Вирусный маркетинг в туристской индустрии: проблемы и перспективы

Материалы XII Междунар. науч.-техн. конф. (науч. чтения, посвящ. П. О. Сухому), Гомель, 22–23 нояб. 2018 г

Molecular Typing and Phenotype Characterization of Methicillin-Resistant Staphylococcus aureus Isolates from Blood in Taiwan

BACKGROUND: Staphylococcus aureus causes a variety of severe infections such as bacteremia and sepsis. At present, 60-80% of S. aureus isolates from Taiwan are methicillin resistant (MRSA). It has been shown that certain MRSA clones circulate worldwide. The goals of this study were to identify MRSA clones in Taiwan and to correlate the molecular types of isolates with their phenotypes. METHODS: A total of 157 MRSA isolates from bacteremic patients were collected from nine medical centers. They were typed based on polymorphisms in agr, SCCmec, MLST, spa, and dru. Phenotypes characterized included Panton-Valentine leucocidin (pvl), inducible macrolide-lincosamide-streptogramin B resistance (MLSBi), vancomycin (VA) and daptomycin (DAP) minimal inhibitory concentrations (MIC), and superantigenic toxin gene profiles. Difference between two consecutive samples was determined by Mann-Whitney-U test, and difference between two categorical variables was determined by Fisher's exact test. RESULTS: Four major MRSA clone complexes CC1, CC5, CC8, and CC59 were found, including 4 CC1, 9 CC5, 111 CC8, and 28 CC59 isolates. These clones had the following molecular types: CC1: SCCmecIV and ST573; CC5: SCCmecII and ST5; CC8: SCCmecIII, ST239, and ST241, and CC59: SCCmecIV, SCCmecV(T), ST59, and ST338. The toxin gene profiles of these clones were CC1: sec-seg-(sei)-sell-selm-(seln)-selo; CC5: sec-seg-sei-sell-selm-(seln)-selp-tst1; CC8: sea-selk-selq, and CC59: seb-selk-selq. Most isolates with SCCmecV(T), ST59, spat437, and dru11 types were pvl(+) (13 isolates), while multidrug resistance (≥4 antimicrobials) were associated with SCCmecIII, ST239, spa t037, agrI, and dru14 (119 isolates) (p<0.001). One hundred and twenty four isolates with the following molecular types had higher VA MIC: SCCmecII and SCCmecIII; ST5, ST239, and ST241; spa t002, t037, and t421; dru4, dru10, dru12, dru13, and dru14 (p<0.05). No particular molecular types were found to be associated with MLSBi phenotype. CONCLUSIONS: Four major MRSA clone complexes were found in Taiwan. Further studies are needed to delineate the evolution of MRSA isolates

Revealing hidden species distribution with pheromones: the case of Synanthedon vespiformis (Lepidoptera: Sesiidae) in Sweden

Synanthedon vespiformis L. (Lepidoptera: Sesiidae) is considered a rare insect in Sweden, discovered in 1860, with only a few observations recorded until a sex pheromone attractant became available recently. This study details a national survey conducted using pheromones as a sampling method for this species. Through pheromone trapping we captured 439 specimens in Southern Sweden at 77 sites, almost tripling the number of previously reported records for this species. The results suggest that S. vespiformis is truly a rare species with a genuinely scattered distribution, but can be locally abundant. Habitat analyses were conducted in order to test the relationship between habitat quality and the number of individuals caught. In Sweden, S. vespiformis is thought to be associated with oak hosts, but our attempts to predict its occurrence by the abundance of oaks yielded no significant relationships. We therefore suggest that sampling bias and limited knowledge on distribution may have led to the assumption that this species is primarily reliant on oaks in the northern part of its range, whereas it may in fact be polyphagous, similar to S. vespiformis found as an agricultural pest in Central and Southern Europe. We conclude that pheromones can massively enhance sampling potential for this and other rare lepidopteran species. Large-scale pheromone-based surveys provide a snapshot of true presences and absences across a considerable part of a species national distribution range, and thus for the first time provide a viable means of systematically assessing changes in distribution over time with high spatiotemporal resolution

Osteotropic cytokines : expression in human gingival fibroblasts and effects on bone

Bone metabolism is regulated by endocrine and paracrine signalling molecules influencing bone cells in the continuously remodelling bone tissue. These molecules include a variety of osteotropic stimulatory and inhibitory cytokines. Degradation of alveolar bone in periodontal disease is believed to be a result of local release of such osteotropic cytokines, although the relative importance of particular cytokines and their cellular origin is currently unknown. The aim of the present project was to study if, and how, pro-inflammatory cytokines in the interleukin-6 (IL-6) family of cytokines, and anti-inflammatory IL-4 and IL-13 type of cytokines, can affect osteoclast differentiation and bone resorption. Additionally, the objective was to study if gingival fibroblasts may influence alveolar bone resorption through secretion of IL-6 type cytokine release and if the secretion is regulated by pro-inflammatory as well as anti-inflammatory mediators such as IL-4 and IL-13. IL-6 in combination with its soluble receptor (sIL-6R) was found to stimulate mouse calvarial bone resorption. Similarly, two other IL-6 family members, leukemia inhibitory factor (LIF) and oncostatin M (OSM) were found to stimulate bone resorption. The stimulatory effect on bone resorption induced by the three cytokines was associated with increased expression of receptor activator of NF- κB ligand (RANKL), a cytokine which is essential in osteoclast formation and activation through binding to receptor activator of NF- κB (RANK) on osteoclastic cells. The interaction between RANKL and RANK can be inhibited by binding of the decoy receptor osteoprotegerin (OPG) to RANKL, and the expression of OPG was also regulated by IL-6, LIF and OSM (Paper I). The two related cytokines IL-4 and IL-13 were found to inhibit osteoclastogenesis and mouse calvarial bone resorption by mechanisms involving a decreased RANKL/OPG ratio in osteoblasts and decreased RANK expression in osteoclastic cells. The results further demonstrated that IL-4 and IL-13 exert their effects on both osteoblasts and osteoclasts by a mechanism involving the transcription factor signal transducer and activator of transcription 6 (STAT6) (Paper II). Constitutional expression of IL-6, LIF and another member of the IL-6 family of cytokines, IL-11, was demonstrated in human gingival fibroblasts. IL-6 type cytokine expression levels were found to be enhanced by IL-1β and tumour necrosis factor-α (TNF-α) (Paper III), whereas IL-4 and IL-13 inhibited IL 11 and LIF release from gingival fibroblasts (Paper IV). In conclusion, IL 6 type cytokines were found to be stimulators and IL-4 and IL-13 inhibitors of bone resorption in vitro via mechanisms involving RANK/RANKL/OPG interactions. Additionally, gingival fibroblasts were able to secrete several cytokines in the IL-6 family. Secretion was further enhanced by pro-inflammatory mediators and inhibited by IL-4 and IL- 13. These findings support the view that resident cells may influence the pathogenesis of periodontal disease through osteotropic cytokine production

Increased Eotaxin and MCP-1 Levels in Serum from Individuals with Periodontitis and in Human Gingival Fibroblasts Exposed to Pro-Inflammatory Cytokines

Periodontitis is a chronic inflammatory disease of tooth supporting tissues resulting in periodontal tissue destruction, which may ultimately lead to tooth loss. The disease is characterized by continuous leukocyte infiltration, likely mediated by local chemokine production but the pathogenic mechanisms are not fully elucidated. There are no reliable serologic biomarkers for the diagnosis of periodontitis, which is today based solely on the degree of local tissue destruction, and there is no available biological treatment tool. Prompted by the increasing interest in periodontitis and systemic inflammatory mediators we mapped serum cytokine and chemokine levels from periodontitis subjects and healthy controls. We used multivariate partial least squares (PLS) modeling and identified monocyte chemoattractant protein-1 (MCP-1) and eotaxin as clearly associated with periodontitis along with C-reactive protein (CRP), years of smoking and age, whereas the number of remaining teeth was associated with being healthy. Moreover, body mass index correlated significantly with serum MCP-1 and CRP, but not with eotaxin. We detected higher MCP-1 protein levels in inflamed gingival connective tissue compared to healthy but the eotaxin levels were undetectable. Primary human gingival fibroblasts displayed strongly increased expression of MCP-1 and eotaxin mRNA and protein when challenged with tumor necrosis factor-alpha (TNF-alpha and interleukin-1 beta (IL-1 beta), key mediators of periodontal inflammation. We also demonstrated that the upregulated chemokine expression was dependent on the NF-kappa B pathway. In summary, we identify higher levels of CRP, eotaxin and MCP-1 in serum of periodontitis patients. This, together with our finding that both CRP and MCP-1 correlates with BMI points towards an increased systemic inflammatory load in patients with periodontitis and high BMI. Targeting eotaxin and MCP-1 in periodontitis may result in reduced leukocyte infiltration and inflammation in periodontitis and maybe prevent tooth loss

Time- and dose-dependent increase of eotaxin and MCP-1 protein expression in gingival fibroblasts stimulated by TNF-α and IL-1β.

<p><b>(A and C)</b> TNF-α (50 ng/ml) stimulates eotaxin and MCP-1 protein expression, and <b>(B and D)</b> IL-1β (100 pg/ml) stimulates eotaxin and MCP-1 protein expression a time-dependent manner. <b>(E and G)</b> TNF-α stimulates eotaxin and MCP-1 protein expression, and <b>(F and H)</b> IL-1β stimulates eotaxin and MCP-1 protein expression in a dose-dependent manner.</p

Schematic figure of the canonical versus non-canonical NF-κB signaling pathways, and downstream targets of inhibitors.

<p>Schematic figure of the canonical versus non-canonical NF-κB signaling pathways, and downstream targets of inhibitors.</p

Pearson correlation coefficients between serum CRP, MCP-1, eotaxin, and BMI in periodontitis (PD) and in periodontally healthy (PH) subjects.

<p>1) Log10 values</p><p>Pearson correlation coefficients between serum CRP, MCP-1, eotaxin, and BMI in periodontitis (PD) and in periodontally healthy (PH) subjects.</p

Characteristics of study participants describing periodontitis (PD) and periodontally healthy (PH) subjects.

<p>a) Distribution of numbers was tested with Chi² test.</p><p>b) Differences between means were tested with Student´s <i>t</i>-test.</p><p>c) Standardized for sex, age and education using general linear modeling.</p><p>d) Standardized for sex, age, education and number of teeth using general linear modeling.</p><p>Characteristics of study participants describing periodontitis (PD) and periodontally healthy (PH) subjects.</p