Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · Apr 2010
ReviewProthymosin alpha as robustness molecule against ischemic stress to brain and retina.
Following stroke or traumatic damage, neuronal death via both necrosis and apoptosis causes loss of functions, including memory, sensory perception, and motor skills. As necrosis has the nature to expand, while apoptosis stops the cell death cascade in the brain, necrosis is considered to be a promising target for rapid treatment for stroke. We identified the nuclear protein, prothymosin alpha (ProTalpha) from the conditioned medium of serum-free culture of cortical neurons as a key protein-inhibiting necrosis. ⋯ In the ischemic brain or retina, ProTalpha showed a potent inhibition of both necrosis and apoptosis. By use of anti-brain-derived neurotrophic factor or anti-erythropoietin IgG, we found that ProTalpha inhibits necrosis, but causes apoptosis, which is in turn inhibited by ProTalpha-induced neurotrophins under the condition of ischemia. From the experiment using anti-ProTalpha IgG or antisense oligonucleotide for ProTalpha, it was revealed that ProTalpha has a pathophysiological role in protecting neurons in stroke.
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The pathophysiology of fibromyalgia (FM) is not completely understood. The disease is characterized by a central sensitization with an amplification of pain perception. A combination of interactions among external stressors, behavioral constructs, neurotransmitters, hormones, immune, and sympathetic nervous systems appears to be involved. ⋯ Recent data highlight the putative role of cytokines in the pathogenesis of FM. The autonomic nervous system is implicated in the maintenance of the physiological homeostasis and sympathetic activity appears increased in FM. Neuropeptide Y and its receptors Y1 and Y2 seem to have a complex role in pain modulation.
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Fibromyalgia (FM) is a chronic pain syndrome characterized by widespread pain, fatigue, sleep alterations, and distress. Emerging evidence points toward augmented pain processing within the central nervous system as having a primary role in the pathophysiology of this disorder. Recent studies have identified distinct FM subgroups on the basis of clinical, neurochemical, and neuroendocrinological abnormalities, including increased cerebrospinal fluid levels of substance P and excitatory amino acids and functional abnormalities in the hypothalamic-pituitary-adrenal axis, and sympathoadrenal (autonomic nervous) system. ⋯ Antidepressants, nonsteroidal anti-inflammatory drugs, opioids, sedatives, muscle relaxants, and alpha2-delta agonists have all been used to treat FM with varying results. Physical exercise and multimodal cognitive-behavioral therapy seem to be the most widely accepted and beneficial forms of nonpharmacological therapy. Studies predicting treatment response indicate that it is useful if not essential to tailor the choice of treatment components to the needs of individual patients.
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Dolichoectasia (dilatative arteriopathy) describes marked elongation, widening, and tortuosity of arteries. The intracranial vertebral and basilar arteries are preferentially involved. ⋯ Flow in dilated arteries can become bidirectional, resulting in reduced antegrade flow and thrombus formation. Elongation and angulation of arteries can stretch and distort the orifices of arterial branches, leading to decreased blood flow, especially in penetrating branches.
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Brain and heart development occur simultaneously in the human fetus. Given the depth and complexity of these shared morphogenetic programs, it is perhaps not surprising that disruption of organogenesis in one organ will impact the development of the other. ⋯ These abnormalities in brain development identified with MRI in newborns with congenital heart disease might reflect abnormalities in cerebral blood flow while in utero. A complete understanding of the mechanisms of white matter injury in the term newborn with congenital heart disease will require further investigation of the timing, extent, and causes of delayed fetal brain development in the presence of congenital heart disease.