Abstract Objective Peri‐implantitis has been attributed to a myriad of factors, including microleakage at the abutment‐implant interface. Implant abutment access channel sealing materials (IACSM) are readily used in implant dentistry, with little evidence on their effect on microleakage. This study aims to evaluate the effect of IACSM on the microbial composition in the implant access channel and the peri‐implant sulcus. Methods A total of n = 8 patients (64 implants) were included in this single‐blinded, randomized controlled trial, whereas four different materials (cotton, polytetrafluoroethylene [PTFE], synthetic foam, or polyvinyl siloxane [PVS]) were randomly placed as an IACSM. Following 6 months, microbial analysis was completed on the IACSM and samples from the peri‐implant sulci via PCR and high‐throughput sequencing. Bacterial samples on the IACSM and in the peri‐implant sulci were classified according to Socransky's microbial complexes. Results There was a preponderance of early colonizing bacteria within the IACSM, while the peri‐implant sulci were dominated by Orange complex bacteria. The proportion of Red and Orange complex members on the IACSM was significantly less than in the peri‐implant sulci. The proportion of Green, Yellow, and Blue complex members found on the IACSM was significantly greater than in the peri‐implant sulci. Atopobium , a diverse species not included in the microbial complexes, was frequently detected in the peri‐implant sulcus samples. Conclusions No detectable effects of IACSM on the microbial community in the peri‐implant sulcus or on the IACSM were identified. Variation of bacterial species was most dependent on the individual patient. No significant differences were found in the periodontal parameters between the different treatment groups.
Deterministic compartmental models are predominantly used in the modeling of infectious diseases, though stochastic models are considered more realistic, yet are complicated to estimate due to missing data. In this paper we present a novel algorithm for estimating the stochastic SIR/SEIR epidemic model within a Bayesian framework, which can be readily extended to more complex stochastic compartmental models. Specifically, based on the infinitesimal conditional independence properties of the model, we are able to find a proposal distribution for a Metropolis algorithm which is very close to the correct posterior distribution. As a consequence, rather than perform a Metropolis step updating one missing data point at a time, as in the current benchmark Markov chain Monte Carlo (MCMC) algorithm, we are able to extend our proposal to the entire set of missing observations. This improves the MCMC methods dramatically and makes the stochastic models now a viable modeling option. A number of real data illustrations and the necessary mathematical theory supporting our results are presented.
We have previously shown that exposure to TiO2 nanoparticles (NPs) reduces the resistance of HeLa cells to bacterial infection. Here we demonstrate that the increased infectivity is associated with enhanced asymmetry in the cholesterol distribution. We applied a new live cell imaging method which uses tunable orthogonal cholesterol sensors to visualize and quantify in-situ cholesterol distribution between the two leaflets of the plasma membrane (PM). In the control culture, we found marked transbilayer asymmetry of cholesterol, with the concentration in the outer plasma membrane (OPM) being 12.5(2.2)-fold higher than that in the inner plasma membrane (IPM). Exposure of the culture to 0.1 mg/mL of rutile TiO2 NPs increased the asymmetry such that the concentration in the OPM was 50.8(9.5) times higher, while the total cholesterol content increased only 20.5(2.4)%. This change in cholesterol gradient may explain the increase in bacterial infectivity in HeLa cells exposed to TiO2 NPs since many pathogens, including Staphylococcus aureus used in the present study, require cholesterol for proper membrane attachment and virulence. RT-PCR indicated that exposure to TiO2 was responsible for upregulation of the ABCA1 and ABCG1 mRNAs, which are responsible for the production of the cholesterol transporter proteins that facilitate cholesterol transport across cellular membranes. This was confirmed by the observation of an overall decrease in bacterial infection in ABCA1 knockout or methyl-β-cyclodextrin-treated HeLa cells, as regardless of TiO2 NP exposure. Hence rather than preventing bacterial infection, TiO2 nanoparticles upregulate genes associated with membrane cholesterol production and distribution, hence increasing infectivity.
The gene for the phosphate-starvation-inducible outer membrane protein OprP, of Pseudomonas aeruginosa was introduced into Caulobacter crescentus CB2A on a plasmid vector. As is the case in P. aeruginosa and Escherichia coli the oprP gene was inducible under conditions of limiting phosphate in C. crescentus. However, the maximal medium concentration of phosphate which still permitted induction of OprP was lower in C. crescentus (50 μM) than in P. aeruginosa (200 μM). Induction of OprP was coincident with the process of stalk elongation, known to occur in C. crescentus under phosphate starvation conditions. When induced, OprP was localized to the cell envelope and became a major membrane protein, indicating that the Pseudomonas promoter was efficiently recognized in C. crescentus and that the gene product was targeted to the appropriate region of the cell. Our data provide support for the hypothesis that the mechanism for regulation of phosphate-starvation-inducible genes is highly conserved amongst the eubacteria.
The lipopolysaccharide (LPS) of the outer membrane of Caulobacter crescentus was purified and analyzed. Two distinct strains of the species, NA 1000 and CB2A, were examined; despite differences in other membrane-related polysaccharides, the two gave similar LPS composition profiles. The LPS was the equivalent of the rough LPS described for other bacteria in that it lacked the ladder of polysaccharide-containing species that results from addition of variable amounts of a repeated sequence of sugars, as detected by gel electrophoresis in smooth LPS strains. The purified LPS contained two definable regions: (i) an oligosaccharide region, consisting of an inner core of three residues of 2-keto-3-deoxyoctonate, two residues of alpha-L-glycero-D-mannoheptose, and one alpha-D-glycero-D-mannoheptose unit and an outer core region containing one residue each of alpha-D-mannose, alpha-D-galactose, and alpha-D-glucose, with the glucose likely phosphorylated and (ii) a region equivalent to the lipid A region of the archetype, consisting primarily of an esterified fatty acid, 3-OH-dodecanoate. The lipid A-like region was resistant to conclusive analysis; in particular, although a variety of analytical methods were used, no amino sugars were detected, as is found in the lipid A of the LPS of most bacteria.
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