scholarly journals Utility of brain CT for predicting delayed encephalopathy after acute carbon monoxide poisoning

2019 ◽  
Author(s):  
Xuqin Du ◽  
Hua Gu ◽  
Fengtong Hao ◽  
Lin Gao ◽  
Jianru Wang ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Brain Ct ◽  
Acute Carbon Monoxide Poisoning ◽  
Delayed Encephalopathy

scholarly journals LRCH1 polymorphisms linked to delayed encephalopathy after acute carbon monoxide poisoning identified by GWAS analysis followed by Sequenom MassARRAY® validation

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Jiapeng Gu ◽  
Jiao Zeng ◽  
Xi Wang ◽  
Xin Gu ◽  
Xiaoli Zhang ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Association Analysis ◽  
Carbon Monoxide Poisoning ◽  
Genetic Models ◽  
Nucleotide Polymorphisms ◽  
Sequenom Massarray ◽  
Acute Carbon Monoxide Poisoning ◽  
Diagnosis And Prognosis ◽  
Increased Risk ◽  
Delayed Encephalopathy

Abstract Background We explored the association of leucine-rich repeats and calponin homology domain containing 1 (LRCH1) gene polymorphisms with genetic susceptibility to delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), which might provide a theoretical basis for the pathogenesis, diagnosis, and prognosis research of DEACMP. Methods Four single nucleotide polymorphisms, rs1539177 (G/A), rs17068697 (G/A), rs9534475 (A/C), and rs2236592 (T/C), of LRCH1, selected as candidate genes through genome-wide association analysis, were genotyped in 661 patients (DEACMP group: 235 cases; ACMP group: 426 cases) using Sequenom Massarray®. The association analysis of four SNPs and LRCH1 was performed under different genetic models. Results LRCH1 polymorphisms (rs1539177, rs17068697, rs9534475) under additive and dominant genetic models were significantly associated with an increased risk of DEACMP, but no significant association under allele and recessive models was found. The LRCH1 rs2236592 polymorphism was susceptible to DEACMP only under the dominant model (TT/TC + CC, OR = 1.616, 95% CI: 1.092–2.390, P = 0.015784). In addition, the A allele gene of rs9534475 polymorphism in LRCH1 might increase the risk for DEACMP (OR = 1.273, 95% CI: 1.013–1.601, P = 0.038445). Conclusions We found a significant association between the four LRCH1 polymorphisms and DEACMP. The allelic A of rs9534475 polymorphism in LRCH1 might be a risk factor for DEACMP.

Risk Factors of Development of Delayed Encephalopathy following Acute Carbon Monoxide Poisoning

1992 ◽  
Vol 1 (5) ◽  
pp. 268-271
Author(s):  
Fengsheng He ◽  
Jie Qin ◽  
Shuyang Chen ◽  
Xiaowen Pan ◽  
Guanghua Xu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Acute Carbon Monoxide Poisoning ◽  
Delayed Encephalopathy

scholarly journals P2Y12 receptor-mediated microglia activation involved in delayed encephalopathy after acute carbon monoxide poisoning

Aging ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 6134-6143
Author(s):  
Wenping Xiang ◽  
Zhigang Yang ◽  
Hui Xue ◽  
Jingbo Wang ◽  
Fanyan Niu ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Microglia Activation ◽  
P2y12 Receptor ◽  
Acute Carbon Monoxide Poisoning ◽  
Delayed Encephalopathy

scholarly journals Buyanghuanwu decoction inhibited TLR4-induced activation of nuclear factor-kappa B in acute carbon monoxide poisoning rats

2015 ◽  
Author(s):  
Weirong Li ◽  
Xiuwei Wang ◽  
Zhen Guan ◽  
Yufei Zheng ◽  
Xiaodong Zhang ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Nuclear Factor Kappa B ◽  
Carbon Monoxide Poisoning ◽  
Intragastric Administration ◽  
Protective Effects ◽  
Hippocampal Region ◽  
Acute Carbon Monoxide Poisoning ◽  
Tnf Α ◽  
Delayed Encephalopathy ◽  
Optimal Treatment Strategy

Acute carbon monoxide poisoning (ACMP) is one of the most common types of poisoning worldwide, and may result in delayed encephalopathy, however, its pathogenesis remains obscure and there is no optimal treatment strategy for the patients with ACMP. Here, we developed the ACMP rat model to observe the protective effects of Buyanghuanwu decoction (BYHWD) on hippocampal neuron. BYHWD (per 5 g/kg) were intragastric administration to rats twice each day for 28 days after ACMP. In ACMP + BYHWD group rats, the neuronal injury in the hippocampal region was significantly less than that of ACMP group’s. BYHWD of intragastric administration also markedly decreased the expression of the TLR4, MyD88, NF-κB P65 after acute carbon monoxide poisoning (P<0.05). TNF-α、IL-1β protein level in ACMP + BYHWD group was lower than that of ACMP group (P<0.05). Our results suggested that decreased the activation of TLR4- NF-κB signal pathway due to BYHWD may partially account for its effect of neuroprotection standing against ACMP, and inhibited the inflammatory reaction to promote the ability recovery of learning and memory in ACMP rats.

scholarly journals Association between Neuron-Specific Enolase Gene Polymorphism and Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Linlin Xu ◽  
Xuejiao Liu ◽  
Jing Zhao ◽  
Jiao Zeng ◽  
Jiapeng Gu ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Gene Polymorphism ◽  
Association Studies ◽  
Carbon Monoxide Poisoning ◽  
Neuron Specific Enolase ◽  
Genetic Models ◽  
Genome Wide Association Studies ◽  
Acute Carbon Monoxide Poisoning ◽  
Increased Risk ◽  
Delayed Encephalopathy

Objective. The aim of this study is to explore the relationship between neuron-specific enolase (NSE) gene polymorphism and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) and provide a theoretical basis for DEACMP pathogenesis, diagnosis, and prognosis. Methods. To investigate this relationship, we screened 6 NSE single nucleotide polymorphisms (SNPs), based on the results of the previous genome-wide association studies (GWAS). A total of 1,201 patients, including 416 in the DEACMP group and 785 in the acute carbon monoxide poisoning (ACMP) group, were detected by the Sequenom MassARRAY® method. The genotype frequencies and alleles of the 6 NSE SNPs (rs2071074, rs2071417, rs2071419, rs11064464, rs11064465, and rs3213434) were compared using different genetic models. Results. In the SNPs rs2071419 and rs3213434, we found that the genotypes and allele frequencies in the two groups significantly correlated with the grouping of patients ( χ 2 = 6.596 , p = 0.037 ; χ 2 = 8.769 , p = 0.012 ). The haplotypes GGTTTC and CCTTTC of ACMP and DEACMP were different ( χ 2 = 6.563 , p = 0.010 ; χ 2 = 4.151 , p = 0.042 ). We also observed that rs2071419 and rs3213434 significantly correlated with DEACMP-increased risk in the dominant, codominant, and overdominant genetic models. In addition, we speculated that the C allele of the rs2071419 polymorphism and the T allele of the rs3213434 polymorphism in NSE may increase the DEACMP risk ( p = 0.011 , p = 0.006 ). Conclusions. The results show that rs2071419 and rs3213434 are susceptible sites of DEACMP. The NSE C allele of rs2071419 and T allele of rs3213434 and the haplotypes GGTTTC and CCTTTC may be risk factors for DEACMP.

scholarly journals After Treatment with Methylene Blue is Effective against Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

2017 ◽  
Vol 122 (5) ◽  
pp. 470-480 ◽  
Author(s):  
Ningjun Zhao ◽  
Pengchong Liang ◽  
Xiaoying Zhuo ◽  
Chenglei Su ◽  
Xuemei Zong ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Acute Carbon Monoxide Poisoning ◽  
Delayed Encephalopathy

scholarly journals Mechanism of delayed encephalopathy after acute carbon monoxide poisoning

2020 ◽  
Vol 15 (12) ◽  
pp. 2286
Author(s):  
Zheng-Rong Peng ◽  
Yan-Qing Huang ◽  
Fang-Ling Huang ◽  
A-Li Yang
Keyword(s):  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Acute Carbon Monoxide Poisoning ◽  
Delayed Encephalopathy

Risk Factors of Development of Delayed Encephalopathy following Acute Carbon Monoxide Poisoning

1992 ◽  
Vol 1 (5) ◽  
pp. 268-271 ◽  
Author(s):  
Fengsheng He ◽  
Jie Qin ◽  
Shuyang Chen ◽  
Xiaowen Pan ◽  
Guanghua Xu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Carbon Monoxide ◽  
Carbon Monoxide Poisoning ◽  
Acute Carbon Monoxide Poisoning ◽  
Delayed Encephalopathy
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