Objective To investigate the impact of intraoperative red blood cell (RBC) transfusion volume on the postoperative oxygenation index in lung transplant recipients. Methods This retrospective study analyzed the clinical data of patients who underwent lung transplantation at Wuxi People's Hospital Affiliated to Nanjing Medical University from 2021 to 2023. Patients were divided into a non-severe primary graft dysfunction (PGD) group and a severe PGD group based on whether their postoperative oxygenation index was>200 mm Hg at 0, 24, and 48 h. General patient data and intraoperative RBC transfusion volumes were compared between the two groups. A binary logistic regression model was constructed to explore the effect size (OR and its 95%CI) of RBC transfusion volume on postoperative oxygenation status at different time points (0, 24, and 48 h). The area under the receiver operating characteristic curve was calculated to evaluate the model's diagnostic performance. Results A total of 351 patients were included (260 males, 91 females), with ages ranging from 20 to 77 years. The OR for the effect of intraoperative RBC transfusion on poor oxygenation was 1.486 (95%CI 0.982 to 2.248, P=0.061) at 0 h postoperatively, 3.111 (95%CI 1.793 to 5.399, P<0.001) at 24 h, and 1.583 (95%CI 1.026 to 2.442, P=0.038) at 48 h. This indicated that as time progressed, the postoperative oxygenation status of lung transplant recipients was affected by the intraoperative transfusion volume. Furthermore, an RBC transfusion volume>975 mLhad a significant impact on patient oxygenation at 24 and 48 h postoperatively. Conclusion The volume of intraoperative RBC transfusion has a significant impact on the oxygenation status at 24 and 48 h postoperatively. Intraoperative RBC transfusion volume is associated with the occurrence of severe PGD after lung transplantation. Controlling the volume of RBC transfusion during lung transplantation may help reduce the incidence of severe PGD.

Objective To investigate the expression profile, prognostic value, gene co-expression network, and immunomodulatory role of BRF1 in a pan-cancer context, and to explore its biological functions and molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC). Methods The pan-cancer dataset from The Cancer Genome Atlas (TCGA) was utilized to analyze the differential expression of BRF1 in tumor versus normal tissues, its association with patient survival, pathway enrichment for co-expressed genes, and immune features (including immune checkpoints, cytokines, and immune cell infiltration). The expression profile of BRF1 in ESCC was validated using the Gene Expression Omnibus (GEO) database. In vitro, BRF1 was knocked down in ESCC cells using siRNA. Cell proliferation and migration were assessed by MTT and Transwell assays, respectively. The expression levels of proliferation- and migration-related proteins were detected by Western blotting. The correlation between BRF1 and ferroptosis was analyzed using TCGA data. Results BRF1 was significantly upregulated in over 20 types of cancer, and its high expression was associated with poor prognosis in patients with adrenocortical carcinoma and prostate adenocarcinoma. BRF1 was found to positively regulate the T-cell-mediated cell death pathway in esophageal adenocarcinoma and was associated with the circadian rhythm regulation pathway in pancreatic adenocarcinoma. The correlation of BRF1 with immune checkpoints, cytokine networks, and immune cell infiltration was found to be cancer type-specific. In vitro experiments demonstrated that knocking down BRF1 significantly inhibited the proliferation of ESCC cells, accompanied by the downregulation of the proliferation marker PCNA. Cell migration was also significantly impaired, with decreased expression of Vimentin and MMPs and increased expression of E-cadherin. Furthermore, the expression of BRF1 was positively correlated with that of ferroptosis-antagonizing genes, such as GPX4, HSPA5, and SLC7A11. Conclusion BRF1 plays complex roles in pan-cancer, participating in the regulation of tumorigenesis, progression, and immune infiltration. BRF1 promotes the proliferation and migration of ESCC cells, a mechanism potentially associated with the regulation of ferroptosis resistance. These findings suggest that BRF1 could be a potential therapeutic target for ESCC.

Antimicrobial resistance (AMR) poses a critical global health threat. This review systematically examines AMR surveillance technology advances, from conventional culture methods to modern molecular diagnostics (e.g., whole-genome sequencing) and artificial intelligence-assisted approaches. It focuses on the current application of mass spectrometry, machine learning predictive models, and real-time surveillance networks. To address challenges including inadequate technical standardization, clinical translation barriers, and data-sharing limitations, we propose integrated ^"genotype-phenotype^" strategies and global standardization framework, while exploring future applications of CRISPR-based portable detection, single-cell sequencing, and blockchain technologies.

Background/Aims: Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation. Methods: We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion. Results: At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites. Conclusions Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

Background/Aims: Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation. Methods: We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion. Results: At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites. Conclusions Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

Background/Aims: Systemic Inflammation (SI) is considered a key mechanism in disease progression and development of complications in decompensated liver cirrhosis. SI is mainly driven by portal hypertension and bacterial translocation. Transjugular intrahepatic portosystemic shunt (TIPS) insertion represents an effective treatment for portal hypertension. This study aims to investigate the impact of TIPS insertion on SI and bacterial translocation. Methods: We prospectively included 59 cirrhotic patients undergoing TIPS insertion. Blood samples were collected at TIPS insertion and follow-up (FU) 1, 3, 6, and 12 months thereafter. At all time points, we performed a comprehensive analysis of SI including 43 soluble inflammatory markers (SIMs), and surrogates of bacterial translocation (sCD14, sCD163). To investigate long-term kinetics of SI, C-reactive protein (CRP) and white blood cells (WBC) were retrospectively analyzed in a cohort of 177 patients up to 3 years after TIPS insertion. Results: At TIPS insertion, 30/43 SIMs, sCD14, and sCD163 measured significantly higher in cirrhotic patients compared to healthy controls. By FU6 25 SIMs and sCD14 measured at significantly lower levels compared to baseline. Interestingly, in patients with TIPS indication of refractory ascites, IL-6 decreased to levels documented in earlier stages of cirrhosis. In long-term follow-up, CRP levels significantly decreased after TIPS insertion, which translated into lower mortality in Cox regression analysis (HR 0.968, p=0.042). Notably, patients with residual ascites post-TIPS showed significantly higher CRP and IL-6 levels across all follow-ups compared to patients with resolved ascites. Conclusions Decreasing portal hypertension via TIPS insertion leads to a significant attenuation of SI and bacterial translocation over time.

Objective:To explore the value of high resolution computed tomography（HRCT） combined with Magnetic Resonance Imaging（MRI） in the diagnosis of inner ear malformation. Methods:HRCT and MRI data of 82 patients with inner ear malformations were analyzed retrospectively. HRCT MPR and CPR reconstruction of the inner ear structure, facial nerve canal and oblique sagittal MRI reconstruction of the internal auditory canal were performed. The inner ear malformations were classified, the conditions of facial nerve canal and cochlear nerve were evaluated. The association between inner ear malformation and cochlear nerve dysplasia were analyzed by Chi-square test with continuity correction. Results:Among the 82 patients with inner ear malformations,there were 49 cases of bilateral symmetry, 11 cases of bilateral asymmetry and 22 cases of unilateral inner ear malformations. Respectively, the most prevalent types were IP-Ⅱ（42.96%）, dilatation of atrium aqueduct（18.31%） and malformations of atrium and semicircular canal 19.72%. Out of 50 cases of cochlear malformations,only 3 were isolated cochlear malformations, and the rest were accompanied by other malformations of varying degrees. In the 67 ears examined by MRI, 26（38.81%） had cochlear nerve deficiency（CND）, and the incidence of CND varied with different types of inner ear malformations. Out of 142 ears, 28（19.72%） had abnormalities of the facial nerve canal. Conclusion:HRCT combined with MRI can accurately distinguish the types of inner ear malformation and effectively evaluate the facial nerve canal and cochlear nerve, and further provides the important finger and Guide value for the clinician to formulate the reasonable treatment and the operation plan.
Humans ; Ear, Inner/diagnostic imaging* ; Magnetic Resonance Imaging/methods* ; Retrospective Studies ; Female ; Male ; Tomography, X-Ray Computed/methods* ; Child ; Adolescent ; Adult ; Child, Preschool ; Cochlear Nerve/diagnostic imaging* ; Facial Nerve/abnormalities* ; Cochlea/abnormalities* ; Infant ; Young Adult

Objective:To investigate the relationship between the Palatopharyngeal Arch Staging System（PASS） and the severity of Obstructive Sleep Apnea（OSA）, as well as the patterns of airway collapse, while further assessing its clinical applicability. Methods:A total of 98 patients diagnosed with OSA at the Department of Otorhinolaryngology Head and Neck Surgery, Shenzhen University Affiliated Shenzhen Hospital, were recruited for this study. Data collected included basic demographic information, oropharyngeal laryngoscopy videos, results from awake laryngoscopy Muller tests, and indicators from sleep respiratory monitoring. The distribution of each PASS stage among patients with varying severities of OSA was compared. Additionally, both objective and subjective sleep indicators along with occurrences of airway collapse in OSA patients across different PASS stages were analyzed. Results:In total, 98 patients participated in this study. Statistically significant differences were observed in neck circumference, weight, Body Mass Index（BMI）, tongue position, and PASS stage when comparing mild-to-moderate OSA patients to those with severe OSA（P<0.05）. Furthermore, there were statistically significant variations in Apnea-Hypopnea Index（AHI）, minimum blood oxygen saturation levels, average blood oxygen saturation levels, oxygen desaturation index values, and total oxygen desaturation indices among OSA patients categorized by different PASS stages. Multiple comparisons revealed statistically significant differences in AHI as well as minimum and average blood oxygen saturation levels between patients at PASS 1 versus those at PASS 3（P<0.05）. Additionally, notable differences regarding oropharyngeal collapse rates among OSA patients across various PASS stages were identified; specifically between those at PASS stage 1 and those at PASS stage 3. Conclusion:The proportion of PASS stages for OSA varies across different severity levels. The severity of OSA and the degree of airway collapse in patients with varying PASS stages also exhibit significant differences. Patients classified as PASS 3 demonstrate a more severe form of OSA compared to those at PASS 1, with stage 3 being more susceptible to oropharyngeal collapse than its stage 1 counterpart. This assessment system is anticipated to address the current limitations in evaluating the lateral pharyngeal wall within the oropharynx.
Humans ; Sleep Apnea, Obstructive/pathology* ; Male ; Severity of Illness Index ; Female ; Middle Aged ; Polysomnography ; Adult ; Pharynx/physiopathology* ; Aged

Abstract Inhibitor of DNA binding 1(ID1) is a crucial regulator of cell differentiation and plays a significant role in maintaining normal hematopoietic differentiation and development. Due to the lack of DNA-binding motif, ID1 functions as a dominant-negative inhibitor of basic helix-loop-helix factors to antagonize their abilities to bind to DNA and transcriptionally regulate target genes. Abnormal expression of ID1 is strongly associated with various hematologic disorders, including myeloid and lymphoblastic leukemia, multiple myeloma and myeloproliferative neoplasms. ID1 acts as a potential oncogene by participating in multiple signaling pathways that promote the malignant proliferation, invasion and therapy resistance in leukemic cells. Significant strides have yielded promising antileukemic effects of ID1 inhibitors, both alone and in combination with targeted therapies against oncogenic signaling pathways. Here, we review the relationship between ID1 expression and the initiation and progression of blood disorders, and summarize the clinical significance of ID1 as a novel therapeutic target and potential prognostic biomarker for hematologic malignancies.

Objective: To investigate the potential therapeutic mechanisms of kaempferol , an active component in the traditional Chinese medicine gardenia , for lung cancer treatment using a network pharmacology approach . Methods: The main active ingredients and potential targets of Gardenia jasminoides were obtained through the Tra⁃ditional Chinese Medicine Pharmacology Database and Analysis Platform (TCMSP) , and combined with the lung cancer related target information collected from Gene Cards and OMIM databases , the intersection targets of Garde⁃nia jasminoides and lung cancer treatment were determined by drawing Venn diagrams . Further screening of core targets was conducted through PPI network analysis , and gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes ( KEGG) pathway enrichment analysis were performed using the Metascape platform . Auto dock software was used to evaluate the binding affinity between the active ingredients of Gardenia jasminoides and target proteins . In terms of experiments , cell proliferation ability was evaluated through CCK⁃8 assay , cell migration and invasion ability were detected through cell scratch healing assay and Transwell assay , and the expression levels of epithelial mesenchymal transition ( EMT) protein and inflammatory factors were detected by Western blot and RT⁃qPCR . Results: The active ingredient kaempferol in Gardenia jasminoides exhibited significant binding ability invasion of lung cancer cells . The results of Western blot and RT⁃qPCR further confirmed that kaempferol could promote an increase in E ⁃cadherin , a decrease in N ⁃cadherin and Vimentin , and reduce the expression of inflam⁃matory factors . Conclusion The active ingredient of Gardenia jasminoides , kaempferol , inhibits the proliferation ,migration and invasion of lung cancer cells by targeting BCL⁃2 , while reversing EMT progression and suppressing the expression levels of inflammatory cytokines in lung cancer cells , thus preventing lung cancer progression .