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Discrete choice models of demand are growing in popularity for understanding markets for seafood, but have thus far been limited to applications using individual-level choice data. The random coefficients logit model is a discrete choice demand model designed for aggregate sales data and imparts a number of theoretical and empirical advantages. Instrumental variables account for price endogeneity, which can arise when there are unobserved product characteristics. Furthermore, correlated preferences can be accommodated in the random coefficients as well as through demographic interactions, which is especially important for seafood where product characteristics are primarily qualitative. We estimate this model for salmon fillets using four years of county-level seafood sales in California, and demonstrate the insights that can be drawn regarding consumer preferences and substitution patterns. Although the model is computationally burdensome, it offers considerable potential for further seafood demand analysis. [ABSTRACT FROM AUTHOR]

Hedonic price functions are frequently used to identify the marginal implicit prices for characteristics of differentiated products, including seafood products. These marginal implicit prices are determined by both consumer preferences and producer costs. When preferences or costs for a single characteristic differ systematically across omitted submarkets, the results are an average of the heterogeneous effects. An empirical test for the joint significance of interaction terms is sufficient to identify the presence of submarkets. We motivate the selection of submarkets on the basis of production differences across salmon species, then use county-level aggregate retailer scanner data for the US state of California from 2013 to 2016 to estimate hedonic price functions. The results indicate that species and production method submarkets exist. Letting differences in production motivate the dimensions for submarkets results in a more accurate picture of the market. [ABSTRACT FROM AUTHOR]

The article presents a speech by Kevin Ray, Of Counsel at the law firm Greenberg Traurig, delivered at the annual symposium for the DePaul Business and Commercial Law Journal, and the Journal of Art Technology and Intellectual Property. Topics of the speech included importance of art-secured loan made by banks in security transactions, the collector loan that is made to an investor and the gallery loan that is secured in the art merchant's gallery.

In New York City, LGBTQ people from different generations have had few opportunities to connect. They have splintered into age-segregated micro-communities, robbing them of opportunities to weave a common history and share strategies that community members have used to survive and thrive.Bridging the Gapwas a community-based intergenerational theatre project designed to address this problem. It was developed and facilitated by a team of three candidates for The City University of New York (CUNY) School of Professional Studies’ MA in Applied Theatre. The project was a partnership between CUNY and SAGE (Services and Advocacy for Gay, Lesbian, Bisexual & Transgender Elders) and culminated in a live performance ofStep Right Up!, an original devised theatre piece. In this paper, we explore our application of the drama strategy, ‘Role on the Wall’, in an intergenerational LGBTQ context. Our various adaptations of the activity allowed for age-related stereotypes to be identified, confronted and disrupted. We further incorporated ‘Role on the Wall’ into the culminating performance. Our dramatisation of the perceptions revealed by ‘Role on the Wall’ allowed us not only to start a dialogue about pertinent subjects within our group, but also to share our dialogue with a wider audience during the performance. [ABSTRACT FROM PUBLISHER]

Abstract: Hyponatremia at time of inpatient admission is associated with increased severity of illness and mortality in patients hospitalized for treatment of medical conditions. This study was conducted to determine the clinical outcome of psychiatric inpatients with admission hyponatremia. The cohort comprised 1000 adults consecutively admitted to a free-standing psychiatric hospital in 2010. Emergency transfer to a general hospital was used as a proxy marker for poor medical outcome. The point prevalence of hyponatremia (sodium level <136mEq/l) at admission was 6.49%. Older age and a diagnosis of arterial hypertension were independent correlates of admission hyponatremia. Medical deteriorations occurred in 26.7% of hyponatremic patients and 13.1% of those with normal sodium levels. Admission hyponatremia is associated with an increased rate of significant medical deteriorations of psychiatric inpatients and should trigger enhanced clinical monitoring to identify and treat somatic disorders. [Copyright &y& Elsevier]

Activating mutations in the Kras gene are commonly found in some but not all epithelial cancers. In order to understand the susceptibility of different epithelial tissues to Kras-induced tumorigenesis, we introduced one of the most common Kras mutations,KrasG12D, broadly in epithelial tissues. We used a mouse model in which the G12D mutation is placed in the endogenous Kras locus controlled by inducible, Cre-mediated recombination in tissues expressing cytokeratin 19 including the oral cavity, GI tract, lungs, and ducts of the liver, kidney, and the pancreas. Introduction of theKrasG12D mutation in adult mouse tissues led to neoplastic changes in some but not all of these tissues. Notably, many hyperplasias, metaplasias and adenomas were observed in the oral cavity, stomach, colon and lungs, suggesting that exposure to products of the outside environment promotesKrasG12D-initiated tumorigenesis. However, environmental exposure did not consistently correlate with tumor formation, such as in the small intestine, suggesting that there are also intrinsic differences in susceptibility to Kras activation. The pancreas developed small numbers of mucinous metaplasias with characteristics of early stage pancreatic intraepithelial neoplasms (PanINs), supporting the hypothesis that pancreatic ducts have the potential to give rise pancreatic cancer. [ABSTRACT FROM AUTHOR]

The development of pancreatic fibrosis has been shown to be a major component in several diseases of the pancreas including pancreatic cancer, chronic pancreatitis, and type 2 diabetes mellitus, but its actual role in the progression of these disorders is still unknown. This fibrosis is characterized by stromal expansion and the excessive deposition of extracellular matrix (ECM) that replaces pancreatic tissue. This eventually leads to dysregulation of ECM turnover, production of cytokines, restriction of blood flow, and often exocrine and endocrine insufficiencies. Activated pancreatic stellate cells (PSCs) have been identified as key mediators in the progression of pancreatic fibrosis, serving as the predominant source of excess ECM proteins. Previously, we found that overexpression of the growth factor heparin-binding epidermal growth factor-like growth factor (HB-EGF) in pancreatic islets led to intraislet fibrosis. HB-EGF binds to and activates two receptors, epidermal growth factor receptor (EGFR) and ErbB4, as well as heparin moieties and CD9/DRAP27. To understand the mechanism underlying the induction of fibrogenesis by HB-EGF, we utilized a hypomorphic allele of Egfr, the Waved-2 allele, to demonstrate that EGFR signaling regulates fibrogenesis in vivo. Using an in vitro cell migration assay, we show that HB-EGF regulates both chemoattraction and stimulation of proliferation of PSCs via EGFR activation. [ABSTRACT FROM AUTHOR]

Reports that Campylobacter fetus, a spiral gram-negative bacterial pathogen, uses multiple loci for DNA inversion within the 5' conserved regions of sap homologs. Effect of mutations on sap inversion frequencies; Movement of the KpnI and NotI sites relative to the sapA promoter; Rearrangement in the FCR downstream of the antibiotic cassettes.

Studies in both humans and rodents have found that insulin+ cells appear within or near ducts of the adult pancreas, particularly following damage or disease, suggesting that these insulin+ cells arise de novo from ductal epithelium. We have found that insulin+ cells are continuous with duct cells in the epithelium that makes up the hyperplastic ducts of both chronic pancreatitis and pancreatic cancer in humans. Therefore, we tested the hypothesis that both hyperplastic ductal cells and their associated insulin+ cells arise from the same cell of origin. Using a mouse model that develops insulin+ cell-containing hyperplastic ducts in response to the growth factor TGFα, we performed genetic lineage tracing experiments to determine which cells gave rise to both hyperplastic ductal cells and duct-associated insulin+ cells. We found that hyperplastic ductal cells arose largely from acinar cells that changed their cell fate, or transdifferentiated, into ductal cells. However, insulin+ cells adjacent to acinar-derived ductal cells arose from pre-existing insulin+ cells, suggesting that islet endocrine cells can intercalate into hyperplastic ducts as they develop. We conclude that apparent pancreatic plasticity can result both from the ability of acinar cells to change fate and of endocrine cells to reorganize in association with duct structures. [ABSTRACT FROM AUTHOR]

Transforming growth factor (TGF)-β family members exert strong effects on restoration of liver mass after injury. Bone morphogenetic proteins (BMPs) are members of the TGF-β family and are found in the liver, suggesting that these proteins may play a role in liver regeneration. We examined BMP signaling in the liver during hepatectomy. We found that BMP4 is constitutively expressed in the peribiliary stroma and endothelial cells of the liver and that expression is decreased after hepatectomy. Mice driven to maintain BMP4 expression in the liver display inhibited hepatocyte proliferation and restoration of liver mass after hepatectomy, suggesting that reduced BMP4 is necessary for normal regeneration. Consistent with this finding, hepatocyte-specific deletion of the BMP receptor activin receptor-like kinase 3 (Alk3) enhances regeneration and reduces phosphorylation of SMAD1/5/8, a transducer of BMP signaling. In contrast to experiments in wild-type mice, maintaining BMP4 levels has no effect on liver regeneration in hepatocyte-specific Alk3 null mice, providing evidence that BMP4 signals through Alk3 to inhibit liver regeneration. Consistent with these findings, the BMP4 antagonist Noggin enhances regeneration. Furthermore, high-dose BMP4 inhibits proliferation of primary hepatocytes and HepG2 cells in culture. These findings elucidate a new, potentially clinically relevant paradigm in which a constitutively expressed paracrine inhibitory factor plays a critical role in liver regeneration. [ABSTRACT FROM AUTHOR]

Presents information on a study which examined the solar cycle dependence of dose in the low-altitude high-latitude 'horns' of the outer zone electron belt. Satellite orbits and dosimeters; Analysis and discussion.

Cerebral blood flow is an important parameter in many diseases and functional studies that can be accurately measured in humans using arterial spin labelling (ASL) MRI. However, although rat models are frequently used for preclinical studies of both human disease and brain function, rat CBF measurements show poor consistency between studies. This lack of reproducibility is due, partly, to the smaller size and differing head geometry of rats compared to humans, as well as the differing analysis methodologies employed and higher field strengths used for preclinical MRI. To address these issues, we have implemented, optimised and validated a multiphase pseudo-continuous ASL technique, which overcomes many of the limitations of rat CBF measurement. Three rat strains (Wistar, Sprague Dawley and Berlin Druckrey IX) were used, and CBF values validated against gold-standard autoradiography measurements. Label positioning was found to be optimal at 45°, while post-label delay was optimised to 0.55 s. Whole brain CBF measures were 109 ± 22, 111 ± 18 and 100 ± 15 mL/100 g/min by multiphase pCASL, and 108 ± 12, 116 ± 14 and 122 ± 16 mL/100 g/min by autoradiography in Wistar, SD and BDIX cohorts, respectively. Tumour model analysis shows that the developed methods also apply in disease states. Thus, optimised multiphase pCASL provides robust, reproducible and non-invasive measurement of CBF in rats. [ABSTRACT FROM AUTHOR]

Stable isotopically labeled (SIL) tryptic peptides, cleavable SIL peptides, and a full-length SIL protein were compared for internal calibration (i.e., as internal calibrators) and external calibration (i.e., as internal standards) when quantifying three forms of unlabeled, human thyroglobulin (Tg) by bottom-up protein analysis. All SIL materials and human proteins were standardized by amino acid analysis to ensure traceability of measurements and allow confident assignment of accuracy. The three forms of human Tg quantified were (1) the primary reference material BCR457 a native protein purified from human thyroids, (2) a commercially available form also purified from human thyroids, and (3) a full-length recombinant form expressed and purified from a human embryonic kidney 293 cell-line. Collectively, the results unequivocally demonstrate the lack of commutability of tryptic and cleavable SIL peptides as internal calibrators across various bottom-up assays (i.e., denaturing/digestion conditions). Further, the results demonstrate the potential during external calibration for surrogate protein calibrators (i.e., recombinant proteins) to produce inaccurate concentration assignments of native protein analytes by bottom-up analysis due to variance in digestion efficiency, which is not alleviated by altering denaturation/digestion stringency and indicates why protein calibrators may not be commutable in bottom-up protein assays. These results have implications regarding the veracity of "absolute" protein concentration assignments by bottom-up assays using peptide calibrators, as well as protein calibrators, given that absolute accuracy was not universally observed. Nevertheless, these results support the use of recombinant SIL proteins as internal standards over SIL peptides due to their ability to better mimic the digestion of human-derived proteins and mitigate bias due to digestion-based matrix effects that were observed during external calibration. [ABSTRACT FROM AUTHOR]

Dicer processes microRNAs (miRs) into active forms in a wide variety of tissues, including the liver. To determine the role of Dicer in liver regeneration, we performed a series of in vivo and in vitro studies in a murine 2/3 hepatectomy model. Dicer was downregulated after 2/3 hepatectomy, and loss of Dicer inhibited liver regeneration associated with decreased cyclin A2 and miR-221, as well as increased levels of the cell cycle inhibitor p27. In vitro, miR-221 inhibited p27 production in primary hepatocytes and increased hepatocyte proliferation. Specific reconstitution of miR-221 in hepatocyte-specific Dicer-null mice inhibited p27 and restored liver regeneration. In wild type mice, targeted inhibition of miR-221 using a cholesterol-conjugated miR-221 inhibited hepatocyte proliferation after 2/3 hepatectomy. These results identify Dicer production of miR-221 as an essential component of a miRNA-dependent mechanism for suppression of p27 that controls the rate of hepatocyte proliferation after partial hepatectomy. NEW & NOTEWORTHY Our findings demonstrate a direct role for microRNAs in controlling the rate of liver regeneration after injury. By deleting Dicer, an enzyme responsible for processing microRNAs into mature forms, we determined miR-221 is a critical microRNA in the physiological process of restoration of liver mass after injury. miR-221 suppresses p27, releasing its inhibitory effects on hepatocyte proliferation. Pharmaceuticals based on miR-221 may be useful to modulate hepatocyte proliferation in the setting of liver injury. [ABSTRACT FROM AUTHOR]

After significant injury, the liver must maintain homeostasis during the regenerative process. We hypothesized the existence of mechanisms to limit hepatocyte proliferation after injury to maintain metabolic and synthetic function. A screen for candidates revealed suppressor of cytokine signaling 2 (SOCS2), an inhibitor of growth hormone (GH) signaling, was strongly induced after partial hepatectomy. Using genetic deletion and administration of various factors we investigated the role of SOCS2 during liver regeneration. SOCS2 preserves liver function by restraining the first round of hepatocyte proliferation after partial hepatectomy by preventing increases in growth hormone receptor (GHR) via ubiquitination, suppressing GH pathway activity. At later times, SOCS2 enhances hepatocyte proliferation by modulating a decrease in serum insulin-like growth factor 1 (IGF-1) that allows GH release from the pituitary. SOCS2, therefore, plays a dual role in modulating the rate of hepatocyte proliferation. In particular, this is the first demonstration of an endogenous mechanism to limit hepatocyte proliferation after injury. [ABSTRACT FROM AUTHOR]

Although bottom-up proteomics using tryplic digests is widely used to locate post-translational modifications (PTM) in proteins, there are cases where the protein has several potential modification sites within a tryptic fragment and MS² strategies fail to pinpoint the location. We report here a method using two proteolytic enzymes, trypsin and pepsin, in combination followed by tandem mass spectrometric analysis to provide fragments that allow one to locate the modification sites. We used this strategy to find a glycosylation site on bovine trypsin expressed in maize (TrypZean). Several glycans are present, and all are attached to a noncon-sensus N-glycosylation site on the protein. [ABSTRACT FROM AUTHOR]

An analysis of differential charging between dielectric surface materials and the frame of a DSCS-III geosynchronous spacecraft is presented. Charging levels measured by surface potential monitors (SPMs) covered with samples of Kapton and Astroquartz have been recorded for one half of a solar cycle. Both seasonal and solar cycle effects are seen in the daily peak levels of the SPM voltages, with local maxima occurring near the equinoxes and a general trend increasing as solar max is approached. Charge neutralization by an onboard Xe plasma contactor was demonstrated to be effective throughout the mission, with a mean voltage reduction of 86% for Astroquartz and 74% for Kapton. Though a statistical analysis shows a general correlation between the fluence of charging electrons with SPM voltages, the event-specific correlation contains enough variance to cast doubt on the usefulness of an electron sensor as a differential charging alarm. We have found that a Kapton-covered SPM may be better suited than an electron sensor as a differential charging alarm. [ABSTRACT FROM AUTHOR]

Provides information on a study which reported on the first year of on-orbit operation of the Compact Environmental Anomaly Sensor. Description of its performance with emphasis on its engineering, hazard-warning function; Instrument overview; On-orbit results.

Focuses on the optically sampled analog-to-digital converters (ADC). Use of a dual-output electrooptic sampling transducer; Benefits of ADC; Domination of thermal noise in the high-resolution low-bandwidth ADC.

Hyperpolarised MRI with Dynamic Nuclear Polarisation overcomes the fundamental thermodynamic limitations of conventional magnetic resonance, and is translating to human studies with several early-phase clinical trials in progress including early reports that demonstrate the utility of the technique to observe lactate production in human brain cancer patients. Owing to the fundamental coupling of metabolism and tissue function, metabolic neuroimaging with hyperpolarised [1-13C]pyruvate has the potential to be revolutionary in numerous neurological disorders (e.g. brain tumour, ischemic stroke, and multiple sclerosis). Through the use of [1-13C]pyruvate and ethyl-[1-13C]pyruvate in naïve brain, a rodent model of metastasis to the brain, or porcine brain subjected to mannitol osmotic shock, we show that pyruvate transport across the blood-brain barrier of anaesthetised animals is rate-limiting. We show through use of a well-characterised rat model of brain metastasis that the appearance of hyperpolarized [1-13C]lactate production corresponds to the point of blood-brain barrier breakdown in the disease. With the more lipophilic ethyl-[1-13C]pyruvate, we observe pyruvate production endogenously throughout the entire brain and lactate production only in the region of disease. In the in vivo porcine brain we show that mannitol shock permeabilises the blood-brain barrier sufficiently for a dramatic 90-fold increase in pyruvate transport and conversion to lactate in the brain, which is otherwise not resolvable. This suggests that earlier reports of whole-brain metabolism in anaesthetised animals may be confounded by partial volume effects and not informative enough for translational studies. Issues relating to pyruvate transport and partial volume effects must therefore be considered in pre-clinical studies investigating neuro-metabolism in anaesthetised animals, and we additionally note that these same techniques may provide a distinct biomarker of blood-brain barrier permeability in future studies. [ABSTRACT FROM AUTHOR]