Nitrogen-Use Dynamics in Switchgrass Grown for Biomass

This work examines N use by switchgrass (Panicum virgatum L.). A study was conducted on two well-established ‘Cave-in-Rock’ switchgrass stands in Blacksburg (37° 11′ N, 80° 25′ W) and Orange (38° 13′ N, 78° 07′ W) Virginia, USA. Plots were fertilized in 2001 (year 1) with 0, 90, 180, or 270 kg N per hectare. No additional N was applied in 2002 (year 2) and 2003 (year 3), and biomass was harvested in July and November for years 2 and 3 (but only in November of year 1). Root and soil samples were collected in May, July, September, and November each year and analyzed for N. Nitrogen fertilization did not increase yields in 2001 (year 1), but it did provide residual benefits in 2002 (year 2) and 2003 (year 3). Root-N levels at 15 cm depth increased with fertilization, fluctuated seasonally between roots and shoots, and root-N was reduced over the course of the study. With two harvests per year, about 100 kg N hectare per year were removed in biomass, even in plots with no N added—suggesting N already present in the soils (at 15 cm depth) contributed to yields; but the soil mineral-N pools were reduced by the end of year 3. Nitrogen-use efficiency, apparent N recovery, and partial factor productivity were reduced with higher N applications. The data support the notion that biomass production can be achieved with minimal N inputs, but stands must be managed to maintain that N reserve over the long term. There is also a need to quantify the N pool to depths greater than 15 cm in other agro-ecoregions.     

H3K27ac bookmarking promotes rapid post-mitotic activation of the pluripotent stem cell program without impacting 3D chromatin reorganization

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Arginine-vasopressin mediates central and peripheral glucose regulation in response to carotid body receptor stimulation with Na-cyanide.

Hypoxic stimulation of the carotid body receptors (CBR) results in a rapid hyperglycemia with an increase in brain glucose retention. Previous work indicates that neurohypophysectomy inhibits this hyperglycemic response. Here, we show that systemic arginine vasopressin (AVP) induced a transient, but significant, increase in blood glucose levels and increased brain glucose retention, a response similar to that observed after CBR stimulation. Comparable results were obtained after intracerebral infusion of AVP. Systemic AVP-induced changes were maintained in hypophysectomized rats but were not observed after adrenalectomy. Glycemic changes after CBR stimulation were inhibited by pharmacological blockage of AVP V1a receptors with a V1a-selective receptor antagonist ([beta-Mercapto-beta,beta-cyclopentamethylenepropionyl1,O-me-Tyr2, Arg8]-vasopressin). Importantly, local application of micro-doses of this antagonist to the liver was sufficient to abolish the hyperglycemic response after CBR stimulation. These results suggest that AVP is a mediator of the hyperglycemic reflex and cerebral glucose retention following CBR stimulation. We propose that hepatic activation of AVP V1a receptors is essential for this hyperglycemic response.