Cloud Workflow Scheduling with Deadlines and Time Slot Availability

[EN] Allocating service capacities in cloud computing is based on the assumption that they are unlimited and can be used at any time. However, available service capacities change with workload and cannot satisfy users' requests at any time from the cloud provider's perspective because cloud services can be shared by multiple tasks. Cloud service providers provide available time slots for new user's requests based on available capacities. In this paper, we consider workflow scheduling with deadline and time slot availability in cloud computing. An iterated heuristic framework is presented for the problem under study which mainly consists of initial solution construction, improvement, and perturbation. Three initial solution construction strategies, two greedy-and fair-based improvement strategies and a perturbation strategy are proposed. Different strategies in the three phases result in several heuristics. Experimental results show that different initial solution and improvement strategies have different effects on solution qualities.This work has been supported by the National Natural Science Foundation of China (Nos. 61572127, 61272377) and the Key Research & Development Program in Jiangsu Province (No. BE2015728). Ruben Ruiz is partially supported by the Spanish Ministry of Economy and Competitiveness, under the project "RESULT - Realistic Extended Scheduling Using Light Techniques" (No. DPI2012-36243-C02-01) partially financed with FEDER funds.Li, X.; Qian, L.; Ruiz García, R. (2018). Cloud Workflow Scheduling with Deadlines and Time Slot Availability. IEEE Transactions on Services Computing. 11(2):329-340. https://doi.org/10.1109/TSC.2016.2518187S32934011

(E)-1-(4-Benzhydrylpiperazin-1-yl)-3-(2-eth­oxy­phen­yl)prop-2-en-1-one

In the title mol­ecule, C28H30N2O2, the piperazine ring adopts a chair conformation and the C=C bond exhibits an E conformation. The dihedral angle between the terminal phenyl rings is 71.4 (2). In the crystal, mol­ecules are linked by C—H⋯O hydrogen bonds, forming [010] chains

Knockdown of TIGAR by RNA interference induces apoptosis and autophagy in HepG2 hepatocellular carcinoma cells

AbstractApoptosis and autophagy are crucial mechanisms regulating cell death, and the relationship between apoptosis and autophagy in the liver has yet to be thoroughly explored. TIGAR (TP53-induced glycolysis and apoptosis regulator), which is a p53-inducible gene, functions in the suppression of ROS (reactive oxygen species) and protects U2OS cells from undergoing cell death. In this study, silencing TIGAR by RNAi (RNA interference) in HepG2 cells down-regulated both TIGAR mRNA (∼75%) and protein levels (∼80%) and led to the inhibition of cell growth (P<0.01) by apoptosis (P<0.001) and autophagy. We demonstrated that TIGAR can increase ROS levels in HepG2 cells. The down-regulation of TIGAR led to the induction of LC-3 II (specific autophagic marker), the formation of the autophagosome, and increased Beclin-1 expression. 3-MA (3-Methyladenine), an inhibitor of autophagic sequestration blocker, inhibited TIGAR siRNA-enhanced autophagy, as indicated by the decrease in LC-3 II levels. Consequently, these data provide the first evidence that targeted silencing of TIGAR induces apoptotic and autophagic cell death in HepG2 cells, and our data raise hope for the future successful application of TIGAR siRNA in patients with hepatocellular carcinoma (HCC)

(E)-1-{4-[Bis(4-bromo­phen­yl)meth­yl]piperazin-1-yl}-3-(4-bromo­phen­yl)prop-2-en-1-one

In the title mol­ecule, C26H23Br3N2O, the piperazine ring adopts a chair conformation and the C=C double bond has an E configuration. In the crystal, mol­ecules are linked through weak inter­molecular C—H⋯O hydrogen bonds

In vivo MRI based prostate cancer localization with random forests and auto-context model

Prostate cancer is one of the major causes of cancer death for men. Magnetic resonance (MR) imaging is being increasingly used as an important modality to localize prostate cancer. Therefore, localizing prostate cancer in MRI with automated detection methods has become an active area of research. Many methods have been proposed for this task. However, most of previous methods focused on identifying cancer only in the peripheral zone (PZ), or classifying suspicious cancer ROIs into benign tissue and cancer tissue. Few works have been done on developing a fully automatic method for cancer localization in the entire prostate region, including central gland (CG) and transition zone (TZ). In this paper, we propose a novel learning-based multi-source integration framework to directly localize prostate cancer regions from in vivo MRI. We employ random forests to effectively integrate features from multi-source images together for cancer localization. Here, multi-source images include initially the multi-parametric MRIs (i.e., T2, DWI, and dADC) and later also the iteratively-estimated and refined tissue probability map of prostate cancer. Experimental results on 26 real patient data show that our method can accurately localize cancerous sections. The higher section-based evaluation (SBE), combined with the ROC analysis result of individual patients, shows that the proposed method is promising for in vivo MRI based prostate cancer localization, which can be used for guiding prostate biopsy, targeting the tumor in focal therapy planning, triage and follow-up of patients with active surveillance, as well as the decision making in treatment selection. The common ROC analysis with the AUC value of 0.832 and also the ROI-based ROC analysis with the AUC value of 0.883 both illustrate the effectiveness of our proposed method

Human pluripotent stem cell-derived epicardial progenitors can differentiate to endocardial-like endothelial cells.

During heart development, epicardial progenitors contribute various cardiac lineages including smooth muscle cells, cardiac fibroblasts, and endothelial cells. However, their specific contribution to the human endothelium has not yet been resolved, at least in part due to the inability to expand and maintain human primary or pluripotent stem cell (hPSC)-derived epicardial cells. Here we first generated CDH5-2A-eGFP knock-in hPSC lines and differentiated them into self-renewing WT1+ epicardial cells, which gave rise to endothelial cells upon VEGF treatment in vitro. In addition, we found that the percentage of endothelial cells correlated with WT1 expression in a WT1-2A-eGFP reporter line. The resulting endothelial cells displayed many endocardium-like endothelial cell properties, including high expression levels of endocardial-specific markers, nutrient transporters and well-organized tight junctions. These findings suggest that human epicardial progenitors may have the capacity to form endocardial endothelium during development and have implications for heart regeneration and cardiac tissue engineering