1.Detection of ESBLs Produced by E. coli in Urinary Tract and Monitoring of Drug Resistance of ESBLs-producing E.coli
Weichan FU ; Dejun ZHAO ; Baojia WANG ; Jinjin YANG ; Jintao YANG ; Yujiang REN
China Pharmacy 1991;0(05):-
OBJECTIVE:To investigate the condition of ESBLs produced by E.coli isolated from urinary tract and the drug resistance of ESBLs-producing E.coli.METHODS:The identification of bacteria was performed using ATB-Expression analysator(France);the susceptibility test was performed using K-B method,and ESBLs were detected using disc diffusion confirmatory test.RESULTS:The detection rate of ESBLs-producing E.coli was 31.8%.All(100%)of the 107 strains of ESBLs-producing E.coli were sensitive to imipenem,however,in which different degree of resistance to other antibiotics was noted.The resistance rate was significantly higher in ESBLs-producing strains than in non-ESBLs-producing strains.CON-CLUSION:In view of the high antibiotic resistance of ESBLs-producing E.coli,great importance should be attached to the detection of the ESBLs.Antibiotics should be used rationally based on the results of susceptibility test.
2.Pathological research progress of sudden unexpected death in epilepsy
Jinhua JI ; Xiaoli WANG ; Weichan WANG ; Xinbo ZHANG ; Na YUAN ; Fengchang LIU ; Yonghong LIU
Chinese Journal of Neurology 2024;57(5):504-510
Sudden unexpected death in epilepsy (SUDEP) refers to the sudden, unexpected and unexplained death of epilepsy patients, which is an important reason for the significant increase of the death risk of epilepsy patients. The risk factors of SUDEP are related to poor control of seizures, nocturnal seizures, prone position, antiepileptic drugs, comorbidity, etc. Epilepsy death caused by SUDEP has become a major public health problem. The latest progress in neuropathology and cardiopulmonary pathology of SUDEP was reviewed in this article.
3.Effects of lead and manganese combined exposure on neurodevelopmental toxicity and JNK expression in zebrafish
Yuan XIA ; Chunyu WANG ; Ziyi LI ; Qin ZHOU ; Jiawei ZHU ; Xiaojing MENG ; Weichan HUANG ; Junyi WANG ; Qingsong CHEN
Journal of Environmental and Occupational Medicine 2023;40(5):583-588
Background Lead and manganese are heavy metal pollutants widely existing in the environment, which can accumulate in the human body through the food chain, exert neurotoxicity, and cause neurodegenerative disorders. Especially in early childhood, the developing blood-brain barrier and nervous system are highly susceptible to environmental chemical pollutants. Most of the previous studies focused on the toxic effects of single heavy metal such as lead or manganese, while the studies on combined toxic effect are still scarce, and involved mechanisms are still unclear. c-Jun N-terminal kinase (JNK) is involved in neuronal development and regeneration, and some studies have found that JNK is involved in lead or manganese induced neurotoxicity. Its role in the toxicity of combined lead and manganese is unknown. Objective To understand the neurodevelopmental toxicity mechanism and to observe changes of JNK expression in zebrafish induced by combined lead and manganese exposure at environmentlly low concentrations. Methods Zebrafish embryos within 2 h post fertilization (hpf) were divided into four groups: control group, lead exposure group (0.1 mg·L−1 lead acetate), manganese exposure group (0.3 mg·L−1 manganous chloride), and lead-manganese combined exposure group (0.1 mg·L−1 lead acetate +0.3 mg·L−1 manganous chloride) and exposed to lead or/and manganese at designed levels for 7 d. Spontaneous movements and motor locomotion were observed, and mortality rate were calculated. The changes of JNK mRNA expression in zebrafish were evaluated. Results The experimental results showed that no significant effect of lead or/and manganese on spontaneous movements and mortality rate was found in zebrafish compared with the control group (P>0.05). The results of locomotion analysis showed that compared with the control group, the activity counts and activity distance of zebrafish in the manganese exposure group were slightly increased (P<0.01); the activity counts and activity distance of zebrafish in the lead exposure group were reduced by 50% and those in the lead-manganese exposure group were reduced by 80% (P<0.01). Compared with the lead exposure group, the activity counts and activity distance of zebrafish in the lead-manganese combined exposure group decreased significantly by 60% (P<0.05). The real-time quantitative PCR results showed that the JNK mRNA expression level was significantly increased in the lead-manganese combined exposure group compared with the control group(P<0.01). Conclusion Lead exposure combined with manganese exposure at environmentlly low concentration can induce neurodevelopmental toxicity to zebrafish. JNK may be involved in neurodevelopmental toxicity induced by the combined exposure to lead and manganese.