OBJECTIVES: The neurotoxicity of carbon monoxide (CO) to the central nervous system is a key pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Our previous study found that retinoic acid (RA) can suppress the neurotoxic effects of CO. This study further explores, in vivo and in vitro, the molecular mechanisms by which RA alleviates CO-induced central nervous system damage. METHODS: A cytotoxic model was established using the mouse hippocampal neuronal cell line HT22 and primary oligodendrocytes exposed to CO, and a DEACMP animal model was established in adult Kunming mice. Cell viability and apoptosis of hippocampal neurons and oligodendrocytes were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Annexin V/propidium iodide (PI) double staining. The transcriptional and protein expression of each gene was detected using real-time fluorescence quantitative PCR (RT-qPCR) and Western blotting. Long noncoding RNA (lncRNA) SNHG15 and LINGO-1 were knocked down or overexpressed to observe changes in neurons and oligodendrocytes. In DEACMP mice, SNHG15 or LINGO-1 were knocked down to assess changes in central nervous tissue and downstream protein expression. RESULTS: RA at 10 and 20 μmol/L significantly reversed CO-induced apoptosis of hippocampal neurons and oligodendrocytes, downregulation of SNHG15 and LINGO-1, and upregulation of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB) (all P<0.05). Overexpression of SNHG15 or LINGO-1 weakened the protective effect of RA against CO-induced cytotoxicity (all P<0.05). Knockdown of SNHG15 or LINGO-1 alleviated CO-induced apoptosis of hippocampal neurons and oligodendrocytes and upregulated BDNF and TrkB expression levels (all P<0.05). Experiments in DEACMP model mice showed that knockdown of SNHG15 or LINGO-1 mitigated central nervous system injury in DEACMP (all P<0.05). CONCLUSIONS RA alleviates CO-induced apoptosis of hippocampal neurons and oligodendrocytes, thereby reducing central nervous system injury and exerting neuroprotective effects. LncRNA SNHG15 and LINGO-1 are key molecules mediating RA-induced inhibition of neuronal apoptosis and are associated with the BDNF/TrkB pathway. These findings provide a theoretical framework for optimizing the clinical treatment of DEACMP and lay an experimental foundation for elucidating its molecular mechanisms.
Animals ; RNA, Long Noncoding/physiology* ; Brain-Derived Neurotrophic Factor/genetics* ; Carbon Monoxide Poisoning/complications* ; Mice ; Tretinoin/pharmacology* ; Nerve Tissue Proteins/metabolism* ; Membrane Proteins/metabolism* ; Apoptosis/drug effects* ; Hippocampus/cytology* ; Receptor, trkB/metabolism* ; Neurons/drug effects* ; Male ; Brain Diseases/etiology* ; Oligodendroglia/drug effects* ; Signal Transduction ; Cell Line

Nitrogen narcosis is a neurological syndrome that manifests when humans or animals encounter hyperbaric nitrogen, resulting in a range of motor, emotional, and cognitive abnormalities. The anterior cingulate cortex (ACC) is known for its significant involvement in regulating motivation, cognition, and action. However, its specific contribution to nitrogen narcosis-induced hyperlocomotion and the underlying mechanisms remain poorly understood. Here we report that exposure to hyperbaric nitrogen notably increased the locomotor activity of mice in a pressure-dependent manner. Concurrently, this exposure induced heightened activation among neurons in both the ACC and dorsal medial striatum (DMS). Notably, chemogenetic inhibition of ACC neurons effectively suppressed hyperlocomotion. Conversely, chemogenetic excitation lowered the hyperbaric pressure threshold required to induce hyperlocomotion. Moreover, both chemogenetic inhibition and genetic ablation of activity-dependent neurons within the ACC reduced the hyperlocomotion. Further investigation revealed that ACC neurons project to the DMS, and chemogenetic inhibition of ACC-DMS projections resulted in a reduction in hyperlocomotion. Finally, nitrogen narcosis led to an increase in local field potentials in the theta frequency band and a decrease in the alpha frequency band in both the ACC and DMS. These results collectively suggest that excitatory neurons within the ACC, along with their projections to the DMS, play a pivotal role in regulating the hyperlocomotion induced by exposure to hyperbaric nitrogen.
Animals ; Gyrus Cinguli/drug effects* ; Male ; Mice, Inbred C57BL ; Locomotion/drug effects* ; Neurons/drug effects* ; Mice ; Nitrogen/toxicity* ; Inert Gas Narcosis/physiopathology* ; Corpus Striatum/physiopathology*

Acute carbon monoxide poisoning (ACMP) is one of the most common gas poisonings in the emergency department, with tens of thousands of people seeking medical attention for carbon monoxide (CO) poisoning each year. The severity of poisoning is dependent upon environmental and human factors, with hypoxia and oxidative stress being important mechanisms of cardiac toxicity induced by CO. Myocardial involvement is common in moderate to severe ACMP, including myocardial injury, myocardial infarction, arrhythmia, and sudden death, which are associated with a high risk of death. Ferroptosis is a cell death mechanism caused by iron-dependent lipid peroxidation (LPO), although ferroptosis has been shown to play a critical role in various cardiovascular diseases, the potential mechanism by which it contributes to ACMP-induced myocardial injury is unclear. This review discusses the established link between ferroptosis and cardiovascular disease and summarizes the potential role of ferroptosis in ACMP-induced myocardial injury and the detrimental effects of ACMP on the heart. Elucidating these mechanisms could guide the development of novel therapeutic strategies that target ferroptosis to mitigate ACMP-induced myocardial injury. This review aims to provide a theoretical foundation for future research on the potential use of ferroptosis as a therapeutic target for ACMP-induced myocardial injury.
Humans ; Carbon Monoxide Poisoning/complications* ; Ferroptosis ; Lipid Peroxidation ; Myocardium/pathology* ; Oxidative Stress

Objective: To observe the effects of transcranial direct current stimulation (tDCS) on nerve injury markers and prognosis in patients with acute severe carbon monoxide poisoning (ASCOP) . Methods: In May 2021, 103 ASCOP patients were treated in the emergency department of Harrison International Peace Hospital of Hebei Medical University from November 2020 to January 2021. The patients were divided into two groups according to whether they received tDCS treatment. The control group (50 cases) were given oxygen therapy (hyperbaric oxygen and oxygen inhalation) , reducing cranial pressure, improving brain circulation and cell metabolism, removing oxygen free radicals and symptomatic support, and the observation group (53 cases) was treated with 2 weeks of tDCS intensive treatment on the basis of conventional treatment. All patients underwent at least 24 h bispectral index (BIS) monitoring, BIS value was recorded at the hour and the 24 h mean value was calculated. Neuron-specific enolase (NSE) and serum S100B calcium-binding protein (S100B) were detected after admission, 3 d, 7 d and discharge. Follow-up for 60 days, the incidence and time of onset of delayed encephalopathy (DEACMP) with acute carbon monoxide poisoning in the two groups were recorded. Results: The NSE and S100B proteins of ASCOP patients were significantly increased at admission, but there was no significant difference between the two groups (P=0.711, 0.326) . The NSE and S100B proteins were further increased at 3 and 7 days after admission. The increase in the observation group was slower than that in the control group, and the difference was statistically significant (P(3 d)=0.045, 0.032, P(7 d)=0.021, 0.000) ; After 14 days, it gradually decreased, but the observation group decreased rapidly compared with the control group, with a statistically significant difference (P=0.009, 0.025) . The 60 day follow-up results showed that the incidence of DEACMP in the observation group was 18.87% (10/53) , compared with 38.00% (19/50) in the control group (P=0.048) ; The time of DEACMP in the observation group[ (16.79±5.28) d] was later than that in the control group[ (22.30±5.42) d], and the difference was statistically significant (P=0.013) . Conclusion: The early administration of tDCS in ASCOP patients can prevent the production of NSE and S100B proteins, which are markers of nerve damage. and can improve the incidence and time of DEACMP.
Humans ; Biomarkers ; Brain Diseases/therapy* ; Carbon Monoxide Poisoning/therapy* ; Oxygen ; Phosphopyruvate Hydratase ; Prognosis ; S100 Calcium Binding Protein beta Subunit ; Transcranial Direct Current Stimulation

Acute carbon monoxide poisoning and its delayed encephalopathy have obvious damage to the central nervous system. There are different neuroimaging changes in different stages of the disease, and they are relatively specific. This article reviews the clinical research progress on the imaging changes of carbon monoxide poisoning and delayed encephalopathy, including computed tomography (CT) , conventional magnetic resonance imaging (MRI) , diffusion weighted imaging (DWI) , diffusion tensor imaging (DTI) , diffusion kurtosis imaging (DKI) , magnetic resonance spectroscopy (MRS) and other imaging changes reflecting the function and metabolic state of the brain tissue.
Humans ; Brain Diseases/etiology* ; Carbon Monoxide Poisoning/diagnostic imaging* ; Diffusion Magnetic Resonance Imaging ; Diffusion Tensor Imaging ; Magnetic Resonance Imaging ; Tomography, X-Ray Computed ; Magnetic Resonance Spectroscopy

Objective: To investigate the poisonous substances and geographical distribution of poisoning in children in China. Methods: A cross-sectional study. The clinical data of 8 385 hospitalized children from January 2016 to December 2020 were extracted from the FUTang Updating Medical Records database. These children aged 0 to 18 years and were admitted due to poisoning. They were grouped according to age (newborns and infants, toddlers, preschoolers, school-age children, adolescents), place of residence (Northeast China, North China, Central China, East China, South China, Southwest China, Northwest China), and mode of discharge (discharge under medical advice, transfer to another hospital under medical advice, discharge without medical advice, death, other). The poisonous substance and causes of poisoning in different groups were analyzed. Results: Among these 8 385 children, 4 734 (56.5%) were male and 3 651 (43.5%) female, with a male-to-female ratio of 1.3∶1. The age was 3 (2, 7) years. The prevalence of poisoning was 51.8% (4 343/8 385) in toddlers, 16.5% (1 380/8 385) in adolescents, 14.8% (1 242/8 385) in preschoolers, 14.4% (1 206/8 385) in school-age children, and 2.5% (214/8 385) in newborns and infants. Drug poisoning accounted for 43.5% (3 649/8 385) and pesticide accounted for 26.8% (2 249/8 385). Drug poisoning was more common in adolescents (684/1 380, 49.6%) and toddlers (2 041/4 343, 47.0%); non-drug poisoning was more common in school-age children (891/1 206, 73.9%), of which carbon monoxide was mainly in newborns and infants (41/214, 19.2%) and food poisoning in children of school age (241/1 206, 20.0%). Regarding regional characteristics, drug poisoning was more frequent in South China (188/246, 64.2%) and non-drug poisoning was more frequent in Southwest China (815/1 123, 72.5%). For drugs, anti-epileptic drugs, sedative-hypnotic drugs and anti-Parkinson's disease drugs had a higher proportion of poisoning in North China (138/1 034, 13.0%) than that in other regions. For non-drug poisoning, pesticides (375/1 123, 33.3%), food poisoning (209/1 123, 18.6%) and contact with poisonous animals (86/1 123, 7.7%) were more common in Southwest China than in other regions; carbon monoxide poisoning was more common in North China (81/1 034, 7.6%) and Northwest China (65/1 064, 6.3%). In Central China, poisoning happened more in toddlers (792/1 295, 61.2%) and less in adolescents (115/1 295, 8.8%) than in other regions. Regarding different age groups, poisoning in adolescent happened more in Northeast China (121/457, 26.5%), North China (240/1 034, 23.2%), and Northwest China (245/1 064, 23.0%). The rate of discharge under medical advice, discharge without medical advice, and mortality rate within the 5 years were 77.0% (6 458/8 385), 20.8% (1 743/8 385), 0.5% (40/8 385), respectively. Conclusions: Poisoning is more common in male and toddlers. Poisonous substances show a regional characteristic and vary in different age groups, with drugs and insecticides as the most common substances.
Infant ; Adolescent ; Animals ; Child ; Male ; Humans ; Infant, Newborn ; Female ; Child, Hospitalized ; Cross-Sectional Studies ; Carbon Monoxide Poisoning/epidemiology* ; Pesticides ; Foodborne Diseases ; Hospitals ; Drug-Related Side Effects and Adverse Reactions ; China/epidemiology*

There have been multiple reports already regarding acute carbon monoxide/CO poisoning in the Philippines secondary to misuse of portable generators, especially during the times of typhoon. We present a case of unintentional carbon monoxide poisoning in a Filipino household wherein three of its members were found dead and leaving other five unconscious before they were rushed to the hospital. The index patient had increased serum fraction percentage of carboxyhemoglobin level and presented with rhabdomyolysis during admission. Neuroimaging confirmed a hypoxic-ischemic encephalopathy secondary to carbon monoxide intoxication. Even without hyperbaric oxygen therapy, patient improved with adequate hydration, early rehabilitation and trauma-focused psychotherapy.
Carbon Monoxide Poisoning ; Carbon Monoxide ; Family Characteristics

Hydrogen sulphide poisoning is an acute poisoning event that occurs frequently in summer. A case of acute hydrogen sulphide poisoning in a confined space in August 2018 was investigated and clinical data were analyzed. This is a typical case of acute hydrogen sulfide gas poisoning in a confined space. The main cause of the accident is the lack of occupational protection and illegal rescue. Among the 5 patients, 3 died, 1 patient had long-term sequelae of nervous system damage such as cortical blindness, and 1 patient was cured.
Accidents ; Accidents, Occupational ; Confined Spaces ; Gas Poisoning ; Humans ; Hydrogen Sulfide ; Poisoning

Objective: To compare the efficacy of high-flow nasal cannula oxygen therapy (HFNC) and non-rebreather face mask (NRFM) in the treatment of mild acute carbon monoxide poisoning (ACOP) in reducing carboxyhemoglobin (COHb) , and to explore the feasibility of HFNC in the treatment of ACOP. Methods: Patients with mild ACOP with COHb >10% who were admitted to the emergency department of Northern Jiangsu People's Hospital from January 2015 to December 2020 were analyzed, and those with altered consciousness, mechanical ventilation and those requiring hyperbaric oxygen therapy were excluded. The patients were divided into HFNC group and NRFM group according to the oxygen therapy used in the emergency department. The COHb decline value and COHb half-life in the two groups were observed. Results: Seventy-one patients were enrolled, including 39 in the NRFM group and 32 in the HFNC group. The baseline COHb in the HFNC group was 24.8%±8.3%, and that in the NRFM group was 22.5%±7.1%, with no significant difference between the two groups (t=1.27, P=0.094) . At 60 min, 90 min and 120 min of treatment, COHb in both groups decreased, but the COHb in HFNC group was lower than that in NRFM group at the same time point (P<0.05) . After 1 h of treatment, the COHb decrease in the HFNC group (16.9%±4.5%) was significantly higher than that in the NRFM group (10.1%±7.8%) (t=4.32, P=0.013) . The mean half-life of COHb in the HFNC group (39.3 min) was significantly lower than that in the NRFM group (61.4 min) (t=4.69, P=0.034) . Conclusion: HFNC treatment of mild ACOP can rapidly reduce blood COHb level, it is a potential oxygen therapy method for clinical treatment of ACOP.
Humans ; Carbon Monoxide Poisoning/therapy* ; Cannula ; Respiration, Artificial ; Masks ; Oxygen Inhalation Therapy/methods* ; Carboxyhemoglobin ; Oxygen/therapeutic use* ; Respiratory Insufficiency/therapy*

Trichloromethane and dichloromethane have toxic effects on the liver, and incidents of toxic liver disease caused by them have been reported from time to time. In November 2021, an occupational chemical poisoning incident occurred in a shoe factory in Huidong County, Guangdong Province. After testing the air at the scene and analyzing the clinical data of the poisoning patients, it was preliminarily determined that the poisoning was caused by a mixed gas poisoning incident dominated by trichoromethane. At admission, the liver function of 7 patients was tested for different degrees of impairment (alanine aminotransferase 145-2501 IU/L, aspartate aminotransferase 66-1286 IU/L). The volatile organic components of on-site raw and auxiliary materials were analyzed. The percentages of trichloromethane and dichloromethane detected in 103A powder glue used in the poisoning workshop site accounted for 21.11% and 6.77% respectively.
Humans ; Alanine Transaminase ; Aspartate Aminotransferases ; Gas Poisoning ; Liver Diseases