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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 762 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1043-4666
    Keywords: Fibrinogen ; IL 1 ; IL-1ra ; IL-6 ; Serum amyloid A
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Cytokine 6 (1994), S. 548 
    ISSN: 1043-4666
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1043-4666
    Keywords: LPS ; cachexia ; interleukin-6 ; tumor necrosis factor
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion Although IL 1 and TNF are biochemically distinct and bind to different cell membrane receptors, they each exhibit only a few distinct biological properties, and have a great number of activities in common. Thus, IL 1 and TNF are radioprotective, have cytocidal effects for some tumor cells, remodel bone and cartilage, induce fever, inflammation, fibroplasia, and angiogenesis. The overlapping effects of IL 1 and TNF are in part due to the induction of the same spectrum of cytokines and their receptors. Both IL 1 and TNF induce IL 2-receptors, IL 6, colony stimulating factors and acute phase proteins which may contribute to their immunoenhancing, inflammatory and radioprotective effects. IL 1 and TNF frequently also are coordinately released by cells and have cooperative effects. For example, IL 1 together with TNF has synergisticin vivo radioprotective effects andin vitro terminal differentiative effects on tumor cell lines. Overall, these data point to the existence of common as well as distinct post-receptor signal transduction pathways for IL 1 and TNF. IL 1 and TNF each can induce a number of cell types to produce IL 6, which appears to act as another “broad spectrum” cytokine. In addition, both IL 1 and TNF induce NAP-1 production by human monocytes and fibroblasts. This novel cytokine which has been purified, sequenced, cloned, expressed and synthesized, may account for some of thein vivo acute inflammatory effects of these cytokines.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-8280
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary and conclusions Our results demonstrate that IL-1 promotes hematopoiesis in normal and radiation compromised animals. IL-1 protected mice from lethal hematopoietic syndrome when given before irradiation. Given after irradiation, IL-1 promoted recovery of mice and primates from radiation injury. A comparison of the effects of IL-1 in three different species indicated that hematopoiesis of mice, monkeys,and dogs is upregulated in a similar fashion by IL-1. These three species, however, vary greatly in their sensitivity to IL-1. Whereas mice and dogs tolerated doses greater than 1000 ⧎g/Kg of IL-1, 10 ⧎g/Kg of IL-1 in rhesus monkeys resulted in considerable toxic effects. Several activities of IL-1 may explain its bone marrow restorative properties. The induction with IL-1 of several hematopoietic growth factors: GM-CSF, G-CSF, M-CSF, IL 3, and IL 6, clearly contributes to the accelerated growth and differentiation of hematopoietic progenitor cells. The induction of scavenger proteins may serve to reduce post irradiation oxidative damage. Our work raised a number of additional questions concerning the potential therapeutic utility of IL-1. The ability of IL-1 to promote engraftment of allogeneic bone marrow cells will require further study. The optimal dosage, schedule, and route for IL-1 induction of hematopoiesis will need to be established. The observed synergy of IL-1 with TNF, IL 6, or CSF's may be useful in reducing the requisite doses of cytokines from pharmacological to physiological levels with concomitant reduction in toxic effects. The choice of proper cytokine combinations, however, may also be dependent on the clinical status of the patients.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1573-2568
    Keywords: zinc ; esophagitis ; H2 antagonist ; interleukin-1 and-6
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Because zinc is an important metabolic requirement for growth and repair of squamous tissue, we questioned whether changes in serum and esophageal tissue zinc were present in patients with reflux esophagitis. To investigate this question, we prospectively studied 49 patients undergoing upper gastrointestinal endoscopy for symptoms of abdominal pain and discomfort; 19 patients were taking H2 antagonists at the time of the study. Blood was obtained to measure serum zinc concentrations prior to endoscopy and tissue zinc levels were obtained from esophageal biopsies from the distal, middle, and proximal esophagus in patients who were either endoscopically normal or who exhibited endoscopic esophagitis. Serum zinc concentrations were significantly lower in patients with endoscopic esophagitis compared to the endoscopically normal group (77±3.8 μg/dl vs 88±2.4 μg/dl,P〈0.02). Distal esophageal tissue concentrations were significantly higher in patients with endoscopic esophagitis compared to the endoscopically normal group (200±30 μg/liter vs 135±15 μg/liter,P〈0.05); whereas there were no differences between values obtained in the proximal or middle esophagus. Serum and tissue zinc concentrations in patients with esophagitis receiving H2 antagonists were more similar to values obtained in patients who were endoscopically normal than to patients with endoscopic esophagitis without treatment. This study suggests that in endoscopic esophagitis: (1) greater amounts of zinc are concentrated in the rapidly proliferating distal esophageal epithelium, (2) the serum zinc pool may serve as a major zinc source, and (3) decreasing esophageal mucosal inflammation with H2 antagonists may decrease zinc loss via the esophageal epithelium.
    Type of Medium: Electronic Resource
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