An AC-AC inverter for high frequency power distribution system

Future computer and telecommunication power distribution systems require the power source to be high frequency ac type and be combined with line current Power Factor Correction that satisfies IEC 1000-3-2 standard. In addition, low power applications require high efficiency, high power density and cost effectiveness. This thesis provides a solution to low power ac-ac inverter for the future computer and telecommunication power distribution systems, which complies with the above requirements. The proposed high frequency ac-ac inverter operates under Zero Voltage Switching (ZVS) throughout the whole range of the line voltage and load. Hence, high efficiency can be realized under high switching frequency. A unified controller is introduced in the proposed ac-ac inverter to control the dc-ac stage and the PFC stage at the same time. The controller is simple and the DC bus voltage can be well limited for A line and load conditions. Hence, cost effectiveness can be realized. In the thesis, two types of PFC stage converters (Boost and Buckboost) are presented to compare the performance of the ac-ac inverter. Principle of operation and steady state analysis of the proposed topology are given. Performance characteristics, design procedures and computer simulation results are presented to guide the design. Experimental results from a prototype of 100kHz, 30V ac /250W output, 90-265V ac input, are presented to confirm the analysis and performance of the proposed ac-ac inverter

PIMT is a Novel and Potent Suppressor of Endothelial Activation

Proinflammatory agonists provoke the expression of cell surface adhesion molecules on endothelium in order to facilitate leukocyte infiltration into tissues. Rigorous control over this process is important to prevent unwanted inflammation and organ damage. Protein L-isoaspartyl O-methyltransferase (PIMT) converts isoaspartyl residues to conventional methylated forms in cells undergoing stress-induced protein damage. The purpose of this study was to determine the role of PIMT in vascular homeostasis. PIMT is abundantly expressed in mouse lung endothelium and PIMT deficiency in mice exacerbated pulmonary inflammation and vascular leakage to LPS(lipopolysaccharide). Furthermore, we found that PIMT inhibited LPS-induced toll-like receptor signaling through its interaction with TNF receptor-associated factor 6 (TRAF6) and its ability to methylate asparagine residues in the coiled-coil domain. This interaction was found to inhibit TRAF6 oligomerization and autoubiquitination, which prevented NF-κB transactivation and subsequent expression of endothelial adhesion molecules. Separately, PIMT also suppressed ICAM-1 expression by inhibiting its N-glycosylation, causing effects on protein stability that ultimately translated into reduced EC(endothelial cell)-leukocyte interactions. Our study has identified PIMT as a novel and potent suppressor of endothelial activation. Taken together, these findings suggest that therapeutic targeting of PIMT may be effective in limiting organ injury in inflammatory vascular diseases

Engineered M13 phage as a novel therapeutic bionanomaterial for clinical applications: From tissue regeneration to cancer therapy

Bacteriophages (phages) are nanostructured viruses with highly selective antibacterial properties that have gained attention beyond eliminating bacteria. Specifically, M13 phages are filamentous phages that have recently been studied in various aspects of nanomedicine due to their biological advantages and more compliant engineering capabilities over other phages. Having nanofiber-like morphology, M13 phages can reach varied target sites and self-assemble into multidimensional scaffolds in a relatively safe and stable way. In addition, genetic modification of the coat proteins enables specific display of peptides and antibodies on the phages, allowing for precise and individualized medicine. M13 phages have also been subjected to novel engineering approaches, including phage-based bionanomaterial engineering and phage-directed nanomaterial combinations that enhance the bionanomaterial properties of M13 phages. In view of these features, researchers have been able to utilize M13 phages for therapeutic applications such as drug delivery, biodetection, tissue regeneration, and targeted cancer therapy. In particular, M13 phages have been utilized as a novel bionanomaterial for precisely mimicking natural tissue environment in order to overcome the shortage in tissue and organ donors. Hence, in this review, we address the recent studies and advances of using M13 phages in the field of nanomedicine as therapeutic agents based upon their characteristics as novel bionanomaterial with biomolecules displayed. This paper also emphasizes the novel engineering approach that enhances M13 phage's bionanomaterial capabilities. Current limitations and future approaches are also discussed to provide insight in further progress for M13 phage-based clinical applications

Ti₃C₂ MXene Nanosheet-Based Dual-Enzyme Cascade Reaction to Facilitate Dual-Stimulation-Mediated Breast Cancer Therapy

Starvation therapy mediated by glucose oxidase is a widely used therapeutic approach for tumor treatment, but it is limited by the simultaneous drawbacks of weak therapeutic efficacy, nonspecificity, and systemic toxicity. Thus, combination therapy was used to complement the widely used therapeutic strategy for anticancer therapy. On the basis of starvation therapy, we designed a catalytic model of nanosheets with biological cascade enzymes synergizing with anticancer drugs. In short, two cascade enzymes (glucose oxidase and horseradish peroxidase) are covalently immobilized on Ti3C2 MXene nanosheet and a cascade enzyme nanoreactor is formed by electrostatically adsorbing positive charged DOX. Finally, the outer layer is coated with hyaluronic acid. By combining glucose oxidase-mediated starvation therapy, photothermal therapy, and chemotherapy, we have achieved the therapeutic effect of “killing three birds with one stone” by combining the dual stimulation response of endogenous and exogenous sources to the tumor site. This method not only achieves the targeting of cancer cells but also improves the systemic toxicity and reduced efficacy of biological enzymes and realizes synergistic cancer therapy with enhanced cascade reactions. It opens up a new path for the research of nanomedicine

In Vitro Antimetastatic Effect of Phosphatidylinositol 3-Kinase Inhibitor ZSTK474 on Prostate Cancer PC3 Cells

Abstract: Tumor metastasis is the main cause of lethality of prostate cancer, because conventional therapies like surgery and hormone treatment rarely work at this stage. Tumor cell migration, invasion and adhesion are necessary processes for metastasis. By providing nutrition and an escape route from the primary site, angiogenesis is also required for tumor metastasis. Phosphatidylinositol 3-kinases (PI3Ks) are well known to play important roles in tumorigenesis as well as metastasis. ZSTK474 is a specific PI3K inhibitor developed for solid tumor therapy. In the present report, antimetastatic activities of ZSTK474 were investigated in vitro by determining the effects on the main metastatic processes. ZSTK474 exhibited inhibitory effects on migration, invasion and adhesive ability of prostate cancer PC3 cells. Furthermore, ZSTK474 inhibited phosphorylation of Akt substrate-Girdin, and the secretion of matrix metalloproteinase (MMP), both of which were reported to be closely involved in migration and invasion. On the other hand, ZSTK474 inhibited theInt. J. Mol. Sci. 2013, 14 1357

Discovery and characterization of functional modules and pathogenic genes associated with the risk of coronary artery disease

An integrated network biology approach for identifying disease risk functional modules and risk pathogenic genes for associated with CAD risk.</p

PIMT is a novel and potent suppressor of endothelial activation

Proinflammatory agonists provoke the expression of cell surface adhesion molecules on endothelium in order to facilitate leukocyte infiltration into tissues. Rigorous control over this process is important to prevent unwanted inflammation and organ damage. Protein L-isoaspartyl O-methyltransferase (PIMT) converts isoaspartyl residues to conventional methylated forms in cells undergoing stress-induced protein damage. The purpose of this study was to determine the role of PIMT in vascular homeostasis. PIMT is abundantly expressed in mouse lung endothelium and PIMT deficiency in mice exacerbated pulmonary inflammation and vascular leakage to LPS(lipopolysaccharide). Furthermore, we found that PIMT inhibited LPS-induced toll-like receptor signaling through its interaction with TNF receptor-associated factor 6 (TRAF6) and its ability to methylate asparagine residues in the coiled-coil domain. This interaction was found to inhibit TRAF6 oligomerization and autoubiquitination, which prevented NF-κB transactivation and subsequent expression of endothelial adhesion molecules. Separately, PIMT also suppressed ICAM-1 expression by inhibiting its N-glycosylation, causing effects on protein stability that ultimately translated into reduced EC(endothelial cell)-leukocyte interactions. Our study has identified PIMT as a novel and potent suppressor of endothelial activation. Taken together, these findings suggest that therapeutic targeting of PIMT may be effective in limiting organ injury in inflammatory vascular diseases