Corn and wheat residue management effects on greenhouse gas emissions in the Mid-Atlantic USA

Greenhouse gas (GHG) emissions from crop residue management have been studied extensively, yet the effects of harvesting more than one crop residue in a rotation have not been reported. Here, we measured the short-term changes in methane (CH4), nitrous oxide (N2O), and carbon dioxide (CO2) emissions in response to residue removal from continuous corn (Zea mays L.) (CC) and corn-wheat (Triticum aestivum L.)-soybean (Glycine max L. Merr.) (CWS) rotations in the Mid-Atlantic USA. A first experiment retained five corn stover rates (0, 3.33, 6.66, 10, and 20 Mg ha-1) in a continuous corn (CC) in Blacksburg, VA, in 2016 and 2017. Two other experiments, initiated during the wheat and corn phases of the CWS rotation in New Kent, VA, utilized a factorial combination of retained corn (0, 3.33, 6.66, and 10.0 Mg ha-1) and wheat residue (0, 1, 2, and 3 Mg ha-1). Soybean residue was not varied. Different crop retention rates did not affect CO2 fluxes in any of the field studies. In Blacksburg, retaining 5 Mg ha-1 stover or more increased CH4 and N2O emissions by ~25%. Maximum CH4 and N2O fluxes (4.16 and 5.94 mg m-2 day-1) occurred with 200% (20 Mg ha-1) retention. Two cycles of stover management in Blacksburg, and one cycle of corn or wheat residue management in New Kent did not affect GHG fluxes. This study is the first to investigate the effects of crop residue on GHG emissions in a multi-crop system in humid temperate zones. Longer-term studies are warranted to understand crop residue management effects on GHG emissions in these systems

Conversion of deoxynivalenol to 3-acetyldeoxynivalenol in barley-derived fuel ethanol co-products with yeast expressing trichothecene 3-O-acetyltransferases

<p>Abstract</p> <p>Background</p> <p>The trichothecene mycotoxin deoxynivalenol (DON) may be concentrated in distillers dried grains with solubles (DDGS; a co-product of fuel ethanol fermentation) when grain containing DON is used to produce fuel ethanol. Even low levels of DON (≤ 5 ppm) in DDGS sold as feed pose a significant threat to the health of monogastric animals. New and improved strategies to reduce DON in DDGS need to be developed and implemented to address this problem. Enzymes known as trichothecene 3-<it>O-</it>acetyltransferases convert DON to 3-acetyldeoxynivalenol (3ADON), and may reduce its toxicity in plants and animals.</p> <p>Results</p> <p>Two <it>Fusarium </it>trichothecene 3-<it>O-</it>acetyltransferases (FgTRI101 and FfTRI201) were cloned and expressed in yeast (<it>Saccharomyces cerevisiae</it>) during a series of small-scale ethanol fermentations using barley (<it>Hordeum vulgare</it>). DON was concentrated 1.6 to 8.2 times in DDGS compared with the starting ground grain. During the fermentation process, FgTRI101 converted 9.2% to 55.3% of the DON to 3ADON, resulting in DDGS with reductions in DON and increases in 3ADON in the Virginia winter barley cultivars Eve, Thoroughbred and Price, and the experimental line VA06H-25. Analysis of barley mashes prepared from the barley line VA04B-125 showed that yeast expressing FfTRI201 were more effective at acetylating DON than those expressing FgTRI101; DON conversion for FfTRI201 ranged from 26.1% to 28.3%, whereas DON conversion for FgTRI101 ranged from 18.3% to 21.8% in VA04B-125 mashes. Ethanol yields were highest with the industrial yeast strain Ethanol Red^®, which also consumed galactose when present in the mash.</p> <p>Conclusions</p> <p>This study demonstrates the potential of using yeast expressing a trichothecene 3-<it>O</it>-acetyltransferase to modify DON during commercial fuel ethanol fermentation.</p

Diagnosis and management of glutaric aciduria type I – revised recommendations

Glutaric aciduria type I (synonym, glutaric acidemia type I) is a rare organic aciduria. Untreated patients characteristically develop dystonia during infancy resulting in a high morbidity and mortality. The neuropathological correlate is striatal injury which results from encephalopathic crises precipitated by infectious diseases, immunizations and surgery during a finite period of brain development, or develops insidiously without clinically apparent crises. Glutaric aciduria type I is caused by inherited deficiency of glutaryl-CoA dehydrogenase which is involved in the catabolic pathways of L-lysine, L-hydroxylysine and L-tryptophan. This defect gives rise to elevated glutaric acid, 3-hydroxyglutaric acid, glutaconic acid, and glutarylcarnitine which can be detected by gas chromatography/mass spectrometry (organic acids) or tandem mass spectrometry (acylcarnitines). Glutaric aciduria type I is included in the panel of diseases that are identified by expanded newborn screening in some countries. It has been shown that in the majority of neonatally diagnosed patients striatal injury can be prevented by combined metabolic treatment. Metabolic treatment that includes a low lysine diet, carnitine supplementation and intensified emergency treatment during acute episodes of intercurrent illness should be introduced and monitored by an experienced interdisciplinary team. However, initiation of treatment after the onset of symptoms is generally not effective in preventing permanent damage. Secondary dystonia is often difficult to treat, and the efficacy of available drugs cannot be predicted precisely in individual patients. The major aim of this revision is to re-evaluate the previous diagnostic and therapeutic recommendations for patients with this disease and incorporate new research findings into the guideline

Genome-wide profiling of p63 DNA-binding sites identifies an element that regulates gene expression during limb development in the 7q21 SHFM1 locus.

Contains fulltext : 88501.pdf (publisher's version ) (Open Access)Heterozygous mutations in p63 are associated with split hand/foot malformations (SHFM), orofacial clefting, and ectodermal abnormalities. Elucidation of the p63 gene network that includes target genes and regulatory elements may reveal new genes for other malformation disorders. We performed genome-wide DNA-binding profiling by chromatin immunoprecipitation (ChIP), followed by deep sequencing (ChIP-seq) in primary human keratinocytes, and identified potential target genes and regulatory elements controlled by p63. We show that p63 binds to an enhancer element in the SHFM1 locus on chromosome 7q and that this element controls expression of DLX6 and possibly DLX5, both of which are important for limb development. A unique micro-deletion including this enhancer element, but not the DLX5/DLX6 genes, was identified in a patient with SHFM. Our study strongly indicates disruption of a non-coding cis-regulatory element located more than 250 kb from the DLX5/DLX6 genes as a novel disease mechanism in SHFM1. These data provide a proof-of-concept that the catalogue of p63 binding sites identified in this study may be of relevance to the studies of SHFM and other congenital malformations that resemble the p63-associated phenotypes