Articles: function.
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The rostral ventromedial medulla (RVM) has a well-documented role in pain modulation and exerts antinociceptive and pronociceptive influences mediated by 2 distinct classes of neurons, OFF-cells and ON-cells. OFF-cells are defined by a sudden pause in firing in response to nociceptive inputs, whereas ON-cells are characterized by a "burst" of activity. Although these reflex-related changes in ON- and OFF-cell firing are critical to their pain-modulating function, the pathways mediating these responses have not been identified. ⋯ Few of these neurons expressed calcitonin gene-related peptide, suggesting that the RVM projection from PB is distinct from that to the amygdala. These data show that a substantial component of "bottom-up" nociceptive drive to RVM pain-modulating neurons is relayed through the PB. While the PB is well known as an important relay for ascending nociceptive information, its functional connection with the RVM allows the spinoparabrachial pathway to access descending control systems as part of a recurrent circuit.
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Semin Respir Crit Care Med · Dec 2016
ReviewThe Role of Streptococcus pneumoniae in Community-Acquired Pneumonia.
Streptococcus pneumoniae (the pneumococcus) remains one of the most common causes of bacterial community-acquired pneumonia (CAP), encompassing infections mild enough to be treated on an outpatient basis, as well as those requiring hospital care, or even intensive care unit admission. This microorganism is associated with a significant burden of disease, causing substantial morbidity and mortality worldwide, and generating considerable health-care costs. ⋯ Such risk factors include extremes of age, lifestyle factors, including smoking and alcohol abuse, and various underlying comorbid conditions, including congenital and acquired immunodeficiencies. This article will review various aspects of pneumococcal CAP, including the burden of pneumococcal disease, risk factors for pneumococcal infection, the occurrence of cardiovascular events in patients with pneumococcal CAP, the apparently pivotal role of pneumolysin, a major virulence factor of the pneumococcus, in the pathogenesis of severe infection and associated cardiac dysfunction, empiric antibiotic treatment for pneumococcal CAP, as well as adjunctive therapies, specifically those which target pneumolysin, and, finally, the mortality of such infections.
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Semin Respir Crit Care Med · Dec 2016
ReviewComplication of Community-Acquired Pneumonia (Including Cardiac Complications).
Community-acquired pneumonia (CAP) represents an important public health problem and carries significant morbidity, mortality, and costs. The incidence of CAP is highest among children and elderly patients, but the mortality is much higher in patients older than 65 years. Despite the advances in medicine, the administration of antimicrobials, and the overall better care, there are still patients with CAP dying due to systemic complications all over the world. ⋯ In this review, we present the characteristics of several CAP-related pulmonary and nonpulmonary organ dysfunction, such as those affecting the heart, kidneys, hematological, neurological, endocrine systems. Multiple severity of illness scores identified a series of systemic findings that indicate the organ dysfunctions and the associated related outcomes. However, further research is required to address the mechanisms, the management, and prevention of organ dysfunction in patients with CAP.
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Critical care medicine · Dec 2016
Multicenter Study Observational StudyAcetaminophen-Induced Changes in Systemic Blood Pressure in Critically Ill Patients: Results of a Multicenter Cohort Study.
We sought to assess the incidence of acetaminophen-induced hypotension. Our secondary objectives were to describe systemic hemodynamic changes and factors associated with this complication. ⋯ Half of the patients who received IV injections of acetaminophen developed hypotension, and up to one third of the observed episodes necessitated therapeutic intervention. Adequately powered randomized studies are needed to confirm our findings, provide an accurate estimation of the consequences of acetaminophen-induced hypotension, and assess the pathophysiologic mechanisms involved.