Characterization of vascular cavity coatings and microscopic tube-shaped structures from Upper Cretaceous dinosaur bone: evidence of a bacterial origin for dinosaur blood vessels""

Recent claims of blood vessels extracted from dinosaur fossils challenge classical views of soft-tissue preservation. Alternatively, these structures may represent postdepositional,diagenetic biofilms that grew on vascular cavity surfaces within the fossil. Similar red, hollow, tube-shaped structures were recovered from well-preserved and poorly-preserved (abraded, desiccated, exposed) Upper Cretaceous dinosaur fossils in this study. Integration of light microscopy, scanning electron microscopy, and energy dispersive x-ray spectroscopy was used to compare these vessel structures to the fossils from which they are derived. Vessel structures are typically 100-400 μm long, 0.5-1.5 μm thick, 10-40 μm in diameter and take on a wide range of straight, curved, andbranching morphologies. Interior surfaces vary from smooth to globular and typically contain spheres, rods, and fibrous structures (< 2 μm in diameter) incorporated into the surface. Exterior surfaces exhibit 2-μm-tall converging ridges, spaced 1-3 μm apart, that are sub-parallel to the long axis of the vessel structure. Fossil vascular cavities are typically coated with a smooth or grainy orange layer that shows a wide range of textures including smooth, globular, rough, ropy, and combinations thereof. Coatings tend to overlay secondary mineral crystals and framboids, confirming they are not primary structures of the fossil. For some cavity coatings, the surface that had been in contact with the bone exhibits a ridged texture, similar to that of vessel structures, having formed as a mold of the intravascular bone surface. Thus, vessel structures are interpreted as intact cavity coatings isolated after the fossil is demineralized. The presence of framboids and structures consistent in size and shape with bacteria cells, the abundance of iron in cavity coatings, and the growth of biofilms directly from the fossil that resemble respective cavity coatings support the hypothesis that vessel structures result from ironconsuming bacteria that form biofilms on the intravascular bone surfaces of fossil dinosaur bone. This also accounts for microstructures resembling osteocytes as some fossil lacunae are filled with the same iron oxide that comprises vessel structures andcoatings. Results of this study show that systematic, high-resolution SEM analyses of vertebrate fossils can provide improved insight on microtaphonomic processes, including the role of bacteria in diagenesis. These results conflict with earlier claims of dinosaurblood vessels and osteocytes.

Inhibition of bacterial degradation of EtG by collection as dried urine spots (DUS)

Ethyl glucuronide (EtG) and ethyl sulfate (EtS) are direct alcohol consumption markers widely used nowadays for clinical and forensic applications. They are detectable in blood and urine even after consumption of trace amounts of ethanol and for a longer time frame, being detectable even when no more ethanol is present. The instability of EtG against bacterial degradation in contaminated urine samples and/or the possible postcollection synthesis of this metabolite in samples containing, e.g., Escherichia coli and ethanol, may cause false identification of alcohol uptake. Therefore, it is of paramount importance to constrict these error sources by inhibition of any bacterial growth causing hydrolization or synthesis of EtG. This study evaluates a new method of collecting urine samples on filter paper, dried urine spots (DUS), for simultaneous detection of EtG, EtS and creatinine, having the great advantage of inhibiting bacterial activity. In addition, a method validation for the determination of EtG and EtS in DUS was performed according to the FDA guidelines. Sterile-filtered urine was spiked with EtG and EtS, inoculated with E. coli and incubated. Liquid and dried urine samples were collected after various time intervals up to 96 h. Liquid samples were frozen immediately after collection, whereas aliquots for DUS were pipetted onto filter paper, allowed to dry and stored at RT until analysis 1 week after. The specimens were analyzed by LC-ESI-MS/MS. As expected, degradation of EtG, but not of EtS, was observed in contaminated liquid urine samples. However, the specimens collected on filter paper and stored at RT showed no degradation during storage. Therefore, collecting urine samples on filter paper for EtG and EtS analysis turns out to be a reliable method to avoid bacterial degradation of EtG and EtS, and consequently, stabilization of these ethanol metabolites is achieved. In addition, simultaneous measurement of creatinine content as an indicator of urine dilution helps to interpret the results. Method validation for EtG and EtS in DUS was satisfactory, showing the linearity of the calibration curves in the studied concentration range, good precision, accuracy and selectivity.

Clinical settings and specialties notifying cases of bacterial sexually transmitted infections in Switzerland: A cross-sectional study

In the next Swiss National HIV and Sexually Transmitted Infection (STI) Strategy 2011-2017, STI control will be integrated with HIV prevention. Information is needed which will improve the targeting of professional education. The objective of this study was to describe the clinical specialities and settings to which patients with bacterial STI present in Switzerland.

Bacterial expression of mutant argininosuccinate lyase reveals imperfect correlation of in-vitro enzyme activity with clinical phenotype in argininosuccinic aciduria

The urea cycle defect argininosuccinate lyase (ASL) deficiency has a large spectrum of presentations from highly severe to asymptomatic. Enzyme activity assays in red blood cells or fibroblasts, although diagnostic of the deficiency, fail to discriminate between severe, mild or asymptomatic cases. Mutation/phenotype correlation studies are needed to characterize the effects of individual mutations on the activity of the enzyme.

Intestinal bacterial colonization induces mutualistic regulatory T cell responses

Mammals harbor a dense commensal microbiota in the colon. Regulatory T (Treg) cells are known to limit microbe-triggered intestinal inflammation and the CD4+ T cell compartment is shaped by the presence of particular microbes or bacterial compounds. It is, however, difficult to distinguish whether these effects reflect true mutualistic immune adaptation to intestinal colonization or rather idiosyncratic immune responses. To investigate truly mutualistic CD4+ T cell adaptation, we used the altered Schaedler flora (ASF). Intestinal colonization resulted in activation and de novo generation of colonic Treg cells. Failure to activate Treg cells resulted in the induction of T helper 17 (Th17) and Th1 cell responses, which was reversed by wild-type Treg cells. Efficient Treg cell induction was also required to maintain intestinal homeostasis upon dextran sulfate sodium-mediated damage in the colon. Thus, microbiota colonization-induced Treg cell responses are a fundamental intrinsic mechanism to induce and maintain host-intestinal microbial T cell mutualism.

NOD2 gene variants are a risk factor for culture-positive spontaneous bacterial peritonitis and monomicrobial bacterascites in cirrhosis

Spontaneous bacterial peritonitis (SBP) is considered as result of bacterial translocation from the gastrointestinal lumen to the mesenteric lymph nodes and subsequent circulation. Variants of the NOD2 gene contribute to bacterial translocation and were associated with SBP in a recent study.

Antimicrobial peptide response to blood translocation of bacterial DNA in Crohn's disease is affected by NOD2/CARD15 genotype

Blood translocation of bacterial-DNA has been described in patients with Crohn's disease (CD). The host's immune cell types cooperate to respond against bacterial insults. Some antimicrobial peptides are inducible after culture with bacterial products and a linkage has been established between them and NOD2/CARD15. The aim was to test whether defensins and cathelicidin (LL-37) expression and NOD2/CARD15 mutations in blood neutrophils are related to molecular bacterial translocation events in CD patients.

Bacterial meningitis: current therapy and possible future treatment options

Despite targeted therapy, case-fatality rates and neurologic sequelae of bacterial meningitis remain unacceptably high. The poor outcome is mainly due to secondary systemic and intracranial complications. These complications seem to be both a consequence of the inflammatory response to the invading pathogen and release of bacterial components by the pathogen itself. Therefore, within the last decades, research has focused on the mechanism underlying immune regulation and the inhibition of bacterial lysis in order to identify new targets for adjuvant therapy. The scope of this article is to give an overview on current treatment strategies of bacterial meningitis, to summarize new insights on the pathophysiology of bacterial meningitis, and to give an outlook on new treatment strategies derived from experimental models.