Preferences for self-service meat among household consumers in metropolitan St. Louis

Also available online.Digitized 2007 AES

Large and seasonally varying biospheric CO₂ fluxes in the Los Angeles megacity revealed by atmospheric radiocarbon

Measurements of Δ¹⁴C and CO₂ can cleanly separate biogenic and fossil contributions to CO₂ enhancements above background. Our measurements of these tracers in air around Los Angeles in 2015 reveal high values of fossil CO₂ and a significant and seasonally varying contribution of CO₂ from the urban biosphere. The biogenic CO₂ is composed of sources such as biofuel combustion and human metabolism and an urban biospheric component likely originating from urban vegetation, including turf and trees. The urban biospheric component is a source in winter and a sink in summer, with an estimated amplitude of 4.3 parts per million (ppm), equivalent to 33% of the observed annual mean fossil fuel contribution of 13 ppm. While the timing of the net carbon sink is out of phase with wintertime rainfall and the sink seasonality of Southern California Mediterranean ecosystems (which show maximum uptake in spring), it is in phase with the seasonal cycle of urban water usage, suggesting that irrigated urban vegetation drives the biospheric signal we observe. Although 2015 was very dry, the biospheric seasonality we observe is similar to the 2006–2015 mean derived from an independent Δ¹⁴C record in the Los Angeles area, indicating that 2015 biospheric exchange was not highly anomalous. The presence of a large and seasonally varying biospheric signal even in the relatively dry climate of Los Angeles implies that atmospheric estimates of fossil fuel–CO₂ emissions in other, potentially wetter, urban areas will be biased in the absence of reliable methods to separate fossil and biogenic CO₂

Large and seasonally varying biospheric CO₂ fluxes in the Los Angeles megacity revealed by atmospheric radiocarbon

Measurements of Δ¹⁴C and CO₂ can cleanly separate biogenic and fossil contributions to CO₂ enhancements above background. Our measurements of these tracers in air around Los Angeles in 2015 reveal high values of fossil CO₂ and a significant and seasonally varying contribution of CO₂ from the urban biosphere. The biogenic CO₂ is composed of sources such as biofuel combustion and human metabolism and an urban biospheric component likely originating from urban vegetation, including turf and trees. The urban biospheric component is a source in winter and a sink in summer, with an estimated amplitude of 4.3 parts per million (ppm), equivalent to 33% of the observed annual mean fossil fuel contribution of 13 ppm. While the timing of the net carbon sink is out of phase with wintertime rainfall and the sink seasonality of Southern California Mediterranean ecosystems (which show maximum uptake in spring), it is in phase with the seasonal cycle of urban water usage, suggesting that irrigated urban vegetation drives the biospheric signal we observe. Although 2015 was very dry, the biospheric seasonality we observe is similar to the 2006–2015 mean derived from an independent Δ¹⁴C record in the Los Angeles area, indicating that 2015 biospheric exchange was not highly anomalous. The presence of a large and seasonally varying biospheric signal even in the relatively dry climate of Los Angeles implies that atmospheric estimates of fossil fuel–CO₂ emissions in other, potentially wetter, urban areas will be biased in the absence of reliable methods to separate fossil and biogenic CO₂

Evaluation of ENTLN Performance Characteristics Based on the Ground Truth Natural and Rocket-Triggered Lightning Data Acquired in Florida

The performance characteristics of the Earth Networks Total Lightning Network (ENTLN) were evaluated by using as ground truth natural cloud-to-ground (CG) lightning data acquired at the Lightning Observatory in Gainesville (LOG) and rocket-triggered lightning data obtained at Camp Blanding (CB), Florida, in 2014 and 2015. Two ENTLN processors (data processing algorithms) were evaluated. The old processor (P2014) was put into use in June 2014 and the new one (P2015) has been operational since August 2015. Based on the natural-CG-lightning data set (219 flashes containing 608 strokes), the flash detection efficiency (DE), flash classification accuracy (CA), stroke DE, and stroke CA for the new processor were found to be 99%, 97%, 96%, and 91%, respectively, and the corresponding values for the old processor were 99%, 91%, 97%, and 68%. The stroke DE and stroke CA for first strokes are higher than those for subsequent strokes. Based on the rocket-triggered lightning data set (36 CG flashes containing 175 strokes), the flash DE, flash CA, stroke DE, and stroke CA for the new processor were found to be 100%, 97%, 97%, and 86%, respectively, while the corresponding values for the old processor were 100%, 92%, 97%, and 42%. The median values of location error and absolute peak current estimation error were 215 m and 15% for the new processor, and 205 m and 15% for the old processor. For both natural and triggered CG lightning, strokes with higher peak currents were more likely to be both detected and correctly classified by the ENTLN

Expression and trans-specific polymorphism of self-incompatibility RNases in Coffea (Rubiaceae)

Self-incompatibility (SI) is widespread in the angiosperms, but identifying the biochemical components of SI mechanisms has proven to be difficult in most lineages. Coffea (coffee; Rubiaceae) is a genus of old-world tropical understory trees in which the vast majority of diploid species utilize a mechanism of gametophytic self-incompatibility (GSI). The S-RNase GSI system was one of the first SI mechanisms to be biochemically characterized, and likely represents the ancestral Eudicot condition as evidenced by its functional characterization in both asterid (Solanaceae, Plantaginaceae) and rosid (Rosaceae) lineages. The S-RNase GSI mechanism employs the activity of class III RNase T2 proteins to terminate the growth of "self" pollen tubes. Here, we investigate the mechanism of Coffea GSI and specifically examine the potential for homology to S-RNase GSI by sequencing class III RNase T2 genes in populations of 14 African and Madagascan Coffea species and the closely related self-compatible species Psilanthus ebracteolatus. Phylogenetic analyses of these sequences aligned to a diverse sample of plant RNase T2 genes show that the Coffea genome contains at least three class III RNase T2 genes. Patterns of tissue-specific gene expression identify one of these RNase T2 genes as the putative Coffea S-RNase gene. We show that populations of SI Coffea are remarkably polymorphic for putative S-RNase alleles, and exhibit a persistent pattern of trans-specific polymorphism characteristic of all S-RNase genes previously isolated from GSI Eudicot lineages. We thus conclude that Coffea GSI is most likely homologous to the classic Eudicot S-RNase system, which was retained since the divergence of the Rubiaceae lineage from an ancient SI Eudicot ancestor, nearly 90 million years ago.United States National Science Foundation [0849186]; Society of Systematic Biologists; American Society of Plant Taxonomists; Duke University Graduate Schoolinfo:eu-repo/semantics/publishedVersio

Polyomic profiling reveals significant hepatic metabolic alterations in glucagon-receptor (GCGR) knockout mice: implications on anti-glucagon therapies for diabetes

<p>Abstract</p> <p>Background</p> <p>Glucagon is an important hormone in the regulation of glucose homeostasis, particularly in the maintenance of euglycemia and prevention of hypoglycemia. In type 2 Diabetes Mellitus (T2DM), glucagon levels are elevated in both the fasted and postprandial states, which contributes to inappropriate hyperglycemia through excessive hepatic glucose production. Efforts to discover and evaluate glucagon receptor antagonists for the treatment of T2DM have been ongoing for approximately two decades, with the challenge being to identify an agent with appropriate pharmaceutical properties and efficacy relative to potential side effects. We sought to determine the hepatic & systemic consequence of full glucagon receptor antagonism through the study of the glucagon receptor knock-out mouse (Gcgr^-/-) compared to wild-type littermates.</p> <p>Results</p> <p>Liver transcriptomics was performed using Affymetric expression array profiling, and liver proteomics was performed by iTRAQ global protein analysis. To complement the transcriptomic and proteomic analyses, we also conducted metabolite profiling (~200 analytes) using mass spectrometry in plasma. Overall, there was excellent concordance (R = 0.88) for changes associated with receptor knock-out between the transcript and protein analysis. Pathway analysis tools were used to map the metabolic processes in liver altered by glucagon receptor ablation, the most notable being significant down-regulation of gluconeogenesis, amino acid catabolism, and fatty acid oxidation processes, with significant up-regulation of glycolysis, fatty acid synthesis, and cholesterol biosynthetic processes. These changes at the level of the liver were manifested through an altered plasma metabolite profile in the receptor knock-out mice, e.g. decreased glucose and glucose-derived metabolites, and increased amino acids, cholesterol, and bile acid levels.</p> <p>Conclusions</p> <p>In sum, the results of this study suggest that the complete ablation of hepatic glucagon receptor function results in major metabolic alterations in the liver, which, while promoting improved glycemic control, may be associated with adverse lipid changes.</p

Molecular Characterisation of Small Molecule Agonists Effect on the Human Glucagon Like Peptide-1 Receptor Internalisation

The glucagon-like peptide receptor (GLP-1R), which is a G-protein coupled receptor (GPCR), signals through both Gαs and Gαq coupled pathways and ERK phosphorylation to stimulate insulin secretion. The aim of this study was to determine molecular details of the effect of small molecule agonists, compounds 2 and B, on GLP-1R mediated cAMP production, intracellular Ca2+ accumulation, ERK phosphorylation and its internalisation. In human GLP-1R (hGLP-1R) expressing cells, compounds 2 and B induced cAMP production but caused no intracellular Ca2+ accumulation, ERK phosphorylation or hGLP-1R internalisation. GLP-1 antagonists Ex(9-39) and JANT-4 and the orthosteric binding site mutation (V36A) in hGLP-1R failed to inhibit compounds 2 and B induced cAMP production, confirming that their binding site distinct from the GLP-1 binding site on GLP-1R. However, K334A mutation of hGLP-1R, which affects Gαs coupling, inhibited GLP-1 as well as compounds 2 and B induced cAMP production, indicating that GLP-1, compounds 2 and B binding induce similar conformational changes in the GLP-1R for Gαs coupling. Additionally, compound 2 or B binding to the hGLP-1R had significantly reduced GLP-1 induced intracellular Ca2+ accumulation, ERK phosphorylation and hGLP-1R internalisation. This study illustrates pharmacology of differential activation of GLP-1R by GLP-1 and compounds 2 and B

Recent Progress in the Use of Glucagon and Glucagon Receptor Antagonists in the Treatment of Diabetes Mellitus

Glucagon is an important pancreatic hormone, released into blood circulation by alpha cells of the islet of Langerhans. Glucagon induces gluconeogenesis and glycogenolysis in hepatocytes, leading to an increase in hepatic glucose production and subsequently hyperglycemia in susceptible individuals. Hyperglucagonemia is a constant feature in patients with T2DM. A number of bioactive agents that can block glucagon receptor have been identified. These glucagon receptor antagonists can reduce the hyperglycemia associated with exogenous glucagon administration in normal as well as diabetic subjects. Glucagon receptor antagonists include isoserine and beta-alanine derivatives, bicyclic 19-residue peptide BI-32169, Des-His1-[Glu9] glucagon amide and related compounds, 5-hydroxyalkyl-4-phenylpyridines, N-[3-cano-6- (1,1 dimethylpropyl)-4,5,6,7-tetrahydro-1-benzothien-2-yl]-2-ethylbutamide, Skyrin and NNC 250926. The absorption, dosage, catabolism, excretion and medicinal chemistry of these agents are the subject of this review. It emphasizes the role of glucagon in glucose homeostasis and how it could be applied as a novel tool for the management of diabetes mellitus by blocking its receptors with either monoclonal antibodies, peptide and non-peptide antagonists or gene knockout techniques

Inactivation of Staphylococcal Phenol Soluble Modulins by Serum Lipoprotein Particles

Staphylococcus aureus virulence has been associated with the production of phenol soluble modulins (PSM). PSM are known to activate, attract and lyse neutrophils. However, the functional characterizations were generally performed in the absence of human serum. Here, we demonstrate that human serum can inhibit all the previously-described activities of PSM. We observed that serum can fully block both the cell lysis and FPR2 activation of neutrophils. We show a direct interaction between PSM and serum lipoproteins in human serum and whole blood. Subsequent analysis using purified high, low, and very low density lipoproteins (HDL, LDL, and VLDL) revealed that they indeed neutralize PSM. The lipoprotein HDL showed highest binding and antagonizing capacity for PSM. Furthermore, we show potential intracellular production of PSM by S. aureus upon phagocytosis by neutrophils, which opens a new area for exploration of the intracellular lytic capacity of PSM. Collectively, our data show that in a serum environment the function of PSM as important extracellular toxins should be reconsidered

Comparative genomics reveals functional transcriptional control sequences in the Prop1 gene

Mutations in PROP1 are a common genetic cause of multiple pituitary hormone deficiency (MPHD). We used a comparative genomics approach to predict the transcriptional regulatory domains of Prop1 and tested them in cell culture and mice. A BAC transgene containing Prop1 completely rescues the Prop1 mutant phenotype, demonstrating that the regulatory elements necessary for proper PROP1 transcription are contained within the BAC. We generated DNA sequences from the PROP1 genes in lemur, pig, and five different primate species. Comparison of these with available human and mouse PROP1 sequences identified three putative regulatory sequences that are highly conserved. These are located in the PROP1 promoter proximal region, within the first intron of PROP1, and downstream of PROP1. Each of the conserved elements elicited orientation-specific enhancer activity in the context of the Drosophila alcohol dehydrogenase minimal promoter in both heterologous and pituitary-derived cells lines. The intronic element is sufficient to confer dorsal expansion of the pituitary expression domain of a transgene, suggesting that this element is important for the normal spatial expression of endogenous Prop1 during pituitary development. This study illustrates the usefulness of a comparative genomics approach in the identification of regulatory elements that may be the site of mutations responsible for some cases of MPHD