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  • 1
    Keywords: Human Genetics ; Lipids ; Human Physiology ; Cytology ; Oncology ; Medicine ; Human Genetics ; Lipidology ; Human Physiology ; Cell Biology ; Cancer Research ; Molecular Medicine ; Springer eBooks
    Description / Table of Contents: Prelims -- Introduction -- Understanding the role of pro-resolving lipid mediators in infectious keratitis -- Immunoresolvent resolvin D1 maintains the health of the ocular surface -- The evolving role of specialized pro-resolving mediators in modulating neuroinflammation in perioperative neurocognitive disorders -- Relationship between specialized pro-resolving mediators and inflammatory markers in chronic cardiac disorders -- Specialized pro-resolving mediators directs cardiac healing and repair with activation of inflammation and resolution program in heart failure -- Novel n-3 docosapentaneoic acid-derived pro-resolving mediators are vasculoprotective and mediate the actions of statins in controlling inflammation -- Aspects of prostaglandin glycerol ester biology -- Targeting the COX/mPGES-1/PGE2 pathway in neuroblastoma -- Metabolomics biomarkers for precision psychiatry -- Cytochrome P450 eicosanoid signaling pathway in colorectal tumorigenesis -- Contributions of 12/15-Lipoxygenase to bleeding in the brain following ischemic stroke -- Systematic understanding of bioactive lipids in neuro-immune interactions: Lessons from an animal model of multiple sclerosis -- Role of bioactive sphingolipids in inflammation and eye diseases -- Roles of ceramides and other sphingolipids in immune cell function and inflammation -- Acute and chronic mild traumatic brain injury differentially changes levels of bioactive lipids in the CNS associated with headache -- Novel anti-inflammatory and vasodilatory ω-3 endocannabinoid epoxide regioisomers -- Overview of lipid biomarkers in Amyotrophic Lateral Sclerosis (ALS) -- Flavonoids ability to disrupt inflammation mediated by lipid and cholesterol oxidation -- Index
    Abstract: This book examines the role of bioactive lipids as pro- and anti-inflammatory mediators in the diagnosis of and as novel therapies for cardiovascular disease, cancer, ocular and neurologic diseases, and inflammatory conditions. The major pathways of arachidonic acid and omega-3 fatty acid metabolism are represented, including cyclooxygenases, lipoxygenases, cytochrome P450 monooxygenases, specialized pro-resolving mediators, endocannabinoids, and ceramide and other sphingolipids. This book would be of great interest to basic and translational researchers, as well as physician-scientists working on selected topics (e.g., cancer, cardiovascular disease, stroke, diabetes, inflammation, etc.) in which the underlying role of lipid mediators in the pathophysiology is known or suspected. This compilation of peer-reviewed manuscripts represents reviews of timely topics presented at the 15th International Conference on Bioactive Lipids in Cancer, Inflammation and Related Diseases. Authors selected are outstanding junior investigators representative of future leaders in the field of bioactive lipids
    Pages: IX, 257 p. 43 illus., 39 illus. in color. : online resource.
    Edition: 1st ed. 2019.
    ISBN: 9783030217358
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  • 2
    Unknown
    Stamford, Conn. : JAI Press
    Call number: QZ200:447/3
    Keywords: Prostatic Neoplasms
    Pages: viii, 264 p. : ill.
    ISBN: 0762303557
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    QZ200:447/3 available
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  • 3
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Indomethacin or 7-oxa-13-prostynoic acid does not alter basal adrenal cortisol output. Preincubation in either, depresses subsequent ACTH-stimulated cortisol output below ACTH alone and controls. Either inhibitor following ACTH preincubation blunts normal ACTH-stimulated cortisol production.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-136X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The hematological modifications occurring as a result of acclimation to increased temperature in the cold water horn shark,Heterodontus francisci, were evaluated. Sharks were maintained under constant conditions except for temperature (15°C and 25°C) in a closed marine system. The total red blood cell (RBC) number decreased in the 25°C sharks. In contrast, hemoglobin concentration, hematocrit, mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) significantly increased at 25°C compared to the control animals. RBC size was increased at 25°C, but the surface area/mm3 whole blood was reduced. Folic acid levels were not different between the groups. Vitamin B12 levels decreased and testosterone increased at 25°C. Blood pH, number of erythroblasts, number of white blood cells (WBC) and WBC differential analyses were essentially unchanged at the two temperatures, except that the relative neutrophil number was increased. The major hematological changes occur in the erythrocytes and appear to be sequential in nature with an initial loss of RBC followed by increased hemoglobin synthesis and increased RBC size, but lack of recovery of RBC numbers.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-7233
    Keywords: prostacyclin ; metastasis ; cicaprost ; platelet
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract More than a decade ago, prostacyclin, a dienoic bicyclic eicosanoid derived from the metabolism of arachidnoic acid, was found to possess potent inhibitory effects on tumor cell metastasis. Thereafter, several laboratories demonstrated the metastasis-suppressive activity of prostacyclin in a wide spectrum of tumor types. Due to the short half-life of prostacyclin, researchers have focused on looking for stable prostacyclin analogues which have extended half lives and increased bioavailabilities. Cicaprost, among other prostacyclin analogues tested, has been demonstrated, like prostacyclin, to effectively inhibit metastasis in several different animal models (i.e., both experimental and spontaneous metastasis models). Prostacyclin as well as cicaprost prevent not only hematogenous, but also lymphatic metastasis. Furthermore, these compounds also inhibit the growth of established micrometastases after removal of the primary tumors. Mechanistic studies revealed that the antimetastatic effects of prostacyclin and its analogues are more related to their interference with tumor cell-host interactions (such as tumor cell induced platelet aggregation, tumor cell adhesion to endothelial cells and subendothelial matrix, tumor cell induced endothelial cell retraction, etc.) than their direct inhibition of the growth of primary tumors. The potent and widespread metastasis-retarding effects of prostacyclin and its stable analogues in animal tumor models warrant their clinical trial in treating human cancer patients and preventing metastasis.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-7233
    Keywords: eicosanoids ; 12-lipoxygenase ; metastasis ; adhesion ; 12(S)-HETE ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Arachidonic acid metabolites have been implicated in multiple steps of carcinogenesis. Their role in tumor cell metastasis, the ultimate challenge for the treatment of cancer patients, are however not well-documented. Arachidonic acid is primarily metabolized through three pathways, i.e., cyclooxygenase, lipoxygenase, and P450-dependent monooxygenase. In this review we focus our attention on one specific lipoxygenase, i.e., 12-lipoxygenase, and its potential role in modulating the metastatic process. In mammalian cells there exist three types of 12-lipoxygenases which differ in tissue distribution, preferential substrates, and profile of their metabolites. Most of these 12-lipoxygenases have been cloned and sequenced, and the molecular and biochemical determinants responsible for catalysis of specific substrates characterized. Solid tumor cells express 12-lipoxygenase mRNA, possess 12-lipoxygenase protein, and biosynthesize 12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid], as revealed by numerous experimental approaches. The ability of tumor cells to generate 12(S)-HETE is positively correlated to their metastatic potential. A large collection of experimental data suggest that 12(S)-HETE is a crucial intracellular signaling molecule that activates protein kinase C and mediates the biological functions of many growth factors and cytokines such as bFGF, PDGF, EGF, and AMF. 12(S)-HETE plays a pivotal role in multiple steps of the metastatic ‘cascade’ encompassing tumor cell-vasculature interactions, tumor cell motility, proteolysis, invasion, and angiogenesis. The fact that 12-lipoxygenase is expressed in a wide diversity of tumor cell lines and 12(S)-HETE is a key modulatory molecule in metastasis provides the rationale for targeting these molecules in anti-cancer and anti-metastasis therapeutic protocols.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cancer and metastasis reviews 3 (1984), S. 249-263 
    ISSN: 1573-7233
    Keywords: cysteine proteinases ; cathepsin B ; metastasis ; invasion ; B16 melanoma ; human tumors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cysteine proteinases are a subclass of endopeptidases which require activation by thiol reagents. A tumor cysteine proteinase which appears to be related to lysosomal cathepsin B has been implicated in the ability of tumor cells to invade the extracellular matrix and to metastasize to secondary sites. Lysosomal cathepsin B can degrade such components of the extracellular matrix as collagen, fibronectin and proteoglycans. Activity of this cathepsin B-like cysteine proteinase (CB) has been correlated with tumor malignancy in a number of tumor lines yet not in all tumor lines studied. CB activity in tumors seems to be associated with the viable tumor cells, probably with the plasma membrane of these tumor cells. CB activity has been measured in the sera, urine, ascites fluid and pancreatic fluid of tumor-bearing patients. CB is released from tumor explants and tumor cells in vitro as well as from normal subcutaneous tissue exposed to tumor-conditioned medium. Cathepsin B from normal tissues is rapidly inactivated above pH 7.0. Therefore, CB in tumor cell membranes or released from tumor cells (or from host cells in response to tumor cells) may not possess proteolytic activity at neutral pH and thus may not facilitate tumor cell invasion. However, CB exhibits enhanced stability at neutral or slightly alkaline pH's. There is not yet definitive proof that CB plays a role in tumor invasion and metastasis. There is, however, an increasing body of correlative evidence relating CB activity and tumor malignancy. This correlative evidence plus preliminary evidence that tumor CB can degrade components of the extracellular matrix in vitro suggests that CB may be one proteinase active in a proteolytic cascade resulting in tumor invasion and metastasis.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Murine 15091A mammary adenocarcinoma cells and membrane vesicles spontaneously shed from these tumor cells in culture can induce aggregation of washed human platelets. A spectrum of proteinase inhibitors was tested for their ability to inhibit 15091A induced platelet aggregation. Of the inhibitors tested the most effective were those selective for cysteine proteinases. The effect of the spectrum of proteinase inhibitors on 15091A induced platelet aggregation was compared to the effect on cathepsin B-like cysteine proteinase activity in homogenates of 15091A tumor cells and their spontaneously shed vesicles. The results suggest that there is a correlation between activity of a cathepsin B-like proteinase in 15091A cells and vesicles and the ability of these cells and vesicles to induce aggregation of washed human platelets.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aggregation of rat platelets was induced in vitro by homologous rat Walker 256 carcinosarcoma cells and the extent of tumor cell-platelet interactions examined ultrastructurally. By 30s there was surface contact between unstimulated platelets and tumor cell microvilli. By midphase aggregation (2–3 min) tumor cells became enmeshed within expanding platelet aggregates. Tumor cell microvilli and platelet pseudopodia interdigitated as aggregation progressed. During the later stages of aggregation (6–10 min) tumor cells formed large processes which penetrated deep into the aggregate. Platelet activation (i.e. degranulation) occurred in gradient fashion and was concentrated near tumor cell membrane sites involved in process formation. At these later stages tumor cells near the aggregate periphery were found to have engulfed platelets or platelet fragments. Tumor cell-platelet interactions in the pulmonary microvasculature were also studied in vivo following injection of murine Lewis lung carcinoma, 16C mammary adenocarcinoma, and B16 amelanotic melanoma tumor cells into the tail vein. Platelets demonstrated a biphasic association with arrested tumor cells with peak interactions occurring at 10–30 min and 4–24h. Ultrastructurally, tumor cells exhibited newly formed processes which interdigitated with the platelet aggregate. Such processes formed only in areas of contact with platelets and not in areas of contact with endothelial cells or other blood elements (i.e. erythrocytes, polymorphonuclear leukocytes). Numerous tumor cell mitochondria were concentrated in the areas of greatest platelet-tumor cell process activity. At early time intervals (2–10 min), intravascular platelet degranulation was observed primarily in platelets associated with tumor cell processes. Tumor cells also were found to have engulfed platelet fragments in vivo.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hematogenous metastasis is a major consideration in the staging, treatment and prognosis of patients with cancer. Key events affecting hematogeneous metastasis occur in the microvasculature. This is a brief, selective review of some interactions involving cancer cells and the microvasculature in pathologic sequence, specifically: (1) intravasation of cancer cells; (2) the arrest of circulating cancer cells in the microvasculature; (3) cancer cell trauma associated with arrest; (4) microvascular trauma; (5) the inflammatory; and (6) the hemostatic coagulative responses associated with arrest, and finally (7) angiogenesis, leading to tumor vascularization. The evidence shows that through a series of complex interactions with cancer cells, the microvasculature acts as a rate-regulator for the metastatic process, in addition to providing routes for cancer cell dissemination and arrest sites for cancer cell emboli.
    Type of Medium: Electronic Resource
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