Regional obesity is associated with obstructive sleep apnea severity, although differently in men and women. In women, a direct influence of neck fat on the upper airway patency is implicated. In men, abdominal obesity appears to be the predominant influence. The apnea-hypopnea index was best predicted by a combination of Dual Energy Absorptiometry-measured mass and traditional anthropometric measurements.
Streptococcus pyogenes secretes many toxins that facilitate human colonization, invasion, and dissemination. NADase (SPN) and streptolysin O (SLO) are two toxins that play important roles in pathogenesis. We previously showed that increased production of SPN and SLO in epidemic serotype M1 and M89 S. pyogenes strains is associated with rapid intercontinental spread and enhanced virulence. The biological functions of SPN and SLO have been extensively studied using eukaryotic cell lines, but the relative contribution of each of these two toxins to pathogenesis of epidemic M1 or M89 strains remains unexplored. Herein, using a genetically representative epidemic M1 strain and a panel of isogenic mutant derivative strains, we evaluated the relative contributions of SPN and SLO toxins to virulence in mouse models of necrotizing myositis, bacteremia, and skin and soft tissue infection. We found that isogenic mutants lacking SPN, SLO, and both toxins are equally impaired in ability to cause necrotizing myositis. In addition, mutants lacking either SPN or SLO are significantly attenuated in the bacteremia and soft tissue infection models, and the mutant strain lacking production of both toxins is further attenuated. The mutant strain lacking both SPN and SLO production is severely attenuated in ability to resist killing by human polymorphonuclear leukocytes. We conclude that both SPN and SLO contribute significantly to S. pyogenes pathogenesis in these virulence assays. (Am J Pathol 2017, 187: 605e613; http://dx.doi.org/10.1016/j.ajpath.2016.11.003) Streptococcus pyogenes (alias group A Streptococcus) is a major bacterial pathogen causing human morbidity and mortality globally. Streptococcus pyogenes produces many virulence factors that facilitate transmission, colonization, invasion, and dissemination.1 NADase (SPN) and streptolysin O (SLO) are two potent cytotoxins secreted by S. pyogenes, and multiple roles in virulence have been attributed to each protein. SPN is actively translocated into the host cells, resulting in cell injury and death via depletion of host cell NAD þ . 2e4 SLO is a cholesteroldependent cytolysin that forms pores in host cell membranes. SPN and SLO inhibit phagocytosis, 3 inhibit maturation of autophagosomes, 5,6 impair neutrophil oxidative burst, 7 and prevent the killing of S. pyogenes by a variety of host immune cells. 3,5e8 SPN and SLO are interconnected in many ways. Several lines of evidence suggest that the SPN and SLO proteins interact physically.4,9e11 Moreover, SPN and SLO toxins are functionally related. For example, translocation of SPN into host cells requires SLO.2 In addition, binding of SPN to the host cell membrane promotes SLOmediated pore formation.
Microtubule glutamylation is an important modulator of microtubule function and has been implicated in the regulation of centriole stability, neuronal outgrowth and cilia motility. Glutamylation of the microtubules is catalyzed by a family of tubulin tyrosine ligase-like (TTLL) enzymes. Analysis of individual TTLL enzymes has led to an understanding of their specific functions, but how activities of the TTLL enzymes are coordinated to spatially and temporally regulate glutamylation remains relatively unexplored. We have undertaken an analysis of the glutamylating TTLL enzymes in C. elegans. We find that although all five TTLL enzymes are expressed in the embryo and adult worm, loss of individual enzymes does not perturb microtubule function in embryonic cell divisions. Moreover, normal dye-filling, osmotic avoidance and male mating behavior indicate the presence of functional amphid cilia and male-specific neurons. A ttll-4(tm3310); ttll-11(tm4059); ttll-5(tm3360) triple mutant, however, shows reduced male mating efficiency due to a defect in the response step, suggesting that these three enzymes function redundantly, and that glutamylation is required for proper function of the male-specific neurons.
Infective endocarditis is an infection of the inner surface or endocardium of the heart, in most instances involving the heart valves or the mural portion of the endocardium. As nonbacterial organisms such as rickettsia, fungi, and even viruses may also cause endocarditis, the term "infective endocarditis" is preferred over the older terminology of "bacterial endocarditis." Despite advancements in medical treatment and surgical therapies over the last few decades, infective endocarditis continues to be associated with a poor prognosis. There are many different factors affecting the clinical outcome in patient with infective endocarditis, including the type of organism and its virulence, patient characteristics, comorbid illness, time to diagnosis and treatment, indications for surgery, and time to surgery when indicated. In this article, we will review the epidemiology of endocarditis, the neurologic complications of infective endocarditis, and the current therapeutic strategies.
Background: Clinical evaluation of hospitalized patients with acute altered mental status (AMS) is
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