Effect analysis of multi-department cooperation in improving etiological submission rates before antibiotic treatment.

Increased bacterial drug resistance has become a serious global public health problem. The application of antibiotics involves various clinical departments, and the rational application of antibiotics is the key to improving their efficacy. To provide a basis for further improving the etiological submission rate and standardizing the rational use of antibiotics, this article discusses the intervention effect of multi-department cooperation in improving the etiological submission rate before antibiotic treatment. A total of 87 607 patients were divided into a control group (n = 45 890) and an intervention group (n = 41 717) according to whether multi-department cooperation management was implemented. The intervention group involved the patients hospitalized from August to December 2021, while the control group involved the patients hospitalized from August to December 2020. The submission rates of the two groups; the rates before antibiotic treatment at the unrestricted use level, the restricted use level, and the special use level in departments; and the timing of submission were compared and analysed. The overall differences in the etiological submission rates before antibiotic treatment at the unrestricted use level (20.70% vs 55.98%), the restricted use level (38.23% vs 66.58%), and the special use level (84.92% vs 93.14%) were statistically significant before and after intervention (P < .05). At a more specific level, the etiological submission rates of different departments before antibiotic treatment at the unrestricted use level, the restricted use level, and the special use level were improved, but the special activities of multi-department cooperation management did not improve the submission timing significantly. Multi-department cooperation can effectively improve the etiological submission rates before antimicrobial treatment, but it is necessary to improve measures for specific departments to improve long-term management and incentive and restraint mechanisms.

CXCL9 regulates acetaminophen-induced liver injury via CXCR3.

Drug-induced liver injury has become a serious public health problem. Although the mechanism of acetaminophen (APAP)-induced liver injury has been studied for decades it has not been fully elucidated. In-depth study into the mechanisms underlying APAP-induced liver injury may provide useful information for more effective prevention and treatment. In the present study, the role of C-X-C motif chemokine ligand-9 (CXCL9) in APAP-induced liver injury was investigated thus providing a novel direction for the prevention and treatment of drug hepatitis. A total of 20 fasting male patients ingested APAP tablets at Nanjing First Hospital. In addition, wild type (WT) mice were treated with 250 mg/kg APAP or isodose PBS for 1, 3, 6 and 12 h, respectively. Results from reverse-transcription-quantitative polymerase chain reaction analyses demonstrated that CXCL9 mRNA levels were increased in the blood of patients who took APAP in a fasting state and in the livers of APAP-treated WT mice, compared with their respective controls. Hepatocyte apoptosis in the liver tissue of APAP-treated mice decreased following administration of a CXCL9 neutralizing antibody. Caspase-3, caspase-8 and phosphorylated-AKT (S437) were activated in primary hepatocytes isolated from WT mice following CXCL9 treatment. However, no significant differences in expression of caspase-3, caspase-8 and p-AKT (S437) were detected in hepatocytes isolated from C-X-C motif chemokine receptor 3 (CXCR3)-/- mice following CXCL9 treatment. After CXCL9 administration, WT mice exhibited higher serum levels of aspartate transaminase and increased caspase-3 and caspase-8 activity in liver tissue compared with controls. The same trends were not observed in CXCR3-/- mice. In conclusion, CXCL9 regulated APAP-induced liver injury through stimulation of hepatocyte apoptosis via binding to CXCR3. These findings provide a novel prevention and treatment strategy for DILI.