Background: There is increasing evidence that, in addition to the well-known effects on musculoskeletal health, vitamin D status may be related to a number of non-skeletal diseases.An international expert panel formulated recommendations on vitamin D for clinical practice, taking into consideration the best evidence available based on published literature today. In addition, where data were limited to smaller clinical trials or epidemiologic studies, the panel made expert-opinion based recommendations.Methods: Twenty-five experts from various disciplines (classical clinical applications, cardiology, autoimmunity, and cancer) established draft recommendations during a 2-day meeting. Thereafter, representatives of all disciplines refined the recommendations and related texts, subsequently reviewed by all panelists. For all recommendations, panelists expressed the extent of agreement using a 5-point scale. Results and conclusion:Recommendations were restricted to clinical practice and concern adult patients with or at risk for fractures, falls, cardiovascular or autoimmune diseases, and

SummaryNeutral lipid accumulation is frequently observed in some Gram-negative prokaryotes like Acinetobacter sp. and most actinomycetes, including the pathogenic Mycobacterium tuberculosis and antibiotic producing streptomycetes. We examined the formation of wax ester-and triacylglycerol (TAG)-bodies in Acinetobacter calcoaceticus and Rhodococcus opacus using microscopic, immunological and biophysical methods. A general model for prokaryotic lipid-body formation is proposed, clearly differing from the current models for the formation of lipid inclusions in eukaryotes and of poly(hydroxyalkanoic acid) (PHA) inclusions in prokaryotes. Formation of lipid-bodies starts with the docking of wax ester synthase/acyl-CoA:diacylglycerol acyltransferase (WS/DGAT) to the cytoplasm membrane. Both, analyses of in vivo and in vitro lipid-body synthesis, demonstrated the formation of small lipid droplets (SLDs), which remain bound to the membraneassociated enzyme. SLDs conglomerated subsequently to membrane-bound lipid-prebodies which are then released into the cytoplasm. The formation of matured lipid-bodies in the cytoplasm occurred by means of coalescence of SLDs inside the lipid prebodies, which are surrounded by a half-unit membrane of phospholipids.

IntroductionSepsis is a complex clinical condition caused by a dysregulated immune response to an infection oftentimes resulting in multiorgan failure with a fatal outcome. 1 Current concepts for the understanding of this dramatic clinical condition suggest that an overwhelming innate inflammatory response to a microbial infection associated with the release of factors such as IL-1, IL-6, TNF-␣, and others early on is involved. 2 Recently, the triggering receptor expressed on myeloid cells 1 (TREM-1) has been identified as an important receptor involved in the innate inflammatory response and in sepsis. [3][4][5][6] TREM-1 is a member of the v-type immunoglobulin super family and expressed on polymorphonuclear leukocytes (PMNs) and monocytes. 7 The expression of TREM-1 is up-regulated upon stimulation with microbial products, and receptor ligation activates the full repertoire of PMN effector functions such as the respiratory burst, phagocytosis, release of IL-8, and myeloperoxidase in synergy with Toll-like receptor (TLR) ligands such as LPS or bacterial lipopeptides. 3,6,8,9 The importance of TREM-1 in the innate inflammatory response is underlined in mouse models for sepsis where the administration of a recombinant soluble TREM-1 fusion protein or a conserved TREM-1 peptide can save the animals from a lethal endotoxic shock or microbial sepsis induced by cecal ligation and puncture. 5,6 The clinical significance of the TREM-1 system is further emphasized by reports that a soluble form of TREM-1 (sTREM-1) is released and detectable in the bronchoalveolar lavage fluid or serum in patients with ventilator-associated pneumonia or sepsis, respectively. 10-12 Among the critically ill patients analyzed in these studies, the determination of sTREM-1 proved to be a useful and highly sensitive parameter for accurate diagnosis. Further studies where sTREM-1 is detected in patients with chronic obstructive pulmonary disease, 13 peptic ulcer disease, 14 or inflammatory bowel disease 15 confirm the involvement of TREM-1 also in noncritically ill patient collectives and suggest that the activation of TREM-1 plays a general role in the innate inflammatory response. 7 However, a deeper understanding of how TREM-1 influences inflammatory responses and sepsis requires the characterization of the natural ligand for TREM-1 and its expression pattern. 7 To this end, we provide evidence that the natural ligand for TREM-1 is present on human platelets. We demonstrate specific binding of recombinant soluble TREM-1 (rsTREM-1) on human platelets. In addition, we show that coincubation of PMNs with platelets in the presence of microbial LPS enhances the neutrophil respiratory burst and release of IL-8 as primary PMN effector functions in a TREM-1-specific manner. Taken together, our results indicate a yet-unrecognized interaction between PMNs and platelets during innate the inflammatory response that is mediated by TREM-1 and its ligand. Materials and methods MaterialsLipopolysaccharide (LPS) from Salmonella typhimurium was obtained fro...

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Infection with the human parvovirus B19 usually results in a mild disease known as erythema infectiosum, or fifth disease