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Strange bodies : a novel
A dizzying novel of deception and metempsychosis by the author of the National Book Award finalist Far North Whatever this is, it started when Nicholas Slopen came back from the dead. In a locked ward of a notorious psychiatric hospital sits a man who insists that he is Dr. Nicholas Slopen, failed husband and impoverished Samuel Johnson scholar. Slopen has been dead for months. Yet nothing can make this man change his story. What begins as a tale of apparent forgery, involving unseen letters by the great Dr. Johnson, grows to encompass a conspiracy between a Silicon Valley mogul and his Russian allies to exploit the darkest secret of Soviet technology: the Malevin Procedure. With echoes of both Jorge Luis Borges and Philip K. Dick, Marcel Theroux's Strange Bodies takes the reader on a dizzying speculative journey that poses questions about identity, authenticity, and what it means to be truly human.
Book
Bodies of summer
\"The existence of an afterlife is now a fact: heaven is the Internet. Death is only an interruption as souls can be uploaded to the Web and new bodies can be purchased by those wishing to reenter the physical world. The need to settle an old score pushes Ramiro Olivaires to move from the comfort of virtual existence back into a human body. Ramiro's grandson, however, can only afford the body of an overweight middle-aged woman. In the shell of this new body, Ramiro must adjust to the dizzying transformations that the world has undergone since his death. Using Ramiro himself as an avatar, Castagnet walks us through a stifling new version of reality where sex, gender, identity, religion, and politics are defined by the limitless possibilities of the human body. Castagnet is considered one of the most promising new voices in Latin American literature and Bodies of Summer shows us why\" -- Provided by publisher.
BOOK
B and T Cells Driving Multiple Sclerosis: Identity, Mechanisms and Potential Triggers
Historically, multiple sclerosis (MS) has been viewed as being primarily driven by T cells. However, the effective use of anti-CD20 treatment now also reveals an important role for B cells in MS patients. The results from this treatment put forward T-cell activation rather than antibody production by B cells as a driving force behind MS. The main question of how their interaction provokes both B and T cells to infiltrate the CNS and cause local pathology remains to be answered. In this review, we highlight key pathogenic events involving B and T cells that most likely contribute to the pathogenesis of MS. These include (1) peripheral escape of B cells from T cell-mediated control, (2) interaction of pathogenic B and T cells in secondary lymph nodes, and (3) reactivation of B and T cells accumulating in the CNS. We will focus on the functional programs of CNS-infiltrating lymphocyte subsets in MS patients and discuss how these are defined by mechanisms such as antigen presentation, co-stimulation and cytokine production in the periphery. Furthermore, the potential impact of genetic variants and viral triggers on candidate subsets will be debated in the context of MS.
Journal Article
Every day : the graphic novel
Every morning A wakes in a different person's body, in a different person's life, learning over the years to never get too attached, until he wakes up in the body of Justin and falls in love with Justin's girlfriend, Rhiannon.
BOOK
Decreased Astrocytic CCL2 Accounts for BAF-312 Effect on PBMCs Transendothelial Migration Through a Blood Brain Barrier in Vitro Model
Disruption of the blood brain barrier (BBB) is a common event in several neurological diseases and in particular, in multiple sclerosis (MS), it contributes to the infiltration of the central nervous system by peripheral inflammatory cells. Sphingosine-1-phosphate (S1P) is a bioactive molecule with pleiotropic effects. Agonists of S1P receptors such as fingolimod and siponimod (BAF-312) are in clinical practice for MS and have been shown to preserve BBB function in inflammatory conditions. Using an in vitro BBB model of endothelial-astrocytes co-culture exposed to an inflammatory insult (tumor necrosis factor-α and interferon-γ; T&I), we show that BAF-312 reduced the migration of peripheral blood mononuclear cells (PBMCs) through the endothelial layer, only in the presence of astrocytes. This effect was accompanied by decreased expression of the adhesion molecule ICAM-1. BAF-312 also reduced the activation of astrocytes, by controlling NF-kB and NLRP3 induction and preventing the increase of proinflammatory cytokine and chemokines. Reduction of CCL2 by BAF-312 may be responsible for the observed effects and, accordingly, addition of exogenous CCL2 was able to counteract BAF-312 effects and rescued T&I responses on PBMC migration, ICAM-1 expression and astrocyte activation. The present results further point out BAF-312 effects on BBB properties, suggesting also the key role of astrocytes in mediating drug effects on endothelial function.
Graphical abstract
Journal Article
Sleep, death, and rebirth : mystical practices of Lurianic Kabbalah
\"In the sixteenth century, the famous kabbalist Isaac Luria transmitted a secret trove of highly complex mystical practices to a select groups of students. These meditations were designed to capitalize on sleep and death states in order to effectively split one's soul into multiple parts, and which, when properly performed, permitted the adept to free oneself from the cycle of rebirth. Through an in-depth analysis of these contemplative practices within the broader context of Lurianic literature, Zvi Ish-Shalom guides us on a penetrating scholarly journey into a realm of mystical teachings and practices never before available in English, illuminating a radically monistic vision of reality at the heart of Kabbalistic metaphysics and practice\"-- Provided by publisher.
BOOK
Three-dimensional microfluidic model for tumor cell intravasation and endothelial barrier function
Entry of tumor cells into the blood stream is a critical step in cancer metastasis. Although significant progress has been made in visualizing tumor cell motility in vivo, the underlying mechanism of cancer cell intravasation remains largely unknown. We developed a microfluidic-based assay to recreate the tumor-vascular interface in three-dimensions, allowing for high resolution, real-time imaging, and precise quantification of endothelial barrier function. Studies are aimed at testing the hypothesis that carcinoma cell intravasation is regulated by biochemical factors from the interacting cells and cellular interactions with macrophages. We developed a method to measure spatially resolved endothelial permeability and show that signaling with macrophages via secretion of tumor necrosis factor alpha results in endothelial barrier impairment. Under these conditions intravasation rates were increased as validated with live imaging. To further investigate tumor-endothelial (TC-EC) signaling, we used highly invasive fibrosarcoma cells and quantified tumor cell migration dynamics and TC-EC interactions under control and perturbed (with tumor necrosis factor alpha) barrier conditions. We found that endothelial barrier impairment was associated with a higher number and faster dynamics of TC-EC interactions, in agreement with our carcinoma intravasation results. Taken together our results provide evidence that the endothelium poses a barrier to tumor cell intravasation that can be regulated by factors present in the tumor microenvironment.
Journal Article
Anglo-Jewry since 1066
This book is a study of the history and memory of Anglo-Jewry from medieval times to the present and explores the construction of identities, both Jewish and non-Jewish, in relation to the concept of place. The introductory chapters provide a theoretical overview focusing on the nature of local studies. The book then moves into a chronological frame, starting with medieval Winchester, moving to early modern Portsmouth, and then it covers the evolution of Anglo-Jewry from emancipation to the twentieth century. Emphasis is placed on the impact on identities resulting from the complex relationship between migration (including transmigration) and the settlement of minority groups. Drawing upon a range of approaches, including history, cultural and literary studies, geography, Jewish and ethnic and racial studies, the book uses extensive sources including novels, poems, art, travel literature, autobiographical writing, official documentation, newspapers and census data.
eBook
CXCL12-mediated monocyte transmigration into brain perivascular space leads to neuroinflammation and memory deficit in neuropathic pain
Emerging clinical and experimental evidence demonstrates that neuroinflammation plays an important role in cognitive impairment associated with neuropathic pain. However, how peripheral nerve challenge induces remote inflammation in the brain remains largely unknown.
The circulating leukocytes and plasma C-X-C motif chemokine 12 (CXCL12) and brain perivascular macrophages (PVMs) were analyzed by flow cytometry, Western blotting, ELISA, and immunostaining in spared nerve injury (SNI) mice. The memory function was evaluated with a novel object recognition test (NORT) in mice and with Montreal Cognitive Assessment (MoCA) in chronic pain patients.
The classical monocytes and CXCL12 in the blood, PVMs in the perivascular space, and gliosis in the brain, particularly in the hippocampus, were persistently increased following SNI in mice. Using the transgenic CCR2
and CX3CR1
mice, we discovered that at least some of the PVMs were recruited from circulating monocytes. The SNI-induced increase in hippocampal PVMs, gliosis, and memory decline were substantially prevented by either depleting circulating monocytes via intravenous injection of clodronate liposomes or blockade of CXCL12-CXCR4 signaling. On the contrary, intravenous injection of CXCL12 at a pathological concentration in naïve mice mimicked SNI effects. Significantly, we found that circulating monocytes and plasma CXCL12 were elevated in chronic pain patients, and both of them were closely correlated with memory decline.
CXCL12-mediated monocyte recruitment into the perivascular space is critical for neuroinflammation and the resultant cognitive impairment in neuropathic pain.
Journal Article