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For patients with dementia, dental care can pose a considerable challenge due to cognitive impairment, behavioral, and psychological symptoms, and (often subsequently) limited autonomous oral care. In this study, we aimed to assess the proficiency of dentists in general practice in the outpatient dental care of these patients. A total of 119 dentists from private practices in Lower Saxony, Germany, participated in this study. Concerning treatment of patients with dementia, they provided details about (1) practice equipment/consultation, (2) training/expertise, and (3) special circumstances of dental treatment. Participating dentists predominantly reported to use medical aids (e.g., positioning cushions) to improve the treatment situation for patients with dementia. Over two thirds (68.6%) offered consultations in nursing homes, and at the patients' homes (47.0%). The training rate was remarkably low in the field of gerodontology for dentists and their practice staff (

The prevalence of infections is supposed to be higher in older patients and to extend the length of hospital stays. This study aimed, first, to test this supposition within a large psychiatric population which we divided into four clusters of psychiatric ICD-10 diagnoses: F00-F03 (dementias), F10 (substance disorders), F20-29 (schizophrenia, schizophreniform and other non-mood psychotic disorders), F32-F33 (major depressive disorders). Second, despite the increasing evidence for the role of infections in psychiatric disorders, it is, to the best of our knowledge, largely unknown whether the rates of infections with pathogens of the four most frequent germ families differ between psychiatric diseases. Thus, in a retrospective study, the results of clinical routine examinations (pap smear, analysis of midstream urine, stool) dependent on symptoms in 8545 patients of a German psychiatric clinic were analyzed in a 12-year dataset. Results show that a longer hospital stay was associated with an increased number of microbiological tests, but led to no significant difference between positive vs. negative findings. Consistent with previous studies, patients with infections were older than patients without infections. For the F10 diagnosis cluster we found a significantly reduced (F10: Staphylococcaceae) and for the F20-29 cluster a heightened risk of infections (Staphylococcaceae, Corynebacteriaceae). Furthermore, patients belonging to the F00-F03 cluster exhibited elevated rates of infections with all four germ families. The latter can be ascribed to patients' age as we found higher age to be associated with these infections, independently of the presence of dementia. Our results suggest that different psychiatric diagnoses are associated with a heightened or lowered risk of bacterial infections and, furthermore, that clinical routine infection-screenings for elderly psychiatric patients seems to be reasonable.

In der Erforschung der Mechanismen der Insulinsekretion ist derzeit allgemein anerkannt, dass der physiologische Hauptstimulus, die Glucose, die Insulinsekretion über eine Depolarisation der Beta-Zellplasmamembran auslöst und zudem noch weitere, bisher noch nicht verstandene Signale produziert, die zu einer Verstärkung der durch die Depolarisation ausgelösten Insulinsekretion führen. Für die Erforschung der verstärkenden („amplifying“) Signale werden Versuchsprotokolle verwendet, in denen die Sekretion zunächst über einen rein depolarisierenden Stimulus ausgelöst und dann der Stoffwechsel durch Glucose bzw. andere Stimuli mit Nährstoffcharakter moduliert wird. Als rein depolarisierender Stimulus wird zumeist eine hohe extrazelluläre Kaliumkonzentration eingesetzt, die eine erstphasenartige Insulinsekretion bewirkt. Es hat sich jedoch gezeigt, dass die mechanistisch scheinbar einfache Kaliumdepolarisation komplexe Effekte ausübt, die sowohl stimulierend als auch hemmend auf die Beta-Zelle wirken. Darum sollte in dieser Arbeit die Rolle der Kaliumdepolarisation für die Auslösung („triggering“) der Depolarisations-induzierten Insulinsekretion genauer geprüft werden. Es hat sich in dieser Arbeit gezeigt, dass die häufig routinemäßig durchgeführte kompensatorische Reduktion der Na+-Konzentration, die die Isoosmolarität des Umströmungsmediums wahren soll, eigene Effekte auf die Nährstoff-induzierte Insulinsekretion ausübt, die nicht durch verstärkte Depolarisation der Plasmamembran erklärt werden können. Dann scheint der Effekt der Kaliumdepolarisation sich nicht in einer Depolarisation der Plasmamembran und dadurch begründbaren Effekten auf spannungsabhängige Ionenkanäle zu erschöpfen. Es kommt bei hohen Kaliumkonzentrationen zu einer qualitativen Änderung des Ca2+-Einstroms, möglicherweise durch eine Verminderung des cytosolischen pH-Wertes bedingt. Somit stellt sich die Frage, inwieweit solche Kaliumdepolarisationen, die bei einer basalen Glucosekonzentration eine Insulinsekretion hervorrufen können, tatsächlich physiologische Ereignisse in der Glucose-induzierten Insulinsekretion imitieren und als pharmakologische Werkzeuge in der weiteren Erforschung der Stimulus-Sekretions-Kopplung brauchbar sind., At present, it is generally recognized that the main physiological stimulus of insulin secretion, glucose, acts by depolarizing the beta cell plasma membrane (“triggering signal”) and producing further, currently only incompletely understood signals, which amplify the secretion elicited by the concurrent depolarization. For the studies on the “amplifying pathway” experimental protocols are used, in which the secretion is elicited by a purely depolarizing stimulus and then the metabolism of the beta cell is modulated by glucose or other nutrient secretagogues. As a purely depolarizing stimulus an increased concentration of the extracellular K+ concentration is employed, which elicits a first phase-like insulin secretion. But the seemingly simple potassium depolarization has been shown to elicit complex effects, both stimulatory and inhibitory, on the beta cell. In this thesis work the potassium depolarization and its consequences on the beta cell were investigated to better understand the “triggering” mechanism of depolarization-induced insulin secretion. In the present work it was found that the compensatory reduction of the sodium concentration, which is often routinely performed to preserve iso-osmolarity during potassium depolarization produces effects of its own on the nutrient-induced insulin secretion. These cannot be explained by an increased depolarization. Furthermore, the potassium depolarization does not only act by the depolarization of the plasma membrane and the consequences thereof on voltage-gated ion channels. At high extracellular potassium concentration a qualitative change of the calcium influx occurs, possibly mediated by the concurrent reduction of the cytosolic pH-value. These observations bring up the question how far such a potassium depolarization, which induces insulin secretion at a basal glucose concentration, actually mimics physiological events in the course of glucose-induced insulin secretion. Also, the role as a pharmacological tool in studies on stimulus-secretion coupling in the beta cell may need reconsideration.

Background. Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) has been shown to induce clinical response and remission in patients with active Crohn’s disease (CD). Moreover the beneficial role of GM-CSF was shown in a mouse model of acute colitis induced by Dextran Sodium Sulfate (DSS). Since it is known that GM-CSF has pleiotropic effects on monocytes and since those cells represent the exclusive source of macrophages in inflamed intestinal mucosa we characterized GM-CSF treated mouse monocytes in vitro and analyzed their function in vivo in a model of chronic DSS colitis. Methods. Mouse bone marrow-derived monocyte precursors were treated for 48 hours with GM-CSF in vitro and phenotypical changes were assessed by real-time polymerase chain reaction (qRT-PCR) and flow cytometry. Functional properties were evaluated in mixed lymphocyte reactions (MLR), by phagocytosis assays, adherence to plastic surface, cytokine production upon lipopolysaccharide (LPS) stimulation and measurement of reactive oxygen species (ROS) production. Therapeutic effects of GM-CSF-treated monocytes were evaluated in a model of chronic colitis induced by repeated oral administration of DSS (2%) on three days per week. GM-CSF treated monocytes were administered i.v. one day prior start of the third DSS treatment cycle and the severity of developed colitis was evaluated by body weight change, colon length, histology and expression of inflammatory markers. The distribution of injected GM-CSF-monocytes across intestine was evaluated by in vivo near infrared imaging. Results. We found that GM-CSF-treated monocytes express higher levels of anti-inflammatory molecules on mRNA and protein levels (e.g. IL1-Ra, IL4-R and ARG1). Functionally, GM-CSF promotes ROS production of the cells but reduces phagocytosis and adherence. In MLR we observed an induction of Foxp3 in naive T cells. Clinically, in chronic DSS-induced colitis, treatment of mice with GM-CSF-monocytes showed an overall better outcome compared to mice treated with control monocytes. This encompasses body weight, colon length, mRNA expression of inflammatory marker molecules (e.g. IL6 and TNF) and histological observations. Using in vivo imaging technology we found that a higher percentage of GM-CSF treated monocytes enter the inflamed intestine compared to control monocytes. In addition, GM-CSF-monocytes persisted longer at sides of inflammation. Conclusion. We showed that the beneficial effects of GM-CSF in CD are probably due to its modifying action especially on monocytes and concomitant anti-inflammatory alterations in phenotype and function of macrophages developed from these cells in an experimental model of colitis.