Nitrogen increases hull rot and interferes with the hull split phenology in almond (Prunus dulcis)

The effect of nitrogen (N) nutrition on the occurrence of hull rot (caused by Rhizopus stolonifer) in almonds was measured in a heavily infected commercial orchard in 2011 and 2012. Starting in 2008, trees were grown under differing N rates (140, 224, 392. kg/ha). In 2011 spurs in these trees were tagged by type (non-fruiting, one-fruiting, two-fruiting) and evaluated for hull rot incidence after harvest. It is demonstrated here that N application in excess of tree demand significantly increased the incidence of hull rot in fruiting spurs in both 2011 and 2012. In 2012, hull split rate was also observationally recorded every other day in the N treatments of 140 and 392. kg/ha. N application rate altered the pattern of fruit development and delayed the transition from the 'closed hulls' stage to the 'beginning of hull split' stage. However, this delay was not critical in the increased incidence of hull rot and hull infection rates did not significantly differ as a function of difference in time spent within different hull split stages. In conclusion, excess N resulted in higher hull rot incidence due to a higher susceptibility of the hulls, but not due to a longer residence time within a particular stage once the fruit started to split. Possible causal mechanisms of N effect on hull rot and the significance of the disease are considered

Nitrogen increases hull rot and interferes with the hull split phenology in almond (Prunus dulcis)

The effect of nitrogen (N) nutrition on the occurrence of hull rot (caused by Rhizopus stolonifer) in almonds was measured in a heavily infected commercial orchard in 2011 and 2012. Starting in 2008, trees were grown under differing N rates (140, 224, 392. kg/ha). In 2011 spurs in these trees were tagged by type (non-fruiting, one-fruiting, two-fruiting) and evaluated for hull rot incidence after harvest. It is demonstrated here that N application in excess of tree demand significantly increased the incidence of hull rot in fruiting spurs in both 2011 and 2012. In 2012, hull split rate was also observationally recorded every other day in the N treatments of 140 and 392. kg/ha. N application rate altered the pattern of fruit development and delayed the transition from the 'closed hulls' stage to the 'beginning of hull split' stage. However, this delay was not critical in the increased incidence of hull rot and hull infection rates did not significantly differ as a function of difference in time spent within different hull split stages. In conclusion, excess N resulted in higher hull rot incidence due to a higher susceptibility of the hulls, but not due to a longer residence time within a particular stage once the fruit started to split. Possible causal mechanisms of N effect on hull rot and the significance of the disease are considered

Angiotensin II plasma levels are linked to disease severity and predict fatal outcomes in H7N9-infected patients

A novel influenza A (H7N9) virus of avian origin emerged in eastern China in the spring of 2013. This virus causes severe disease in humans, including acute and often lethal respiratory failure. As of January 2014, 275 cases of H7N9-infected patients had been reported, highlighting the urgency of identifying biomarkers for predicting disease severity and fatal outcomes. Here, we show that plasma levels of angiotensin II, a major regulatory peptide of the renin-angiotensin system, are markedly elevated in H7N9 patients and are associated with disease progression. Moreover, the sustained high levels of angiotensin II in these patients are strongly correlated with mortality. The predictive value of angiotensin II is higher than that of C-reactive protein and some clinical parameters such as the PaO2/FiO2 ratio (partial pressure of arterial oxygen to the fraction of inspired oxygen). Our findings indicate that angiotensin II is a biomarker for lethality in flu infections