Acute Flaccid Paralysis Associated with Novel Enterovirus C105.

An outbreak of acute flaccid paralysis among children in the United States during summer 2014 was tentatively associated with enterovirus D68 infection. This syndrome in a child in fall 2014 was associated with enterovirus C105 infection. The presence of this virus strain in North America may pose a diagnostic challenge.

Extensive clonal spread and extreme longevity in saw palmetto, a foundation clonal plant.

The lack of effective tools has hampered out ability to assess the size, growth and ages of clonal plants. With Serenoa repens (saw palmetto) as a model, we introduce a novel analytical framework that integrates DNA fingerprinting and mathematical modelling to simulate growth and estimate ages of clonal plants. We also demonstrate the application of such life-history information of clonal plants to provide insight into management plans. Serenoa is an ecologically important foundation species in many Southeastern United States ecosystems; yet, many land managers consider Serenoa a troublesome invasive plant. Accordingly, management plans have been developed to reduce or eliminate Serenoa with little understanding of its life history. Using Amplified Fragment Length Polymorphisms, we genotyped 263 Serenoa and 134 Sabal etonia (a sympatric non-clonal palmetto) samples collected from a 20 × 20 m study plot in Florida scrub. Sabal samples were used to assign small field-unidentifiable palmettos to Serenoa or Sabal and also as a negative control for clone detection. We then mathematically modelled clonal networks to estimate genet ages. Our results suggest that Serenoa predominantly propagate via vegetative sprouts and 10,000-year-old genets may be common, while showing no evidence of clone formation by Sabal. The results of this and our previous studies suggest that: (i) Serenoa has been part of scrub associations for thousands of years, (ii) Serenoa invasion are unlikely and (ii) once Serenoa is eliminated from local communities, its restoration will be difficult. Reevaluation of the current management tools and plans is an urgent task.

Surfactant administration prior to one lung ventilation: physiological and inflammatory correlates in a piglet model.

OBJECTIVES: To test the hypothesis that surfactant, when given prophylactically during one lung ventilation (OLV), improves physiological stability and reduces inflammation. METHODS: Prospective controlled animal study. After 30 min of mechanical ventilation, surfactant was administered to the left lung of the treatment group. Right lung mechanical ventilation continued for 3 hr, after which the left lung was unblocked. Bilateral mechanical ventilation was continued for 30 min thereafter. Physiological parameters and biomarkers of inflammation in plasma, lung tissue homogenates, and bronchoalveolar lavage (BAL) were measured. MEASUREMENTS AND MAIN RESULTS: Oxygenation improved in the surfactant group, reaching statistical significance at 3 hr of OLV and again after 30 min of bilateral mechanical ventilation following the OLV. Plasma levels of interleukin (IL)-1 ß, IL-6, and tumor necrosis factor (TNF)-α showed a trend for reduction. The lung homogenates from the ventilated lungs had significantly lower levels of IL-1 ß (P < 0.01) and IL-6 (P < 0.01). The BAL specimen showed an overall reduction in the cytokine levels; IL-1 ß was significantly lower in the ventilated lungs (P < 0.01). CONCLUSIONS: Surfactant administration improves oxygenation and decreases inflammation, as evidenced by a decrease in several inflammatory cytokines both in the plasma and lungs of a piglet model of OLV.

Protective ventilation to reduce inflammatory injury from one lung ventilation in a piglet model.

OBJECTIVES: To test the hypothesis that protective ventilation strategy (PVS) as defined by the use of low stretch ventilation (tidal volume of 5 ml x kg(-1) and employing 5 cm of positive end expiratory pressure (PEEP) during one lung ventilation (OLV) in piglets would result in reduced injury compared to a control group of piglets who received the conventional ventilation (tidal volume of 10 ml x kg(-1) and no PEEP). BACKGROUND: PVS has been found to be beneficial in adults to minimize injury from OLV. We designed the current study to test the beneficial effects of PVS in a piglet model of OLV. METHODS: Ten piglets each were assigned to either 'Control' group (tidal volume of 10 ml x kg(-1) and no PEEP) or 'PVS' group (tidal volume of 5 ml x kg(-1) during the OLV phase and PEEP of 5 cm of H2O throughout the study). Experiment consisted of 30 min of baseline ventilation, 3 h of OLV, and again 30 min of bilateral ventilation. Respiratory parameters and proinflammatory markers were measured as outcome. RESULTS: There was no difference in PaO2 between groups. PaCO2 (P < 0.01) and ventilatory rate (P < 0.01) were higher at 1.5 h OLV and at the end point in the PVS group. Peak inflating pressure (PIP) and pulmonary resistance were higher (P < 0.05) in the control group at 1.5 h OLV. tumor necrosis factor-alpha (P < 0.04) and IL-8 were less (P < 0.001) in the plasma from the PVS group, while IL-6 and IL-8 were less (P < 0.04) in the lung tissue from ventilated lungs in the PVS group. CONCLUSIONS: Based on this model, PVS decreases inflammatory injury both systemically and in the lung tissue with no adverse effect on oxygenation, ventilation, or lung function.