FEMS immunology and medical microbiology最新文献

{"title":"Characterization of the PCR inhibitory effect of bile to optimize real-time PCR detection of Helicobacter species","authors":"Waleed Abu Al-Soud,&nbsp;Ibn-Sina Ouis,&nbsp;Dai-Qing Li,&nbsp;Åsa Ljungh,&nbsp;Torkel Wadström","doi":"10.1016/j.femsim.2004.12.004","DOIUrl":"10.1016/j.femsim.2004.12.004","url":null,"abstract":"<div><p><span>The inhibitory effect of human and porcine bile samples to detect Helicobacter DNA was studied by adding different concentrations of bile samples to PCR mixtures of six thermostable DNA polymerases containing </span><em>cagA</em> specific primers and <span><em>Helicobacter pylori</em></span> DNA. PCR products were amplified by using the Rotorgene system and SYBR Green I. Among the six DNA polymerases tested, r<em>Tth</em> had the lowest sensitivity to bile inhibitors, whereas <em>Taq</em> and <em>Tfl</em> had the highest sensitivity. Bile proteins did not inhibit Ampli<em>Taq</em><span> DNA polymerase, whereas the fraction containing mainly bile acids and their salts inhibited the amplification capacity of Ampli</span><em>Taq</em>. Heating human bile at 98<!--> <span>°C and adding casein and formamide to the reaction mixture reduced the PCR inhibitory effect of bile. Therefore, a pre-PCR treatment based on dilution and heating of bile, adding casein and formamide to the reaction mixture of r</span><em>Tth</em> DNA polymerase was found efficient to amplify DNA directly in bile.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.12.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25089019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenesis and host response in Helicobacter infections","authors":"Karen A. Krogfelt,&nbsp;Leif Percival Andersen (Secretary and Chair of the local Scientific Committee, respectively),&nbsp;J.G. Kusters (Editor)","doi":"10.1016/j.femsim.2005.02.006","DOIUrl":"10.1016/j.femsim.2005.02.006","url":null,"abstract":"","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2005.02.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88880541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Minimizing the release of proinflammatory and toxic bacterial products within the host: A promising approach to improve outcome in life-threatening infections","authors":"Roland Nau ,&nbsp;Helmut Eiffert","doi":"10.1016/j.femsim.2005.01.001","DOIUrl":"10.1016/j.femsim.2005.01.001","url":null,"abstract":"<div><p><span><span>Various bacterial components (e.g., endotoxin<span>, teichoic and lipoteichoic acids, </span></span>peptidoglycans<span><span>, DNA) induce or enhance inflammation by stimulating the innate immune system and/or are directly toxic in eukariotic cells (e.g., hemolysins). When antibiotics which inhibit bacterial </span>protein synthesis kill bacteria, smaller quantities of proinflammatory or toxic compounds are released in vitro and in vivo than during killing of bacteria by β-lactams and other cell-wall active drugs. In general, high antibiotic concentrations liberate lower quantities of bacterial proinflammatory or toxic compounds than concentrations close to the minimum inhibitory concentration. In animal models of </span></span><span><em>Escherichia coli </em><em>Pseudomonas aeruginosa</em></span> and <span><em>Staphylococcus aureus</em></span> peritonitis/sepsis and of <span><em>Streptococcus pneumoniae</em></span><span> meningitis, a lower release of proinflammatory bacterial compounds was associated with a reduced mortality or neuronal injury. Pre-treatment with a bacterial protein synthesis inhibitor reduced the strong release of bacterial products usually observed during treatment with a β-lactam antibiotic. Data available strongly encourage clinical trials comparing antibiotic regimens with different release of proinflammatory/toxic bacterial products. The benefit of the approach to reduce the liberation of bacterial products should be greatest in patients with a high bacterial load.</span></p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2005.01.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25017157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological importance of the two Toll-like receptors, TLR2 and TLR4, in macrophage response to infection with Candida albicans","authors":"Elisabetta Blasi ,&nbsp;Anna Mucci ,&nbsp;Rachele Neglia ,&nbsp;Francesco Pezzini ,&nbsp;Bruna Colombari ,&nbsp;Danuta Radzioch ,&nbsp;Andrea Cossarizza ,&nbsp;Enrico Lugli ,&nbsp;Gianfranco Volpini ,&nbsp;Giuseppe Del Giudice ,&nbsp;Samuele Peppoloni","doi":"10.1016/j.femsim.2004.12.005","DOIUrl":"10.1016/j.femsim.2004.12.005","url":null,"abstract":"<div><p><span><span><span>The aim of this study was to assess the role of TLR2<span>, TLR4<span> and MyD88 accessory molecule in the effector and secretory response of macrophages to viable microbial agents. Using TLR-deleted </span></span></span>macrophage cell lines generated from the bone marrow of </span>genetically engineered mice (TLR4 gene-deficient, MyD88- and TLR2-knockout mice) and wild-type control mice, we found that TLR2-deleted macrophages exhibit increased ability to contain </span><span><em>Candida albicans</em></span><span> infection compared to TLR2+/+ counterpart. In contrast, both MyD88−/− and TLR4−/− macrophages retain levels of functional activity comparable to that of the respective wild-type MyD88+/+ and TLR4+/+ controls. The difference in anticandidal effector functions observed between TLR2−/− and TLR2+/+ macrophages is abrogated upon opsonization of the fungal target and interestingly is not observed when using other microbial targets, such as </span><span><em>Streptococcus pneumoniae</em></span> and <span><em>Helicobacter pylori</em></span>. When tested for secretory response to <em>C. albicans</em><span>, TLR2-deleted macrophages show a pattern of cytokine production similar to that of TLR2+/+ controls. Finally, flow cytometry analysis reveals that TLR2-deleted macrophages express only TLR4, while, as expected, TLR2+/+ macrophages are both TLR2 and TLR4 positive; in no cases, modulation of such markers occurs in macrophages exposed to </span><em>C. albicans</em> infection. In conclusion, these data indicate that TLR2 and TLR4 have different biological relevance, in which TLR2 but not TLR4, is involved in the accomplishment of macrophage-mediated anticandidal activity, while the secretory response to <em>C. albicans</em> appears to be TLR4 but not TLR2-dependent.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.12.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25074144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of Porphyromonas gingivalis-induced monocyte chemoattractant protein-1 expression in endothelial cells","authors":"Eun-Kyoung Choi ,&nbsp;Sun-Ah Park ,&nbsp;Won-Mann Oh ,&nbsp;Ho-Cheol Kang ,&nbsp;Howard K. Kuramitsu ,&nbsp;Byung-Gook Kim ,&nbsp;In-Chol Kang","doi":"10.1016/j.femsim.2004.12.003","DOIUrl":"10.1016/j.femsim.2004.12.003","url":null,"abstract":"<div><p><span>Monocyte chemoattractant protein-1 (MCP-1) is expressed in vascular endothelial cells<span><span> of inflamed gingival tissues and plays an important role in periodontal pathogenesis. </span>Endothelial cells produce high levels of MCP-1 in response to </span></span><span><em>Porphyromonas gingivalis</em></span><span><span>, an important periodontal pathogen. The present study investigated the mechanisms involved in MCP-1 production by </span>human umbilical vein endothelial cells (HUVEC) following infection with </span><em>P. gingivalis</em>. In contrast to <span><em>P. gingivalis, </em><em>Bacteroides forsythus</em></span> only weakly stimulated MCP-1 production while <span><em>Treponema denticola</em></span><span> could not induce MCP-1 in HUVEC. The MCP-1 production was independent of endogenous interleukin (IL)-1α as IL-1 receptor antagonist treatment did not reduce MCP-1 production by </span><em>P. gingivalis</em><span>. Meanwhile, antioxidant treatment and inhibition of NAD(P)H oxidase significantly reduced MCP-1 production. Pharmacological inhibition of p38 mitogen-associated protein (MAP) kinase, c-Jun N-terminal kinase (JNK), nuclear factor-κB (NF-κB) or activator protein-1 (AP-1) also substantially attenuated </span><em>P. gingivalis</em>-induced MCP-1 expression by HUVEC. Indeed, activation of NF-κB and AP-1 was observed in <em>P. gingivalis</em>-infected HUVEC. These results suggest that MCP-1 expression is upregulated in <em>P. gingivalis</em>-infected endothelial cells via reactive oxygen species, p38 MAP kinase, JNK, NF-κB, and AP-1.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.12.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25016215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strain-dependent disruption of blood–cerebrospinal fluid barrier by Streptoccocus suis in vitro","authors":"Tobias Tenenbaum ,&nbsp;Rüdiger Adam ,&nbsp;Ingo Eggelnpöhler ,&nbsp;David Matalon ,&nbsp;Annette Seibt ,&nbsp;Gerd E. K. Novotny ,&nbsp;Hans-Joachim Galla ,&nbsp;Horst Schroten","doi":"10.1016/j.femsim.2004.12.006","DOIUrl":"10.1016/j.femsim.2004.12.006","url":null,"abstract":"<div><p><span><em>Streptococcus suis</em></span><span><span> capsular type 2 is an important agent of diseases including meningitis among pigs worldwide, and is also a zoonotic agent. The barrier function of the </span>choroid plexus<span> epithelium that constitutes the structural basis for the blood-cerebrospinal fluid (CSF) barrier has not been elucidated yet in bacterial meningitis. We investigated the influence of various </span></span><em>S. suis</em><span> isolates on the barrier function of cultured porcine choroid plexus epithelial cells with respect to the transepithelial resistance and paracellular [</span>³H]-mannitol flux. Preferentially apical application of <em>S. suis</em> isolates significantly decreased transepithelial resistance and significantly increased paracellular [³H]-mannitol flux in a time-, dose- and strain-dependent manner. Viable <em>S. suis</em><span><span> isolates caused cytotoxicity determined by lactate dehydrogenase assay and </span>electron microscopy, whereas </span><em>S. suis</em> sonicates and UV-inactivated <em>S. suis</em><span> did not cause cytotoxicity. The observed effects on porcine choroid plexus epithelial cells barrier function could not exclusively be ascribed to known virulence factors of </span><em>S. suis</em> such as suilysin. In conclusion, <em>S. suis</em> isolates induce loss of blood–cerebrospinal fluid barrier function in an in vitro model. Thus, <em>S. suis</em> may facilitate trafficking of bacteria and leucocytes across the blood–cerebrospinal fluid barrier. The underlying mechanisms for the barrier breakdown have yet to be determined.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.12.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25016212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of a peroxiredoxin–glutaredoxin by Haemophilus influenzae in biofilms and during human respiratory tract infection","authors":"Timothy F. Murphy ,&nbsp;Charmaine Kirkham ,&nbsp;Sanjay Sethi ,&nbsp;Alan J. Lesse","doi":"10.1016/j.femsim.2004.12.008","DOIUrl":"10.1016/j.femsim.2004.12.008","url":null,"abstract":"<div><p>Evidence is mounting that nontypeable <em>Haemophilus influenzae</em><span> grows as a biofilm in the middle ear of children with otitis media<span> and the airways of adults with chronic obstructive pulmonary disease. To begin to assess antigens expressed by </span></span><span><em>H. influenzae</em></span> in biofilms, cell envelopes of bacteria grown as a biofilm were compared to those grown planktonically. A ∼30<!--> <span>kDa peroxiredoxin–glutaredoxin was present in greater abundance during growth in biofilms. Mutants deficient in expression of peroxiredoxin–glutaredoxin were constructed by homologous recombination in four clinical isolates. The mutants showed a 25–50% reduction in biofilm formation compared to the corresponding parent strains. To study in vivo expression of peroxiredoxin–glutaredoxin during human respiratory tract infection, paired pre- and post-exacerbation serum from adults with chronic obstructive pulmonary disease and </span><em>H. influenzae</em><span> in sputum were assayed using an enzyme-linked immunosorbent assay and purified recombinant peroxiredoxin–glutaredoxin. Eight from 18 (44.4%) paired serum samples showed a significant increase in antibody to peroxiredoxin–glutaredoxin from pre- to post-infection. These results indicate that (1) peroxiredoxin–glutaredoxin is present in greater abundance in </span><em>H. influenzae</em> biofilms compared to planktonically grown bacteria; (2) peroxiredoxin–glutaredoxin is involved in biofilm formation by <em>H. influenzae</em> and the degree of involvement varies among strains; and (3) peroxiredoxin–glutaredoxin is expressed by <em>H. influenzae</em> during infection of the human respiratory tract and is recognized by the human immune system.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.12.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25016217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High relative content of lysophospholipids of Helicobacter pylori mediates increased risk for ulcer disease","authors":"Tone Tannaes ,&nbsp;Ida K. Bukholm ,&nbsp;Geir Bukholm","doi":"10.1016/j.femsim.2004.10.003","DOIUrl":"10.1016/j.femsim.2004.10.003","url":null,"abstract":"<div><p><span><span>Helicobacter pylori</span></span><span><span><span> phospholipase A<span><span> (OMPLA) degrades bacterial membrane phospholipids to </span>lysophospholipids. High levels of lysophospholipids are associated with higher </span></span>hemolytic activity, increased release of </span>urease and vacA and better adherence to epithelial cells in vitro. The phospholipase A gene (</span><em>pldA</em><span>) displays phase variation due to a slippage in a homopolymeric tract. The aim of this study was to determine if the relative amount of lysophospholipids in the cell wall is associated with ulcer disease, and to further investigate the significance of </span><em>pldA</em> phase variation. <em>H. pylori</em> isolates of 40 patients were examined. The relative lysophospholipid content of each isolate was determined and the <em>pldA</em> gene was sequenced. The study indicated that <em>H. pylori</em> can regulate its OMPLA activity by phase variation in the <em>pldA</em> gene or by protein level regulation among phase variants in the <em>pldA</em> ‘ON’ status. We found a significant difference between the relative amount of lysophospholipids of the ulcer group and the non-ulcer group (<em>p</em> <!-->=<!--> <!-->0.022). When the lysophospholipid/phospholipid ratios were compared with outcome, the OR for ulcer disease was 9.0 (95% CI 1.6–49.4; <em>p</em> <!-->=<!--> <!-->0.014). Isolates with a high OMPLA activity are significantly associated with patients with ulcer disease.</p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.10.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25016211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of anti-β-glucan antibody in host defense against fungi","authors":"Ken-ichi Ishibashi ,&nbsp;Masaharu Yoshida ,&nbsp;Iwao Nakabayashi ,&nbsp;Hiroyasu Shinohara ,&nbsp;Noriko N. Miura ,&nbsp;Yoshiyuki Adachi ,&nbsp;Naohito Ohno","doi":"10.1016/j.femsim.2004.12.012","DOIUrl":"10.1016/j.femsim.2004.12.012","url":null,"abstract":"<div><p>We have recently detected an anti-β-glucan antibody in normal human and normal mouse sera. The anti-β-glucan antibody showed reactivity to pathogenic fungal <span><em>Aspergillus</em></span> and <em>Candida</em><span> cell wall glucan. Anti-β-glucan antibody could bind whole </span><em>Candida</em><span> cells. It also enhanced the candidacidal activity of macrophages in vitro. The anti-β-glucan antibody titer of DBA/2 mice intravenously administered either </span><em>Candida</em> or <em>Aspergillus</em><span> solubilized cell wall β-glucan decreased remarkably dependent on dose. Moreover, in deep mycosis<span> patients, the anti-β-glucan antibody titer decreased, and this change correlated with clinical symptoms and other parameters such as C-reactive protein. It was suggested that the anti-β-glucan antibody formed an antigen–antibody complex and participated in the immune response as a molecule recognizing pathogenic fungi.</span></span></p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.12.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25016578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Altered T helper 1 reaction but not increase of virus load in patients with dengue hemorrhagic fever","authors":"Rong-Fu Chen ,&nbsp;Jien-Wei Liu ,&nbsp;Wen-Ting Yeh ,&nbsp;Lin Wang ,&nbsp;Jen-Chieh Chang ,&nbsp;Hong-Ren Yu ,&nbsp;Jiin-Tsuey Cheng ,&nbsp;Kuender D. Yang","doi":"10.1016/j.femsim.2004.11.012","DOIUrl":"10.1016/j.femsim.2004.11.012","url":null,"abstract":"<div><p><span>To investigate whether dengue-2 patients with and without dengue </span>hemorrhagic fever<span> had different virus load, immune mediators, or T helper (Th) reaction, we simultaneously measured virus load, immune mediators and the Th1/Th2 transcription factors T-bet/GATA-3 mRNA expression in a large outbreak of dengue-2 infections in Southern Taiwan. Results showed that virus load was not significantly different between patients with and without dengue hemorrhagic fever. Patients with dengue fever had higher IFN-γ levels, but patients with dengue hemorrhagic fever had significantly higher IL-10 levels. Further studies showed that patients with dengue hemorrhagic fever had a significantly lower T-bet than those with dengue fever, but GATA-3 mRNA expression in peripheral blood leukocytes was not significant difference between both groups. In conclusion, altered Th1 reaction as reflected by lower T-bet mRNA expression associated with higher IL-10 levels might be involved in the pathogenesis of dengue hemorrhagic fever.</span></p></div>","PeriodicalId":12220,"journal":{"name":"FEMS immunology and medical microbiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.femsim.2004.11.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25016214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}