Author name: Romeo Mariano, M.D.

Autoimmune thyrotoxicosis or Graves’ disease (GD) is the most common cause of hyperthyroidism in the United States. GD occurs more often in women (ratio 5:1) and has a population prevalence of 1-2%. GD is a systemic autoimmune thyroid disorder characterized by the infiltration of immune effector cells and thyroid-antigen-specific T cells into the thyroid and thyroid stimulating hormone receptor (TSHR) expressing tissues, i.e. orbit, skin, with the production of autoantibodies to well-defined thyroidal antigens. Diagnosis of GD is straightforward in a patient with a diffusely enlarged, heterogeneous, hypervascular (increased Doppler flow on neck ultrasound) thyroid gland, associated orbitopathy, biochemically confirmed thyrotoxicosis, positive TSHR autoantibodies, and often a family history of autoimmune disorders.

Untreated maternal depression was associated with slower rates of fetal body and head growth. Pregnant mothers treated with SSRIs had fewer depressive symptoms and their fetuses had no delay in body growth but had delayed head growth and were at increased risk for preterm birth.

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.

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.

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.

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 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.

Bidirectional communication between the brain and the immune system is carried out through a complex network of autonomic nerves, endocrine hormones, and cytokines. Insomnia perturbs the functioning of this network and therefore contribute to elevations in inflammatory mediators which lead to cardiovascular disease.

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.

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. …

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