Search Results Heading

MBRLSearchResults

mbrl.module.common.modules.added.book.to.shelf
Title added to your shelf!
View what I already have on My Shelf.
Oops! Something went wrong.
Oops! Something went wrong.
While trying to add the title to your shelf something went wrong :( Kindly try again later!
Are you sure you want to remove the book from the shelf?
Oops! Something went wrong.
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
    Done
    Filters
    Reset
  • Discipline
      Discipline
      Clear All
      Discipline
  • Is Peer Reviewed
      Is Peer Reviewed
      Clear All
      Is Peer Reviewed
  • Series Title
      Series Title
      Clear All
      Series Title
  • Reading Level
      Reading Level
      Clear All
      Reading Level
  • Year
      Year
      Clear All
      From:
      -
      To:
  • More Filters
      More Filters
      Clear All
      More Filters
      Content Type
    • Item Type
    • Is Full-Text Available
    • Subject
    • Country Of Publication
    • Publisher
    • Source
    • Target Audience
    • Donor
    • Language
    • Place of Publication
    • Contributors
    • Location
164,367 result(s) for "Bruno"
Sort by:
Microgrid dynamics and control
This book discusses relevant microgrid technologies in the context of integrating renewable energy and also addresses challenging issues. The authors summarize long term academic and research outcomes and contributions. In addition, this book is influenced by the authors' practical experiences on microgrids (MGs), electric network monitoring, and control and power electronic systems. A thorough discussion of the basic principles of the MG modeling and operating issues is provided. The MG structure, types, operating modes, modelling, dynamics, and control levels are covered. Recent advances in DC microgrids, virtual synchronousgenerators, MG planning and energy management are examined. The physical constraints and engineering aspects of the MGs are covered, and developed robust and intelligent control strategies are discussed using real time simulations and experimental studies.
Pathophysiology of diabetic dyslipidaemia: where are we?
Cardiovascular disease is a major cause of morbidity and mortality in patients with type 2 diabetes mellitus, with a two- to fourfold increase in cardiovascular disease risk compared with non-diabetic individuals. Abnormalities in lipid metabolism that are observed in the context of type 2 diabetes are among the major factors contributing to an increased cardiovascular risk. Diabetic dyslipidaemia includes not only quantitative lipoprotein abnormalities, but also qualitative and kinetic abnormalities that, together, result in a shift towards a more atherogenic lipid profile. The primary quantitative lipoprotein abnormalities are increased triacylglycerol (triglyceride) levels and decreased HDL-cholesterol levels. Qualitative lipoprotein abnormalities include an increase in large, very low-density lipoprotein subfraction 1 (VLDL 1 ) and small, dense LDLs, as well as increased triacylglycerol content of LDL and HDL, glycation of apolipoproteins and increased susceptibility of LDL to oxidation. The main kinetic abnormalities are increased VLDL 1 production, decreased VLDL catabolism and increased HDL catabolism. In addition, even though LDL-cholesterol levels are typically normal in patients with type 2 diabetes, LDL particles show reduced turnover, which is potentially atherogenic. Although the pathophysiology of diabetic dyslipidaemia is not fully understood, the insulin resistance and relative insulin deficiency observed in patients with type 2 diabetes are likely to contribute to these lipid changes, as insulin plays an important role in regulating lipid metabolism. In addition, some adipocytokines, such as adiponectin or retinol-binding protein 4, may also contribute to the development of dyslipidaemia in patients with type 2 diabetes.
NF-kappaB Is Involved in the Regulation of EMT Genes in Breast Cancer Cells
The metastatic process in breast cancer is related to the expression of the epithelial-to-mesenchymal transition transcription factors (EMT-TFs) SNAIL, SLUG, SIP1 and TWIST1. EMT-TFs and nuclear factor-κB (NF-κB) activation have been associated with aggressiveness and metastatic potential in carcinomas. Here, we sought to examine the role of NF-κB in the aggressive properties and regulation of EMT-TFs in human breast cancer cells. Blocking NF-κB/p65 activity by reducing its transcript and protein levels (through siRNA-strategy and dehydroxymethylepoxyquinomicin [DHMEQ] treatment) in the aggressive MDA-MB-231 and HCC-1954 cell lines resulted in decreased invasiveness and migration, a downregulation of SLUG, SIP1, TWIST1, MMP11 and N-cadherin transcripts and an upregulation of E-cadherin transcripts. No significant changes were observed in the less aggressive cell line MCF-7. Bioinformatics tools identified several NF-κB binding sites along the promoters of SNAIL, SLUG, SIP1 and TWIST1 genes. Through chromatin immunoprecipitation and luciferase reporter assays, the NF-κB/p65 binding on TWIST1, SLUG and SIP1 promoter regions was confirmed. Thus, we suggest that NF-κB directly regulates the transcription of EMT-TF genes in breast cancer. Our findings may contribute to a greater understanding of the metastatic process of this neoplasia and highlight NF-κB as a potential target for breast cancer treatment.
Deep strong light–matter coupling in plasmonic nanoparticle crystals
In the regime of deep strong light–matter coupling, the coupling strength exceeds the transition energies of the material 1 – 3 , fundamentally changing its properties 4 , 5 ; for example, the ground state of the system contains virtual photons and the internal electromagnetic field gets redistributed by photon self-interaction 1 , 6 . So far, no electronic excitation of a material has shown such strong coupling to free-space photons. Here we show that three-dimensional crystals of plasmonic nanoparticles can realize deep strong coupling under ambient conditions, if the particles are ten times larger than the interparticle gaps. The experimental Rabi frequencies (1.9 to 3.3 electronvolts) of face-centred cubic crystals of gold nanoparticles with diameters between 25 and 60 nanometres exceed their plasmon energy by up to 180 per cent. We show that the continuum of photons and plasmons hybridizes into polaritons that violate the rotating-wave approximation. The coupling leads to a breakdown of the Purcell effect—the increase of radiative damping through light–matter coupling—and increases the radiative polariton lifetime. The results indicate that metallic and semiconducting nanoparticles can be used as building blocks for an entire class of materials with extreme light–matter interaction, which will find application in nonlinear optics, the search for cooperative effects and ground states, polariton chemistry and quantum technology 4 , 5 . Photons and plasmons hybridize into polaritons in three-dimensional crystals of plasmonic nanoparticles, leading to deep strong light–matter coupling and the breakdown of the Purcell effect.
Tumor angiogenesis and vascular normalization: alternative therapeutic targets
Tumor blood vessels are a key target for cancer therapeutic management. Tumor cells secrete high levels of pro-angiogenic factors which contribute to the creation of an abnormal vascular network characterized by disorganized, immature and permeable blood vessels, resulting in poorly perfused tumors. The hypoxic microenvironment created by impaired tumor perfusion can promote the selection of more invasive and aggressive tumor cells and can also impede the tumor-killing action of immune cells. Furthermore, abnormal tumor perfusion also reduces the diffusion of chemotherapeutic drugs and radiotherapy efficiency. To fight against this defective phenotype, the normalization of the tumor vasculature has emerged as a new therapeutic strategy. Vascular normalization, by restoring proper tumor perfusion and oxygenation, could limit tumor cell invasiveness and improve the effectiveness of anticancer treatments. In this review, we investigate the mechanisms involved in tumor angiogenesis and describe strategies used to achieve vascular normalization.