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 investigate the phenotypes, molecular types and drug-resistance genes of erythromycin (ERY)-resistant group B Streptococcus (GBS) in pregnant women in late pregnancy in Zhengzhou and provide basic data for the prevention, control and treatment of GBS infection. Methods:This study retrospectively collected 86 GBS strains isolated from the vaginal secretions of pregnant women in late pregnancy at Maternal and Child Health Hospital of Henan Province from 2021 to 2022. ERY-resistant GBS strains were selected using the ERY disk diffusion method, and their susceptibility to 10 different antibiotics was tested. Whole-genome sequencing was performed to analyze their molecular features including molecular types, clonal complex groups and drug-resistance genes. Drug-resistance genes carried by GBS strains belonging to different clonal complex groups were compared.Results:There were 70 ERY-resistant GBS strains. Among them, 7.14%(5/70) exhibited an inducible resistance phenotype to macrolide-lincosamide-streptogramin B (MLSB) antibiotics; 84.29%(59/70) showed constitutive resistance to MLSB antibiotics; 8.57%(6/70) were resistant to macrolides but susceptible to lincosamides. The resistance rates of these strains to clindamycin (CLI), tetracycline (TE) and levofloxacin (LEV) were 91.43%(64/70), 54.29%(38/70) and 60.00%(42/70), respectively. These ERY-resistant strains exhibited multidrug resistance patterns with 40.00%(28/70) showing ERY-CLI-LEV resistance phenotype and 30.00%(21/70) showing ERY-CLI-TE resistance phenotype. The major drug-resistance genes carried by the 70 GBS strains were macrolide/lincosamide resistance genes mreA (100.00%) and ermB (53/70, 75.71%), aminoglycoside resistance genes ant (6)-Ⅰ a (22/70, 31.43%) and aph(3′)-Ⅲ (18/70, 25.71%), and tetracycline resistance genes tetM (22/70, 31.43%) and tetO (13/70, 18.57%). These strains belonged to 12 sequence types derived from seven clonal complexes (CCs) and 48.57%(34/70) of them were clustered into CC12. All CC12 strains harbored ermB, but none carried ermA. The positive rates of lsaE, lunB, and aac (6′)- aph(2" ) in CC19 and CC651 strains, ant (6)-Ⅰ a in CC651 and CC452 strains, and mefA and msrD in CC19 and CC23 strains were significantly higher than those in CC12 strains ( P<0.001). Conclusions:ERY-resistant GBS in Zhengzhou exhibited diverse drug resistance phenotypes and molecular types. CC12 was the most prevalent clonal complex in this region. The constitutive MLSB resistance phenotype and ermB gene were the most common ERY resistance phenotype and genotype, respectively, and tetM gene was related to tetracycline resistance. Furthermore, the drug-resistance genes varied in GBS strains of different clonal complexes. This study suggested that close attention should be paid to the epidemiological situation of GBS in this region and the effectiveness of antibiotics used for clinical prevention and treatment of GBS infection should be carefully evaluated.

Objective: To observe continuous and intermittent application of lamivudine or entecavir resistance mutations in patients with chronic hepatitis B. Methods: Data of patients with active stage of chronic hepatitis B over the past 6 years were collected and analyzed retrospectively. The incidence of drug resistance mutation and related factors between patients taking LAM or ETV continuously and intermittently were compared with those taking LAM or ETV. Data comparison was performed using χ² test. Results: Patients with HBV DNA≥10⁵ copies / ml at the time of initial treatment had higher resistance mutation rates than those with HBV DNA < 10⁵ copies / ml at either continuous or intermittent treatment, and patients with intermittent treatment had higher resistance mutation rates than those with continuous treatment. Simultaneously, the incidence of drug resistance mutation in LAM and ETV in the first, second and third years were significantly higher in intermittent treatment than that of continuous treatment (P < 0.05). There was a positive correlation between the frequency of drug withdrawal and the rate of drug resistance mutation. There were no individual difference and drug difference between LAM and ETV. Conclusion In the treatment of chronic hepatitis B with oral nucleoside analogues, drug resistance may occur in either continuous or intermittent treatment. When comparing continuous with intermittent treatment, it suggests that intermittent is more likely to cause viral resistance mutation.

Adult ; Aged ; Carcinoma, Hepatocellular ; epidemiology ; Female ; Hepatitis B, Chronic ; drug therapy ; Humans ; Liver Neoplasms ; epidemiology ; Male ; Middle Aged ; Nucleosides ; administration & dosage ; therapeutic use

Objective To probe the diagnostic efficacy of fetal eehocardiography for characterizing complex congenital heart diseases.Methods Fetal echocardiography was performed on 49 cases of fetal complex congenital heart disease, the ultrasonic diagnosis was compared retrospectively with pathological results after autopsy.Results Antenatal sonographic diagnosis was in agreement with the pathological results in 42 cases (85.71 %), 7 cases were disagreed with pathological diagnosis (antenatal sonographic diagnosis was discrepancy in 3 cases, 4 cases were partially mis-classified).Twenty-four cases were combined with extra-cardiac malformations.Nine cases had chromosomal abnormality.Conclusions Fetal echocardiography is highly accurate for antenatal diagnosis of complex congenital heart disease, but it is hard to detect some type of cardiac anomalies.