Trending Articles
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Twenty-four basic and clinical studies and case reports are included in this quarterly review of the myofascial pain literature. The majority of publications focus on invasive techniques, especially dry needling. ⋯ While some physiotherapists have bought into the notion that hands-on approaches are a thing of the past, since "pain is in the brain" and "the issues are not in the tissues," there is also a body of research that aims to combine so-called top-down and bottom-up therapies. Combining manual therapy and dry needling with pain neuroscience education is likely the preferred method using a multimodal approach (Puentedura and Flynn, 2016; Lluch Girbes et al., 2015).
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Comparative Study
Up-regulation of P2X4 receptors in spinal microglia after peripheral nerve injury mediates BDNF release and neuropathic pain.
ATP is a known mediator of inflammatory and neuropathic pain. However, the mechanisms by which specific purinergic receptors contribute to chronic pain states are still poorly characterized. Here, we demonstrate that in response to peripheral nerve injury, P2X(4) receptors (P2X(4)R) are expressed de novo by activated microglia in the spinal cord. ⋯ Furthermore, ATP stimulation is unable to stimulate BDNF release from P2X(4)-deficient mice microglia in primary cultures. These results indicate that P2X(4)R contribute to chronic pain through a central inflammatory pathway. P2X(4)R might thus represent a potential therapeutic target to limit microglia-mediated inflammatory responses associated with brain injury and neurodegenerative disorders.
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To protect the ischemic penumbra, guidelines have recommended against treating all but the severest elevations in blood pressure during acute ischemic stroke. ⋯ Most patients with acute ischemic stroke are treated with antihypertensive agents despite the absence of severe hypertension. Although low blood pressure is common among treated patients, frank hypotension is unusual.
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The rise in life expectancy worldwide has been accompanied by an increased incidence of age-related diseases, representing an enormous burden on healthcare services and society. All vital organs lose function with age, and this is well described in the lung, with a progressive decline in pulmonary function after the age of about 25 years. The lung ages, like any other organ, with progressive functional impairment and reduced capacity to respond to environmental stresses and injury. ⋯ However, COPD shows striking age-associated features, such as an increase in cellular senescence, stem cell exhaustion, increased oxidative stress, alteration in the extracellular matrix and a reduction in endogenous antiageing molecules and protective pathways such as autophagy. In this review we discuss the evidence showing how oxidative stress induces accelerated ageing by upregulating the phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT/mechanistic target of rapamycin signalling pathway resulting in depletion of stem cells, defective autophagy, reduced antioxidant responses and defective mitochondrial function thus generating further oxidative stress. Understanding the mechanisms of accelerated ageing in COPD may identify novel therapeutic approaches.
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This review discusses combined pulmonary fibrosis and emphysema (CPFE) in the setting of connective tissue disease. ⋯ The syndrome of CPFE is a distinct pulmonary manifestation in the spectrum of lung diseases associated with connective tissue diseases, especially in smokers or ex-smokers.