Chronic lung allograft dysfunction (CLAD) is a common complication after lung transplantation, which severely impairs the long-term survival of patients. At present, effective therapeutic approaches remain lacking. Dysregulation of the lung microbiome acts as a pathogenic factor for a variety of pulmonary diseases. Accumulating studies have demonstrated that the compositional characteristics of the lung microbiome after lung transplantation are closely associated with CLAD. Therefore, this article reviews the definition of CLAD, characteristics of the lung microbiome, the influence of the lung microbiome on the occurrence and progression of CLAD, the potential mechanisms underlying the lung microbiome in the pathogenesis of CLAD, and microbiome-based intervention strategies for CLAD. It aims to provide novel insights for the prevention and treatment of CLAD following lung transplantation and further improve the prognosis of lung transplant recipients.

Objective To analyze the characteristics of postoperative hospital-acquired infections and drug sensitivity in lung transplant recipients over the past 5 years in a single center. Methods A total of 724 lung transplant recipients at Wuxi People's Hospital from January 2019 to December 2023 were selected. Based on the principles of hospital-acquired infection diagnosis, a retrospective analysis was conducted on the hospital infection situation and infection sites of lung transplant recipients, and an analysis of the distribution of hospital-acquired infection pathogens and their antimicrobial susceptibility test status was performed. Results Among the 724 lung transplant recipients, 275 cases of hospital-acquired infection occurred, with an infection rate of 38.0%. The case-time infection rate decreased from 54.2% in 2019 to 22.8% in 2023, showing a downward trend year by year (Z=30.98, P<0.001). The main infection site was the lower respiratory tract, accounting for 73.6%. The pathogens were mainly Gram-negative bacteria, with the top four being Acinetobacter baumannii (37.1%), Pseudomonas aeruginosa (17.3%), Klebsiella pneumoniae (13.7%), and Stenotrophomonas maltophilia (13.4%), with imipenem resistance rates of 89%, 53%, 58% and 100%, respectively. Gram-positive bacteria were mainly Staphylococcus aureus (3.6%), with a methicillin resistance rate of 67%. Conclusions Over the past 5 years, the hospital-acquired infections in lung transplant recipients have shown a downward trend, mainly involving lower respiratory tract infections, with the main pathogens being Acinetobacter baumannii, Pseudomonas aeruginosa and Klebsiella pneumoniae, all of which have high resistance rates to imipenem.

ObjectiveTo investigate how Xiaoyao Shukun decoction （XYSKD） regulates the formation and release of neutrophil extracellular traps （NETs） via the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway， thereby reducing inflammation， inhibiting the excessive proliferation of fibroblasts in pelvic adhesion tissue， decreasing adhesion and fibrosis， and repairing the tissue damage in sequelae of pelvic inflammatory disease （SPID）. MethodsA total of 84 Wistar rats were randomly allocated into seven groups： blank， model， XYSKD （8 mg·kg^-1）， mTOR agonist （10 mg·kg^-1）， mTOR agonist + XYSKD （10 mg·kg^-1+8 mg·kg^-1）， mTOR inhibitor （2 mg·kg^-1）， and mTOR inhibitor + XYSKD （2 mg·kg^-1+8 mg·kg^-1）. The rat model of SPID was constructed by starvation， fatigue， and ascending Escherichia coli infection. After 14 days of drug intervention， the ultrastructure of fibroblasts in the pelvic adhesion tissue was observed by transmission electron microscopy. The general morphology of the uterus， fallopian tube， and ovary was observed by laparotomy. The levels of interleukin-1β （IL-1β）， interleukin-17 （IL-17）， and tumor necrosis factor-α （TNF-α） in the peritoneal flushing fluid were determined by enzyme-linked immunosorbent assay （ELISA）. The expression of myeloperoxidase （MPO） and citrullinated histone 3 （H3） in the fallopian tube was detected by immunofluorescence. Western blot and Real-time quantitative polymerase chain reaction （Real-time PCR） were employed to determine the relative protein and mRNA levels， respectively， of neutrophil elastase （NE）， intercellular adhesion molecule-1 （CD54）， α-smooth muscle actin （α-SMA）， H3， PI3K， and Akt. ResultsCompared with the blank group， the model group presented a large number of collagen fibers in bundles， numerous cytoplasmic folds of fibroblasts， reduced or absent mitochondrial cristae， and disordered and expanded endoplasmic reticulum. By laparotomy， extensive pelvic congestion， connective tissue hyperplasia， thickening and hardening of the tubal end near the uterus， and tubal and ovarian adhesion or cyst were observed in the model group. In addition， the model group showed raised levels of IL-1β， IL-17， and TNF-α in the peritoneal flushing fluid （P<0.01）， increased average fluorescence intensities of MPO and H3 （P<0.01）， and up-regulated protein and mRNA levels of NE， H3， CD54， PI3K， and Akt （P<0.01）. Compared with the model group， the mTOR agonist group showed increased fibroblasts and cytoplasmic folds， absence of mitochondrial cristae， endoplasmic reticulum dilation， and evident collagen fiber hyperplasia. Pelvic adhesions were observed to cause aggravated damage to the uterine， fallopian tube， and ovarian tissues. The levels of IL-1β， IL-17， and TNF-α in the peritoneal lavage fluid elevated （P<0.01） and the average fluorescence intensities of MPO and H3 enhanced （P<0.01） in the mTOR agonist group. In contrast， the XYSKD group and the mTOR inhibitor group showcased decreased fibroblasts and collagen fibers， alleviated mitochondrial crista loss and endoplasmic reticulum dilation， improved morphology and appearance of the uterine， fallopian tube， and ovarian tissues， lowered levels of IL-1β， IL-17， and TNF-α in the peritoneal lavage fluid （P<0.01）， decreased average fluorescence intensities of MPO and H3 （P<0.01）， and down-regulated protein and mRNA levels of NE， H3， CD54， PI3K， and Akt （P<0.05）. Compared with the mTOR agonist group， the mTOR agonist + XYSKD group showed alleviated pathological changes in the pelvic tissue， declined levels of IL-1β， IL-17， and TNF-α （P<0.01）， decreased average fluorescence intensities of MPO and H3 （P<0.01）， and down-regulated protein levels of NE， H3， CD54， α-SMA， p-PI3K/PI3K， and p-Akt/Akt （P<0.01） and mRNA levels of NE， H3， CD54， α-SMA， PI3K， and Akt （P<0.01）. Compared with the mTOR inhibitor group， the mTOR inhibitor + XYSKD group demonstrated reduced pathological severity of the pelvic tissue， reduced levels of IL-1β， IL-17， and TNF-α （P<0.01）， decreased average fluorescence intensities of MPO and H3 （P<0.01）， and down-regulated protein and mRNA levels of NE and CD54 （P<0.05）. ConclusionXYSKD can inhibit the excessive formation and release of NETs via PI3K/Akt/mTOR to ameliorate the inflammatory environment and reduce fibrosis and adhesion of the pelvic tissue， thereby playing a role in the treatment of SPID. It may exert the effects by lowering the levels of IL-1β， IL-17， and TNF-α and down-regulating the expression of NE， H3， CD54， α-SMA， PI3K， and Akt in the pelvic adhesion tissue.

Objective To discuss the factors influencing the occurrence of frailty in patients with acute myocardial infarction(AMI)after receiving interventional treatment,and to construct a prediction model,to draw a nomogram,and to make the validation of the model.Methods Using convenient sampling method,a total of 462 patients with AMI,who were admitted to the Department of Cardiovascular Medicine of three Grade Ⅲ-A hospitals in Shandong Province of China from July 2023 to January 2024,were selected as the study subjects.Among them,324 AMI patients encountered from July 2023 to November 2023 were selected as modeling group,and logistic regression was used to construct a risk prediction model and draw a nomogram to visualize the model.The remaining 138 AMI patients encountered from December 2023 to January 2024 were used as the validation group.The receiver operating characteristic(ROC)curve and Hosmer-Lemeshow testing were adopted to verify the predictive effect of the model.Results Of 324 patients in the modeling group,170(52.47％)developed frailty.Univariate analysis showed that significant differences in age,education level,body mass index(BMI),Charlson comorbidity index,grip strength,walking speed,brain natriuretic peptide precursor level,physical exercise,multiple medication,and kinesophobia existed between the two groups(all P＜0.05).Multivariate logistic regression analysis revealed that age,BMI,Charlson comorbidity index,grip strength,walking speed,NT-ProBNP precursor level,physical exercise,multiple medication,and kinesophobia were the influencing factors of frailty in patients with AMI after receiving interventional treatment,with an OR value of 1.061,0.630,1.529,0.931,0.005,0.358,1.783,2.929,and 0.497 respectively.The above nine factors were used as independent variables to draw the nomogram,the area under ROC curve of the model was 0.851(95％CI:0.809-0.892),the optimal critical value was 0.562,the sensitivity was 84.1％,and the specificity was 72.1％.Hosmer-Lemeshow goodness of fit testing showed that the model had anx2=12.957 and P=0.113.Conclusion The frailty condition of AMI patients after receiving interventional treatment is at a low to medium levels.The frailty risk prediction model constructed in this study has good prediction effect,which can provide guidance for clinical nurses to timely identify high-risk patients and to promptly adopt interventional measures.

Arthritis, encompassing osteoarthritis (OA), rheumatoid arthritis (RA), and gouty arthritis (GA), is a prevalent inflammatory disease that significantly impacts quality of life. Natural products (NPs), derived from animals, plants, marine organisms, and microorganisms, have demonstrated beneficial effects in arthritis treatment both domestically and internationally. These natural compounds offer advantages in drug discovery due to their skeletal diversity, structural complexity, and multi-effect, multi-target, and low-toxicity properties compared to conventional small-molecule medicines. However, unclear mechanisms have hindered the development and clinical application of NPs. This review summarizes recent experimental studies from the past decade on natural medicine for arthritis treatment, emphasizing key NPs with therapeutic effects on OA, RA, and GA. It examines the effects and molecular mechanisms of NPs acting on different cells to treat arthritis. Furthermore, this review provides insights into the future prospects of NP research in this field, which is crucial for advancing NP-based arthritis treatments.
Humans ; Biological Products/therapeutic use* ; Animals ; Arthritis, Rheumatoid/drug therapy* ; Arthritis, Gouty/drug therapy* ; Arthritis/drug therapy* ; Osteoarthritis/drug therapy*

Objective To investigate the effects of music therapy on cognitive function and immunity of sleep-deprived mice and the potential underlying mechanisms.Methods A novel music therapy was developed by integrating elements from both Western and Chinese music.A sleep-deprived mouse model was established to explore the effects of the music combination on learning and memory of mice using Morris water maze experiments.ELISA was used to detect immune-endocrine indicators in the blood and saliva of mice and to study the effects of this music combination on IgA levels.Transcriptome high-throughput sequencing and B-cell receptor(BCR)repertoire sequencing were adopted to explore the potential mechanisms through which music therapy influenced IgA production.Results The Morris water maze test revealed that the novel music therapy could promote the recovery of cognition and memory of sleep-deprived mice.Additionally,it was found that the music combination could increase IgA levels in both blood and saliva.Transcriptome high-throughput sequencing and BCR sequencing analysis showed that the music combination enhanced the abundance of the IgA immunoglobulin light chain variable region(Igkv4-53)and heavy chain constant region(Igha).Conclusion Music therapy can help restore cognitive function and increase IgA levels in sleep-deprived mice.The mechanism may be related to the enhanced abundance of immunoglobulin light chain variable region(Igkv4-53)and heavy chain constant region(Igha).