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Fodor's essential Iceland
\"Whether you want to soak in a hot spring, experience Reykjavik nightlife, or hike glaciers, the local Fodor's travel experts in Iceland are here to help! This guidebook is packed with maps, carefully curated recommendations, and everything else you need to simplify your trip-planning process and make the most of your time. This brand-new Iceland guide has been designed with an easy-to-read layout, fresh information, and beautiful color photos. An illustrated ultimate experiences guide to the top things to see and do. Photo-filled \"best of\" features on the best waterfalls, craft beer, and museums. Color photos throughout to spark your wanderlust! Up-to-date and honest recommendations for the best sights, restaurants, hotels, and more. Illustrated features on Iceland's musicians past and present, as well as Icelandic mythology. Multiple itineraries to effectively organize your days and maximize your time. Special features on how to save money in this expensive country, and guides to the country's fascinating wildlife and geology. Best road trips in Iceland has an entire chapter dedicated to it. Covers: Reykjavik, the Highlands, the Blue Lagoon, the East and West Fjords, the Golden Circle, Snµfellsnes Peninsula, Snµfellsjèokull National Park, and more. More than 20 detailed maps and a free fullout map to navigate confidently, trip-planning tools and practical tips on when to go, getting around, beating the crowds, and saving time and money, historical and cultural insights providing rich context on the art, architecture, cuisine, music, geography, mythology, and more, local writers to help you find the under-the-radar gems, Icelandic language primer with useful words and essential phrases\"-- Publisher's description.
Book
Mast Cell Biology at Molecular Level: a Comprehensive Review
Mast cells (MCs) are portions of the innate and adaptive immune system derived from bone marrow (BM) progenitors that are rich in cytoplasmic granules. MC maturation, phenotype, and function are determined by their microenvironment. MCs accumulate at inflammatory sites associated with atopy, wound healing, and malignancies. They interact with the external environment and are predominantly located in close proximity of blood vessels and sensory nerves. MCs are key initiators and modulators of allergic, anaphylactic, and other inflammatory reactions, by induction of vasodilation, promoting of vascular permeability, recruitment of inflammatory cells, facilitation of adaptive immune responses, and modulation of angiogenesis, and fibrosis. They express a wide range of receptors, e.g., for IgE (FcεRI), IgG (FcγR), stem cell factor (SCF) (KIT receptor or CD117), complement (including C5aR), and cytokines, that upon activation trigger various signaling pathways. The final consequence of such ligand receptor–based activation of MCs is the release of a broad array of mediators which are classified in three categories. While some mediators are preformed and remain stored in granules such as heparin, histamine, and enzymes mainly chymase and tryptase, others are de novo synthesized only after activation including LTB4, LTD4, PDG2, and PAF, and the cytokines IL-10, IL-8, IL-5, IL-3, IL-1, GM-CSF, TGF-β, VEGF, and TNF-α. Depending on the stimulus, MCs calibrate their pattern of mediator release, modulate the amplification of allergic inflammation, and are involved in the resolution of the immune responses. Here, we review recent findings and reports that help to understand the MC biology, pathology, and physiology of diseases with MC involvement.
Journal Article
Role of Mast Cells in Shaping the Tumor Microenvironment
Early mast cell (MC) infiltration has been reported in a wide range of human and animal tumors particularly malignant melanoma and breast and colorectal cancer. The consequences of their presence in the tumor microenvironment (TME) or at their margins still remain unclear as it is associated with a good or poor prognosis based on the type and anatomical site of the tumor. Within the tumor, MC interactions occur with infiltrated immune cells, tumor cells, and extracellular matrix (ECM) through direct cell-to-cell interactions or release of a broad range of mediators capable of remodeling the TME. MCs actively contribute to angiogenesis and induce neovascularization by releasing the classical proangiogenic factors including VEGF, FGF-2, PDGF, and IL-6, and nonclassical proangiogenic factors mainly proteases including tryptase and chymase. MCs support tumor invasiveness by releasing a broad range of matrix metalloproteinases (MMPs). MC presence within the tumor gained additional significance when it was assumed that controlling its activation by tyrosine kinase inhibitors (imatinib and masitinib) and tryptase inhibitors (gabexate and nafamostat mesylate) or controlling their interactions with other cell types may have therapeutic benefit.
Journal Article
Mast Cell-Mediated Orchestration of the Immune Responses in Human Allergic Asthma: Current Insights
Improving the lung function after experimental allergen challenge by blocking of mast cell (MC) mediators and the capability of MC mediators (including histamine, prostaglandin (PG) D2, and leukotriene (LT) C4) in induction of mucosal edema, bronchoconstriction, and mucus secretion provide evidence that MCs play a key role in pathophysiology of asthma. In asthma, the number of MCs increases in the airways and infiltration of MCs in a variety of anatomical sites including the epithelium, the submucosal glands, and the smooth muscle bundles occurs. MC localization within the ASM is accompanied with the hypertrophy and hyperplasia of the layer, and smooth muscle dysfunction that is mainly observed in forms of bronchial hyperresponsiveness, and variable airflow obstruction. Owing to the expression of a wide range of surface receptors and releasing various cytoplasmic mediators, MCs orchestrate the pathologic events of the disease. MC-released preformed mediators including chymase, tryptase, and histamine and de novo synthesized mediators such as PGD2, LTC4, and LTE4 in addition of cytokines mainly TGFβ1, TSLP, IL-33, IL-4, and IL-13 participate in pathogenesis of asthma. The release of MC mediators and MC/airway cell interactions during remodeling phase of asthma results in persistent cellular and structural changes in the airway wall mainly epithelial cell shedding, goblet cell hyperplasia, hypertrophy of ASM bundles, fibrosis in subepithelial region, abnormal deposition of extracellular matrix (ECM), increased tissue vascularity, and basement membrane thickening. We will review the current knowledge regarding the participation of MCs in each stage of asthma pathophysiology including the releasing mediators and their mechanism of action, expression of receptors by which they respond to stimuli, and finally the pharmaceutical products designed based on the strategy of blocking MC activation and mediator release.
Journal Article
A Review of the Contribution of Mast Cells in Wound Healing: Involved Molecular and Cellular Mechanisms
Mast cells (MCs), apart from their classic role in allergy, contribute to a number of biologic processes including wound healing. In particular, two aspects of their histologic distribution within the skin have attracted the attention of researchers to study their wound healing role; they represent up to 8% of the total number of cells within the dermis and their cutaneous versions are localized adjacent to the epidermis and the subdermal vasculature and nerves. At the onset of a cutaneous injury, the accumulation of MCs and release of proinflammatory and immunomodulatory mediators have been well documented. The role of MC-derived mediators has been investigated through the stages of wound healing including inflammation, proliferation, and remodeling. They contribute to hemostasis and clot formation by enhancing the expression of factor XIIIa in dermal dendrocytes through release of TNF-α, and contribute to clot stabilization. Keratinocytes, by secreting stem cell factor (SCF), recruit MCs to the site. MCs in return release inflammatory mediators, including predominantly histamine, VEGF, interleukin (IL)-6, and IL-8, that contribute to increase of endothelial permeability and vasodilation, and facilitate migration of inflammatory cells, mainly monocytes and neutrophils to the site of injury. MCs are capable of activating the fibroblasts and keratinocytes, the predominant cells involved in wound healing. MCs stimulate fibroblast proliferation during the proliferative phase via IL-4, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) to produce a new extracellular matrix (ECM). MC-derived mediators including fibroblast growth factor-2, VEGF, platelet-derived growth factor (PDGF), TGF-β, nerve growth factor (NGF), IL-4, and IL-8 contribute to neoangiogenesis, fibrinogenesis, or reepithelialization during the repair process. MC activation inhibition and targeting the MC-derived mediators are potential therapeutic strategies to improve wound healing through reduced inflammatory responses and scar formation.
Journal Article
Chitin and Its Effects on Inflammatory and Immune Responses
Chitin, a potential allergy-promoting pathogen-associated molecular pattern (PAMP), is a linear polymer composed of N-acetylglucosamine residues which are linked by β-(1,4)-glycosidic bonds. Mammalians are potential hosts for chitin-containing protozoa, fungi, arthropods, and nematodes; however, mammalians themselves do not synthetize chitin and thus it is considered as a potential target for recognition by mammalian immune system. Chitin is sensed primarily in the lungs or gut where it activates a variety of innate (eosinophils, macrophages) and adaptive immune cells (IL-4/IL-13 expressing T helper type-2 lymphocytes). Chitin induces cytokine production, leukocyte recruitment, and alternative macrophage activation. Intranasal or intraperitoneal administration of chitin (varying in size, degree of acetylation and purity) to mice has been applied as a routine approach to investigate chitin’s priming effects on innate and adaptive immunity. Structural chitin present in microorganisms is actively degraded by host true chitinases, including acidic mammalian chitinases and chitotriosidase into smaller fragments that can be sensed by mammalian receptors such as FIBCD1, NKR-P1, and RegIIIc. Immune recognition of chitin also involves pattern recognition receptors, mainly via TLR-2 and Dectin-1, to activate immune cells to induce cytokine production and creation of an immune network that results in inflammatory and allergic responses. In this review, we will focus on various immunological aspects of the interaction between chitin and host immune system such as sensing, interactions with immune cells, chitinases as chitin degrading enzymes, and immunologic applications of chitin.
Journal Article
Crosstalk Between Mast Cells and Adipocytes in Physiologic and Pathologic Conditions
Excessive fatty acids and glucose uptake support the infiltration of adipose tissue (AT) by a variety of immune cells including neutrophils, pro-inflammatory M1 macrophages, and mast cells (MCs). These cells promote inflammation by releasing pro-inflammatory mediators. The involvement of MCs in AT biology is supported by their accumulation in the AT of obese individuals along with significantly higher serum levels of MC-derived tryptase. AT-resident MCs under the influence of locally derived adipokines such as leptin become activated and release pro-inflammatory cytokines including TNFα that worsens the inflammatory state. MCs support angiogenesis in AT by releasing chymase and inducing preadipocyte differentiation and also the proliferation of adipocytes through 15-deoxy-delta PGJ2/PPARγ interaction. Additionally, they contribute to the remodeling of the AT extracellular matrix (ECM) and play a role in the recruitment and activation of leukocytes. MC degranulation has been linked to brown adipocyte activation, and evidence indicates an important link between MCs and the appearance of BRITE/beige adipocytes in white AT. Cell crosstalk between MCs and AT-resident cells, mainly adipocytes and immune cells, shows that these cells play a critical role in the regulation of AT homeostasis and inflammation.
Journal Article
Degradation of phenol via ortho-pathway by Kocuria sp. strain TIBETAN4 isolated from the soils around Qinghai Lake in China
Based on the feature of high-altitude permafrost topography and the diverse microbial ecological communities of the Qinghai-Tibetan Plateau, soil samples from thirteen different collection points around Qinghai lake were collected to screen for extremophilic strains with the ability to degrade phenol, and one bacterial strain recorded as TIBETAN4 that showed effective biodegradation of phenol was isolated and identified. TIBETAN4 was closely related to Kocuria based on its observed morphological, molecular and biochemical characteristics. TIBETAN4 grew well in the LB medium at pH 7-9 and 0-4% NaCl showing alkalophilicity and halophilism. The isolate could also tolerate up to 12.5 mM phenol and could degrade 5 mM phenol within 3 days. It maintained a high phenol degradation rate at pH 7-9 and 0-3% NaCl in MSM with 5 mM phenol added as the sole carbon source. Moreover, TIBETAN4 could maintain efficient phenol degradation activity in MSM supplemented with both phenol and glucose and complex water environments, including co-culture Penicillium strains or selection of non-sterilized natural lake water as a culture. It was found that TIBETAN4 showed enzymatic activity of phenol hydroxylase and catechol 1,2-dioxygenase after induction by phenol and the corresponding genes of the two enzymes were detected in the genome of the isolate, while catechol 2,3-dioxygenase or its gene was not, which means there could be a degradation pathway of phenol through the ortho-pathway. The Q-PCR results showed that the transcripts of both the phenol hydroxylase gene and catechol 1,2-dioxygenase gene were up-regulated under the stimulation of phenol, demonstrating again that the strain degraded phenol via ortho-degradation pathway.
Journal Article
Role of Mast Cells in Regulation of T Cell Responses in Experimental and Clinical Settings
Mast cells secrete a wide spectrum of stored or newly synthesized pro-inflammatory, anti-inflammatory, and/or immunosuppressive mediators and express several costimulatory and inhibitory surface molecules. Mast cells finely tune activities of T cells, B cells, and regulatory cells and effectively contribute to the development of different T cell-associated responses by influencing their recruitment, activation, proliferation, and differentiation. The interaction between mast cells and T cells, with regard to cellular functionality and immune responses, can be assessed in both activating and inhibitory regulations. While Th2 cytokines, including IL-5 and IL-9, stimulate stem cell factor (SCF)-dependent proliferation of mast cells, Th1 cytokine IFN-γ suppresses SCF-mediated differentiation of mast cell progenitors. Mast cell mediators such as CCL5 have a role in the recruitment of CD8+ T cells to viral infection sites where their ability in clearance of viral reservoirs is needed. The capacity of mast cells in presenting antigens by classes I and II MHC molecules to CD4+ and CD8+ T cells respectively is considered one of the main antigen-dependent interactions of mast cells with T cells. Interestingly, Tregs recruit mast cells to different sites through secretion of IL-9, while the OX40L (expressed on mast cell)-OX40(expressed on T cell) interaction inhibits the extent of the mast cell degranulation. Recently, the capability of exosomes to carry regulatory receptors of the mast cell surface and their role in T cell activation has been investigated. Functional interplay between mast cells and T cell subsets has been suggested primarily by investigating their co-localization in inflamed tissues and involvement of mast cells in autoimmune diseases. In this review, the interactions of mast cells with T cells are reviewed in cell-to-cell, cytokine, and exosome categories.
Journal Article
Significance of Mast Cell Formed Extracellular Traps in Microbial Defense
Mast cells (MCs) are critically involved in microbial defense by releasing antimicrobial peptides (such as cathelicidin LL-37 and defensins) and phagocytosis of microbes. In past years, it has become evident that in addition MCs may eliminate invading pathogens by ejection of web-like structures of DNA strands embedded with proteins known together as extracellular traps (ETs). Upon stimulation of resting MCs with various microorganisms, their products (including superantigens and toxins), or synthetic chemicals, MCs become activated and enter into a multistage process that includes disintegration of the nuclear membrane, release of chromatin into the cytoplasm, adhesion of cytoplasmic granules on the emerging DNA web, and ejection of the complex into the extracellular space. This so-called ETosis is often associated with cell death of the producing MC, and the type of stimulus potentially determines the ratio of surviving vs. killed MCs. Comparison of different microorganisms with specific elimination characteristics such as S pyogenes (eliminated by MCs only through extracellular mechanisms), S aureus (removed by phagocytosis), fungi, and parasites has revealed important aspects of MC extracellular trap (MCET) biology. Molecular studies identified that the formation of MCET depends on NADPH oxidase-generated reactive oxygen species (ROS). In this review, we summarize the present state-of-the-art on the biological relevance of MCETosis, and its underlying molecular and cellular mechanisms. We also provide an overview over the techniques used to study the structure and function of MCETs, including electron microscopy and fluorescence microscopy using specific monoclonal antibodies (mAbs) to detect MCET-associated proteins such as tryptase and histones, and cell-impermeant DNA dyes for labeling of extracellular DNA. Comparing the type and biofunction of further MCET decorating proteins with ETs produced by other immune cells may help provide a better insight into MCET biology in the pathogenesis of autoimmune and inflammatory disorders as well as microbial defense.
Journal Article