An H∞ design for dynamic pricing in the smart grid.

An H∞ design for dynamic pricing in the smart grid is proposed. This design jointly considers the operation of a distribution network operator and a market operator. In the design, a ratio of the regulated output energy to the disturbance energy is minimized to address the worst-case scenario. Linear matrix inequality approaches are used to formulate the design problem as a convex problem. Fuzzy interpolation techniques are integrated into the design procedure so that nonlinear grid dynamics can be addressed. In contrast with existing designs, the proposed design can yield a more reliable and practical pricing scheme as shown via simulations

Functional Effects of let-7g Expression in Colon Cancer Metastasis.

MicroRNA regulation is crucial for gene expression and cell functions. It has been linked to tumorigenesis, development and metastasis in colorectal cancer (CRC). Recently, the let-7 family has been identified as a tumor suppressor in different types of cancers. However, the function of the let-7 family in CRC metastasis has not been fully investigated. Here, we focused on analyzing the role of let-7g in CRC. The Cancer Genome Atlas (TCGA) genomic datasets of CRC and detailed data from a Taiwanese CRC cohort were applied to study the expression pattern of let-7g. In addition, in vitro as well as in vivo studies have been performed to uncover the effects of let-7g on CRC. We found that the expression of let-7g was significantly lower in CRC specimens. Our results further supported the inhibitory effects of let-7g on CRC cell migration, invasion and extracellular calcium influx through store-operated calcium channels. We report a critical role for let-7g in the pathogenesis of CRC and suggest let-7g as a potential therapeutic target for CRC treatment

Effects of Metformin on the Cerebral Metabolic Changes in Type 2 Diabetic Patients

Metformin, a widely used antidiabetic drug, has numerous effects on human metabolism. Based on emerging cellular, animal, and epidemiological studies, we hypothesized that metformin leads to cerebral metabolic changes in diabetic patients. To explore metabolism-influenced foci of brain, we used 2-deoxy-2-[18F]fluoro-D-glucose (FDG) positron emission tomography for type 2 diabetic patients taking metformin (MET, n=18), withdrawing from metformin (wdMET, n=13), and not taking metformin (noMET, n=9). Compared with the noMET group, statistical parametric mapping showed that the MET group had clusters with significantly higher metabolism in right temporal, right frontal, and left occipital lobe white matter and lower metabolism in the left parahippocampal gyrus, left fusiform gyrus, and ventromedial prefrontal cortex. In volume of interest (VOI-) based group comparisons, the normalized FDG uptake values of both hypermetabolic and hypometabolic clusters were significantly different between groups. The VOI-based correlation analysis across the MET and wdMET groups showed a significant negative correlation between normalized FDG uptake values of hypermetabolic clusters and metformin withdrawal durations and a positive but nonsignificant correlation in the turn of hypometabolic clusters. Conclusively, metformin affects cerebral metabolism in some white matter and semantic memory related sites in patients with type 2 diabetes

An H∞ design for dynamic pricing in the smart grid

An H∞ design for dynamic pricing in the smart grid is proposed. This design jointly considers the operation of a distribution network operator and a market operator. In the design, a ratio of the regulated output energy to the disturbance energy is minimized to address the worst-case scenario. Linear matrix inequality approaches are used to formulate the design problem as a convex problem. Fuzzy interpolation techniques are integrated into the design procedure so that nonlinear grid dynamics can be addressed. In contrast with existing designs, the proposed design can yield a more reliable and practical pricing scheme as shown via simulations

Genomic-Analysis-Oriented Drug Repurposing in the Search for Novel Antidepressants

From inadequate prior antidepressants that targeted monoamine neurotransmitter systems emerged the discovery of alternative drugs for depression. For instance, drugs targeted interleukin 6 receptor (IL6R) in inflammatory system. Genomic analysis-based drug repurposing using single nucleotide polymorphism (SNP) inclined a promising method for several diseases. However, none of the diseases was depression. Thus, we aimed to identify drug repurposing candidates for depression treatment by adopting a genomic-analysis-based approach. The 5885 SNPs obtained from the machine learning approach were annotated using HaploReg v4.1. Five sets of functional annotations were applied to determine the depression risk genes. The STRING database was used to expand the target genes and identify drug candidates from the DrugBank database. We validated the findings using the ClinicalTrial.gov and PubMed databases. Seven genes were observed to be strongly associated with depression (functional annotation score = 4). Interestingly, IL6R was auspicious as a target gene according to the validation outcome. We identified 20 drugs that were undergoing preclinical studies or clinical trials for depression. In addition, we identified sarilumab and satralizumab as drugs that exhibit strong potential for use in the treatment of depression. Our findings indicate that a genomic-analysis-based approach can facilitate the discovery of drugs that can be repurposed for treating depression

Adaptor protein Shc acts as an immune-regulator for the LPS-stimulated maturation of bone marrow-derived dendritic cells

<p>Abstract</p> <p>Background</p> <p>The Shc isoforms is known to mediate immune responses and has been indicated as a negative regulator of autoimmunity and lymphocyte activation. We aimed to evaluate the immune-regulatory role of Shc in rat bone marrow-derived DCs in the maturation process triggered by LPS.</p> <p>Results</p> <p>We found that, in response to LPS, expression of Shc proteins was induced and that neutralization of Shc inhibited the LPS-induced transient phosphorylation of p52Shc on pTyr239/240 in DCs of Lewis (LEW; RT1^l) rats. Moreover, the significantly enhanced expression of IL-10 and the surface level of costimulatory molecule CD80, as well as suppressed expression of IL-6 and IL-12 in the Shc-silenced DCs were also observed. Similar IκB phosphorylation occurred in Shc-silenced DCs primed by LPS, indicating Shc is not associated with NF-κB pathway. We further demonstrate that Shc blockade on LPS-treated DCs results in significant increase of the overall STAT3 phosphorylation and the relative levels of phospho-STAT3 in the nuclear fraction. STAT3 activation by LPS with or without Shc blockade was totally abolished by SU6656, a selective Src family kinases inhibitor, underscoring the critical role of Src-mediated activation.</p> <p>Conclusions</p> <p>We conclude that Shc blockade in LPS-primed DC leads to the development of tolerogenic DC via Src-dependent STAT3 activation and that adaptor protein Shc might play a pivotal role in mediating immunogenic and tolerogenic properties of DCs.</p

Device Thrombogenicity Emulation: A Novel Method for Optimizing Mechanical Circulatory Support Device Thromboresistance

Mechanical circulatory support (MCS) devices provide both short and long term hemodynamic support for advanced heart failure patients. Unfortunately these devices remain plagued by thromboembolic complications associated with chronic platelet activation – mandating complex, lifelong anticoagulation therapy. To address the unmet need for enhancing the thromboresistance of these devices to extend their long term use, we developed a universal predictive methodology entitled Device Thrombogenicity Emulation (DTE) that facilitates optimizing the thrombogenic performance of any MCS device – ideally to a level that may obviate the need for mandatory anticoagulation