaction. This can also be triggered by noninfectious stimuli, e.g. a large surgical intervention and cause severe tissue destruction and organ dysfunction. The organism cannot distinguish many stimuli that are released during a large surgical intervention from exogenous pathogens. Therefore, there is a high risk for the occurrence of systemic inflammatory reactions, particularly in large surgical interventions. This excessive immune response leads to release of proinflammatory cytokines, endothelial dysfunction, damage to the glycocalyx, activation of leukocytes as well as tissue and organ destruction. This article summarizes the molecular principles of the surgery-associated inflammatory reaction, the differentiation from other inflammatory complications and treatment options. [ABSTRACT FROM AUTHOR]

Copyright of Parodontologie: die Zeitschrift für die Praxis (Berlin, Germany) is the property of Quintessenz Verlags GmbH and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In this study, effects of dietary supplementation of dried tomato powder (DTP) and red pepper powder (DPP) on the antioxidant mechanisms, immune system, cytokines, egg production performance, and egg quality were investigated in a total of 90, 30-week-old hens. The study groups were fed on a diet containing 4% DTP and 4% DPP, respectively for 30 days, while the control group received a commercial laying hen feed. Egg production and egg quality parameters, differential leukocyte count, heterophil functions, serum cytokine, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), ascorbic acid, and glutathione peroxidase (GSH-Px) levels were measured. It was determined that serum tumor necrosis factor-alpha (TNF-α) levels increased (P = 0.018) and heterophil (P = 0.033) and monocyte (P = 0.020) percentages decreased in the DPP group compared to both control and DTP groups. In the same hens, serum transforming growth factor-beta (TGF-β) level (P = 0.029) and oxidative burst (P = 0.021) increased compared to the control group, but interleukin-4 (IL-4) (P = 0.014) level and SOD activity (P = 0.021) increased compared to the DTP group. Phagocytic activity was higher in the DTP group compared to other groups (P = 0.003). In addition, it was observed that serum catalase level (P = 0.008), and egg yolk colour (P = 0.001) increased in both experimental groups compared to the control group. It was concluded that DPP and DTP used in this study strengthen the antioxidant defence system, increase heterophil functions, and positively affect cytokine production and egg colour, so it can be used as a safe feed additive in chickens. [ABSTRACT FROM AUTHOR]

Copyright of Rheuma Plus is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Herz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In the present study the effect of inclusion of different levels of dietary Tenebrio molitor larvae meal (TM) as a dietary protein source on laying performance, egg quality, amino acid and fatty acid profile of egg yolk, haematological traits, cytokines, and faecal noxious gas emission was investigated in laying hen. One hundred and ninety-two 41 weeks old laying hens (Hy-Line Brown; average BW 1973 ± 28 g) with similar egg production were randomly divided into 4 treatments, including control (without TM), TM1 (1%), TM2 (2%), and TM3 (3%) with 6 replicates per treatment and 8 hens per replicate. The feeding study lasted 56 days. Yolk colour increased linearly when TM was added to the diet (P < 0.05). Concentration of yolk histidine was linearly increased as the TM level increased. An increase in the palmitoleic acid and oleic acid ratio of egg yolk (P < 0.01) and a linear increase in the ratio of linoleic acid were observed with increasing dietary TM levels. In addition, the a-linolenic acid content of egg yolk was quadratically affected (P < 0.05) by an increase in dietary TM. There was also a linear increase (P < 0.05) in total polyunsaturated fatty acid of egg yolk, however, total short-chain and monounsaturated fatty acids were not affected. A linear decrease was observed in the plasma concentration of IL-4 with increasing dietary levels of TM at week 4. Plasma IL-2 concentration decreased linearly (P < 0.01) with increasing dietary TM-levels at week 8. In conclusion, in this study dietary TM-supplementation induced no improvement in egg production but positively affected the egg quality by improving the yolk colour and increasing the yolk content of linolenic acid and unsaturated fatty acid. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Orofacial Orthopedics/Fortschritte der Kieferorthopadie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of German Journal of Sports Medicine / Deutsche Zeitschrift fur Sportmedizin is the property of Verein zur Forderung der Sportmedizin Hannover e.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Diabetologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

During the past few decades, cardiovascular research has increasingly focused on systemic inflammatory mechanisms, particularly in the field of atherosclerosis but also in association with cardiac arrhythmogenesis. Objective inflammatory markers including C‑reactive protein and cytokines, also called "biomarkers," seem to serve as predictors of onset and prognosis of cardiac arrhythmias. This review gives an overview of potential mechanisms underlying inflammatory processes and arrhythmias, especially atrial fibrillation, which is the most common sustained arrhythmia in daily clinical routine. The association between inflammatory pathways and cardiac arrhythmia is highly complex and includes direct as well as indirect pathways. While past research into arrhythmia focused on fibrosis, altered action potential properties, and ischemia, novel concepts include coagulation and inflammation in cardiac tissue. The underlying mechanisms are altered electrophysiological properties, including ion channel disturbance, early and late afterdepolarizations, as well as enhanced fibrosis and structural remodeling in cardiomyopathies. These pathophysiological factors favor the occurrence of ectopic pacemakers as well as re-entry tachycardia. Further studies are essential to better understand the main inflammatory signal cascades and the exact proarrhythmic effect of interacting key mediators. This will facilitate the evaluation of future anti-inflammatory therapeutic approaches for arrhythmias, analogous to recent developments in atherosclerosis. [ABSTRACT FROM AUTHOR]

Independent of the underlying cause, pulmonary hypertension (PH) remains a devastating condition that is characterized by limited survival. Cumulating evidence indicates that in addition to a dysbalance of mediators regulating vascular tone and growth factors promoting vascular remodeling, failure to resolve inflammation and altered immune processes play a pivotal role in the development and progression of PH. Here, we highlight the role of key inflammatory pathways in the pathobiology of vascular remodeling and PH, and discuss potential therapeutic interventions that may halt disease progression or even reverse pulmonary vascular remodeling. Perivascular inflammation is present in all forms of PH, and inflammatory pathways involve numerous mediators and cell types including macrophages, neutrophils, T cells, dendritic cells, and mast cells. Dysfunctional bone morphogenic protein receptor 2 (BMPR2) signaling and dysregulated immunity enable the accumulation of macrophages and other inflammatory cells in obliterative vascular lesions. Regulatory T cells (Tregs) were shown to be of particular relevance in the control of inflammatory responses. Key cytokines/chemokines include interleukin-6, functioning via classic or trans-signaling, macrophage migratory inhibitory factor (MIF), but also other mediators such as neutrophil-derived myeloperoxidase. The expanding knowledge on this topic has resulted in multiple opportunities for sophisticated therapeutic interventions. [ABSTRACT FROM AUTHOR]

Inflammation plays a central role in the development of heart failure, especially in heart failure with preserved ejection fraction (HFpEF). Furthermore, the inflammatory response enables the induction of regenerative processes following acute myocardial injury. Recent studies in humans and animals have greatly advanced our understanding of the underlying mechanisms behind these adaptations. Importantly, inflammation can have both beneficial and detrimental effects, dependent on its extent, localization, and duration. Therefore, modulation of cardiac inflammation has been suggested as an attractive target for the treatment of heart failure, which has been investigated in numerous clinical trials. This review discusses key inflammatory mechanisms contributing to the pathogenesis of heart failure and their potential impact as therapeutic targets. [ABSTRACT FROM AUTHOR]

Copyright of Der Schmerz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der MKG-Chirurg is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: Th2‐biasing CD1d ligands are attractive potential candidates for adjuvants and therapeutic drugs. However, the number of potent ligands is limited, and their biasing mechanism remain unclear. Herein, a series of novel Th2‐biasing CD1d glycolipid ligands, based on modification of their lipid part, have been identified. These have shown high binding affinities and efficient Th2 cytokine production. Importantly, the truncated acyl chain containing variants still retain their binding affinities and agonistic activities, which can be associated with an “anchoring effect,” that is, formation of a buried hydrogen bond between a polar group on the acyl chain and the CD1d lipid‐binding pocket. The analysis indicated that the appearance rates of ligand–CD1d complexes on the cell surface were involved in Th2‐biasing responses. The designed ligands, having the anchor in the shorter lipid part, are one of the most potent Th2‐biasing ligands among the known ligands. [ABSTRACT FROM AUTHOR]

Copyright of Monatsschrift Kinderheilkunde is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Ophthalmologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of HNO is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: For head and neck squamous cell cancer (HNSCC), standard therapy consists of surgery, radiation, and/or chemotherapy. Antineoplastic immunotherapy could be an option in an adjuvant setting and is already in palliation. A functional immune system is a prerequisite for successful immunotherapy. However, effects of the standard-of-care therapy on the patients' immune system are not fully understood.Methods: Peripheral blood mononuclear cells (PBMC) were collected from patients with HNSCC (n = 37) and healthy controls (n = 10). PBMC were stimulated with staphylococcal enterotoxin B (SEB). Simultaneous expression of various cytokines was measured in CD4+ and CD8+ T cells by multicolor flow cytometry, and polyfunctional cytokine expression profiles were determined on a single-cell basis.Results: Expression levels of all measured cytokines in CD4+ T cells were higher in patients after chemoradiotherapy (CRT) as compared to untreated HNSCC patients or normal controls. After CRT, the frequency of polyfunctional CD4+ T cells, which simultaneously expressed multiple cytokines, was significantly increased as compared to untreated patients (p < 0.01).Conclusion: CRT increases polyfunctionality of CD4+ T cells in HNSCC patients, suggesting that standard-of-care therapy can promote immune activity in immune cells. These polyfunctional CD4+ T cells in the blood of treated HNSCC patients are expected to be responsive to subsequent immunotherapeutic approaches. [ABSTRACT FROM AUTHOR]

Copyright of Der Hautarzt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Sepsis is a systemic inflammatory response usually correlated with multi-organ failure. Myocardial dysfunction is one of the adverse outcomes in septic patients and results in high mortality rates. The aim of this study was to investigate the impact of irbesartan in attenuation of cardiac depression during polymicrobial sepsis via decreased activation of the phospho-p38MAPK/nuclear factor (NF)-κB signaling pathway.Materials and methods: A model of polymicrobial sepsis induced via cecal ligation and puncture (CLP) with 8- to 12-week-old albino mice was used. Mice were treated with i.p. irbesartan (3 mg/kg) 1 h before CLP. Using a micro-tipped transducer catheter, the following hemodynamic parameters were evaluated after CLP: heart rate, ejection fraction, left ventricular (LV) end-diastolic pressure, LV systolic pressure, and cardiac output. Plasma levels of proinflammatory cytokines, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, monocyte chemoattractant protein-1 (MCP-1), and cardiac troponin I (cTn-I), were measured via ELISA analysis. The degree of p38MAPK and NF-κB phosphorylation was assessed via Western blotting.Results: Mice treated with irbesartan displayed improvement in LV function (ejection fraction: 42.4 ± 1.1% vs. 27.8 ± 3% in CLP mice). The attenuation of cardiac depression in irbesartan-treated mice was associated with lower levels of MCP-1 in plasma and a reduction in the levels of TNF-alpha, IL-1beta, and IL-6. Furthermore, irbesartan-treated mice displayed lower expression levels of p38-MAPK and NF-κB phosphorylation.Conclusion: Irbesartan can attenuate cardiac dysfunction during polymicrobial sepsis possibly via a reduction of proinflammatory cytokines through decreased activation of the p38MAPK/NF-κB pathways. [ABSTRACT FROM AUTHOR]