34 research outputs found

    Interfacial behavior of lipid nanocapsules spread on model membrane monolayers

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    The lipid nanocapsules (LNCs) spread at the air–water interface (A/W) undergo destabilization and disaggregation leading to formation of a triglyceride (TG) surface film. The kinetics of reorganization and formation of TG surface film were followed by measuring either the change of surface pressure at constant area or the surface area at constant surface pressure. From the obtained experimental data were determined the effectiveness of TG spreading and the rate of LNC disaggregation at A/W interface covered with preformed model membrane monolayers of DPPC, Curosurf®, and mucus. Partial LNC stabilization due to their interaction with the model membrane monolayers was observed and characterized by atomic force microscopy (AFM). The obtained results demonstrated that the LNCs spread on mucus surface layer, which models the epithelial surface were more stable than if they were spread either on DPPC or Curosurf® surface layers, which emulate the alveolar surface

    Effect of 67 kDa calcimedin on caldesmon functioning

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    AbstractInteraction of smooth muscle caldesmon with calmodulin, troponin C, S-100 protein and 67 kDa calcimedin was analyzed. Native gel electrophoresis and crosslinking revealed the complex formation between caldesmon and three EF-hand Ca-binding proteins, whereas calcimedin did not interact with caldesmon. In the presence of Ca2+, calcimedin binds to actin-tropomyosin without affecting the interaction of caldesmon with this complex. Although calcimedin reversed the inhibitory action of caldesmon on the actomyosin ATPase activity at a lower concentration than three other Ca-binding proteins, this effect only slightly depends on Ca2+ and was observed at the concentration of calcimedin comparable to that of actin. It is concluded that calcimedin itself cannot be responsible for Ca-dependent regulation of caldesmon functioning, but actin bundling induced by calcimedin (or by other actin binding proteins) decreases the inhibitory action of caldesmon on the actomyosin ATPase activity

    Spread of Q fever within dairy cattle herds: key parameters inferred using a Bayesian approach

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    Q fever is a worldwide zoonosis caused by Coxiella burnetii. Although ruminants are recognized as the most important source of human infection, no previous studies have focused on assessing the characteristics of the bacterial spread within a cattle herd and no epidemic model has been proposed in this context. We assess the key epidemiological parameters from field data in a Bayesian framework that takes into account the available knowledge, missing data and the uncertainty of the observation process owing to the imperfection of diagnostic tests. We propose an original individual-based Markovian model in discrete time describing the evolution of the infection for each animal. Markov chain Monte Carlo methodology is used to estimate parameters of interest from data consisting of individual health states of 217 cows of five chronically infected dairy herds sampled every week for a four-week period. Outputs are the posterior distributions of the probabilities of transition between health states and of the environmental bacterial load. Our findings show that some herds are characterized by a very low infection risk while others have a mild infection risk and a non-negligible intermittent shedding probability. Moreover, the antibody status seems to be a key point in the bacterial spread (shedders with antibodies shed for a longer period of time than shedders without antibodies). In addition to the biological insights, these estimates also provide information for calibrating simulation models to assess control strategies for C. burnetii infection

    Genomic characterization of MDR/XDR-TB in Kazakhstan by a combination of high-throughput methods predominantly shows the ongoing transmission of L2/Beijing 94-32 central Asian/Russian clusters

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    International audienceBACKGROUND: Kazakhstan remains a high-burden TB prevalence country with a concomitent high-burden of multi-drug resistant tuberculosis. For this reason, we performed an in depth genetic diversity and population structure characterization of Mycobacterium tuberculosis complex (MTC) genetic diversity in Kazakhstan with both patient and community benefit. METHODS: A convenience sample of 700 MTC DNA cultures extracts from 630 tuberculosis patients recruited from 12 out of 14 regions in Kazakhstan, between 2010 and 2015, was independently studied by high-throughput hybridization-based methods, TB-SPRINT (59-Plex, n = 700), TB-SNPID (50-Plex, n = 543). DNA from 391 clinical isolates was successfully typed by two methods. To resolve the population structure of drug-resistant clades in more detail two complementary assays were run on the L2 isolates: an IS6110-NTF insertion site typing assay and a SigE SNP polymorphism assay. RESULTS: Strains belonged to L2/Beijing and L4/Euro-American sublineages; L2/Beijing prevalence totaled almost 80%. 50% of all samples were resistant to RIF and to INH., Subtyping showed that: (1) all L2/Beijing were "modern" Beijing and (2) most of these belonged to the previously described 94-32 sublineage (Central Asian/Russian), (3) at least two populations of the Central Asian/Russian sublineages are circulating in Kazakhstan, with different evolutionary dynamics. CONCLUSIONS: For the first time, the global genetic diversity and population structure of M. tuberculosis genotypes circulating in Kazakhstan was obtained and compared to previous local studies. Results suggest a region-specific spread of a very limited number of L2/Beijing clonal complexes in Kazakhstan many strongly associated with an MDR phenotype
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