American journal of respiratory and critical care medicine
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Medical problems occur at high altitude because of the low inspired Po(2), which is caused by the reduced barometric pressure. The classical physiological responses to high altitude include hyperventilation, polycythemia, hypoxic pulmonary vasoconstriction-increased intracellular oxidative enzymes, and increased capillary density in muscle. However, with the discovery of hypoxia-inducible factors (HIFs), it is apparent that there is a multitude of responses to cellular hypoxia. ⋯ An alternative strategy is to increase the barometric pressure as in aircraft cabins. A hybrid approach combining both strategies shows promise but has never been used. Mines that are being developed at increasingly high altitudes pose great medical problems.
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Am. J. Respir. Crit. Care Med. · Dec 2012
Comparative StudyNoninvasive ventilation in acute hypercapnic respiratory failure caused by obesity hypoventilation syndrome and chronic obstructive pulmonary disease.
Noninvasive ventilation (NIV) is widely used in episodes of acute hypercapnic respiratory failure (AHRF) in patients with chronic obstructive pulmonary disease (COPD). However, there is no evidence on the efficacy of NIV during similar episodes in obesity hypoventilation syndrome (OHS). Objectives: To compare the efficacy of NIV in episodes of AHRF caused by OHS and COPD. ⋯ Patients with OHS can be treated with NIV during an episode of AHRF with similar efficacy and better outcomes than patients with COPD.
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Am. J. Respir. Crit. Care Med. · Dec 2012
High levels of virus-specific CD4+ T cells predict severe pandemic influenza A virus infection.
T-cell responses have been implicated in control and exacerbation of lung injury during influenza A virus (IAV) infection. ⋯ High levels of circulating virus-specific CD4(+) T cells to two viral internal proteins (nucleoprotein and matrix) in the first phase of infection are associated with subsequent development of severe IAV infection. This finding could be an early and specific marker for ensuing clinical deterioration. Contrasting levels of antigen-specific CD8(+) T cells in lungs and blood have implications on design and analysis of clinical trials for T-cell vaccines because measurements of T cells in the periphery may not reflect events in the lungs.
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The exploration of the endogenous regenerative potential of the diseased adult human lung represents an innovative and exciting task. In this pulmonary perspective, we discuss three major components essential for endogenous lung repair and regeneration: epithelial progenitor populations, developmental signaling pathways that regulate their reparative and regenerative potential, and the surrounding extracellular matrix in the human diseased lung. Over the past years, several distinct epithelial progenitor populations have been discovered within the lung, all of which most likely respond to different injuries by varying degrees. ⋯ Third, endogenous progenitor cells and developmental signaling pathways act in close spatiotemporal synergy with the extracellular matrix. These three components define and refine the highly dynamic microenvironment of the lung, which is altered in a disease-specific fashion in several chronic lung diseases. The search for the right mixture to induce efficient and controlled repair and regeneration of the diseased lung is ongoing and will open completely novel avenues for the treatment of patients with chronic lung disease.