Money, Real Interest Rates, and Output: A Reinterpretation of Postwar U.S. Data

This paper reexamines both monthly and quarterly U.S. postwar data to investigate if the observed comovements between money, real interestrates, prices and output are compatible with the money-real interest-output link suggested by existing monetary theories of output, which include both Keynesian and equilibrium models.The major empirical findings are these;1) In both monthly and quarterly data, we cannot reject the hypothesis that the ex ante real rate is exogenous, or Granger-causally prior in the context of a four-variable system which contains money, prices, nominal interest rates and industrial production.2) In quarterly data, there is significantly more information con-tained in either the levels of expected inflation or the innovationof this variable for predicting future output, given current and lagged output, than in any other variable examined (money, actualinflation, nominal interest rates, or ex ante real rates). The effect of an inflation innovation on future output is unambiguously negative. The first result casts strong doubt on the empirical importance of existing monetary theories of output, which imply that money should have a causal role on the ex ante real rates. The second result would appear incompatible with most demand driven models of output.In light of these results, we propose an alternative structural model which can account for the major dynamic interactions among the variables.This model has two central features: i) output is unaffected by money supply;and ii) the money supply process is motivated by short-run price stability.

Massively parallel approximate Gaussian process regression

We explore how the big-three computing paradigms -- symmetric multi-processor (SMC), graphical processing units (GPUs), and cluster computing -- can together be brought to bare on large-data Gaussian processes (GP) regression problems via a careful implementation of a newly developed local approximation scheme. Our methodological contribution focuses primarily on GPU computation, as this requires the most care and also provides the largest performance boost. However, in our empirical work we study the relative merits of all three paradigms to determine how best to combine them. The paper concludes with two case studies. One is a real data fluid-dynamics computer experiment which benefits from the local nature of our approximation; the second is a synthetic data example designed to find the largest design for which (accurate) GP emulation can performed on a commensurate predictive set under an hour.Comment: 24 pages, 6 figures, 1 tabl

Human interleukin-1 receptor antagonist is expressed in liver

AbstractUsing PCR and Northern blot analysis, an IL-1 receptor antagonist specific transcript was amplified from HepG2- and liver mRNA, cDNA clones coding for IL-1 receptor antagonist were isolated from a liver cDNA library and sequence comparison revealed complete identity with the secreted, monocytic form of IL-1 receptor antagonist

Predominantly Fibrous Malignant Mesothelioma in a Cat

Malignant mesotheliomas are rare tumours in domestic cats. They occur within the abdominal or thoracic cavity and are regularly associated with pleural or peritoneal effusions. The histopathological diagnosis can be quite challenging, as these neoplasms may resemble other epithelial or mesenchymal neoplasms. However, differentiation can be achieved by immunohistochemistry in most cases. Here we describe the rare case of a malignant mesothelioma of the fibrous subtype in the thoracic cavity of a cat and discuss differential diagnoses and treatment options for this tumor type

Altered platelet alpha2-adrenoceptors in patients with angina pectoris

The alpha2-adrenoceptor located on noradrenergic neurons regulates the release of norepinephrine by negative feedback. This receptor is also located on human blood platelets, and the number of these receptors is correlated with the plasma norepinephrine content. The purpose of this study was to determine the status of platelet alpha2-adrenoceptors in patients with symptomatic and asymptomatic coronary artery disease. It was hypothesized that patients with symptomatic coronary disease might have a decrease in alpha2-adrenoceptor number that might be related to increased neuronal norepinephrine release. Specific, high-affinity binding of the alpha2-agonist, 3H-clonidine, and the alpha2-antagonist, 3H-yohimbine, to isolated platelet membranes was used to determine the maximal number of binding sites (in fmol/mg protein ± standard error of the mean) and the dissociation constant (in nM) of the alpha2-receptors.In normal subjects, the number of binding sites for 3H-clonidine was 32 ± 2 and the dissociation constant was 5.5 ± 0.6 (n = 26); the maximal number of binding sites for 3H-yohimbine was 165 ±12 and the dissociation constant was 4.0 ± 0.5 (n = 16). In patients with symptomatic coronary artery disease, there was a 38% decrease in 3H-clonidine binding (number of binding sites = 20 ± 3; dissociation constant = 6.6 ± 1.2; n = 9; p < 0.05) and a 44% decrease in 3H-yohimbine binding (number of binding sites = 93 ± 8; dissociation constant = 4.5 ± 0.3; n = 18; p < 0.005). In patients with asymptomatic coronary artery disease, there were no significant changes from the normal population in binding with either ligand (3H-clonidine: number of binding sites = 30 ± 2; dissociation constant = 6.9 ± 1.9; n = 6 and 3H-yohimbine: number of binding sites = 137 ±11; dissociation constant = 5.1 ± 0.6; n = 10). Five patients were studied during a symptomatic phase of their disease and then restudied during a quiescent period. In this group, the number of alpha2-adrenoceptors increased markedly as shown in 3H-clonidine from 16 ± 3 to 29 ± 3 (44%, p < 0.005) and in 3H-yohimbine from 69 ± 22 to 127 ± 17 (46%, p < 0.05).The affinity constants and plasma norepinephrine concentrations did not differ among the three groups. If similar changes in receptor number occur on nerve terminals, this may represent a primary abnormality that permits enhanced release of norepinephrine or a secondary down regulation of receptor number in response to increased synaptic levels of norepinephrine

Nocturia as an Unrecognized Symptom of Uncontrolled Hypertension in Black Men Aged 35 to 49&nbsp;Years.

Background Hypertension is assumed to be asymptomatic. Yet, clinically significant nocturia (≥2 nightly voids) constitutes a putative symptom of uncontrolled hypertension. Black men with hypertension may be prone to nocturia because of blunted nocturnal blood pressure ( BP ) dipping, diuretic drug use for hypertension, and comorbidity that predisposes to nocturia. Here, we test the hypothesis that nocturia is a common and potentially reversible symptom of uncontrolled hypertension in black men. Methods and Results We determined the strength of association between nocturia (≥2 nightly voids) and high BP (≥135/85&nbsp;mm&nbsp;Hg) by conducting in-person health interviews and measuring BP with an automated monitor in a large community-based sample of black men in their barbershops. Because nocturia is prevalent and steeply age-dependent after age 50&nbsp;years, we studied men aged 35 to 49&nbsp;years. Among 1673 black men (mean age, 43±4&nbsp;years [ SD ]), those with hypertension were 56% more likely than men with normotension to have nocturia after adjustment for diabetes mellitus and sleep apnea (adjusted odds ratio, 1.56; 95% CI , 1.25-1.94 [ P&lt;0.0001]). Nocturia prevalence varied by hypertension status, ranging from 24% in men with normotension to 49% in men whose hypertension was medically treated but uncontrolled. Men with untreated hypertension were 39% more likely than men with normotension to report nocturia ( P=0.02), whereas men whose hypertension was treated and controlled were no more likely than men with normotension to report nocturia ( P=0.69). Conclusions Uncontrolled hypertension was an independent determinant of clinically important nocturia in a large cross-sectional community-based study of non-Hispanic black men aged 35 to 49&nbsp;years. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unqiue identifier: NCT 02321618

A human polymorphism affects NEDD4L subcellular targeting by leading to two isoforms that contain or lack a C2 domain

<p>Abstract</p> <p>Background</p> <p>Ubiquitination serves multiple cellular functions, including proteasomal degradation and the control of stability, function, and intracellular localization of a wide variety of proteins. NEDD4L is a member of the HECT class of E3 ubiquitin ligases. A defining feature of NEDD4L protein isoforms is the presence or absence of an amino-terminal C2 domain, a class of subcellular, calcium-dependent targeting domains. We previously identified a common variant in human <it>NEDD4L </it>that generates isoforms that contain or lack a C2 domain.</p> <p>Results</p> <p>To address the potential functional significance of the <it>NEDD4L </it>common variant on NEDD4L subcellular localization, NEDD4L isoforms that either contained or lacked a C2 domain were tagged with enhanced green fluorescent protein, transfected into <it>Xenopus laevis </it>kidney epithelial cells, and imaged by performing confocal microscopy on live cells. We report that the presence or absence of this C2 domain exerts differential effects on the subcellular distribution of NEDD4L, the ability of C2 containing and lacking NEDD4L isoforms to mobilize in response to a calcium stimulus, and the intracellular transport of subunits of the NEDD4L substrate, ENaC. Furthermore, the ability of the C2-containing isoform to influence β-ENaC mobilization from intracellular pools involves the NEDD4L active site for ubiquitination. We propose a model to account for the potential impact of this common genetic variant on protein function at the cellular level.</p> <p>Conclusion</p> <p>NEDD4L isoforms that contain or lack a C2 domain target different intracellular locations. Additionally, whereas the C2-containing NEDD4L isoform is capable of shuttling between the plasma membrane and intracellular compartments in response to calcium stimulus the C2-lacking isoform can not. The C2-containing isoform differentially affects the mobilization of ENaC subunits from intracellular pools and this trafficking step requires NEDD4L ubiquitin ligase activity. This observation suggests a new mechanism for the requirement for the PY motif in cAMP-mediated exocytosis of ENaC. We have elucidated how a common genetic variant can underlie significant functional diversity in NEDD4L at the cellular level. We propose a model that describes how that functional variation may influence blood pressure. Moreover, our observations regarding differential function of the NEDD4L isoforms may impact other aspects of physiology that involve this ubiquitin ligase.</p

A Modular System of Algorithms for Unconstrained Minimization ; CU-CS-240-82

We describe a new package, UNCMIN, for finding a local minimizer of a real valued function of more than one variable. The novel feature of UNCMIN is that it is a modular system of algorithms, containing three different step selection strategies (line search, dogleg, and optimal step) that may be combined with either analytic or finite difference gradient evaluation and with either analytic, finite difference, or BFGS Hessian approximation. We present the results of a comparison of the three step selection strategies on the problems in More, Garbow, and Hillstrom in two separate cases: using finite difference gradients and Hessians, and using finite difference gradients with BFGS Hessian approximations. We also describe a second package, REVMIN, that uses optimization algorithms identical to UNCMIN but obtains values of user-supplied functions by reverse communication.</jats:p