Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
TRIT1 encodes a tRNA isopentenyl transferase that allows a strong interaction between the mini helix and the codon. Recent reports support the TRIT1 bi-allelic alterations as the cause of an autosomal recessive disorder, named combined oxydative phophorylation deficiency 35, with microcephaly, developmental disability, and epilepsy. The phenotype is due to decreased mitochondrial function, with deficit of i6A37 in cytosolic and mitochondrial tRNA. Only 10 patients have been reported. We report on two new patients with four novel variants, and confirm the published clinical TRIT1 deficient phenotype stressing the possibility of both very severe, with generalized pharmaco-resistant seizures, and mild phenotypes.
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Source |
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http://dx.doi.org/10.1016/j.ejmg.2022.104603 | DOI Listing |
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