Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · Feb 2009
ReviewArthrocentesis and synovial fluid analysis in clinical practice: value of sonography in difficult cases.
Joint aspiration, or arthrocentesis, is one of the most useful and commonly performed procedures for the diagnosis and treatment of joint diseases. The synovial fluid aspirated may be examined to evaluate the degree of inflammation and, mainly, to detect the presence of some relevant pathogenic agents, such as crystals or microorganisms. In these cases, synovial fluid analysis still represents the best diagnostic procedure. ⋯ The most recent recommendations on arthrocentesis confirm the need for the procedure in the presence of synovial effusion of unknown origin, especially if septic or crystal arthritis is suspected. Owing to the importance of this analysis, it is clearly recommended that ultrasonography should be used to facilitate arthrocentesis in difficult cases. Furthermore, ultrasonography may be useful in revealing the presence of synovial fluid before the joint aspiration and, subsequently, distinguishing some aspects characteristic of crystal-induced arthropathies.
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SNAP-25 (synaptosomal-associated protein of 25 kDa) is a plasma membrane protein that, together with syntaxin and the synaptic vesicle protein VAMP/synaptobrevin, forms the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) docking complex for regulated exocytosis. SNAP-25 also modulates different voltage-gated calcium channels, representing therefore a multifunctional protein that plays essential roles in neurotransmitter release at different steps. Recent genetic studies of human populations and of some mouse models implicate alterations in SNAP-25 gene structure, expression, and/or function in contributing directly to these distinct neuropsychiatric and neurological disorders.
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Ann. N. Y. Acad. Sci. · Dec 2008
Neuroendocrine activation during combined mental and physical stress in women depends on trait anxiety and the phase of the menstrual cycle.
The aim of this study was to investigate the influence of trait anxiety and menstrual cycle phase on neuroendocrine activation during combined mental and physical stress procedure in 40 healthy female subjects. Women at the upper (anxious) and lower (nonanxious) limits of the normal range of a trait anxiety scale were exposed to the stress procedure consisting of a mental component (Stroop test) and handgrip exercise. Salivary cortisol levels, cardiovascular parameters, and cognitive performance in the Stroop test were evaluated. ⋯ In contrast, a negative correlation trend was observed in anxious subjects. Thus, in subjects with low but not high trait anxiety, enhanced cortisol concentrations seem to be associated with better cognitive performance. The results suggest that women with high trait anxiety exhibit greater cardiovascular and hormonal sensitivity to stress stimuli during the follicular phase.
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Ann. N. Y. Acad. Sci. · Dec 2008
ReviewFrom Hans Selye's discovery of biological stress to the identification of corticotropin-releasing factor signaling pathways: implication in stress-related functional bowel diseases.
Selye pioneered the concept of biological stress in 1936, culminating in the identification of the corticotropin-releasing factor (CRF) signaling pathways by Vale's group in the last two decades. The characterization of the 41 amino-acid CRF and other peptide members of the mammalian CRF family, urocortin 1, urocortin 2, and urocortin 3, and the cloning of CRF(1) and CRF(2) receptors, which display distinct affinity for CRF ligands, combined with the development of selective CRF receptor antagonists enable us to unravel the importance of CRF(1) receptor in the stress-related endocrine (activation of pituitary-adrenal axis), behavioral (anxiety/depression, altered feeding), autonomic (activation of sympathetic nervous system), and immune responses. The activation of CRF(1) receptors is also one of the key mechanisms through which various stressors impact the gut to stimulate colonic propulsive motor function and to induce hypersensitivity to colorectal distension as shown by the efficacy of the CRF(1) receptor antagonists in blunting these stress-related components. The importance of CRF(1) signaling pathway in the visceral response to stress in experimental animals provided new therapeutic approaches for treatment of functional bowel disorder such as irritable bowel syndrome, a multifactor functional disorder characterized by altered bowel habits and visceral pain, for which stress has been implicated in the pathophysiology and is associated with anxiety-depression in a subset of patients.
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Ann. N. Y. Acad. Sci. · Dec 2008
ReviewReduced hypothalamo-pituitary-adrenal axis stress responses in late pregnancy: central opioid inhibition and noradrenergic mechanisms.
In late pregnancy, the hypothalamo-pituitary-adrenal (HPA) axis is less responsive to a range of psychological and physical stressors as a result of reduced central drive to the corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN). Most stressors activate the brain stem noradrenergic system, which innervates the majority of networks involved in regulating stress responses, including the PVN. Forced swimming, systemic interleukin-1beta (IL-1beta), and cholecystokinin (CCK) all activate brain stem noradrenergic cell groups, stimulate noradrenaline release in the PVN, and activate the HPA axis in nonpregnant rats. ⋯ HPA axis responses to IL-1beta and CCK can be reinstated in pregnant rats by systemic administration of the opioid receptor antagonist naloxone, and when infused directly into the PVN, naloxone restores noradrenaline release in the PVN following IL-1beta treatment. Adrenaline release into the blood following stress is also attenuated in late pregnancy, despite increased adrenomedullary expression of tyrosine hydroxylase mRNA at this time. This review describes the mechanisms underlying attenuated HPA axis stress responses in pregnancy, focusing on the role of endogenous opioids and the central noradrenergic system.