Nationwide Study on the Course of Influenza A (H1N1) Infections in Hospitalized Children in the Netherlands During the Pandemic 2009-2010.

BACKGROUND: The influenza H1N1 pandemic of 2009-2010, provided a unique opportunity to assess the course of disease, as well as the analysis of risk factors for severe disease in hospitalized children (< 18 years). METHODS: Retrospective national chart study on hospitalized children with H1N1 infection during the 2009-2010 pH1N1 outbreak. RESULTS: Nine hundred forty patients (56% boys), median age 3.0 years, were enrolled; the majority were previously healthy. Treatment consisted of supplemental oxygen (24%), mechanical ventilation (5%) and antiviral therapy (63%). Fifteen patients died (1.6%), 5 of whom were previously healthy. Multivariable analyses confirmed pre-existent heart and lung disease as risk factors for intensive care unit admission. Risk factors for mortality included children with a neurologic or oncologic disease and psychomotor retardation. CONCLUSIONS: This nationwide overview of hospitalized children confirms known risk groups for severe influenza infections. However, most of the acute and severe presentations of influenza occurred in previously healthy children.

Mice deficient for soluble adenylyl cyclase are infertile because of a severe sperm-motility defect.

To acquire the ability to fertilize, spermatozoa undergo complex, but at present poorly understood, activation processes. The intracellular rise of cAMP produced by the bicarbonate-dependent soluble adenylyl cyclase (sAC) has been suggested to play a central role in initiating the cascade of the events that culminates in spermatozoa maturation. Here, we show that targeted disruption of the sAC gene does not affect spermatogenesis but dramatically impairs sperm motility, leading to male sterility. sAC mutant spermatozoa are characterized by a total loss of forward motility and are unable to fertilize oocytes in vitro. Interestingly, motility in sAC mutant spermatozoa can be restored on cAMP loading, indicating that the motility defect observed is not caused by a structural defect. We, therefore, conclude that sAC plays an essential and nonredundant role in the activation of the signaling cascade controlling motility and, therefore, in fertility. The crucial role of sAC in fertility and the absence of any other obvious pathological abnormalities in sAC-deficient mice may provide a rationale for developing inhibitors that can be applied as a human male contraceptive.