The mechanisms underlying diabetic encephalopathy are only partially understood. This review tries to address the mechanisms of diabetes-induced cell and tissue damage in the brain, and discusses whether docosahexaenoic acid (DHA) could attenuate the degenerative changes observed in the diabetic brain. DHA, the main omega-3 fatty acid, is concentrated and avidly retained in membrane phospholipids of the nervous system. DHA is involved in brain and retina physiological functions, aging, and neurological and behavioral illnesses. Neuroprotectin D1 (NPD1), the first identified stereoselective bioactive product of DHA, exerts neuroprotection in models of experimental diabetes. Photoreceptor membranes display the highest content of DHA of any cell. Retinal pigment epithelial cells participate in the phagocytosis of the tips of photoreceptor cells (photoreceptor outer segment renewal). There is a DHA retrieval-intercellular mechanism between both types of cells that conserves this fatty acid during this process. NPD1 promotes the homeostatic regulation of the integrity of these two cells, particularly during oxidative stress, and this protective signaling may be relevant in retinal degenerative diseases. Moreover, neurotrophins are NPD1-synthesis agonists, and NPD1 content is decreased in the CA1 region of the hippocampus of Alzheimer's patients. Overall, NPD1 promotes brain cell survival via the induction of anti-apoptotic and neuroprotective gene expression programs that suppress neurotoxicity. Thus, NPD1 elicits potent cell-protective, anti-inflammatory, prosurvival and repair signaling.
In 1949, as Cold War tensions in Europe mounted, French intellectual and former Buchenwald inmate David Rousset called upon fellow concentration camp survivors to denounce the Soviet Gulag as a "hallucinatory repetition" of Nazi Germany's most terrible crime. In Political Survivors, Emma Kuby tells the riveting story of what followed his appeal, as prominent members of the wartime Resistance from throughout Western Europe united to campaign against the continued existence of inhumane internment systems around the world. The International Commission against the Concentration Camp Regime brought together those originally deported for acts of anti-Nazi political activity who believed that their unlikely survival incurred a duty to bear witness for other victims. Over the course of the next decade, these pioneering activists crusaded to expose political imprisonment, forced labor, and other crimes against humanity in Franco's Spain, Maoist China, French Algeria, and beyond. Until now, the CIA's secret funding of Rousset's movement has remained in the shadows. Kuby reveals this clandestine arrangement between European camp survivors and American intelligence agents. She also brings to light how Jewish Holocaust victims were systematically excluded from Commission membership – a choice that fueled the group's rise, but also helped lead to its premature downfall. The history that she unearths provides a striking new vision of how wartime memory shaped European intellectual life and ideological struggle after 1945, showing that the key lessons Western Europeans drew from the war centered on "the camp," imagined first and foremost as a site of political repression rather than ethnic genocide. Political Survivors argues that Cold War dogma and acrimony, tied to a distorted understanding of WWII's chief atrocities, overshadowed the humanitarian possibilities of the nascent anti-concentration camp movement as Europe confronted the violent decolonizing struggles of the 1950s.
Complete PET is the most authentic exam preparation course available. Each unit of the Student's Book covers one part of each PET paper and provides thorough exam practice. Grammar and vocabulary exercises target areas that cause most problems for PET candidates, based on data from the Cambridge Learner Corpus, taken from real candidate scripts. The CD-ROM provides additional exam-style practice.'--Publisher's description.
The mechanisms underlying diabetic encephalopathy are only partially understood. This review tries to address the mechanisms of diabetes-induced cell and tissue damage in the brain, and discusses whether docosahexaenoic acid (DHA) could attenuate the degenerative changes observed in the diabetic brain. DHA, the main omega-3 fatty acid, is concentrated and avidly retained in membrane phospholipids of the nervous system. DHA is involved in brain and retina physiological functions, aging, and neurological and behavioral illnesses. Neuroprotectin D1 (NPD1), the first identified stereoselective bioactive product of DHA, exerts neuroprotection in models of experimental diabetes. Photoreceptor membranes display the highest content of DHA of any cell. Retinal pigment epithelial cells participate in the phagocytosis of the tips of photoreceptor cells (photoreceptor outer segment renewal). There is a DHA retrieval-intercellular mechanism between both types of cells that conserves this fatty acid during this process. NPD1 promotes the homeostatic regulation of the integrity of these two cells, particularly during oxidative stress, and this protective signaling may be relevant in retinal degenerative diseases. Moreover, neurotrophins are NPD1-synthesis agonists, and NPD1 content is decreased in the CA1 region of the hippocampus of Alzheimer's patients. Overall, NPD1 promotes brain cell survival via the induction of anti-apoptotic and neuroprotective gene expression programs that suppress neurotoxicity. Thus, NPD1 elicits potent cell-protective, anti-inflammatory, prosurvival and repair signaling.
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