With the widespread use of antimicrobial agents, bacterial drug resistance has become an increasingly severe issue, posing significant challenges to global healthcare. Traditional Chinese medicine (TCM) has emerged as a research focus in the field of bacterial resistance due to its broad sources, high safety profile, low toxicity, and antimicrobial mechanisms distinct from those of chemical drugs. Studies have shown that various TCM herbs, such as Scutellaria baicalensis, exert antibacterial effects through multiple pathways, including disrupting the integrity of bacterial cell walls and membranes, inhibiting nucleic acid and protein synthesis, and impairing energy production and metabolism. Additionally, certain TCM herbs, including Scutellaria baicalensis, Coptis chinensis, and Fritillaria thunbergii, can reverse antimicrobial resistance by eliminating resistant plasmids, inhibiting bacterial efflux pump function, and suppressing β-lactamase activity. TCM holds promising potential for antibacterial applications and synergistically reversing antimicrobial resistance, though systematic analyses remain limited. This review summarizes the mechanisms of antibacterial action of TCM and current research on its synergistic use with antimicrobial agents to reverse drug resistance, aiming to provide insights for developing novel TCM-based antimicrobials and addressing bacterial resistance.

To analyze the biological characteristics of Pasteurella multocida in bovine respiratory tract and its prevalence in large-scale cattle farms,bacterial isolation,culture,and morphological observation were conducted on the lungs and liver samples of dead cows suffering from respiratory diseases in Hohhot,Inner Mongolia.The isolated strains were studied through biochemical testing,16S rRNA gene sequencing,specific primer PCR identification,capsule serotyping,pathogenicity testing,virulence gene testing,drug sensitivity testing,and drug resistance gene detection methods.The results showed that six strains of Pasteurella multocida serotype A were isolated and identi-fied from the lungs of diseased and dead cows.After sequencing the 16S rRNA sequence of the bac-teria,it was found that the six strains of Pasteurella multocida had the closest genetic relationship with the Chongqing isolate CQ2(CP033599.1).The results of mouse pathogenicity test and viru-lence gene detection showed that all isolates were pathogenic and carried at least 16 or more related virulence genes such as exbB,nanB,sodC,oma 87,etc.,but no hsf1 and toxA were detected.The results of drug sensitivity tests and resistance gene detection showed that the isolated strains were sensitive to different degrees of antibiotics such as ciprofloxacin,ofloxacin,and cefotaxime.They were resistant to streptomycin,clindamycin,and lincomycin,and resistance genes of str A,strB,and tet(H)were detected.The results indicate that there is a certain correlation between the pathoge-nicity and virulence genes,drug resistance phenotype,and drug resistance genes of Pasteurellamultocida type A in cattle.It is recommended to use quinolones(such as ciprofloxacin)and cepha-losporins(such as cefotaxime)antibacterial drugs in clinical practice,which can provide scientific basis and prevention and control plans for the prevention and treatment of respiratory diseases caused by Pasteurella multocida in cattle farms,and lay a foundation for the epidemiological mo-nitoring of bovine respiratory multocida pasteurellosis.

Objective: To explore the clinical features of hepatocerebral mitochondrial DNA depletion syndrome (MDS). Methods: The clinical data of 6 hepatocerebral MDS patients diagnosed in the Jinshan Hospital of Fudan University from January 2012 to December 2019 were retrospectively collected and analyzed. Related literature published before January 2020 were searched with the key words of "DGUOK""MPV17""POLG""C10orf2" in PubMed, China national knowledge infrastructure (CNKI) and Wanfang database. Results: All the 6 hepatocerebral MDS cases were male. The age of onset ranged from 3 days to 8 months. The most common initial symptoms were cholestasis and developmental retrogression. The main clinical manifestations included hepatomegaly (4 cases), hypotonia (3 cases), growth retardation (4 cases), cholestasis (5 cases), coagulopathy (5 cases), hypoalbuminemia (3 cases), hypoglycemia (4 cases), hyperlactacidemia (5 cases), and abnormal blood metabolism screening (6 cases). The isotope hepatobiliary imaging revealed no gallbladder and intestinal tract development within 24 hours in 2 patients. Regarding the cranial imaging examination, the head CT found widening of the extracranial space in 1 case, the brain magnetic resonance imaging (MRI) found ventricular enlargement in 2 cases, and the brain ultrasound found peripheral white matter injury in 1 case. Two cases were lost to follow-up, one died of liver failure, and three died of multiple organ failure due to aggravated infection. Among the 6 cases, there were 3 with MPV17 variation (c.182T>C and c.279G>C were novel), 1 with POLG variation (c.2993G>A was novel), 1 with DGUOK variation (c.679G>A homozygous mutation, parthenogenetic diploid of chromosome 2) and 1 with C10orf2 variation (c.1186C>T and c.1504C>T were novel). The literature review found that 129, 100, 51 and 12 cases of hepatocerebral MDS were caused by DGUOK, MPV17, POLG and C10orf2 gene variations, respectively. And the most common clinical manifestations were liver dysfunction presented with cholestasis and elevated transaminase, metabolic disorders including hypoglycemia and hyperlactacidemia, and diverse neurologic symptoms including developmental retardation, hypotonia, epilepsy and peripheral neuropathy. Besides, 1/3 of the patients with C10orf2 variation developed renal tubular injury. Conclusions: Hepatocerebral MDS mainly present with liver dysfunction, metabolic disorder and neuromuscular impairment. Different genotypes show specific clinical manifestations.
Cholestasis ; DNA, Mitochondrial/genetics* ; Female ; Humans ; Hypoglycemia/genetics* ; Infant ; Liver Diseases/genetics* ; Male ; Mitochondrial Diseases ; Muscle Hypotonia ; Retrospective Studies

Objective　To evaluate the effects of hsa-miR-642b-3p on cerebral microvascular endothelial cells under hypoxia/reoxygenation (H/R).Methods　The H/R model of brain microvascular endothelial cells was established to analyze the expression alteration of hsa-miR-642b-3p,and the intervention was carried out accordingly.Cell death was detected by trypan blue staining,cell proliferation was detected by CCK8,cell permeability was detected by FITC-albumin,and potential GO and KEGG function enrichment of hsa-miR-642b-3p was analyzed by bioinformatics.Results　The expression of hsa-miR-642b-3p was elevated in H/R condition.After administration of hsa-miR-642b-3p inhibitor,we found the cell death was reduced,cell proliferation was increased and cell permeability was decreased under H/R condition.In addition,GO and KEGG functional enrichment analysis showed that hsa-miR-642b-3p may be involved in multiple biological functions and signal pathways such as RNA regulation,cell adhesion,TGF-β pathway and others.Conclusion　Abnormal expression of hsa-miR-642b-3p in cerebral microvascular endothelial cells under H/R may have certain value for ischemic stroke.

Objective:To analyze the epidemiological characteristics of an aggregational gastroenteritis and determine the genotypes of sapovirus， and to provide scientific basis for formulating effective control strategies. Methods:Unified case definition， active case search and descriptive epidemiology were used to analyze the epidemic. Feces or anal swabs of untreated students， teachers， canteen staff as well as canteen environment samples were collected. Norovirus and sapovirus nucleic acid tests were conducted by real-time fluorescent RT-PCR， and sapovirus nucleic acid was amplified by conventional RT-PCR. The gene region of capsid protein was analyzed by MEGA7.0 software and phylogenetic tree was constructed. Results:A total of 12 cases were reported in the epidemic， and the incidence rate was 44.44%. All reported cases， with vomiting symptoms， were found in the same class. The epidemic showed a point-based outbreak. The first case became the source of infection in class， and the epidemic lasted for 8 days. Real-time fluorescent RT-PCR assay confirmed that five children's feces were positive for sapovirus nucleic acid， and the first-episode children's feces were positive for sapovirus and GII norovirus nucleic acid. Sequence alignment result showed that the sapovirus strains belonged to GI.1 type with homologous genes. Conclusion:Based on the clinical manifestations， field epidemiological investigation and laboratory test results， we confirm that the first case of the epidemic in class is caused by GI.1 sapovirus infection. The epidemic is effectively controlled by comprehensive measures such as case isolation and disinfection.