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Study on the mechanism of brain injury caused by acute diquat poisoning based on metabolomics.

Toxicol Appl Pharmacol

January 2025

West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, Sichuan, China; Department of Emergency and Critical Care Medicine, West China School of Public Health, West China Fourth Hospital, Si Chuan, China; West China-PUMC C.C. Chen Institute of Health, Sichuan University, Chengdu 610041, Si Chuan, China. Electronic address:

Article Synopsis
  • Diquat poisoning is linked to increased brain injuries and high mortality, leading researchers to study metabolomics in brain tissue from poisoned rats to understand its effects.
  • The analysis identified significant changes in metabolites, with some upregulated and downregulated in both high and low-dose groups, suggesting altered metabolic pathways in brain injury cases.
  • Three specific metabolites (sedoheptulose-7-phosphate, (2R)-2-hydroxy-3-(phosphonatooxy)propanoate, and 3-hydroxybenzoic acid) showed strong potential as diagnostic markers for brain injury from diquat poisoning and correlated with clinical indicators.
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Background: BK polyomavirus-associated nephropathy (BKPyVAN) is an important cause of allograft dysfunction and failure in kidney transplant recipients (KTRs) and there are no proven effective treatments. Case reports and in vitro data support the potential activity of cidofovir against BK polyomavirus (BKPyV).

Methods: We report the results of a phase I/II, double-blind, placebo-controlled randomized dose-escalation trial of cidofovir in KTRs with biopsy-confirmed BKPyVAN and estimated glomerular filtration rate ≥30 mL/min.

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Pseudomonas aeruginosa (P. aeruginosa) is a gram-negative biofilm-forming opportunistic human pathogen whose vital mechanism is biofilm formation for better survival. PelA and PelB proteins of the PEL operon are essential for bacterial-synthesized pellicle polysaccharide (PEL), which is a vital structural component of the biofilm.

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Improving outcomes for older patients with acute myeloid leukaemia remains an unmet need. As part of the LI-1 trial, we evaluated lenalidomide (LEN) in combination with low-dose cytosine arabinoside (LDAC) in patients aged >60 years unfit for intensive therapy and compared this to LDAC alone. Two hundred and two patients, randomised 1:1, were evaluable.

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