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MySQL Error: 1194 (Table 'pwn_comment' is marked as crashed and should be repaired)
#0 dbbase_sql->halt(Invalid SQL: select count(id) from pwn_comment where pid='548322' and iffb='1') called at [D:\wwwroot\hs21cn2043\wwwroot\includes\db.inc.php:54] #1 dbbase_sql->query(select count(id) from {P}_comment where pid='548322' and iffb='1') called at [D:\wwwroot\hs21cn2043\wwwroot\comment\module\CommentContent.php:65] #2 CommentContent() called at [D:\wwwroot\hs21cn2043\wwwroot\includes\common.inc.php:551] #3 printpage() called at [D:\wwwroot\hs21cn2043\wwwroot\comment\html\index.php:13]
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Warning: mysql_query() [function.mysql-query]: Unable to save result set in D:\wwwroot\hs21cn2043\wwwroot\includes\db.inc.php on line 50
Database error: Invalid SQL: select * from pwn_comment where pid='548322' and iffb='1' order by id limit 0,10
MySQL Error: 1194 (Table 'pwn_comment' is marked as crashed and should be repaired)
#0 dbbase_sql->halt(Invalid SQL: select * from pwn_comment where pid='548322' and iffb='1' order by id limit 0,10) called at [D:\wwwroot\hs21cn2043\wwwroot\includes\db.inc.php:54] #1 dbbase_sql->query(select * from {P}_comment where pid='548322' and iffb='1' order by id limit 0,10) called at [D:\wwwroot\hs21cn2043\wwwroot\comment\module\CommentContent.php:167] #2 CommentContent() called at [D:\wwwroot\hs21cn2043\wwwroot\includes\common.inc.php:551] #3 printpage() called at [D:\wwwroot\hs21cn2043\wwwroot\comment\html\index.php:13]
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网友点评-Unctionally related to that of L. pneumophila to-线缆测高仪,超声波测高仪, 手持式测高仪-上海交通大学科技园上海野豹企业发展公司
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发布于:2018-9-19 20:26:39  访问:71 次 回复: 篇
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Unctionally related to that of L. pneumophila to
The inflammasome is another cytosolic immune response which is robustly activated and plays a important role in controlling a variety of pathogens, including L. pneumophila (116). In contrast to L. pneumophila, C. burnetii doesn‘t possess flagellin (117), a potent activator in the NAIP5 inflammasome (71, 72). It was unknown, nevertheless, if C. burnetii, like L. pneumophila, possesses other stimulators of inflammasome activation. We identified that even though C. burnetii NMII induces pro-IL-1 production, it will not induce inflammasome MLN1117 chemical information activation in WT B6 macrophages, in agreement having a not too long ago published study (45). Additionally, NMII didn‘t induce inflammasome activation in Tlr2 / macrophages that support NMII replication, suggesting that the inability of NMII to trigger inflammasome activation in B6 macrophages is not as a result of an inability to replicate within this cell form. One possibility for the lack of inflammasome activation is that C. burnetii may not express PAMPs which might be recognized by inflammasome-associated PRRs. For example, caspase-11 recognizes hexa- or penta-acylated LPS (100, 101), whereas C. burnetii generates tetra-acylated LPS (58), despite the fact that a recent study indicated that purified C. burnetii LPS transfected into macrophages could activate caspase-11 (45). Alternatively, C. burnetii may employ T4SS effectors to actively inhibit inflammasome activation. It was not too long ago shown that the C. burnetii T4SS effector protein, IcaA, can inhibit caspase-11 activation in mouse macrophages when expressed in L. pneumophila (45). Interestingly, an IcaA-deficient C. burnetii NMII strain is unable to inhibit noncanonical inflammasome activation induced by L. pneumophila coinfection, but there EHop-016 Purity nonetheless is no proof of inflammasome activation PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/21411495 in mouse macrophages infected withIcaA-deficient C. burnetii alone, suggesting that you can find added mechanisms employed by C. burnetii to evade inflammasome activation (45). It has been shown, on the other hand, that major human alveolar macrophages create mature IL-1 in response to NMII but not phase I C. burnetii, suggesting that human and mouse inflammasome sensors or different cell types differ in their responses to NMII PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26891946 infection (54). The discovering that NMII does not induce inflammasome activation in mouse cells may possibly give some insight in to the observation that neutrophil recruitment is delayed in mice infected with phase I or phase II C. burnetii till 1 week postinfection (118), as inflammasome-derived IL-1 is a crucial regulator of neutrophil recruitment during other bacterial infections, which include pulmonary L. pneumophila infection (68, 90?92). Further research are warranted to identify the further mechanisms by which C. burnetii evades inflammasome activation in mouse macrophages. A lot of intracellular bacteria trigger cytosolic nuc.Unctionally similar to that of L. pneumophila to translocate effector proteins into B6 BMDMs (59, 115), we subsequent asked whether B6 BMDMs make use of cytosolic immunosurveillance pathways to detect and restrict NMII infection. In contrast to what was observed for L. pneumophila, we did not observe a clear requirement for the C. burnetii NMII T4SS in enhancing cytokine responses. Instead, we observed a slight decrease in TNF and IL-6 production in response to T4SS-expressing NMII in comparison with that of a T4SS-deficient strain.
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