Structure and Emplacement of the Eocene Golden Horn Batholith, North Cascades, Washington

The 48 Ma Golden Horn batholith is a ~310 km2, shallow intrusion constructed of sub-horizontal sheets in the crystalline core of the North Cascades of Washington. It is the only large body of granite in an orogen dominated by 96-45 Ma tonalite, and probably intruded during ridge subduction. The oldest and structurally highest unit of the batholith is diorite, followed by alkaline granite, one feldspar-biotite granite, two feldspar-biotite granite, and finally granodiorite, the youngest and structurally lowest unit. The batholith displays a weak NE-striking foliation restricted to the center of the intrusion and a stronger NW-striking foliation formed throughout the batholith with an associated weak, NW-trending and shallowly plunging lineation. Foliation is coupled across the northwestern and parts of the southern contact, and likely records a NE-SW shortening component in an overall transtensional regime. Most Golden Horn dikes intruding host rock are felsic, but there are some mafic dikes. These steeply dipping dikes tend to form swarms and strike NE and E-W. The NE-striking dikes reflect regional NW-SE extension. Parts of the southern contact are marked by xenolith-rich zones, which are ~100 m wide and several km long, and lend evidence to stoping as an emplacement mechanism. The diking, stoped blocks, and lack of a ductile aureole are compatible with shallow batholith emplacement models

Showcase Panel III: The States and Administrative Law

2018 National Lawyers Convention Transcripts “We live in a system where regulators make the rules, investigate alleged violations of the rules, and then adjudicate those violations before Administrative Law Judges. If the matter ever gets to court, courts generally defer to the agency on questions of law “and fact.” As a result, agencies know that their regulations are unlikely to face challenge and, if they are challenged, will likely be upheld. In this system, critics argue, the predictable result is more and more irrational regulations and enforcement actions. Arizona has first-of-its-kind legislation to “reverse” Chevron and to instruct courts to give no deference to agency decisions on questions of law. On a related note, Arizona also passed the Right to Earn a Living Act, creating a cause of action to challenge occupational licensing decisions under a heightened standard of review. Some contend that the result of this new law has been significant in that regulators are reviewing and improving rules, or repealing them outright, rather than face litigation. Could these measures serve as a model other states and the federal government in reducing the size and scope of, and otherwise improving, the Administrative State?” Speakers:Prof. Nestor Davidson, Albert A. Walsh Chair in Real Estate, Land Use, and Property Law; Faculty Director, Urban Law Center, Fordham University School of Law Prof. Chris Green, Associate Professor of Law and H.L.A. Hart Scholar in Law and Philosophy, University of Mississippi School of Law Prof. Miriam Seifter, Professor of Law, University of Wisconsin Law School Hon. Jeffrey Sutton, United States Court of Appeals, Sixth Circuit Moderator: Hon. Michael Scudder, United States Court of Appeals, Seventh Circuit Credit: The Federalist Society, https://fedsoc.org/conferences/2018-national-lawyers-convention#agenda-item-showcase-panel-iii-the-states-administrative-la

Effect of pituitary‐dependent hypercortisolism on the survival of dogs treated with radiotherapy for pituitary macroadenomas

Background: Radiotherapy (RT) is an effective treatment for dogs presented with neurologic signs caused by pituitary tumors. However, its impact on the outcome of concurrent pituitary-dependent hypercortisolism (PDH) is controversial. Objectives: Determine whether dogs with PDH have longer survival after pituitary RT compared with dogs with nonhormonally active pituitary masses and to evaluate whether clinical, imaging, and RT variables affect survival. Animals: Ninety-four dogs divided into 2 groups: PDH and non-PDH, based on the presence of hypercortisolism. Forty-seven dogs were allocated to the PDH group and 47 to the non-PDH group. Methods: Retrospective cohort study in which clinical records of dogs undergoing RT for pituitary macroadenomas between 2008 and 2018 at 5 referral centers were retrospectively evaluated. Results: Survival was not statistically different between PDH and non-PDH groups (median survival time [MST], 590 days; 95% confidence interval [CI], 0-830 days and 738 days; 95% CI, 373-1103 days, respectively; P = .4). A definitive RT protocol was statistically associated with longer survival compared with a palliative protocol (MST 605 vs 262 days, P = .05). The only factor statistically associated with survival from multivariate Cox proportional hazard analysis was total radiation dose (Gy) delivered (P < .01). Conclusions and Clinical Importance: No statistical difference in survival was identified between the PDH and non-PDH groups, and longer survival was associated with higher Gy delivered

Transsphenoidal hypophysectomy for the treatment of hypersomatotropism secondary to a pituitary somatotroph adenoma in a dog

AbstractPituitary‐dependent hypersomatotropism is rarely diagnosed in dogs and surgical treatment is not reported. A 6‐year‐10‐month male neutered Patterdale Terrier presented with polyuria, polydipsia, progressive pharyngeal stertor, excessive hair growth and widened facial features and paws. Serum insulin‐like growth factor‐1 concentration via radioimmunoassay was consistent with hypersomatotropism (1783 ng/mL). A pituitary mass was identified on magnetic resonance and computed tomography imaging. Six weeks later, glucosuria, starved hyperglycemia and serum fructosamine above the reference range (467.6 μmol/L, RI 177‐314) were documented, consistent with diabetes mellitus. Transsphenoidal hypophysectomy was performed under general anesthesia without complications. Pituitary histopathology identified an acidophil neoplasm, with positive immunostaining for growth hormone. Postoperatively, there was rapid resolution of clinical, biochemical and morphologic changes of hypersomatotropism with persistence of diabetes mellitus. This case demonstrates successful resolution of hypersomatotropism with ongoing diabetes mellitus in a dog after surgical treatment by transsphenoidal hypophysectomy.</jats:p

HELP: the Herschel Extragalactic Legacy Project

We present the Herschel Extragalactic Legacy Project (HELP). This project collates, curates, homogenizes, and creates derived data products for most of the premium multiwavelength extragalactic data sets. The sky boundaries for the first data release cover 1270 deg2 defined by the Herschel SPIRE extragalactic survey fields; notably the Herschel Multi-tiered Extragalactic Survey (HerMES) and the Herschel Atlas survey (H-ATLAS). Here, we describe the motivation and principal elements in the design of the project. Guiding principles are transparent or ‘open’ methodologies with care for reproducibility and identification of provenance. A key element of the design focuses around the homogenization of calibration, meta data, and the provision of information required to define the selection of the data for statistical analysis. We apply probabilistic methods that extract information directly from the images at long wavelengths, exploiting the prior information available at shorter wavelengths and providing full posterior distributions rather than maximum-likelihood estimates and associated uncertainties as in traditional catalogues. With this project definition paper, we provide full access to the first data release of HELP; Data Release 1 (DR1), including a monolithic map of the largest SPIRE extragalactic field at 385 deg2 and 18 million measurements of PACS and SPIRE fluxes. We also provide tools to access and analyse the full HELP data base. This new data set includes far-infrared photometry, photometric redshifts, and derived physical properties estimated from modelling the spectral energy distributions over the full HELP sky. All the software and data presented is publicly available

Miscellany

Art Writings I Believe Roy F. Powell Awardshttps://digitalcommons.georgiasouthern.edu/miscell/1002/thumbnail.jp

Sensitivity of the Natriuretic Peptide/cGMP System to Hyperammonaemia in Rat C6 Glioma Cells and GPNT Brain Endothelial Cells.

C-type natriuretic peptide (CNP) is the major natriuretic peptide of the central nervous system and acts via its selective guanylyl cyclase-B (GC-B) receptor to regulate cGMP production in neurons, astrocytes and endothelial cells. CNP is implicated in the regulation of neurogenesis, axonal bifurcation, as well as learning and memory. Several neurological disorders result in toxic concentrations of ammonia (hyperammonaemia), which can adversely affect astrocyte function. However, the relationship between CNP and hyperammonaemia is poorly understood. Here, we examine the molecular and pharmacological control of CNP in rat C6 glioma cells and rat GPNT brain endothelial cells, under conditions of hyperammonaemia. Concentration-dependent inhibition of C6 glioma cell proliferation by hyperammonaemia was unaffected by CNP co-treatment. Furthermore, hyperammonaemia pre-treatment (for 1 h and 24 h) caused a significant inhibition in subsequent CNP-stimulated cGMP accumulation in both C6 and GPNT cells, whereas nitric-oxide-dependent cGMP accumulation was not affected. CNP-stimulated cGMP efflux from C6 glioma cells was significantly reduced under conditions of hyperammonaemia, potentially via a mechanism involving changed in phosphodiesterase expression. Hyperammonaemia-stimulated ROS production was unaffected by CNP but enhanced by a nitric oxide donor in C6 cells. Extracellular vesicle production from C6 cells was enhanced by hyperammonaemia, and these vesicles caused impaired CNP-stimulated cGMP signalling in GPNT cells. Collectively, these data demonstrate functional interaction between CNP signalling and hyperammonaemia in C6 glioma and GPNT cells, but the exact mechanisms remain to be established

Natriuretic Peptide Expression and Function in GH3 Somatolactotropes and Feline Somatotrope Pituitary Tumours.

Patients harbouring mutations in genes encoding C-type natriuretic peptide (CNP; NPPC) or its receptor guanylyl cyclase B (GC-B, NPR2) suffer from severe growth phenotypes; loss-of-function mutations cause achondroplasia, whereas gain-of-function mutations cause skeletal overgrowth. Although most of the effects of CNP/GC-B on growth are mediated directly on bone, evidence suggests the natriuretic peptides may also affect anterior pituitary control of growth. Our previous studies described the expression of NPPC and NPR2 in a range of human pituitary tumours, normal human pituitary, and normal fetal human pituitary. However, the natriuretic peptide system in somatotropes has not been extensively explored. Here, we examine the expression and function of the CNP/GC-B system in rat GH3 somatolactotrope cell line and pituitary tumours from a cohort of feline hypersomatotropism (HST; acromegaly) patients. Using multiplex RT-qPCR, all three natriuretic peptides and their receptors were detected in GH3 cells. The expression of Nppc was significantly enhanced following treatment with either 100 nM TRH or 10 µM forskolin, yet only Npr1 expression was sensitive to forskolin stimulation; the effects of forskolin and TRH on Nppc expression were PKA- and MAPK-dependent, respectively. CNP stimulation of GH3 somatolactotropes significantly inhibited Esr1, Insr and Lepr expression, but dramatically enhanced cFos expression at the same time point. Oestrogen treatment significantly enhanced expression of Nppa, Nppc, Npr1, and Npr2 in GH3 somatolactotropes, but inhibited CNP-stimulated cGMP accumulation. Finally, transcripts for all three natriuretic peptides and receptors were expressed in feline pituitary tumours from patients with HST. NPPC expression was negatively correlated with pituitary tumour volume and SSTR5 expression, but positively correlated with D2R and GHR expression. Collectively, these data provide mechanisms that control expression and function of CNP in somatolactotrope cells, and identify putative transcriptional targets for CNP action in somatotropes