Articles: chronic.
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Am. J. Respir. Crit. Care Med. · Feb 2014
Deficiency of MDA5 Results in Exacerbated Chronic Post-Viral Lung Inflammation.
Respiratory viral infections can result in the establishment of chronic lung diseases. Understanding the early innate immune mechanisms that participate in the development of chronic postviral lung disease may reveal new targets for therapeutic intervention. The intracellular viral sensor protein melanoma differentiation-associated protein 5 (MDA5) sustains the acute immune response to Sendai virus, a mouse pathogen that causes chronic lung inflammation, but its role in the development of postviral chronic lung disease is unknown. ⋯ MDA5 modulates the development of chronic lung inflammation by regulating the early inflammatory response in the lung.
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Curr Opin Anaesthesiol · Feb 2014
ReviewBronchoscopic treatment of end-stage chronic obstructive pulmonary disease.
Chronic obstructive pulmonary disease (COPD) is a progressive, debilitating disease that in its final stages cripples the patient. The disappointing results of the National Emphysema Treatment Trial study led to a decrease in the acceptance of lung volume reduction surgery as a therapy. Thus, it became clear that debilitated COPD patients would need innovative alternative nonsurgical procedures to potentially alleviate their symptoms. This review will address the various techniques of bronchoscopic lung volume reduction (BLVR). ⋯ BLVR appears to be safer than surgery and presents an attractive alternative for the treatment of COPD patients. Unfortunately, the outcome data to date are inconclusive; the procedures remain experimental and any benefits unproven. However, the data that are emerging continue to appear promising.
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This review article explores the need for specialized pain care for children and adolescents and provides some historical context for our current knowledge base and clinical practice. ⋯ Awareness of children's pain has increased dramatically over the past three decades, and Canadians have performed a leadership role in much of the research. Specific multidisciplinary teams are a more recent phenomenon, but they are shown to be more effective and probably more cost effective than traditional treatment models. Important gaps in availability of resources to manage these patients remain.
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Review
The transition from acute to chronic pain: understanding how different biological systems interact.
Although pain is an adaptive sensory experience necessary to prevent further bodily harm, the transition from acute to chronic pain is not adaptive and results in the development of a chronic clinical condition. How this transition occurs has been the focus of intense study for some time. The focus of the current review is on changes in neuronal plasticity as well as the role of immune cells and glia in the development of chronic pain from acute tissue injury and pain. ⋯ A better understanding of how chronic pain develops at a mechanistic level can aid clinicians in treating their patients by showing how the underlying biology of chronic pain contributes to the clinical manifestations of pain. A thorough understanding of how chronic pain develops may also help identify new targets for future analgesic drugs.
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Am. J. Respir. Crit. Care Med. · Feb 2014
Regulation of Hypoxia-Induced Pulmonary Hypertension by Vascular Smooth Muscle HIF-1alpha.
Chronic hypoxia induces pulmonary vascular remodeling, pulmonary hypertension, and right ventricular hypertrophy. At present, little is known about mechanisms driving these responses. Hypoxia-inducible factor-1α (HIF-1α) is a master regulator of transcription in hypoxic cells, up-regulating genes involved in energy metabolism, proliferation, and extracellular matrix reorganization. Systemic loss of a single HIF-1α allele has been shown to attenuate hypoxic pulmonary hypertension, but the cells contributing to this response have not been identified. ⋯ These results indicate that HIF-1α in smooth muscle contributes to pulmonary vascular remodeling and pulmonary hypertension in chronic hypoxia. However, loss of HIF-1 function in smooth muscle does not affect hypoxic cardiac remodeling, suggesting that the cardiac hypertrophy response is not directly coupled to the increase in pulmonary artery pressure.