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Furthermore, this group was associated with a higher incidence of cardiac deaths (p = 0.001) and major adverse cardiac events (p less then 0.001). The supervised models predicted reduced LV ejection fraction ( less then 50%) and global longitudinal strain ( less then 16%) with area under the receiver-operator-characteristics curves (ROC AUC) of 0.83 and 0.87 in the hold-out test set, respectively. Furthermore, the presence of myocardial fibrosis was predicted from only ultrasound myocardial texture with an ROC AUC of 0.84 (sensitivity 86.4% and specificity 83.3%) in the test set. INTERPRETATION Ultrasound texture-based myocardial tissue characterization identified phenotypic features of LV remodeling from still ultrasound images. Further clinical validation may address critical barriers in the adoption of ultrasound techniques for myocardial tissue characterization. FUNDING None. BACKGROUND Mesenchymal stem cells (MSCs) selectively differentiate into adipocytes or osteoblasts, and several molecules control the fate determination of MSCs. Understanding these key checkpoints greatly contributes to the ability to induce specific MSC differentiation for clinical applications. In this study, we aimed to explore whether TNF receptor-associated factor 4 (TRAF4) affects MSC adipogenic differentiation, which we previously reported that could positively regulated the osteogenic differentiation. METHODS Western blotting and Real-time Polymerase Chain Reaction were used to detected the expression pattern of TRAF4 during adipogenic differentiation. Lentivirus was constructed to regulate TRAF4 expression, and oil red O staining and Western blotting were used to assess its role in adipogenesis, which was confirmed in vivo by implanting an MSC-matrigel mixture into nude mice. Western blotting was used to detect the activated signaling pathways, and a specific inhibitor and agonist were used to clear n, and suggests that TRAF4 may be a novel target of MSCs in clinical use and may also illuminate the underlying mechanisms of bone metabolic diseases. FUNDING This study was supported by the National Natural Science Foundation of China (81871750 and 81971518) and the Science and Technology Project of Guangdong Province (2019B02023600 and 2017A020215070). BACKGROUND Triple-negative breast cancer (TNBC) is aggressive and has a poor prognosis. Kynurenine 3-monooxygenase (KMO), a crucial kynurenine metabolic enzyme, is involved in inflammation, immune response and tumorigenesis. We aimed to study the role of KMO in TNBC. METHODS KMO alteration and expression data from public databases were analyzed. KMO expression levels in TNBC samples were analyzed using immunohistochemistry. Knockdown of KMO in TNBC cells was achieved by RNAi and CRISPR/Cas9. KMO functions were examined by MTT, colony-forming, transwell migration/invasion, and mammosphere assays. The molecular events were analyzed by cDNA microarrays, Western blot, quantitative real-time PCR and luciferase reporter assays. Tumor growth and metastasis were detected by orthotopic xenograft and tail vein metastasis mouse models, respectively. FINDINGS KMO was amplified and associated with worse survival in breast cancer patients. KMO expression levels were higher in TNBC tumors compared to adjacent normal mammary tissues. In vitro ectopic KMO expression increased cell growth, colony and mammosphere formation, migration, invasion as well as mesenchymal marker expression levels in TNBC cells. In addition, KMO increased pluripotent gene expression levels and promoter activities in vitro. Mechanistically, KMO was associated with β-catenin and prevented β-catenin degradation, thereby enhancing the transcription of pluripotent genes. KMO knockdown suppressed tumor growth and the expression levels of β-catenin, CD44 and Nanog. Furthermore, mutant KMO (known with suppressed enzymatic activity) could still promote TNBC cell migration/invasion. Importantly, mice bearing CRISPR KMO-knockdown TNBC tumors showed decreased lung metastasis and prolonged survival. INTERPRETATION KMO regulates pluripotent genes via β-catenin and plays an oncogenic role in TNBC progression. V.BACKGROUND Multiagent therapies, due to their ability to delay or overcome resistance, are a hallmark of treatment in multiple myeloma (MM). The growing number of therapeutic options in MM requires high-throughput combination screening tools to better allocate treatment, and facilitate personalized therapy. METHODS A second-order drug response model was employed to fit patient-specific ex vivo responses of 203 MM patients to single-agent models. A novel pharmacodynamic model, developed to account for two-way combination effects, was tested with 130 two-drug combinations. We have demonstrated that this model is sufficiently parameterized by single-agent and fixed-ratio combination responses, by validating model estimates with ex vivo combination responses for different concentration ratios, using a checkerboard assay. This new model reconciles ex vivo observations from both Loewe and BLISS synergy models, by accounting for the dimension of time, as opposed to focusing on arbitrary time-points or drug effect. Cncer Center (P30-CA076292), the Pentecost Family Foundation, and Miles for Moffitt Foundation. 4-HNE The adsorption of proteins to silica surface is a common process mainly governed by the electrostatic attractive interaction between the pH-dependent negatively silica surface and the positive charges of the biomolecule. This process often reduces the conformational stability of the adsorbed protein and may reduce its biological functionality mostly due to multimolecular processes such as aggregation and fibrillation. Here we show that high-density charge cationic polyelectrolytes may successfully compete with the protein for the silica surface containing deprotonated-silanol groups. Therefore, the coating of silica surfaces with these cationic polyelectrolytes precludes the adsorption of the protein to the solid surface. Intensive water washing of the polyelectrolyte-coated silica surfaces had does not result in polyelectrolyte release (even at moderate ionic strength) maintaining the solid surface protected from protein adsorption.