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Background: The incidence of incidental pulmonary embolism (IPE) has greatly increased, but its clinical characteristics and outcomes are still controversial. This study aimed to compare the clinical characteristics and outcomes between cancer patients with IPE and patients with symptomatic pulmonary embolism (SPE). Patients/Methods: Clinical data of 180 consecutive patients with cancer complicated with pulmonary embolism admitted to Beijing Cancer Hospital from July 2011 to December 2019 were retrospectively collected and analysed. General characteristics, diagnosis time of pulmonary embolism (PE), location of PE, concurrent deep venous thrombosis, anticoagulant treatment, impact of PE on anti-tumor treatment, recurrent venous thromboembolism, rate of bleeding after anticoagulation therapy, survival and risk factors of IPE were compared with SPE. Results: Of 180 patients, 88 (49%) had IPEs and 92 (51%) had SPEs. Patients with IPE and SPE did not differ in age, sex, tumor type, or tumor stage. Median diagnosis times of IPE and SPE after cancer were 108 (45, 432) days and 90 (7, 383) days, respectively. Compared to SPE, IPE tended to be central (44% versus 26%; P < 0.001), isolated (31.8% versus 0.0%; P < 0.001), and unilateral (67.1% versus 12.8%; P < 0.00). The rate of bleeding after anticoagulation therapy did not differ between IPE and SPE. Patients with IPE had a better prognosis than patients with SPE in terms of 30-, and 90-day mortality, as well as overall survival after diagnosis of PE (median: 314.5 vs. 192.0 days, log-rank P = 0.004) and cancer (median: 630.0 vs. 450.5 days, log-rank P = 0.018). SPE (compared to IPE) was an independent risk factor for poor survival after diagnosis of PE in multivariate analysis (hazard ratio [HR] = 1.564, 95% confidence interval [CI]: 1.008–2.425, p = 0.046). Conclusions: IPE accounts for nearly one half of PE cases among Chinese cancer patients. With active anticoagulation treatment, IPE is expected to achieve better survival rates than SPE. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease frequently coexist and share pathophysiological manifestations. This study aimed to explore the association between T2DM status and prevalence of liver steatosis and fibrosis, identified using the controlled attenuation parameter and liver stiffness measurement attained via liver ultrasound transient elastography. Methods: This was a cross-sectional analysis of data collected in the National Health and Nutrition Examination Survey for 2017–2018. Multivariable logistic regression model was used to evaluate the association between T2DM and prevalence of liver steatosis and fibrosis. Subgroup analyses, stratified by sex age, race, and body mass index (BMI), were further performed. Results: Of the 2,780 participants aged ≥ 40 years enrolled, 749 had T2DM, and 2,031 did not. After adjustment for potential confounders, T2DM was associated with a higher prevalence of liver steatosis (OR = 1.7, 95% CI, 1.3–2.1). This T2DM-related prevalence was higher among women (OR = 1.8, 95% CI, 1.3–2.5) and in the non-Hispanic Black (OR = 1.8, 95% CI, 1.1–3.0), other race (OR = 1.9, 95% CI, 1.2–3.0), and BMI < 25 kg/m2 (OR = 2.0, 95% CI, 1.1–3.8) groups. T2DM was also associated with a significantly higher prevalence of fibrosis (OR = 2.0, 95% CI, 1.5–2.7), with this association being more prominent for the other race (OR = 2.9, 95% CI, 1.5–5.5) and BMI < 25 kg/m2 (OR = 3.3, 95% CI: 1.3–8.8) groups. Conclusions: Our findings indicated a positive association between T2DM status and prevalence of hepatic steatosis and fibrosis. This association was more prominent for individuals with a BMI < 25 kg/m2 and was influenced by race-specific effects. [ABSTRACT FROM AUTHOR]

Background: To develop a clinical model for predicting high axillary nodal burden in patients with early breast cancer by integrating ultrasound (US) and clinicopathological features. Methods and materials: Patients with breast cancer who underwent preoperative US examination and breast surgery at the Affiliated Hospital of Nantong University (centre 1, n = 250) and at the Affiliated Hospital of Jiangsu University (centre 2, n = 97) between January 2012 and December 2016 and between January 2020 and March 2022, respectively, were deemed eligible for this study (n = 347). According to the number of lymph node (LN) metastasis based on pathology, patients were divided into two groups: limited nodal burden (0–2 metastatic LNs) and heavy nodal burden (≥ 3 metastatic LNs). In addition, US features combined with clinicopathological variables were compared between these two groups. Univariate and multivariate logistic regression analysis were conducted to identify the most valuable variables for predicting ≥ 3 LNs in breast cancer. A nomogram was then developed based on these independent factors. Results: Univariate logistic regression analysis revealed that the cortical thickness (p < 0.001), longitudinal to transverse ratio (p = 0.001), absence of hilum (p < 0.001), T stage (p = 0.002) and Ki-67 (p = 0.039) were significantly associated with heavy nodal burden. In the multivariate logistic regression analysis, cortical thickness (p = 0.001), absence of hilum (p = 0.042) and T stage (p = 0.012) were considered independent predictors of high-burden node. The area under curve (AUC) of the nomogram was 0.749. Conclusion: Our model based on US variables and clinicopathological characteristics demonstrates that can help select patients with ≥ 3 LNs, which can in turn be helpful to predict high axillary nodal burden in early breast cancer patients and prevent unnecessary axillary lymph node dissection. [ABSTRACT FROM AUTHOR]

Background: Adenomyosis (AM) is a common benign chronic gynaecological disorder; however, the precise pathogenesis of adenomyosis is still poorly understood. Single-cell RNA sequencing (scRNA-seq) can uncover rare subpopulations, explore genetic and functional heterogeneity, and reveal the uniqueness of each cell. It provides us a new approach to reveal biological issues from a more detailed and microscopic perspective. Here, we utilize this revolutionary technology to identify the changes of gene expression patterns between ectopic lesions and the eutopic endometrium at the single-cell level and explore a potential novel pathogenesis of AM. Methods: A control endometrium (sample with leiomyoma excluding endometrial disorders, n = 1), eutopic endometrium and ectopic lesion (from a patient with adenomyosis, n = 1) samples were analysed by scRNA-seq, and additional leiomyoma (n = 3) and adenomyosis (n = 3) samples were used to confirm colocalization and vasculogenic mimicry (VM) formation. Protein colocalization was visualized by immunofluorescence, and CD34-periodic acid-Schiff (PAS) double staining was used to assess the formation of VM. Results: The scRNA-seq results suggest that cancer-, cell motility- and inflammation- (CMI) associated terms, cell proliferation and angiogenesis play important roles in the progression of AM. Moreover, the colocalization of EPCAM and PECAM1 increased significantly in the ectopic endometrium group (P < 0.05), cell subpopulation with high copy number variation (CNV) levels possessing tumour-like features existed in the ectopic lesion sample, and VNN1- and EPCAM-positive cell subcluster displayed active cell motility in endometrial epithelial cells. Furthermore, during the transformation of epithelial cells to endothelial cells, we observed the significant accumulation of VM formation (positively stained with PAS but not CD34, P < 0.05) in ectopic lesions. Conclusions: In the present study, our results support the theory of adenomyosis derived from the invasion and migration of the endometrium. Moreover, cell subcluster with high CNV level and tumour-associated characteristics is identified. Furthermore, epithelial-endothelial transition (EET) and the formation of VM in tumours, the latter of which facilitates the blood supply and plays an important role in maintaining cell growth, were also confirmed to occur in AM. These results indicated that the inhibition of EET and VM formation may be a potential strategy for AM management. [ABSTRACT FROM AUTHOR]

Background: Kawasaki disease (KD) is a systemic vasculitis, and the formation of coronary artery lesions(CAL) is its most common sequela. Both genetic and environmental factors are considered to be important factors of in KD. Integrin α2 (ITGA2) is a transmembrane receptor that is associated with susceptibility to several diseases, but its relevance to KD with CAL is unclear. Methods: We genotyped ITGA2 rs1126643 in 785 KD patients with the CAL and no-CAL(NCAL) (300 patients with CAL, and 485 age- and sex-matched patients with NCAL). OR (95% CI) and adjusted OR (95% CI) were used to evaluate the intensity of the association. Results: We found a significantly increased risk of KD with CAL associated with ITGA2 rs1126643 genotypes (CT vs CC: adjusted OR = 1.57, 95% CI = 1.16–2.12, P = 0.0032; CT/TT vs CC: adjusted OR = 1.49, 95% CI = 1.12–2.00, P = 0.0068; T vs C: adjusted OR = 1.66, 95% CI = 1.16–2.51, P = 0.0165). Moreover, we found that carriers of the CT/TT genotype had a significant risk of KD with coronary artery lesion susceptibility for children ≤60 months of age, and the CT/TT genotype was significantly associated with an increased risk of SCAL formation and MCAL formation when compared with the CC genotype. Conclusion: ITGA2 rs1126643 was associated with increased susceptibility and severity of CAL in KD. [ABSTRACT FROM AUTHOR]

Background: A growing body of evidence supports neutrophils as having an active role in the development of diabetic kidney disease (DKD). However, the clinical relevance of neutrophils and DKD in autoimmune diabetes remains unknown. This study aimed to investigate the relationship between circulating neutrophils and DKD in autoimmune diabetes. Methods: Patients with type 1 diabetes (T1D, n = 226) and latent autoimmune diabetes in adults (LADA, n = 79) were enrolled and stratified according to the urinary albumin to creatinine ratio (ACR). Circulating levels of white blood cells (WBCs), including neutrophils, were measured in a central laboratory, and the neutrophil-to-lymphocyte ratio (NLR) was calculated. The risk factors associated with DKD were analysed by logistic regression. Results: In T1D and LADA patients, the peripheral neutrophil counts increased in parallel with DKD advancement. The neutrophil counts in the patients with macroalbuminuria were significantly higher than those in the patients with normoalbuminuria for each type of diabetes. Furthermore, neutrophil counts positively correlated with ACR in T1D. In addition, neutrophils were independently associated with DKD in T1D in the logistic regression analysis, when various well-known risk factors, including age, gender, disease duration, hypertension, dyslipidemia and smoking status, were adjusted. Conclusions: Neutrophil counts are closely associated with DKD in patients with autoimmune diabetes, suggesting that neutrophil-mediated inflammation may be involved in the pathogenesis of DKD in patients with autoimmune diabetes. [ABSTRACT FROM AUTHOR]