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  • 1
    Keywords: Clinical biochemistry. ; Medical genetics. ; Human physiology. ; Proteins. ; Medical Biochemistry. ; Medical Genetics. ; Human Physiology. ; Proteins.
    Description / Table of Contents: 1. The disease-modifying role of taurine and its therapeutic potential in Coronavirus Disease 2019 (COVID-19) -- 2. Examination of taurine chloramine and taurine on LPS-induced acute pulmonary inflammation in mice -- 3. Synergism between taurine and dexamethasone in anti-inflammatory response in LPS-activated macrophages -- 4. Regulation of CXCR4 expression by taurine in macrophage-like cells -- 5. Taurine chloramine inhibits leukocyte migration by suppressing actin polymerization and extracellular signal regulated kinase -- 6. Taurine alleviates LPS-induced acute lung injury by suppressing TLR-4/NFKB pathway -- 7. Intervention effect of taurine on LPS-induced intestinal mechanical barrier injury in piglets -- 8. Current opinion on the therapeutic capacity of taurine containing halogen derivatives in infectious and inflammatory diseases -- 9. Taurine and N-bromotaurine in topical treatment of psoriasis -- 10. Taurine deficiency in tissues aggravates radiation-induced gastrointestinal syndrome -- 11. Taurine and its anti-cancer functions: In vivo and in vitro study -- 12. Taurine supplementation inhibits the expression of Atrogin-1 and MuRF-1, protein degradation marker genes, in skeletal muscle of C26-induced cachexia mouse model -- 13. Bioavailability of tauropine after oral ingestion in mouse -- 14. Taurine prevents liver injury by reducing oxidative stress and cytochrome c mediated apoptosis in broilers under low temperature -- 15. Effects of taurine on serum indexes of broilers with chronic heat stress -- 16. Antioxidant effect of taurine on chronic heat stressed broilers -- 17. Grading of Japanese diet intakes by 24-hour urine analysis of taurine and soy isoflavones in relation to cardiovascular risks -- 18. Perinatal taurine supplementation preserves the benefits of dynamic exercise training on cardiovascular and metabolic functions and prevents organ damage in adult male exercised rats -- 19. Impaired bile acid synthesis in a taurine-deficient cat model -- 20. Characterization of bone tissue and bone morphology in taurine transporter knockout mice -- 21. Blood taurine dynamics in captive lions: relationship with feed and bile acid composition -- 22. Taurine ameliorates apoptosis via Akt pathway in the kidney of diabetic rats -- 23. Taurine ameliorates oxidative stress in spinal cords of diabetic rats via Keap-Nrf2 signaling -- 24. Assessment of in vitro tests as predictors of the antioxidant effects of insulin, metformin and taurine in the brain of diabetic rats -- 25. Potential binding sites for taurine on the insulin receptor: A molecular docking study -- 26. Dietary protein modulates the efficacy of taurine supplementation on adaptive islet function and morphology in obesity -- 27. Taurine and exercise: Synergistic effects on adipose tissue metabolism and inflammatory processes in obesity -- 28. The taurine conjugated bile acid (TUDCA) normalizes insulin secretion in pancreatic b-cells exposed to fatty acids: Role of mitochondrial metabolism -- 29. Effect of taurine on the regulation of glucose uptake in skeletal muscle -- 30. Differences between physiological and pharmacological actions of taurine -- 31. Taurine and the brain -- 32. Electrophysiological evidence for anti-epileptic property of taurine -- 33. Observation of acupuncture effects on the expression of taurine transporter and taurine in the senescence-accelerated mouse brain: A pilot study -- 34. The regulatory effects of taurine on neurogenesis and apoptosis of neural stem cells in the hippocampus of rats -- 35. Brain-derived neurotrophic factor potentiates entorhinal-dentate but not hippocampus CA1 pathway in adult male rats: A mechanism of taurine-modulated BDNF on learning and memory -- 36. Influences of taurine pharmacodynamics and sex on active avoidance learning and memory -- 37. The effects of dietary taurine-containing jelly supplementation on cognitive function and memory ability of the elderly with subjective cognitive decline -- 38. Effects of dietary taurine-containing jelly supplementation on academic-related characteristics and academic achievement in Korean college entrance examinees: a pilot study -- 39. Improvement in willingness to purchase taurine-containing jelly needs high degrees of interest and preference: focused on Korean college students -- 40. Positive eusocial impacts on ants by taurine derivatives -- 41. Taurine prevents AFB1-induced renal injury by inhibiting oxidative stress and apoptosis -- 42. Taurine-derived compounds produce anxiolytic effects in rats following developmental lead exposure -- 43. Developmental lead exposure in rats causes sex-dependent changes in neurobiological and anxiety-like behaviors that are improved by taurine co-treatment -- 44. In vivo sex-dependent effects of perinatal Pb2+ exposure on pilocarpine-induced seizure susceptibility and taurine neuropharmacology -- 45. Taurine prevents LPS-induced liver injury in weaned piglets.
    Abstract: This volume gathers a selection of original articles and reviews on timely topics about the application of Taurine in human health written by members of the International Taurine Society, including COVID-19, cancer, heart disease, and diabetes, among others. Chapters are written by Taurine experts across the globe in North and South America, Asia, and Europe. A majority of the articles are based on original studies recently carried out in individual laboratories worldwide. The book is divided into eight parts, each covering a unique aspect of Taurine. Each section will highlight new research findings on Taurine and its application in various human systems, including the nervous system, immune system, and cardiovascular system, to combat disease. The first section covers COVID-19, the dominant health event of 2020. Experts will explore and clarify the potential therapeutic effectiveness of Taurine against COVID-19. The volume will promote further research into the application of Taurine in human health, and will be of use to a wide audience, including basic and clinical scientists, pharmaceutical and nutraceutical companies, and libraries. .
    Type of Medium: Online Resource
    Pages: XII, 518 p. 181 illus., 68 illus. in color. , online resource.
    Edition: 1st ed. 2022.
    ISBN: 9783030933371
    Series Statement: Advances in Experimental Medicine and Biology, 1370
    DDC: 612.015
    Language: English
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  • 2
    ISSN: 1573-4919
    Keywords: mitochondria ; transport ; non-insulin-dependent diabetes mellitus ; streptozotocin ; liposome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The effect of non-insulin-dependent diabetes mellitus (i.e., NIDDM; type 2 diabetes) on the levels of functional mitochondrial anion transport proteins has been determined utilizing a chemically-induced neonatal model of NIDDM. We hypothesized that moderate insulin deficiency exacerbated by the insulin resistance, which is characteristic of NIDDM, would cause changes in mitochondrial anion transporter function that were similar to those we have previously shown to occur in insulin-dependent diabetes mellitus (i.e., IDDM; type 1 diabetes) (Arch. Biochem. Biophys. 280: 181–191, 1990). Our experimental approach consisted of the extraction of the pyruvate, dicarboxylate and citrate transport proteins from the mitochondrial inner membrane with Triton X-114 using rat liver mitoplasts (prepared from diabetic and control animals) as the starting material, followed by the functional reconstitution of each transporter in a proteoliposomal system. This strategy permitted the quantification of the functional levels of these three transporters in the absence of the complications that arise when such measurements are carried out with intact mitochondria (or mitoplasts). We found that experimental NIDDM did not cause significant changes in the extractable and reconstitutable specific (and total) transport activities of the pyruvate, dicarboxylate, and citrate transporters. These results are in marked contrast to our previous findings obtained using rats with IDDM and negated our hypothesis. The present results, in combination with our earlier findings, allow us to conclude that insulin plays an important role in the regulation of mitochondrial anion transporter function. Accordingly, in this model of NIDDM, where the level of insulin is not profoundly deficient, transporter function is unaltered, whereas in IDDM, where a profound insulinopenia exists, transporter function is altered. Furthermore, the present studies suggest that in the neonatal model of NIDDM the three mitochondrial transporters investigated are neither affected by, nor are they the sites of the well documented hepatic post-receptor insulin resistance which is characteristic of this disease.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 176 (1997), S. 219-225 
    ISSN: 1573-4919
    Keywords: diabetes mellitus ; cardiomyopathy ; protein kinase C ; glucose metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The activity of the β isoform of protein kinase C (PKCβ) is reduced in the diabetic heart. Since this isozyme has been implicated in insulin action, we tested the hypothesis that PKCβ contributes to the development of impaired glucose metabolism by the noninsulin-dependent diabetic heart. Exposure of the diabetic heart to buffer containing the protein kinase C activator, phorbol myristate acetate, increased PKCβ activity in the membrane. Associated with the improvement in PKCβ activity was a biphasic change in glucose metabolism. The initial phase was characterized by a breakdown in glycogen stores, a stimulation in glucose oxidation and a decrease in endogenous fatty acid oxidation. This was followed by a second phase in which the uptake of glucose was modestly stimulated. Nonetheless, since the phorbol ester did not overcome the diabetes-linked defect in pyruvate dehydrogenase, the increase in glycolytic flux was not associated with a rise in glucose oxidation. Consequently, nearly 50% of the triose units were diverted into lactate and pyruvate production and the generation of ATP from glucose was restricted. Since insulin promotes not only glucose uptake, but also glycogen synthesis and glucose oxidation, the phorbol ester and insulin effects are very different. Thus, the data do not support a role for PKCβ in the development of glucose metabolic defects in the hearts of noninsulin-dependent diabetic rats.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 107 (1991), S. 1-20 
    ISSN: 1573-4919
    Keywords: noninsulin-dependent diabetic cardiomyopathy ; glucose transport ; insulin resistance ; protein phosphatase 1 and membrane phosphorylation ; calcium transport and overload ; myosin isozymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Summary Cardiovascular disease represents the major cause of morbidity and mortality in noninsulin-dependent diabetic patients. While it was once thought that atherosclerotic vascular disease was responsible for all of these adverse effects, recent studies support the notion that one of the major adverse complications of diabetes is the development of a diabetic cardiomyopathy characterized by defects in both diastolic and systolic function. Contributing to the development of the cardiomyopathy is a shift in myosin isozyme content in favor of the least active V3 form. Also defective in the noninsulin-dependent diabetic heart is regulation of calcium homeostasis. While transport of calcium by the sarcolemmal and sarcoplasmic reticular calcium pumps are minimally affected by noninsulin-dependent diabetes, significant impairment occurs in sarcolemmal Na+-Ca2+ exchanger activity. This defect limits the ability of the diabetic heart to extrude calcium, contributing to an elevation in [Ca2+]i. Also promoting the accumulation of calcium by the diabetic cell is a decrease in Na+, K+ ATPase activity, which is known to increase [Ca2+]i secondary to a rise in [Na+]i. In addition, calcium influx via the calcium channel is stimulated. Although the molecular mechanisms underlying these defects are presently unknown, the possibility that they may be related to aberrations in glucose or lipid metabolism are considered. The evidence suggests that classical theories of glucose toxicity, such as excessive polyol production or glycosylation, appear to be insignificant factors in heart. Also insignificant are defects in lipid metabolism leading to accumulation of toxic lipid amphiphiles or triacylglycerol. Rather, the major defects involve membrane changes, such as phosphatidylethanolamine N-methylation and protein phosphorylation, which can be attributed to the state of insulin resistance.
    Type of Medium: Electronic Resource
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  • 5
    Publication Date: 2005-01-01
    Print ISSN: 0300-8177
    Electronic ISSN: 1573-4919
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Springer
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  • 6
    Publication Date: 2016-03-29
    Print ISSN: 0300-8177
    Electronic ISSN: 1573-4919
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Springer
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  • 7
    Publication Date: 1991-09-01
    Print ISSN: 0300-8177
    Electronic ISSN: 1573-4919
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Springer
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  • 8
    Publication Date: 1991-09-01
    Print ISSN: 0300-8177
    Electronic ISSN: 1573-4919
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Springer
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  • 9
    Publication Date: 2015-01-28
    Electronic ISSN: 1932-6203
    Topics: Medicine , Natural Sciences in General
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  • 10
    Publication Date: 1978-02-01
    Print ISSN: 0003-2697
    Electronic ISSN: 1096-0309
    Topics: Biology , Chemistry and Pharmacology
    Published by Elsevier
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