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International handbook of migration and population distribution
This Handbook offers a comprehensive collection of essays that cover essential features of geographical mobility, from internal migration, to international migration, to urbanization, to the adaptation of migrants in their destinations. Part I of the collection introduces the range of theoretical perspectives offered by several social science disciplines, while also examining the crucial relationship between internal and international migration. Part II takes up methods, ranging from how migration data are best collected to contemporary techniques for analyzing such data. Part III of the handbook contains summaries of present trends across all world regions. Part IV rounds out the volume with several contributions assessing pressing issues in contemporary policy areas. The volume's editor Michael J. White has spent a career studying the pattern and process of internal and international migration, urbanization and population distribution in a wide variety of settings, from developing societies to advanced economies. In this Handbook he brings together contributors from all parts of the world, gathering in this one volume both geographical and substantive expertise of the first rank. The Handbook will be a key reference source for established scholars, as well as an invaluable high-level introduction to the most relevant topics in the field for emerging scholars.-- Provided by Publisher.
BOOK
Cancer exome analysis reveals a T-cell-dependent mechanism of cancer immunoediting
Exome analysis of chemical-carcinogen-induced mouse tumours provides evidence for T-cell-mediated immunoselection as a mechanism of immunoediting.
The anticancer potential of immunoediting
Two groups reporting in this issue of
Nature
use contrasting approaches to come to many of the same conclusions about the process of cancer immunoediting, in which an individual is protected from cancer though the elimination and immunogenic modification of cancerous cells. Matsushita
et al
. use whole-exon sequencing of mouse sarcomas induced by chemical carcinogens to obtain evidence for T-cell-mediated immuno-selection as a mechanism of immune editing. DuPage
et al
. demonstrate that immunosurveillance and immunoediting can occur in an oncogene-driven endogenous tumour model provided that the tumours carry strong neoantigens that are not present in the host.
Cancer immunoediting, the process by which the immune system controls tumour outgrowth and shapes tumour immunogenicity, is comprised of three phases: elimination, equilibrium and escape
1
,
2
,
3
,
4
,
5
. Although many immune components that participate in this process are known, its underlying mechanisms remain poorly defined. A central tenet of cancer immunoediting is that T-cell recognition of tumour antigens drives the immunological destruction or sculpting of a developing cancer. However, our current understanding of tumour antigens comes largely from analyses of cancers that develop in immunocompetent hosts and thus may have already been edited. Little is known about the antigens expressed in nascent tumour cells, whether they are sufficient to induce protective antitumour immune responses or whether their expression is modulated by the immune system. Here, using massively parallel sequencing, we characterize expressed mutations in highly immunogenic methylcholanthrene-induced sarcomas derived from immunodeficient
Rag2
−/−
mice that phenotypically resemble nascent primary tumour cells
1
,
3
,
5
. Using class I prediction algorithms, we identify mutant spectrin-β2 as a potential rejection antigen of the d42m1 sarcoma and validate this prediction by conventional antigen expression cloning and detection. We also demonstrate that cancer immunoediting of d42m1 occurs via a T-cell-dependent immunoselection process that promotes outgrowth of pre-existing tumour cell clones lacking highly antigenic mutant spectrin-β2 and other potential strong antigens. These results demonstrate that the strong immunogenicity of an unedited tumour can be ascribed to expression of highly antigenic mutant proteins and show that outgrowth of tumour cells that lack these strong antigens via a T-cell-dependent immunoselection process represents one mechanism of cancer immunoediting.
Journal Article
The traumatic colonel : the founding fathers, slavery, and the phantasmatic Aaron Burr
\"In American political fantasy, the Founding Fathers loom large, at once historical and mythical figures. In The Traumatic Colonel, Michael J. Drexler and Ed White examine the Founders as imaginative fictions, characters in the specifically literary sense, whose significance emerged from narrative elements clustered around them. From the revolutionary era through the 1790s, the Founders took shape as a significant cultural system for thinking about politics, race, and sexuality. Yet after 1800, amid the pressures of the Louisiana Purchase and the Haitian Revolution, this system could no longer accommodate the deep anxieties about the United States as a slave nation. Drexler and White assert that the most emblematic of the political tensions of the time is the figure of Aaron Burr, whose rise and fall were detailed in the literature of his time: his electoral tie with Thomas Jefferson in 1800, the accusations of seduction, the notorious duel with Alexander Hamilton, his machinations as the schemer of a breakaway empire, and his spectacular treason trial. The authors venture a psychoanalytically-informed exploration of post-revolutionary America to suggest that the figure of 'Burr' was fundamentally a displaced fantasy for addressing the Haitian Revolution. Drexler and White expose how the historical and literary fictions of the nation's founding served to repress the larger issue of the slave system and uncover the Burr myth as the crux of that repression. Exploring early American novels, such as the works of Charles Brockden Brown and Tabitha Gilman Tenney, as well as the pamphlets, polemics, tracts, and biographies of the early republican period, the authors speculate that this flourishing of political writing illuminates the notorious gap in U.S. literary history between 1800 and 1820\"-- Provided by publisher.
BOOK
Correction: Trypsin, Tryptase, and Thrombin Polarize Macrophages towards a Pro-Fibrotic M2a Phenotype
[This corrects the article DOI: 10.1371/journal.pone.0138748.].
Journal Article
The Maine coon's haiku : and other poems for cat lovers
Via haiku, depicts twenty different breeds of cats, whether mischievous or mysterious, comical or commanding.
Book
Laminin heparin-binding peptides bind to several growth factors and enhance diabetic wound healing
Laminin, as a key component of the basement membrane extracellular matrix (ECM), regulates tissue morphogenesis. Here, we show that multiple laminin isoforms promiscuously bind to growth factors (GFs) with high affinity, through their heparin-binding domains (HBDs) located in the α chain laminin-type G (LG) domains. These domains also bind to syndecan cell-surface receptors, promoting attachment of fibroblasts and endothelial cells. We explore the application of these multifunctional laminin HBDs in wound healing in the type-2 diabetic mouse. We demonstrate that covalent incorporation of laminin HBDs into fibrin matrices improves retention of GFs and significantly enhances the efficacy of vascular endothelial cell growth factor (VEGF-A165) and platelet-derived growth factor (PDGF-BB) in promoting wound healing in vivo, under conditions where the GFs alone in fibrin are inefficacious. This laminin HBD peptide may be clinically useful by improving biomaterial matrices as both GF reservoirs and cell scaffolds, leading to effective tissue regeneration.
Laminins are important regulators of epidermal wound healing. Here, the authors show that laminins bind to multiple growth factors via their heparin-binding domains, and that incorporation of these domains into fibrin matrices increases growth factor retention, promoting wound healing in type 2 diabetic mouse models.
Journal Article
VEGF-A, PDGF-BB and HB-EGF engineered for promiscuous super affinity to the extracellular matrix improve wound healing in a model of type 1 diabetes
Chronic non-healing wounds, frequently caused by diabetes, lead to lower quality of life, infection, and amputation. These wounds have limited treatment options. We have previously engineered growth factors to bind to exposed extracellular matrix (ECM) in the wound environment using the heparin-binding domain of placental growth factor-2 (PlGF-2123–144), which binds promiscuously to ECM proteins. Here, in the type 1 diabetic (T1D) NOD mouse model, engineered growth factors (eGFs) improved both re-epithelialization and granulation tissue formation. eGFs were even more potent in combination, and the “triple therapy” of vascular endothelial growth factor-A (VEGF-PlGF-2123–144), platelet-derived growth factor-BB (PDGF-BB-PlGF-2123–144), and heparin-binding epidermal growth factor (HB-EGF-PlGF-2123–144) both improved wound healing and remained at the site of administration for significantly longer than wild-type growth factors. In addition, we also found that changes in the cellular milieu of a wound, including changing amounts of M1 macrophages, M2 macrophages and effector T cells, are most predictive of wound-healing success in the NOD mouse model. These results suggest that the triple therapy of VEGF-PlGF-2123–144, PDGF-BB-PlGF-2123–144, and HB-EGF-PlGF-2123–144 may be an effective therapy for chronic non-healing wounds in that occur as a complication of diabetes.
Journal Article
Star destroyers : big ships blowing things up
\"In space, size matters. Boomers. Ships of the Line. Star Destroyers. The bigger the ship, the better the bang. From the dawn of history onward, commanding the most powerful ship around has been a dream of admirals, sultans, emperors, kings, generalissimos, and sea captains everywhere. For what the intimidation factor alone doesn't achieve, a massive barrage from super-weapons probably will. Thus it was, and ever shall be, even into the distant future. From the oceans of Earth, to beneath the ice of Europa, to the distant reaches of galactic empires, it is the great warships and their crews that sometimes keep civilization safe for the rest of us -- but sometimes become an extinction-level event in and of themselves\"--Back cover.
Book
Blocking antibodies against integrin-α3, -αM, and -αMβ2 de-differentiate myofibroblasts, and improve lung fibrosis and kidney fibrosis
Fibrosis is involved in 45% of deaths in the United States, and no treatment exists to reverse the progression of lung or kidney fibrosis. Myofibroblasts are key to the progression and maintenance of fibrosis. We investigated features of cell adhesion necessary for monocytes to differentiate into myofibroblasts, seeking to identify pathways key to myofibroblast differentiation. Blocking antibodies against integrins α3, αM, and αMβ2 de-differentiate myofibroblasts in vitro, lower the pro-fibrotic secretome of myofibroblasts, and treat lung fibrosis and inhibit kidney fibrosis in vivo. Decorin’s collagen-binding peptide can be used to direct functionalized blocking antibodies (against integrins-α3, -αM, -αMβ2) to both fibrotic lungs and fibrotic kidneys, reducing the dose of antibody necessary to treat fibrosis. This targeted immunotherapy blocking key integrins may be an effective therapeutic for the treatment of fibrosis.
Journal Article