Characteristics and Prevalence of Vancomycin-variable Enterococcus faecium bacteremia in southern Taiwan.

BACKGROUND: Vancomycin-variable enterococci (VVE) are vanA-carrying Enterococcus faecium that are phenotypically susceptible to vancomycin and can only be detected using molecular methods, leading to the possibility of treatment failure and posing threats to infection control. This study aimed to determine the prevalence of VVE and its associated clinical risk factors. METHODS: This retrospective study was conducted in two hospitals in southern Taiwan. Patients with phenotypically vancomycin-susceptible E. faecium bacteremia were enrolled between 2017 and 2021. VVEs were defined as isolates harboring the vanA gene that were phenotypically susceptible to vancomycin. Vancomycin-susceptible E. faecium (VSE) isolates were phenotypically susceptible to vancomycin and lacked vanA or vanB genes. RESULTS: Of the 142 enrolled patients, 121 (85.2%) had VSE and 21 (14.8%) had VVE. Resistance rates to penicillin, tetracycline, and fosfomycin were higher in VVE isolates. Malignancy (adjusted odds ratio [aOR] = 4.87; 95% confidence interval [CI] 1.54-15.41, p = 0.007) and central venous catheter usage (aOR = 4.69; 95% CI 1.49-14.78, p = 0.008) were the independent risk factors associated with VVE bacteremia. Being male (aOR = 0.12, CI 0.03-0.44, p = 0.002) was less likely to be associated with VVE bacteremia. Although VVE was not associated with 30-day mortality (38.1% [VVE] vs. 35.5% [VSE], p = 0.822), one case of subsequent vancomycin-resistant enterococci infection in the VVE group with vancomycin treatment (4.8%, 1/21) was identified, which led to subsequent mortality. CONCLUSIONS: The prevalence of VVE was high among E. faecium isolates with vancomycin-susceptible phenotypes in southern Taiwan. Although the current study revealed that VVE bacteremia was not associated with poor clinical outcome, further multicenter surveillance survey is recommended to evaluate the possible impact of VVE on public health in Taiwan.

Correlation between Baseline Conventional Ultrasounds, Shear-Wave Elastography Indicators, and Neoadjuvant Therapy Efficacy in Triple-Negative Breast Cancer.

In patients with triple-negative breast cancer (TNBC)-the subtype with the poorest prognosis among breast cancers-it is crucial to assess the response to the currently widely employed neoadjuvant treatment (NAT) approaches. This study investigates the correlation between baseline conventional ultrasound (US) and shear-wave elastography (SWE) indicators and the pathological response of TNBC following NAT, with a specific focus on assessing predictive capability in the baseline state. This retrospective analysis was conducted by extracting baseline US features and SWE parameters, categorizing patients based on postoperative pathological grading. A univariate analysis was employed to determine the relationship between ultrasound indicators and pathological reactions. Additionally, we employed a receiver operating characteristic (ROC) curve analysis and multivariate logistic regression methods to evaluate the predictive potential of the baseline US indicators. This study comprised 106 TNBC patients, with 30 (28.30%) in a nonmajor histological response (NMHR) group and 76 (71.70%) in a major histological response (MHR) group. Following the univariate analysis, we found that T staging, dmax values, volumes, margin changes, skin alterations (i.e., thickening and invasion), retromammary space invasions, and supraclavicular lymph node abnormalities were significantly associated with pathological efficacy (p < 0.05). Combining clinical information with either US or SWE independently yielded baseline predictive abilities, with AUCs of 0.816 and 0.734, respectively. Notably, the combined model demonstrated an improved AUC of 0.827, with an accuracy of 76.41%, a sensitivity of 90.47%, a specificity of 55.81%, and statistical significance (p < 0.01). The baseline US and SWE indicators for TNBC exhibited a strong relationship with NAT response, offering predictive insights before treatment initiation, to a considerable extent.

Prediction of clinical response to neoadjuvant therapy in advanced breast cancer by baseline B-mode ultrasound, shear-wave elastography, and pathological information.

Background: Neoadjuvant therapy (NAT) is the preferred treatment for advanced breast cancer nowadays. The early prediction of its responses is important for personalized treatment. This study aimed at using baseline shear wave elastography (SWE) ultrasound combined with clinical and pathological information to predict the clinical response to therapy in advanced breast cancer. Methods: This retrospective study included 217 patients with advanced breast cancer who were treated in West China Hospital of Sichuan University from April 2020 to June 2022. The features of ultrasonic images were collected according to the Breast imaging reporting and data system (BI-RADS), and the stiffness value was measured at the same time. The changes were measured according to the Response evaluation criteria in solid tumors (RECIST1.1) by MRI and clinical situation. The relevant indicators of clinical response were obtained through univariate analysis and incorporated into a logistic regression analysis to establish the prediction model. The receiver operating characteristic (ROC) curve was used to evaluate the performance of the prediction models. Results: All patients were divided into a test set and a validation set in a 7:3 ratio. A total of 152 patients in the test set, with 41 patients (27.00%) in the non-responders group and 111 patients (73.00%) in the responders group, were finally included in this study. Among all unitary and combined mode models, the Pathology + B-mode + SWE model performed best, with the highest AUC of 0.808 (accuracy 72.37%, sensitivity 68.47%, specificity 82.93%, P<0.001). HER2+, Skin invasion, Post mammary space invasion, Myometrial invasion and Emax were the factors with a significant predictive value (P<0.05). 65 patients were used as an external validation set. There was no statistical difference in ROC between the test set and the validation set (P>0.05). Conclusion: As the non-invasive imaging biomarkers, baseline SWE ultrasound combined with clinical and pathological information can be used to predict the clinical response to therapy in advanced breast cancer.

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Breast cancer has now become the leading cancer in women. The development of breast ultrasound artificial intelligence (AI) diagnostic technology is conducive to promoting the precise diagnosis and treatment of breast cancer and alleviating the heavy medical burden due to the unbalanced regional development in China. In recent years, on the basis of improving diagnostic efficiency, AI technology has been continuously combined with various clinical application scenarios, thereby providing more comprehensive and reliable evidence-based suggestions for clinical decision-making. Although AI diagnostic technologies based on conventional breast ultrasound gray-scale images and cutting-edge technologies such as three-dimensional (3D) imaging and elastography have been developed to some extent, there are still technical pain points, diffusion difficulties and ethical dilemmas in the development of AI diagnostic technologies for breast ultrasound.

RAGE mediates airway inflammation via the HDAC1 pathway in a toluene diisocyanate-induced murine asthma model.

BACKGROUND: Exposure to toluene diisocyanate (TDI) is a significant pathogenic factor for asthma. We previously reported that the receptor for advanced glycation end products (RAGE) plays a key role in TDI-induced asthma. Histone deacetylase (HDAC) has been reported to be important in asthmatic pathogenesis. However, its effect on TDI-induced asthma is not known. The aim of this study was to determine the role of RAGE and HDAC in regulating airway inflammation using a TDI-induced murine asthma model. METHODS: BALB/c mice were sensitized and challenged with TDI to establish an asthma model. FPS-ZM1 (RAGE inhibitor), JNJ-26482585 and romidepsin (HDAC inhibitors) were administered intraperitoneally before each challenge. In vitro, the human bronchial epithelial cell line 16HBE was stimulated with TDI-human serum albumin (TDI-HSA). RAGE knockdown cells were constructed and evaluated, and MK2006 (AKT inhibitor) was also used in the experiments. RESULTS: In TDI-induced asthmatic mice, the expression of RAGE, HDAC1, and p-AKT/t-AKT was upregulated, and these expressions were attenuated by FPS-ZM1. Airway reactivity, Th2 cytokine levels in lymph supernatant, IgE, airway inflammation, and goblet cell metaplasia were significantly increased in the TDI-induced asthmatic mice. These increases were suppressed by JNJ-26482585 and romidepsin. In addition, JNJ-26482585 and romidepsin ameliorated the redistribution of E-cadherin and ß-catenin in TDI-induced asthma. In TDI-HSA-stimulated 16HBE cells, knockdown of RAGE attenuated the upregulation of HDAC1 and phospho-AKT (p-AKT). Treatment with the AKT inhibitor MK2006 suppressed TDI-induced HDAC1 expression. CONCLUSIONS: These findings indicate that RAGE modulates HDAC1 expression via the PI3K/AKT pathway, and that inhibition of HDAC prevents TDI-induced airway inflammation.