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Background: The healing of a bone injury is a highly complex process involving a multitude of different tissue and cell types, including immune cells, which play a major role in the initiation and progression of bone regeneration. Methods: We histologically analyzed the spatio-temporal occurrence of cells of the innate immune system (macrophages), the adaptive immune system (B and T lymphocytes), and bone cells (osteoblasts and osteoclasts) in the fracture area of a femoral osteotomy over the healing time. This study was performed in a bone osteotomy gap mouse model. We also investigated two key challenges of successful bone regeneration: hypoxia and revascularization. Results: Macrophages were present in and around the fracture gap throughout the entire healing period. The switch from initially pro-inflammatory M1 macrophages to the anti-inflammatory M2 phenotype coincided with the revascularization as well as the appearance of osteoblasts in the fracture area. This indicates that M2 macrophages are necessary for the restoration of vessels and that they also play an orchestrating role in osteoblastogenesis during bone healing. The presence of adaptive immune cells throughout the healing process emphasizes their essential role for regenerative processes that exceeds a mere pathogen defense. B and T cells co-localize consistently with bone cells throughout the healing process, consolidating their crucial role in guiding bone formation. These histological data provide, for the first time, comprehensive information about the complex interrelationships of the cellular network during the entire bone healing process in one standardized set up. With this, an overall picture of the spatio-temporal interplay of cellular key players in a bone healing scenario has been created. Conclusions: A spatio-temporal distribution of immune cells, bone cells, and factors driving bone healing at time points that are decisive for this process—especially during the initial steps of inflammation and revascularization, as well as the soft and hard callus phases—has been visualized. The results show that the bone healing cascade does not consist of five distinct, consecutive phases but is a rather complex interrelated and continuous process of events, especially at the onset of healing.

Background. Because of changes in gut physiology, immune system reactivity, and diet, elderly people are more susceptible to gastrointestinal infections than are younger adults. The gut microflora, which provides a natural defense against invading microorganisms, changes in elderly people with the development of potentially damaging bacterial populations, which may lead to alterations in bacterial metabolism and higher levels of infection. Methods. A randomized, double-blind, controlled feeding trial was done with 18 healthy elderly volunteers (age, >62 years) using a synbiotic comprising Bifidobacterium bifidum BB-02 and Bifidobacterium lactis BL-01 (probiotics) together with an inulin-based prebiotic (Synergy 1; Orafti). Real-time PCR was employed to quantitate total bifidobacteria, B. bifidum, and B. lactis in fecal DNA before, during, and after synbiotic consumption. Counting all viable anaerobes, bifidobacteria, and lactobacilli and identification of bacterial isolates to species level was also done. Results. Throughout feeding, both bifidobacteria species were detected in fecal samples obtained from all subjects receiving the synbiotic, with significant increases in the number of copies of the 16S rRNA genes of B. bifidum, B. lactis, and total bifidobacteria, compared with the control week and the placebo group. At least 1 of these species remained detectable in fecal samples 3 weeks after feeding in individuals that had no fecal B. bifidum and/or B. lactis in the control week, indicating that the probiotics persisted in the volunteers. Counting of viable organisms showed significantly higher total numbers of fecal bifidobacteria, total numbers of lactobacilli, and numbers of B. bifidum during synbiotic feeding. Conclusion. Synbiotic consumption increased the size and diversity of protective fecal bifidobacterial populations, which are often very much reduced in older people.

The intracellular location of the membrane-bound nitrite oxidoreductase of Nitrobacter hamburgensis X14 was determined by electron microscopic immunocytochemistry. Post-embedding labeling performed on ultrathin sections revealed that the enzyme was located at the cytoplasmic membrane and at the intracytoplasmic membranes. As shown by immunonegative staining of isolated membranes the labeling of the monoclonal antibodies named Hyb 153-2 and Hyb 153-3 was located at the cytoplasmic side of the membranes. Using Hyb 153-2, which recognize the α-subunit of nitrite oxidoreductase, the labeling was found at the surface of the paniculate membranes. In contrast, Hyb 153-3, recognizing the β-subunit of nitrite oxidoreductase, bound preferably at the periphery of the membrane fragments. Besides Nitrobacter, Hyb 153-3 also recognized the nitrite-oxidizing system in two strains of Nitrospira. No reaction was found with Nitrospina and Nitrococcus.

Abstract The intracellular location of the membrane-bound nitrite oxidoreductase of Nitrobacter hamburgensis X14 was determined by electron microscopic immunocytochemistry. Post-embedding labeling performed on ultrathin sections revealed that the enzyme was located at the cytoplasmic membrane and at the intracytoplasmic membranes. As shown by immunonegative staining of isolated membranes the labeling of the monoclonal antibodies named Hyb 153-2 and Hyb 153-3 was located at the cytoplasmic side of the membranes. Using Hyb 153-2, which recognize the α-subunit of nitrite oxidoreductase, the labeling was found at the surface of the paniculate membranes. In contrast, Hyb 153-3, recognizing the β-subunit of nitrite oxidoreductase, bound preferably at the periphery of the membrane fragments. Besides Nitrobacter, Hyb 153-3 also recognized the nitrite-oxidizing system in two strains of Nitrospira. No reaction was found with Nitrospina and Nitrococcus.

Der Band befasst sich mit Stand und Perspektiven von Fachkräften der Gesundheitswirtschaft in Berlin-Brandenburg, neuen Berufsbildern und Ausbildungsgängen und der Entwicklung und Einführung neuer Gesundheitsstudiengänge. (IAB) Inhaltsverzeichnis: I. Stand und Perspektive von Fachkräften in Berlin-Brandenburg Marion Hass, Stefanie Richter: Zur Fachkräftesituation in der Gesundheitswirtschaft in Berlin-Brandenburg. Eine Feldstudie der IHK; Stephan Padberg, Thomas Winschuh: Entwicklungstrends in der Berliner Gesundheitswirtschaft und ihre Folgen für Organisations- und Personalentwicklung; Anja Walter, Carsten Kampe, Markus Höhne: Branchenspezifische Fachkräftebedarfsanalysen als Instrument einer gestaltenden Arbeitsmarktpolitik in Berlin-Brandenburg am Beispiel der Gesundheitswirtschaft; Igor Koscak, Dennis Alexander Ostwald, Anja Ranscht: Methodische Überlegungen zur Realisierung eines Fachkräftemonitorings für die Gesundheitswirtschaft; II. Neue Berufsbilder und Ausbildungsgänge Tobias Funk: Gesundheit ist mehr - Berufsausbildungen im Bereich der Gesundheitswirtschaft; Lukas Schmid, Olaf Schenk, Jochen Sieper, Parwis Fotuhi: Entwicklungsoptionen im Bereich Pflege am Beispiel der Modularen Weiterbildung der HELIOS Kliniken; Neeltje van den Berg, Claudia Meinke, Adina Dreier, Wolfgang Hoffmann: Das Konzept AGnES. Unterstützung von Hausärzten in ländlichen Regionen; Karl Hartmann, Gunter Frenzel: Der Campus Berlin-Buch - Neue Wege der Aus- und Weiterbildung in der Gesundheitswirtschaft; III. Entwicklung und Einführung neuer Gesundheitsstudiengänge Karin Gavin-Kramer: Studium Gesundheit in Berlin und Brandenburg. Wie ein transdisziplinärer Führer entstehen kann; Georg Duda, Sabine Bartosch: Interdisziplinäre Graduiertenschule für Regenerative Therapien in Berlin-Brandenburg. Von der Grundlagenforschung zu neuen Behandlungsmethoden; Eva-Maria Neumann: Innovations- und Steuerfähigkeit im demografischen Wandel: Gerontologische Leitungsqualifikation für Gesundheits- und Sozialberufe durch den Masterstudiengang Gerontologie an der Fachschule Lausitz; Karsten Schulz: Kommunikation im Zentrum der Managementausbildung: Der MBA in Health Communication Management an der FHTW Berlin.

NLRP3 is a pattern recognition receptor with a well-documented role in inducing inflammasome assembly in response to cellular stress. Deregulation of its activity leads to many inflammatory disorders including gouty arthritis, Alzheimer disease, and cancer. Whereas its role in the context of cancer has been mostly explored in the immune compartment, whether NLRP3 exerts functions unrelated to immunity in cancer development remains unexplored. Here, we demonstrate that NLRP3 interacts with the ATM kinase to control the activation of the DNA damage response, independently of its inflammasome activity. NLRP3 down-regulation in both broncho- and mammary human epithelial cells significantly impairs ATM pathway activation, leading to lower p53 activation, and provides cells with the ability to resist apoptosis induced by acute genotoxic stress. Interestingly, NLRP3 expression is down-regulated in non-small cell lung cancers and breast cancers, and its expression positively correlates with patient overall survival. Our findings identify a novel non-immune function for NLRP3 in maintaining genome integrity and strengthen the concept of a functional link between innate immunity and DNA damage sensing pathways to maintain cell integrity.

The DNA damage response (DDR) is essential to preserve genomic integrity and acts as a barrier to cancer. The ATM pathway orchestrates the cellular response to DNA double strand breaks (DSBs), and its attenuation is frequent during tumorigenesis. Here, we show that NLRP3, a Pattern Recognition Receptor known for its role in the inflammasome complex formation, interacts with the ATM kinase to control the early phase of DDR, independently of its inflammasome activity. NLRP3 down-regulation in human bronchial epithelial cells impairs ATM pathway activation as shown by an altered ATM substrate phosphorylation profile, and due to impaired p53 activation, confers resistance to acute genomic stress. Moreover, we found that NLRP3 is down-regulated in Non-Small Cell Lung Cancer (NSCLC) tissues and NLRP3 expression is correlated with patient overall survival. NLRP3 re-expression in NSCLC cells restores appropriate ATM signaling. Our findings identify a non-immune function for NLRP3 in genome integrity surveillance and strengthen the concept of a functional link between innate immunity and DNA damage sensing pathways. Competing Interest Statement The authors have declared no competing interest.