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| http://dx.doi.org/10.2337/db12-0091 | DOI Listing |
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Department of Integrative Medicine and Neurobiology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
In patients with major depressive disorder (MDD) and animal models of depression, key pathological hallmarks include activation of microglia as well as atrophy and loss of astrocytes. Under certain pathological conditions, microglia can inflict damage to neurons and astrocytes. However, the precise mechanisms underlying how activated microglia induced astrocyte atrophy and loss remain enigmatic.
View Article and Find Full Text PDFCirculating biomarkers of nitrosative stress, protein glycoxidation and inflammation in maxillofacial surgery patients treated with titanium implants.
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Department of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, Poland.
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View Article and Find Full Text PDFGlucagon-Like Peptide-1 Links Ingestion, Homeostasis, and the Heart.
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Glucagon-like peptide-1 (GLP-1), a hormone released from enteroendocrine cells in the distal small and large intestines in response to nutrients and other stimuli, not only controls eating and insulin release, but is also involved in drinking control as well as renal and cardiovascular functions. Moreover, GLP-1 functions as a central nervous system peptide transmitter, produced by preproglucagon (PPG) neurons in the hindbrain. Intestinal GLP-1 inhibits eating by activating vagal sensory neurons directly, via GLP-1 receptors (GLP-1Rs), but presumably also indirectly, by triggering the release of serotonin from enterochromaffin cells.
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School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Environmental factors are linked to aging and age-related diseases. Emerging evidence suggests that enhancing body's resistance to xenobiotics might be an anti-aging strategy. The constitutive androstane receptor (CAR) regulates drug-metabolizing enzymes and transporters, coordinating metabolism and immune responses to adapt to stress triggered by exogenous exposure.
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