Objective To analyze drug resistance and clustering of environmental and clinical isolates of Acinetobacter baumannii (A. baumannii) in ICU of a medical institution in Shanghai. Methods The isolates of A. baumannii from ICU environments and clinic were used to analyze the contamination and distribution in 2021-2024. Antimicrobial susceptibility testing was carried out with microbroth dilution method. Whole genome sequencing was performed out of strains for MLST typing and SNP clustering. Results The detection rate of contamination in ICU environment was 7.67%, and the most serious contamination was found in pillows, bedding, hospital gowns and other items that patients directly contacted. Clinical isolates were predominantly from sputum specimens. The environmental and clinical isolates had a high level of resistance to third generation cephalosporins, third generation quinolones and carbapenems (more than 85%). Environmental isolates had a low level of resistance to polymyxin B, but none of the clinical isolates were resistant. MLST typing showed that ST2 was the dominant clone (66.67%), and SNP clustering found that isolates from different sources but with the same ST type were clustered together. Conclusion ST2 is the dominant clone of A. baumannii isolates in this medical institution, and there is cross-contamination between different samples. Monitoring of drug resistance and disinfection should be further strengthened to prevent the emergence and spread of pan-resistant or even fully resistant strains.

Rheumatoid arthritis(RA)is characterized by bidi-rectional bone remodeling imbalance,clinically termed the "high resorption-low formation" paradox,stemming not only from osteoclast hyperactivation but also critically involving pro-found suppression of osteoblast differentiation and function.No-tably,this suppression cannot be fully attributed to osteoclast hyperactivity;synovium-resident immune cells exert a pivotal regulatory influence through distinct mechanisms.This review systematically examines how synovial immune cells orchestrate bone remodeling in RA through both paracrine cytokine networks and direct cell-cell communication with bone lineage cells,thereby perturbing physiological homeostasis and driving patho-logical progression.These mechanistic revelations yield innova-tive perspectives on RA pathogenesis,positioning immune-medi-ated osteoimmune dysregulation as a promising therapeutic fron-tier for targeted intervention.

Aim To investigate the effect of icariin(ICA)on chronic ulcerative colitis(UC)in mice.Methods Male SPF-grade C57BL/6J mice were ran-domly divided into the control group,model group,low-dose ICA group,and high-dose ICA group.Except for the control group,the rest of the mice were established as chronic UC models.Expressions of tight junction proteins,inflammatory factors,fibrosis markers,macro-phage markers,and MAPK signaling pathways in the colonic epithelium of each group were determined by Western blot,qPCR,immunohistochemistry;the degree of intestinal damage and fibrosis was detected by HE and Masson staining;the co-localization of different macrophage markers with related factors was examined by immunofluorescence.Results Treatment of ICA significantly improved the general condition of chronic UC mice,decreased the infiltration of M1-type macro-phages and the secretion of pro-inflammatory factors,inhibited the MAPK signaling pathway,reduced the co-localization expression of M1-type macrophages with the MAPK signaling pathway,and downregulated the infiltration of M2-type macrophages and the secretion of pro-fibrotic factors in the colon.Conclusion ICA mitigates the inflammatory damage and fibrosis of colon in chronic UC mice.

Purpose To develop and validate a nomogram based on 18F-FDG PET/CT for predicting spread through air space(STAS)in stage IA lung adenocarcinoma(LUAD),providing imaging support for surgical decision-making.Materials and Methods This retrospective study analyzed 155 patients with pathologically confirmed stage IA LUAD from the Fifth People's Hospital of Chongqing,Affiliated Hospital of Zunyi Medical University and Cavalier Hospital(December 2019 to December 2023).Patients were stratified into STAS-positive and STAS-negative groups based on postoperative histopathological evaluation.Univariate and multivariate binary Logistic regression analyses identified risk factors for STAS from clinical characteristics,PET/CT semantic features,and metabolic parameters.A nomogram predicting preoperative STAS status was developed and internally validated using bootstrap resampling.Model performance was assessed in training and internal validation sets using receiver operating characteristic analysis,calibration curves and decision curve analysis.Results Among 155 stage IA LUAD patients,20(12.9%)were STAS-positive.Multivariate analysis identified tumor mean diameter(OR=0.618,P=0.024),solid component proportion(OR=2.678,P=0.033),and maximum standardized uptake value(OR=3.437,P=0.028)as independent STAS predictors.The nomogram demonstrated excellent discrimination,with areas under the curve of 0.912(95%CI 0.855-0.942)and 0.843(95%CI 0.805-0.923)in training and validation sets,respectively.Hosmer-Lemeshow goodness-of-fit test indicated satisfactory calibration(χ2=5.591,P=0.693).Decision curve analysis showed substantial net clinical benefit across threshold probabilities of 5%-91%.Conclusion The nomogram incorporating tumor diameter,solid component proportion,and maximum standardized uptake value from 18F-FDG PET/CT effectively predicts STAS status in stage IA LUAD,demonstrating high preoperative predictive performance.

Aim To investigate the effect of icariin(ICA)on chronic ulcerative colitis(UC)in mice.Methods Male SPF-grade C57BL/6J mice were ran-domly divided into the control group,model group,low-dose ICA group,and high-dose ICA group.Except for the control group,the rest of the mice were established as chronic UC models.Expressions of tight junction proteins,inflammatory factors,fibrosis markers,macro-phage markers,and MAPK signaling pathways in the colonic epithelium of each group were determined by Western blot,qPCR,immunohistochemistry;the degree of intestinal damage and fibrosis was detected by HE and Masson staining;the co-localization of different macrophage markers with related factors was examined by immunofluorescence.Results Treatment of ICA significantly improved the general condition of chronic UC mice,decreased the infiltration of M1-type macro-phages and the secretion of pro-inflammatory factors,inhibited the MAPK signaling pathway,reduced the co-localization expression of M1-type macrophages with the MAPK signaling pathway,and downregulated the infiltration of M2-type macrophages and the secretion of pro-fibrotic factors in the colon.Conclusion ICA mitigates the inflammatory damage and fibrosis of colon in chronic UC mice.

Purpose To develop and validate a nomogram based on 18F-FDG PET/CT for predicting spread through air space(STAS)in stage IA lung adenocarcinoma(LUAD),providing imaging support for surgical decision-making.Materials and Methods This retrospective study analyzed 155 patients with pathologically confirmed stage IA LUAD from the Fifth People's Hospital of Chongqing,Affiliated Hospital of Zunyi Medical University and Cavalier Hospital(December 2019 to December 2023).Patients were stratified into STAS-positive and STAS-negative groups based on postoperative histopathological evaluation.Univariate and multivariate binary Logistic regression analyses identified risk factors for STAS from clinical characteristics,PET/CT semantic features,and metabolic parameters.A nomogram predicting preoperative STAS status was developed and internally validated using bootstrap resampling.Model performance was assessed in training and internal validation sets using receiver operating characteristic analysis,calibration curves and decision curve analysis.Results Among 155 stage IA LUAD patients,20(12.9%)were STAS-positive.Multivariate analysis identified tumor mean diameter(OR=0.618,P=0.024),solid component proportion(OR=2.678,P=0.033),and maximum standardized uptake value(OR=3.437,P=0.028)as independent STAS predictors.The nomogram demonstrated excellent discrimination,with areas under the curve of 0.912(95%CI 0.855-0.942)and 0.843(95%CI 0.805-0.923)in training and validation sets,respectively.Hosmer-Lemeshow goodness-of-fit test indicated satisfactory calibration(χ2=5.591,P=0.693).Decision curve analysis showed substantial net clinical benefit across threshold probabilities of 5%-91%.Conclusion The nomogram incorporating tumor diameter,solid component proportion,and maximum standardized uptake value from 18F-FDG PET/CT effectively predicts STAS status in stage IA LUAD,demonstrating high preoperative predictive performance.

Diamond-Blackfan anemia(DBA),also known as congenital pure red cell aplasia,is a rare genetic disorder characterized by bone marrow failure,congenital anomalies,and severe red blood cell abnormalities.The rarity of the condition,and consequently limited patient pool and scarcity of research models,means that the pathogenic mechanisms associated with genetic mutations in DBA remain uncertain,and the clinical treatment options are limited.This review synthesizes the findings from zebrafish,mouse,and human cellular models of DBA mutations.We clarify the pathogenic mechanisms and monitor the progression of drugs into clinical trials,thereby aiding further in-depth explorations into the etiology and therapeutic advancements for DBA.

Rheumatoid arthritis(RA)is characterized by bidi-rectional bone remodeling imbalance,clinically termed the "high resorption-low formation" paradox,stemming not only from osteoclast hyperactivation but also critically involving pro-found suppression of osteoblast differentiation and function.No-tably,this suppression cannot be fully attributed to osteoclast hyperactivity;synovium-resident immune cells exert a pivotal regulatory influence through distinct mechanisms.This review systematically examines how synovial immune cells orchestrate bone remodeling in RA through both paracrine cytokine networks and direct cell-cell communication with bone lineage cells,thereby perturbing physiological homeostasis and driving patho-logical progression.These mechanistic revelations yield innova-tive perspectives on RA pathogenesis,positioning immune-medi-ated osteoimmune dysregulation as a promising therapeutic fron-tier for targeted intervention.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Infiltration of a large number of inflammatory cells in the synovial tissue of rheumatoid arthritis(RA)promotes vascu-lar neovascularisation and the formation of aggressive pannus,which ultimately lead to bone erosion and cartilage destruction,causing irreversible damage to the joints.Numerous studies have demonstrated the role of proangiogenic factors such as growth factors,adhesion factors,angiopoietin 2,matrix metalloproteinas-es,and macrophage migration inhibitory factors in stimulating vascular opacification formation during RA progression.In re-cent years,a variety of traditional Chinese medicines have dem-onstrated inhibitory effects on the formation of pannus.In this paper,we elucidate the mechanism of pro-angiogenic factors in RA and review the latest research results on traditional Chinese medicines that inhibit the formation of pannus through the above mechanisms,so as to provide more research ideas for the treat-ment of RA.