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Correction of stress-depended changes of glucoproteid platelet receptors activity by electromagnetic radiation of terahertz range  [PDF]
V.F. Kirichuk,E.V. Andronov,A.N. Ivanov,S.V. Svistunov
Saratov Journal of Medical Scientific Research , 2010,
Abstract: The research goal is correction of stress-depended changes of glucoproteid (Gp) platelet receptors activity by electromagnetic radiation of terahertz range. Influence of electromagnetic waves of terahertz range at the frequency of molecular spectrum of radiation and absorption of nitrogen oxide on lectin-induced platelet aggregation of white rats in the stressed condition was investigated
The Design of GP 2
Detlef Plump
Electronic Proceedings in Theoretical Computer Science , 2012, DOI: 10.4204/eptcs.82.1
Abstract: This papers defines the syntax and semantics of GP 2, a revised version of the graph programming language GP. New concepts are illustrated and explained with example programs. Changes to the first version of GP include an improved type system for labels, a built-in marking mechanism for nodes and edges, a more powerful edge predicate for conditional rule schemata, and functions returning the indegree and outdegree of matched nodes. Moreover, the semantics of the branching and loop statement have been simplified to allow their efficient implementation.
THE EFFECTS OF DIAZEPAM ON THE ELEVATED T-MAZE ARE DEPENDED ON THE ESTROUS CYCLE OF RATS
Amauri Gouveia Jr, Gabriela Antunes, Caio Maximino, Silvio Morato
Psychology & Neuroscience , 2009,
Abstract: In order to determine the modulation of anxiolytic and panicolytic effects of diazepam by the hormonal cycle of female rats, male and female rats – the latter divided per estrous cycle phase (estrus, diestrus, metaestrus and proestrus) – were tested in the elevated T-maze, a behavioral model of panic and anxiety. Diazepam (0.5, 1.0 and 2.0 mg/kg) or saline solution was injected in individual animals that were submitted to one session in the elevated T-maze 25 min after drug/saline administration. The test consisted of three avoidance trials and one escape trial, separated by a 30 s interval, during which the animals were isolated in individual cages. The avoidance trials began with the animal being placed at the end of the maze's enclosed arm. The time necessary for the animal to leave the central square was considered as the response's latency. The trials that exceeded 300 s were considered as failures. Results demonstrate a decrease in the effects of diazepam in inhibitory avoidance (anxiety) trials in females in diestrus and proestrus, but no relation of gender or estrous cycle on diazepam effects on escape trials (fear). The results support the hypothesis of down-regulation of GABAA receptors by activation of nuclear estrogen receptors and induction of PKC-mediated GABAA receptor phosphorylation by activation of surface estrogen receptors in raphe neurons underlie the modulation of diazepam sensitivity by estrogen.
Asymmetric Deactivation of HIV-1 gp41 following Fusion Inhibitor Binding  [PDF]
Kristen M. Kahle,H. Kirby Steger,Michael J. Root
PLOS Pathogens , 2009, DOI: 10.1371/journal.ppat.1000674
Abstract: Both equilibrium and nonequilibrium factors influence the efficacy of pharmaceutical agents that target intermediate states of biochemical reactions. We explored the intermediate state inhibition of gp41, part of the HIV-1 envelope glycoprotein complex (Env) that promotes viral entry through membrane fusion. This process involves a series of gp41 conformational changes coordinated by Env interactions with cellular CD4 and a chemokine receptor. In a kinetic window between CD4 binding and membrane fusion, the N- and C-terminal regions of the gp41 ectodomain become transiently susceptible to inhibitors that disrupt Env structural transitions. In this study, we sought to identify kinetic parameters that influence the antiviral potency of two such gp41 inhibitors, C37 and 5-Helix. Employing a series of C37 and 5-Helix variants, we investigated the physical properties of gp41 inhibition, including the ability of inhibitor-bound gp41 to recover its fusion activity once inhibitor was removed from solution. Our results indicated that antiviral activity critically depended upon irreversible deactivation of inhibitor-bound gp41. For C37, which targets the N-terminal region of the gp41 ectodomain, deactivation was a slow process that depended on chemokine receptor binding to Env. For 5-Helix, which targets the C-terminal region of the gp41 ectodomain, deactivation occurred rapidly following inhibitor binding and was independent of chemokine receptor levels. Due to this kinetic disparity, C37 inhibition was largely reversible, while 5-Helix inhibition was functionally irreversible. The fundamental difference in deactivation mechanism points to an unappreciated asymmetry in gp41 following inhibitor binding and impacts the development of improved fusion inhibitors and HIV-1 vaccines. The results also demonstrate how the activities of intermediate state inhibitors critically depend upon the final disposition of inhibitor-bound states.
Temperature Depended Role of Shigella flexneri Invasion Plasmid on the Interaction with Acanthamoeba castellanii  [PDF]
Amir Saeed,David Johansson,Gunnar Sandstr m,Hadi Abd
International Journal of Microbiology , 2012, DOI: 10.1155/2012/917031
Abstract: Shigella flexneri is a Gram-negative bacterium causing the diarrhoeal disease shigellosis in humans. The virulence genes required for invasion are clustered on a large 220 kb plasmid encoding type three secretion system (TTSS) apparatus and virulence factors such as adhesions and invasion plasmid antigens (Ipa). The bacterium is transmitted by contaminated food, water, or from person to person. Acanthamoebae are free-living amoebae (FLA) which are found in diverse environments and isolated from various water sources. Different bacteria interact differently with FLA since Francisella tularensis, Vibrio cholerae, Shigella sonnei, and S. dysenteriae are able to grow inside A. castellanii. In contrast, Pseudomonas aeruginosa induces both necrosis and apoptosis to kill A. castellanii. The aim of this study is to examine the role of invasion plasmid of S. flexneri on the interaction with A. castellanii at two different temperatures. A. castellanii in the absence or presence of wild type, IpaB mutant, or plasmid-cured strain S. flexneri was cultured at 30°C and 37°C and the interaction was analysed by viable count of both bacteria and amoebae, electron microscopy, flow cytometry, and statistical analysis. The outcome of the interaction was depended on the temperature since the growth of A. castellanii was inhibited at 30°C, and A. castellanii was killed by invasion plasmid mediated necrosis at 37°C.
Temperature Depended Role of Shigella flexneri Invasion Plasmid on the Interaction with Acanthamoeba castellanii  [PDF]
Amir Saeed,David Johansson,Gunnar Sandstr?m,Hadi Abd
International Journal of Microbiology , 2012, DOI: 10.1155/2012/917031
Abstract: Shigella flexneri is a Gram-negative bacterium causing the diarrhoeal disease shigellosis in humans. The virulence genes required for invasion are clustered on a large 220?kb plasmid encoding type three secretion system (TTSS) apparatus and virulence factors such as adhesions and invasion plasmid antigens (Ipa). The bacterium is transmitted by contaminated food, water, or from person to person. Acanthamoebae are free-living amoebae (FLA) which are found in diverse environments and isolated from various water sources. Different bacteria interact differently with FLA since Francisella tularensis, Vibrio cholerae, Shigella sonnei, and S. dysenteriae are able to grow inside A. castellanii. In contrast, Pseudomonas aeruginosa induces both necrosis and apoptosis to kill A. castellanii. The aim of this study is to examine the role of invasion plasmid of S. flexneri on the interaction with A. castellanii at two different temperatures. A. castellanii in the absence or presence of wild type, IpaB mutant, or plasmid-cured strain S. flexneri was cultured at C and C and the interaction was analysed by viable count of both bacteria and amoebae, electron microscopy, flow cytometry, and statistical analysis. The outcome of the interaction was depended on the temperature since the growth of A. castellanii was inhibited at C, and A. castellanii was killed by invasion plasmid mediated necrosis at C. 1. Introduction Shigella flexneri is a Gram-negative bacterium and a human intestinal pathogen, causing the diarrhoeal disease bacillary dysentery (shigellosis), which is a worldwide health problem [1–4]. Shigellosis is characterized by invasion of, massive inflammation in, and destruction of the colonic mucosa. The genes required for invasion are clustered on a large 220?kb invasion plasmid that encodes the type three secretion system (TTSS) apparatus and the effectors’ proteins, which implicate in the mechanism of characteristic cellular invasion of Shigella virulence such as adhesions and invasion plasmid antigens (Ipa) [5–7]. It is well known that S. flexneri utilises TTSS to invade the epithelial layer of the colonic mucosa [7–9]. Infection of the macrophage and epithelial cells has been shown to be the responsible for TTSS effector Ipa proteins [10–12]. The bacteria escape from the phagocytic vacuoles shortly after entry into infected cells, but the outcome of the invasion process depends on the targeted cell [13]. In macrophages, IpaB activates series of reactions, which triggers the apoptosis of the macrophages. Unlike the situation in macrophages, the invasion of
Absence of Metalloprotease GP63 Alters the Protein Content of Leishmania Exosomes  [PDF]
Kasra Hassani, Marina Tiemi Shio, Caroline Martel, Denis Faubert, Martin Olivier
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0095007
Abstract: Protozoan parasites of Leishmania genus are able to successfully infect their host macrophage due to multiple virulence strategies that result in its deactivation. Recent studies suggest Leishmania GP63 to be a critical virulence factor in modulation of many macrophage molecules, including protein tyrosine phosphatases (PTPs) and transcription factors (TFs). Additionally, we and others recently reported that Leishmania-released exosomes can participate in pathogenesis. Exosomes are 40–100 nm vesicles that are freed by many eukaryotic cells. To better understand the GP63-dependent immune modulation of the macrophage by Leishmania parasites and their exosomes, we compared the immunomodulatory properties of Leishmania major (WT) and L. major gp63?/? (KO) as well as their exosomes in vitro and in vivo. Importantly, we observed that Leishmania exosomes can modulate macrophage PTPs and TFs in a GP63-dependent manner. In addition, our qRT-PCR analyses showed that WT parasites were able to downregulate multiple genes involved in the immune response, especially cytokines and pattern recognition receptors. KO parasites showed a strongly reduced modulatory capacity compared to WT parasites. Furthermore, comparison of WT versus KO exosomes also showed divergences in alteration of gene expression, especially of chemokine receptors. In parallel, studying the in vivo inflammatory recruitment using a murine air pouch model, we found that exosomes have stronger proinflammatory properties than parasites and preferentially induce the recruitment of neutrophils. Finally, comparative proteomics of WT and KO exosomes surprisingly revealed major differences in their protein content, suggesting a role for GP63 in Leishmania exosomal protein sorting. Collectively our data clearly establish the crucial role of GP63 in dampening the innate inflammatory response during early Leishmania infection, and also provides new insights in regard to the role and biology of exosomes in Leishmania host-parasite interactions.
Structural Plasticity and Conformational Transitions of HIV Envelope Glycoprotein gp120  [PDF]
Anil Korkut, Wayne A. Hendrickson
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0052170
Abstract: HIV envelope glycoproteins undergo large-scale conformational changes as they interact with cellular receptors to cause the fusion of viral and cellular membranes that permits viral entry to infect targeted cells. Conformational dynamics in HIV gp120 are also important in masking conserved receptor epitopes from being detected for effective neutralization by the human immune system. Crystal structures of HIV gp120 and its complexes with receptors and antibody fragments provide high-resolution pictures of selected conformational states accessible to gp120. Here we describe systematic computational analyses of HIV gp120 plasticity in such complexes with CD4 binding fragments, CD4 mimetic proteins, and various antibody fragments. We used three computational approaches: an isotropic elastic network analysis of conformational plasticity, a full atomic normal mode analysis, and simulation of conformational transitions with our coarse-grained virtual atom molecular mechanics (VAMM) potential function. We observe collective sub-domain motions about hinge points that coordinate those motions, correlated local fluctuations at the interfacial cavity formed when gp120 binds to CD4, and concerted changes in structural elements that form at the CD4 interface during large-scale conformational transitions to the CD4-bound state from the deformed states of gp120 in certain antibody complexes.
Fixed-Point Theorem For Mappings Satisfying a General Contractive Condition Of Integral Type Depended an Another Function  [PDF]
S. Moradi
Mathematics , 2009,
Abstract: We established a fixed-point theorem for mapping satisfying a general contractive inequality of integral type depended an another function. This theorem substantially extend the theorem due to Branciari (2003) and Rhoades (2003)
Kannan Fixed-Point Theorem On Complete Metric Spaces And On Generalized Metric Spaces Depended an Another Function  [PDF]
S. Moradi
Mathematics , 2009,
Abstract: We obtain sufficient conditions for existence of unique fixed point of Kannan type mappings on complete metric spaces and on generalized complete metric spaces depended an another function.
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