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Filename: drivers/Session_files_driver.php
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File: /var/www/html/index.php
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Filename: Session/Session.php
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File: /var/www/html/index.php
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Function: require_once
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Message: Undefined array key "choices"
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 249
Backtrace:
File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
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Message: strpos(): Passing null to parameter #1 ($haystack) of type string is deprecated
Filename: models/Detail_model.php
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Function: strpos
File: /var/www/html/application/controllers/Detail.php
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Function: insertAPISummary
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Filename: helpers/my_audit_helper.php
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File: /var/www/html/application/controllers/Detail.php
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Filename: controllers/Detail.php
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Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
Line Number: 256
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File: /var/www/html/application/controllers/Detail.php
Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Undefined array key "usage"
Filename: controllers/Detail.php
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Line: 257
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 257
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
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Function: file_get_contents
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Objective: Endoplasmic reticulum (ER) stress plays important roles not only in stress avoidance, but also in cell differentiation and maturation, cell proliferation, and promotion of bone formation. This study aimed to investigate the involvement of ER stress in the onset of pulpitis.
Methods: Immunohistochemical analysis was conducted on human teeth extracted for orthodontic reasons. The effects of tunicamycin (TM), an inducer of ER stress, lipopolysaccharide (LPS), and 4μ8c, an inhibitor of inositol-requiring enzyme 1 (IRE1) on cultured human dental pulp cells (hDPCs) were also examined.
Results: The expressions of two ER stress markers, X-box binding protein (XBP)-1 and binding immunoglobulin protein (BiP)/78 kDa glucose-regulated protein (GRP78), were found in the human pulp tissues of a decayed tooth that had not developed irreversible acute pulpitis, but not in an impacted tooth without inflammation in pulp tissue. Both TM and LPS increased the mRNA levels of XBP-1, interleukin (IL)-6, and IL-8, whereas TM, but not LPS, enhanced the mRNA expression of BiP/GRP78 in hDPCs. 4μ8c significantly suppressed the increased level of XBP-1 by LPS.
Conclusion: This study is the first to demonstrate that XBP-1, in addition to inflammatory cytokines, may participate in the onset of pulpitis through IRE1. These findings provide a more comprehensive understanding of pulpitis pathogenesis through the cooperation of ER stress and inflammatory cytokines.
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Source |
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http://dx.doi.org/10.14744/eej.2024.49344 | DOI Listing |
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