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Books on the topic 'Diabetes Cataract Oxidative stress'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Carla, Costa, and SpringerLink (Online service), eds. Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome. Dordrecht: Springer Netherlands, 2009.

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2

Preedy, Victor R. Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology, 2020.

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3

Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2013.

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4

Preedy, Victor R. Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2020.

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5

Preedy, Victor R. Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier Science & Technology Books, 2013.

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6

Diabetes: Oxidative Stress and Dietary Antioxidants. Elsevier, 2014. http://dx.doi.org/10.1016/c2012-0-02421-0.

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7

(Editor), Lester Packer, Peter Rosen (Editor), Hans J. Tritschler (Editor), George L. King (Editor), Glenn A. King (Editor), and Angelo Azzi (Editor), eds. Antioxidants in Diabetes Management (Oxidative Stress & Disease). CRC, 2000.

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8

Keaneyjr, John F. Oxidative Stress and Vascular Disease. Springer, 2012.

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9

(Editor), Lester Packer, and Helmut Sies (Editor), eds. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome (Oxidative Stress and Disease). CRC, 2007.

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10

C, Opara Emmanuel, ed. Nutrition & diabetes: Pathophysiology & management. Boca Raton: Taylor and Francis, 2005.

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11

F, Keaney John, ed. Oxidative stress and vascular disease. Boston: Kluwer Academic Publishers, 1999.

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12

Nutrition and diabetes: Pathophysiology and management. Boca Raton, FL: CRC/Taylor & Francis, 2006.

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13

Opara, Emmanuel. Nutrition and Diabetes: Pathophysiology and Management. CRC, 2005.

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14

Jana, Varvaøovská, ed. Impact of oxidative stress on diabetes mellitus and inflammatory bowel diseases. New York: Nova Science, 2007.

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15

Davison, Gareth William. Exercise and oxidative stress: Implications in health and disease. 2002.

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16

M, Matata Bashir, and Elahi Maqsood M, eds. Oxidative stress: A focus on cardiovascular disease pathogensis. Hauppauge, N.Y: Nova Science, 2010.

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17

Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. Boca Raton, FL: CRC Press/Taylor & Francis, 2007.

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18

Lester, Packer, and Sies H. 1942-, eds. Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. Boca Raton: CRC Press, 2008.

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19

Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome. London: Taylor and Francis, 2007.

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20

Sies, Helmut, ed. Oxidative Stress and Inflammatory Mechanisms in Obesity, Diabetes, and the Metabolic Syndrome. CRC Press, 2007. http://dx.doi.org/10.1201/9781420043792.

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21

Oxidative stress and inflammatory mechanisms in obesity, diabetes, and the metabolic syndrome. Boca Raton: CRC Press, 2008.

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22

Soares, Raquel, and Carla Costa. Oxidative Stress, Inflammation and Angiogenesis in the Metabolic Syndrome. Springer, 2010.

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23

Jr, John F. Keaney. Oxidative Stress and Vascular Disease (Developments in Cardiovascular Medicine). Springer, 2000.

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24

Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insulin signaling and the effects of glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are also implicated.

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25

Ho, Vanessa P., and Philip S. Barie. Acute acalculous cholecystitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0188.

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Acute acalculous cholecystitis (AAC) may occur in surgical or injured, critically-ill, and systemically-ill patients, with diabetes mellitus, malignant disease, abdominal vasculitis, congestive heart failure, cholesterol embolization, shock, and cardiac arrest. Children may also be affected, especially following a viral illness. The pathogenesis of AAC is complex and multifactorial. Ischaemia/reperfusion injury and the associated pro-inflammatory response and oxidative tissue stress, appear to be the central mechanisms, but bile stasis, opioid therapy, positive-pressure ventilation, and parenteral nutrition may all contribute to development of the disease. Ultrasound of the gallbladder is most accurate for the diagnosis of AAC in the critically-ill patient. Computed tomography is probably of comparable accuracy, but carries both advantages and disadvantages. Percutaneous cholecystostomy is now the treatment of choice, controlling AAC in about 85% of patients, despite the known high prevalence of gallbladder infarction (~50%) and perforation (~10%). Rapid improvement may be expected when AAC is diagnosed correctly and cholecystostomy is performed timely. The mortality (historically ~30%) of percutaneous and open cholecystostomy are similar, reflecting the severity of illness, but improved resuscitation and critical care may portend a decreased risk of death.

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