WorldCat Identities

黃宜侯

Overview
Works: 76 works in 82 publications in 2 languages and 123 library holdings
Genres: Academic theses 
Roles: Author, Other, Contributor
Classifications: G155.A8, 338.479194
Publication Timeline
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Most widely held works by 黃宜侯
A comparison of value at risk approaches and a new method with extreme value theory and kernel estimator by Yi-Hou Huang( )

1 edition published in 2006 in English and held by 26 WorldCat member libraries worldwide

Domestic overnight leisure travel : recent trends and challenges by Justin Marshall( Book )

1 edition published in 2005 in English and held by 11 WorldCat member libraries worldwide

IPhone 3G Master Book wan xiang zhi( Book )

1 edition published in 2009 in Chinese and held by 7 WorldCat member libraries worldwide

In Vivo Observations of Resident Microglia and Blood Derived Macrophages in the Brain and Spinal Cord by Teresa A Evans-Campbell( )

2 editions published in 2014 in English and held by 2 WorldCat member libraries worldwide

Microglia and macrophages are two phagocytic cell types that found in the Central Nervous System (CNS). Microglia are present in the normal CNS and play a role in both homeostasis and disease while macrophages are not present in large numbers in the healthy CNS. After an insult, microglia become activated and macrophages infiltrate into the tissue from the circulation. Both of these cell types express many of the same markers and display similar morphology, making them so difficult to distinguish that they are often lumped into one group. Here, we observed microglia and macrophages in the healthy CNS and in several different injury models. First, we describe interactions of both microglia and macrophages with damaged axons in traumatic spinal cord injury. Previously, it has been shown that damaged axons die back from the center of a spinal cord lesion over the first few days after injury by an immune mediated process. We have shown that this dieback occurs by loss of axonal material from the damaged end of the axon after contact with CX3CR1 GFP expressing, bone marrow derived, macrophages but not after contact with resident microglia independent of the CCR2 chemokine receptor. Second, we investigated a possible role for microglia in the presentation of antigen across the blood brain barrier. Current thought maintains that antigen presentation from within the CNS is completed without direct interaction between microglia and T-cells. We have observed microglial projections that leave the compartment defined by the blood brain barrier and extend into blood vessels, representing a potential route for antigen presentation to circulating T-cells. These projections increase in number in an autoimmune condition, experimental autoimmune encephalomyelitis, and did not increase in cases of sterile trauma or tumor infiltration, presumably due to differences in activation of antigen presentation in these models. Together, these descriptions identify previously unknown differences between microglia and macrophages and propose a new function for microglia. As these two separate cell populations are further investigated and separate identities established, this understanding may lead to more targeted therapies for CNS disorders
Identifying predictors for postoperative clinical outcome in lumbar spinal stenosis patients using smart-shoe technology by Sunghoon I Lee( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

The prevalence of hypertension and abnormal kidney function in children with sickle cell disease -a cross sectional review by Prasad Bodas( )

1 edition published in 2013 in English and held by 2 WorldCat member libraries worldwide

Electrical Characteristics of 10-kV 4H-SiC MPS Rectifiers with High Schottky Barrier Height by Feng Jiang( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Lymphocyte trafficking, homing and function : insights into the in vivo behavior of regulatory t and natural killer cells by Alexander Andrew Tong( )

2 editions published in 2017 in English and held by 2 WorldCat member libraries worldwide

The immune system exists as an elaborate network of organized tissue and mobile cellular elements working in concert to defend the host against foreign pathogens and self-derived cancer cells. At the core of how the immune system works is the complex choreography of mobile immune cells actively finding their way into and out of tissues in order to exert their function. As we enter the era of immunotherapy, understanding the fundamental processes of how lymphocytes in concert with antigen presenting cells dynamically and efficiently patrol the comparatively vast body of the host is critical for discovering how to meaningfully perturb their behavior for clinical gain in cancer, infection, and autoimmune disease. Here, we study the trafficking and homing of two important lymphocyte populations: regulatory T cells (Tregs) and natural killer (NK) cells. We first describe the unique trafficking and transit properties of Tregs in peripheral lymph nodes, comparing their behavior to that of conventional T cells. Previous work has shown differences between the CD4+ and CD8+ conventional T cell subsets in terms of LN trafficking times and dendritic cell (DC) contact. We have now demonstrated using classic immunologic tools that a "resident" subpopulation of Tregs has an especially prolonged LN dwell time with concomitantly poor LN homing kinetics. Utilizing a novel imaging platform allowing first-in-kind intravital 2-photon laser scanning microscopy (2PLSM) of gut secondary lymphoid organs, we also find increased resident Treg contact with DC in mesenteric as well as other peripheral LN. Second, we study the homing and efficacy of ex vivo-expanded NK (eNK) cells for the therapy of metastatic Ewing's sarcoma (ES). We observe that eNK cells have a strong lung, spleen, and liver homing tropism and are able to significantly reduce pulmonary metastases of ES. While this is incredibly promising for clinical purposes, eNKs are ultimately unable to penetrate the primary tumor site, likely due to a lack of appropriate homing receptors and cues. These data underscore the pressing need to uncover mechanisms by which we might be able to drive desired lymphocyte populations into the tumor microenvironment. As we investigate and understand more about why certain lymphocyte populations reside in or quickly transit through different tissues, we hope the knowledge gained will help lead to more effective cellular immunotherapies in cancer and other diseases
Telling in-tune from out-of-tune: widespread evidence for implicit absolute intonation by Stephen C Van Hedger( )

1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide

Unobtrusive and Continuous Monitoring of Alcohol-impaired Gait Using Smart Shoes( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

Implantation of a second glaucoma drainage device by Brian A Francis( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Regulation of macrophages by Mycobacterium tuberculosis and the ERK MAP kinase signaling pathway by Edward Thompson, III Richardson( )

2 editions published in 2015 in English and held by 2 WorldCat member libraries worldwide

Mycobacterium tuberculosis, the cause of tuberculosis, survives for long periods in a latent state in infected individuals, and the immune system is typically able to control but not eliminate the bacteria. Latency is a complex phenomenon but involves, in part, interactions of the bacteria and its unique lipoproteins and lipoglycans with macrophages, the main cells that become infected. The purpose of this dissertation was to expand understanding of how M. tuberculosis engages with macrophages. In the first part, we characterized the lipoglycan binding function of M. tuberculosis lipoprotein LprG. We determined the binding properties of these M. tuberculosis lipoglycans to LprG using surface plasmon resonance. We also verified the presence of a non-acyl chain dependent binding mode to LprG, and determined that LprG also binds mannan. Finally, we determined that one function of LprG is to facilitate exposure of LAM on the bacterial cell surface for interaction with macrophages. LprG-deficient M. tuberculosis had reduced surface-exposed lipoarabinomannan, and had reduced ability to block phagolysosome maturation, a known immune evasion mechanism that requires lipoarabinomannan. These studies contribute to understanding of LprG, and develop increased knowledge of how M. tuberculosis lipoarabinomannan is exposed to macrophages to block phagolysosome fusion, a process involved in bacterial persistence and intracellular survival. In the second part, we studied the TLR2 signaling response of macrophages to M. tuberculosis. We determined that TLR2 was required for M. tuberculosis to trigger NF-¿B and ERK, and that TLR2 signaling results in balanced downstream effects. NF-¿B is required for expression of pro-inflammatory IL-12, and M. tuberculosis-stimulated Tpl2-ERK signaling suppressed IL-12 while inducing anti-inflammatory IL-10. These effects reduced CD4+ T cell responses against M. tuberculosis. Tpl2-deficient macrophages expressed IL-12 in response to M. tuberculosis, and were more potent at stimulating antigen-specific T cells, upon initial stimulation and recall. These findings contribute to understanding of the signaling triggered by M. tuberculosis, and the role of the macrophage-intrinsic ERK cascade in inhibiting T cell-mediated host defense. Together, these studies expand understanding of the regulation of macrophages by M. tuberculosis in ways that promote long-term survival of the bacteria, and may potentiate latent infection
Defining the role of immune therapy in pediatric CNS malignancy by Rodney Dixon, Jr Dorand( )

2 editions published in 2015 in English and held by 2 WorldCat member libraries worldwide

Understanding the mechanisms tumors employ to escape detection by both the innate and adaptive immune systems is imperative for developing new immune based therapeutics. Available evidence now favors the view that physiological immune surveillance by members of the innate and adaptive immune systems play an essential role in suppressing tumor development in vivo, and the failure of immune surveillance mechanisms favors tumor development and metastasis formation (1, 2). Whether it is altering cell surface markers, secreting cytokines, or even altering its genome, tumors can evolve much faster than the immune system. New and innovative approaches to cancer therapy are necessary to combat all cancer types, but especially solid tumors as current immunotherapies are more effective at targeting non-solid tumors. Even further complicating physiologic immune surveillance, tumors that develop within the central nervous system (CNS) do so behind the blood brain barrier (BBB) that can serve as an impediment to both the small molecules employed in immunotherapeutics, as well as, the infiltrating lymphocytes necessary for tumor elimination. Medulloblastoma (MB) is the most common malignant CNS neoplasm in the pediatric setting, accounting for 20% of pediatric CNS malignancies overall. It is a WHO-Grade IV primitive neuroectodermal tumor (PNET) that develops in the cerebellum and often invades into surrounding structures including the fourth ventricle and brain stem (3). While treatment modalities and, more importantly, post treatment cognitive instruction has improved outcomes, surviving patients still suffer cognitive sequelae (4). Unique to CNS neoplasms are microglia, an additional immune cell type that plays a pivotal role in normal immune surveillance of the CNS, phagocytosis, and neuroinflammation (5). Microglia reside in the brain parenchyma and help maintain the homeostatic immunosuppressive environment partially due to their expression of CX3CR1. Fractalkine (FKN) is constitutively expressed by neurons and astrocytes leading to tonic inhibition of microglial activation (6). In the presence of malignancy, FKN signaling is disrupted and we found MB can even express FKN itself. Understanding the intricacies of the FKN signaling axis may provide the key signals leading to immune suppression in the CNS in the context of malignant tumors. Furthermore, strategies that augment physiologic immune surveillance, such as the development of tumor vaccines and the addition of small molecule inhibitors, have the potential to benefit therapeutic approaches for CNS malignancies. Whether using a conventional ex vivo vaccine approach (7), or new in situ approaches centered around plant viral nanoparticles (8), vaccination strategies hold great possibilities for enhancing CNS tumor surveillance by vigorously activating the adaptive immune system. To ensure continued activation of the immune response, other therapeutic approaches focus on targeting known immune checkpoint molecules such as CTLA-4, PD-1, or PD-L1, which are expressed on the surface of either immune cells or tumors and inhibit the immune response (9, 10). Additionally, novel approaches can be employed to disrupt the very signaling mechanisms that lead to the surface expression of these immune checkpoint molecules (11). Understanding both the basics of CNS immune cell physiology and how combining targeted immunotherapy with supplemental treatment can counteract suppressive mechanisms is imperative to prevent tumor immune evasion. Enhanced immunotherapeutic approaches to malignant diseases in the CNS have the potential to produce significant increases in overall survival and better prognosis for brain tumor patients
CCL3 Augments Antitumor Responses in CT26 by Enhancing Cellular Trafficking and Interferon-Gamma Expression by Frederick, Jr Allen( )

2 editions published in 2018 in English and held by 2 WorldCat member libraries worldwide

Cancer evolves and thrives due to the failures of multiple intracellular and extracellular self-control mechanisms, and as such, often requires a multifaceted approach for complete eradication. An effective vaccine consists of specific, well-developed, and robust CD8+ T cell responses. However, while inducing tumor reactive CD8+ T cells in vitro or in vivo is achievable, the potential benefits often fail to translate into better patient outcomes. One of the major difficulties stems from the tumor's ability to induce immune tolerance. Studies have shown that immune cells can be induced to promote tumor growth or regression and chemokines are often integral organizers and modulators of these events. The ability for tumors to maintain a tolerant environment or for immunotherapy to promote strong long-lived antitumor CD8+ T cell responses is dependent on the tumor types and also the chemokines associated within the tumor milieu. Clinical data has shown that increased number of lymph nodes (LNs) infiltrated by tumors directly correlates with poor patient outcomes. Therefore, deciphering the complexities of immune interactions within LNs are essential to understanding how many tumors can redirect or suppress immune responses. Chemokines, such as CCL3, have the ability to attract naive CD8+ T cells and modulate their immune responses. CCL3 is also integral in orchestrating nonrandom naive CD8+ T cell contacts with dendritic cells (DCs) in the draining LNs (DLNs) of vaccinated mice9. These events lead to increased CD8+ T cell-DC surveillance time, decreases effector response time, and enhanced memory T cell generation; all of which are important in building an effective vaccine response. Furthermore, CCL3 has also been directly implicated in facilitating the clearance of some tumor models. These findings suggest possible therapeutic roles for CCL3 in redirecting tumor-tolerant milieus toward a tumor-immunogenic one by conditioning immune cells to induce an inflammatory response to tumor antigens (Ag). The body of work presented here discusses various dynamic cellular responses that occur during Ag capture, and subsequent early and late phase adaptive immune development in the tumor-DLN (TDLN) and at the primary tumor site (PTS) in response to CCL3 therapy
Liang anIC she ji chan ye jing he ji jing ying ji xiao fen xi = Co-opetition and Firm Performance in IC Design Industry by Sunyanling( Book )

1 edition published in 2017 in Chinese and held by 1 WorldCat member library worldwide

Ji yi ti chan ye zhi fa zhan yu zhuan xing : yi tai wan chang shang wei li = The Development and Transformation of DRAM Industry :Case Study on Taiwanese Companies by Yangxiaozhen( Book )

1 edition published in 2018 in Chinese and held by 1 WorldCat member library worldwide

Feng ge tou zi yu zi chan cheng zhang yin zi = Style Investing Based on Asset Growth by Panjianlin( Book )

1 edition published in 2019 in Chinese and held by 1 WorldCat member library worldwide

Mechanobiology of Leukocyte Adhesion by Bryan Lauck Benson( )

2 editions published in 2019 in English and held by 1 WorldCat member library worldwide

Splitting their lives between the chaotic, dynamic environment within the bloodstream and the calm, stable waters of tissues, leukocytes face unique challenges in integrating and responding to mechanical forces across their lifespan. The bloodstream affords leukocytes rapid transit. In order to be useful, leukocytes must exit from the bloodstream and enter lymphoid organs for antigen surveillance or sites of inflammation to respond to threats. This process, extravasation via the leukocyte adhesion cascade, consists of at least 8 steps and each involves dynamic interactions with plasma, erythrocytes, platelets, other leukocytes, endothelial cells, and cells of the tissue parenchyma. To navigate this process, leukocytes make use of an array of signaling, cytoskeletal, motor, and adhesion molecules, and emergent in the literature is the understanding that each of these has different functions in different contexts: intravascular vs. extravascular, in different tissues, and in different leukocyte subsets. Of these, by far the most important are the integrins, which bind to adhesion molecules on endothelia and are critically involved in every step of the cascade. Blockade of integrins with the monoclonal antibodies natalizumab and efalizumab results in almost complete ablation of leukocyte transmigration into tissue and marked clinical benefit in autoimmune diseases, but also carries risks of rare but potentially fatal progressive multifocal leukencephalopathy. The focus of the present work is on understanding the responses of leukocytes to physical forces in the adhesion cascade, with emphasis on shear stress, erythrocyte collisions, and leukocyte cytoskeleton-coupled motor protein activity. We first generated biomimetic in vitro models of the post-capillary venule, the anatomical site of leukocyte adhesion. These models afforded us the experimental control needed to demonstrate three insights. First, chemokines and cytokines cannot spread laterally within the convective context of the bloodstream, and therefore inflammation must be propagated by extravascular means. Second, collisions with erythrocytes are the most significant forces acting on leukocytes in post-capillary venules, and are essential for efficient adhesion. Finally, the mechanosensitive ion channel PIEZO1 is necessary for a feedback loop that transduces myosin activity and allows coordinated release of high affinity integrin bonds during leukocyte intravascular crawling
 
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Alternative Names
Huang, Alex YiHou

Huang, Yi Hou

Huang, YiHou

YiHou, Huang

YiHou Huang, Alex

Languages