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Higher Levels of Adipocytokines Increase the Risk for Stroke

Higher plasma levels of resistin, adipsin, and total adiponectin were associated with an increased 10-year risk of ischemic stroke among healthy middle-aged men. Resistin, adipsin, and total adiponectin, but not leptin, were independent predictors of ischemic stroke. The performance of a traditional risk factor model predicting ischemic stroke was significantly improved by the simultaneous inclusion of resistin, adipsin, and total adiponectin.

Inflammatory prostaglandin E(2) Signaling on EP3 Receptors Lead to Pro-inflammatory Changes Contributing to Alzheimer's Disease

There is significant evidence for a central role of inflammation in the development of Alzheimer disease (AD). Chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) reduces the risk of developing AD. Stimulation of the the PGE(2) EP3 receptor activates proinflammatory, proamyloidogenic, and synaptotoxic signaling pathways. Deletion of the PGE(2) EP3 receptor in a model of Aβ(42) peptide-induced neuroinflammation reduced proinflammatory gene expression, cytokine production, and oxidative stress. Deletion of the EP3 receptor blocked induction of proinflammatory gene and protein expression and lipid peroxidation, and levels of Aβ peptides were significantly decreased, as were β-secretase and β C-terminal fragment levels.

Psychoneuroimmunology of Psoriasis

Bi-directional communication between the Central Nervous System and the Endocrine System has been known for many years. Some of the hormones, themselves, are secreted by the Brain. The CNS and Endocrine System are also involved in a bi-directional communication with the Immune System. This has been a target of intense research in recent decades. Psychological states are related to changes in immune meidators. These influence the development of diseases. This review looks at the role of psychoneuroimmunology in psoriasis.

Stress Activates Immune System Pro-inflammatory Changes Contributing to Coronary Artery Disease

The evidence for the effects of acute and chronic psychological stress on the onset and progression of CAD is consistent and convincing. Psychological stressors change endothelial function and lead to chemotaxis. Acute psychological stressors lead to leukocytosis, increased natural killer cell cytotoxicity and reduced proliferative response to mitogens. Psychological stressors will increase haemostatic factors and acute phase proteins, possibly leading to thrombus formation and myocardial infarction.

Obesity results in chronic low-grade pro-inflammatory signaling that contributes to anxiety and depressive behaviors

Obesity is characterized by chronic low-grade inflammation that may lead to emotional distress and behavioural symptoms. At baseline, body mass index (BMI) was positively correlated with inflammatory markers and adipokines. Regression analyses adjusting for age and diabetes revealed that baseline concentrations of IL-6 and hsCRP were associated with the depression and anxiety facets of neuroticism, with higher inflammation predicting higher anxiety and depression.

Insomnia exacerbates fatigue, depression, pain, and rheumatoid arthritis.

This study provides the first evidence of an exaggerated increase in symptoms of mood and pain in patients with rheumatoid arthritis after sleep loss, along with an activation of rheumatoid arthritis-related joint pain. Given the reciprocal relationship between sleep disturbances and pain, clinical management of pain in patients with rheumatoid arthritis should include an increased focus on the prevention and treatment of sleep disturbance in this clinical population.

Sulfasalazine Inhibits Activation of NF-κB in Basolateral Amygdala, Impairing Memory Persistance in Auditory Fear Conditioning

Activation of NF-κB in Basolateral Amygdala Is Required for Memory Reconsolidation in Auditory Fear ConditioningPLoS One. 2012;7(9):e43973. Epub 2012 Sep 5.Si J, Yang J, Xue L, Yang C, Luo Y, Shi H, Lu L.Source Abstract Posttraumatic stress disorder (PTSD) is characterized by acute and chronic changes in the stress response, manifested as conditioned fear memory. …

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