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  • 1
    Keywords: Life sciences ; Human Physiology ; Biochemistry ; Life sciences ; Biochemistry, general ; Human Physiology ; Springer eBooks
    Description / Table of Contents: Erythropoietin and Engineered Innate Repair Activators -- Epo and Non-hematopoietic Cells: What Do We Know? -- Tissue Protective Cytokines: Structure and Evolution -- The Regenerative Activity of Interleukin-6 -- Brain Ischemic Injury in Rodents: The Protective Effect of EPO -- Experımental Traumatıc Spınal Cord Injury -- Erythropoietin as a Neuroprotectant for Neonatal Brain Injury: Animal Models -- Evaluating Effects of EPO in Rodent Behavioral Assays Related to Depression -- Erythropoietin and Cytoprotective Cytokines in Experimental Traumatic Brain Injury -- Therapeutic Efficacy of Erythropoietin in Experimental Autoimmune Encephalomyelitis in Mice, a Model of Multiple Sclerosis -- Deciphering the Intracellular Signaling of Erythropoietin in Neuronal Cells -- Assessment of Allodynia Relief by Tissue-protective Molecules in a Rat Model of Nerve Injury-induced Neuropathic Pain -- Intra-Epidermal Nerve Fibres Density and Nociception in EPO-treated Type 1 Diabetic Rats with Peripheral Neuropathy -- ARA290 in a Rat Model of Inflammatory Pain -- In Vivo Angiogenic Activity of Erythropoietin -- Photoreceptor Degeneration in Mice: Adeno-associated Viral (AAV) Vector-Mediated Delivery of Erythropoietin -- Myocardial Infarction - Cardioprotection by Erythropoietin -- Using Plethysmography to Determine Erythropoietin’s Impact on Neural Control of Ventilation -- Cerebral Malaria: Protection by Erythropoietin
    Abstract: While many cytokines are known for their inflammatory action, there is a growing interest in the tissue-protective effects of some cytokines. The prototypic tissue-protective cytokine is EPO. Initially described as neuro-protective, it is beneficial in animal models of ischemic and other types of injury. Scientists had to overcome the notion that EPO had only erythropoietic actions, was only produced by the kidney, and that its receptor was only present in erythroid progenitor cells. The use of in vitro and in vivo disease models was essential to demonstrate the protective effects of EPO. Reproducible models will be needed for the further study of the mechanism of action of EPO and for the identification of other tissue-protective cytokines. ℗ In Tissue-Protective Cytokines: Methods and Protocols, expert researchers in the field detail the key models that have been used to characterize the tissue-protective actions of cytokines. Written in the highly successful Methods in Molecular Biologý„Ø series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, provide step-by-step laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls. ℗ Thorough and intuitive, Tissue Protective Cytokines: Methods and Protocols aids scientists in continuing to study tissue-protection that will be a new field of interest of cytokine biology, both in discovering novel actions of known cytokines and in developing new drugs
    Pages: XI, 328 p. 55 illus., 18 illus. in color. : digital.
    ISBN: 9781627033084
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    ISSN: 0304-4165
    Keywords: (Human lens) ; Aging ; Browning product ; Maillard reaction
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Trends in Biochemical Sciences 11 (1986), S. 311-314 
    ISSN: 0968-0004
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 47 (1979), S. 75-79 
    ISSN: 1432-0533
    Keywords: Neurotoxicity ; Cyanate ; Demyelination ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of sodium cyanate (NaNCO) on the nervous system of Maccaca nemestrina were studied at 2, 4, and 6 months of administration of the drug. The two groups injected with daily doses of 35 and 25 mg/kg/day of Na-cyanate developed a predominantly demyelinating lesion in the pyramidal tracts of the spinal cord. No neuronal changes were observed in the motor cortex, basal ganglia, midbrain, medulla or anterior horn cells of the spinal cord. There was no evidence of peripheral neuropathy. A comparison between the cyanate induced neuropathy in the rat and in the primate was drawn. Ultrastructurally, both species developed a demyelinating process of central or peripheral myelin characterized by vacuolation of the myelin sheath, removal of myelin debris by macrophages and re-myelination. There was little evidence of axoplasmic damage except for an occasional distended fiber containing abundant dense bodies and whorls of neurofilaments. Oligodendrocytes and Schwann cells were electron microscopically intact and participated actively in remyelination. Maccacas maintained at 15 mg/day and sham animals remained normal clinically and anatomically. The predominantly myelinotoxic effect of cyanate is similar to that produced by other myelinotoxic agents and is attributed to a selective modification of myelin proteins by carbamylation.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Diabetic control ; urine ; glycopeptides ; affinity chromatography ; non-enzymatic glycosylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship between improvement in diabetic control and changes in levels of glycosylated urinary peptides was investigated. Eight poorly controlled Type 1 (insulin-dependent) diabetic patients were studied as optimal metabolic control was achieved. Mean daily blood glucose values and weekly haemoglobin A1 levels were determined simultaneously. Urinary glycosylated peptide levels fell 50% in 15 days, compared with 23 days for haemoglobin A1. Levels of glycosylated urinary peptides were sensitive to increased mean blood glucose concentrations of 9.72 mmol/l and increased linearly up to 20.0 mmol/l (r=0.98) when compared with mean blood glucose levels obtained 8–9 days earlier. A similar correlation was found with haemoglobin A1 levels. Levels of glycosylated urinary peptides before and after optimal control were compared, and a decrease of 40% was observed (pre-control: 269±44 μmol/day, optimal control: 162±45 μmol/day, mean±SEM). The lag time between the fall in mean blood glucose level and the parallel fall in glycosylated urinary peptides was 8–9 days, suggesting that measurement of these compounds may become a useful clinical laboratory technique for monitoring short-term integrated glycaemia in diabetic patients.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0673
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics , Physics
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0673
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics , Physics
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Alloxan ; diabetes ; mice ; glucose tolerance ; genetic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Alloxan was administered at dosages of 25 to 100 mg/kg to C57BL/6J (6J) and C57BL/KsJ (KsJ) mice to determine the dose dependence of alloxan-induced diabetes in these strains. KsJ mice were more susceptible to alloxan: the effective dose (ED) with respect to the likelihood of 50% of the treated mice becoming hyperglycaemic by 2 days was 42 mg/ kg for KsJ mice, compared with 59 mg/kg for 6J mice (P〈0.001). The dose response curves for the two strains were parallel, and mice receiving equieffective alloxan dosages studied, which were approximately the ED1, ED20, ED80, and ED99, blood glucose levels at 2 days did not differ significantly between KsJ and 6J mice. Although the initial severity of hyperglycaemia and polydipsia was indistinguishable in KsJ and 6J mice administered the ED80 alloxan dosages, there were two major differences in the long term course of their diabetes. First, only 13 of 23 diabetic KsJ mice survived for three months following alloxan administration compared with all 23 diabetic 6J mice (P〈0.001). Second, 9 of 23 diabetic 6J mice gradually became normoglycaemic, compared with none of the diabetic KsJ mice (P〈0.001). These observations support an earlier hypothesis that these two strains of mice differ in their capacity to adapt to diabetogenic stimuli.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0835
    Keywords: 35J20 ; 49F15 ; 58E05
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Notes: Abstract We use Morse theory to estimate the number of positive solutions of an elliptic problem in an open bounded setΩ ∉ ℝN. The number of solutions depends on the topology ofΩ, actually onP t (Ω), the Poincaré polynomial ofΩ. More precisely, we obtain the following Morse relations: $$\sum\limits_{u \in K} {t^{\mu \left( u \right)} } = tP_t \left( \Omega \right) + t^2 [P_t \left( \Omega \right) - 1] + t\left( {1 + t} \right)\underset{\raise0.3em\hbox{$\smash{\scriptscriptstyle\thicksim}$}}{O} \left( t \right)$$ , where $$\underset{\raise0.3em\hbox{$\smash{\scriptscriptstyle\thicksim}$}}{O} \left( t \right)$$ is a polynomial with non-negative integer coefficients,K is the set of positive solutions of our problem andμ(u) is the Morse index of the solutionu.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 320 (1986), S. 584-588 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] In response to invasive stimuli, macrophages secrete cachectin, a multipotent protein. Prominent among its biological effects is the ability to induce wasting (cachexia) as well as a lethal state of shock. The identity of cachectin and tumour necrosis factor has led to a new view of its therapeutic ...
    Type of Medium: Electronic Resource
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