PRICE VERSUS QUOTA REDUCTIONS: U.S. FLUE-CURED TOBACCO POLICY

Declining domestic cigarette consumption, increased global competition, and loss of import restrictions indicate decreased demand for U.S. flue-cured tobacco. The effects of 10% declines in domestic and export demand are evaluated under a policy of reducing quota to maintain price versus a policy of allowing price to fall to maintain quota. Changes in prices, quantities, revenues, and economic rents are simulated. Losses to nonfarming quota owners are minimized under a policy of price maintenance, while losses in revenues to tobacco-producing areas are minimized by a policy of quota maintenance. Aggregate losses to tobacco growers are greater under a policy of quota maintenance.Flue-cured, Policy, Price reduction, Quota, Tobacco, Agricultural and Food Policy,

Penalties Off the Field: Exploring Social Media Policies for Student Athletes at Universities

University student-athletes and their teams rely on social media to communicate with their fans, and these interactions may be beneficial for teams and athletes alike. But social media use also carries risk if an offensive photo or statement goes viral. Using frameworks from social cognitive, privacy, and uses and gratification theories, this article captures the status of university social media policies for athletes through content analysis and interviews. The findings outline strategies for monitoring, penalizing and rewarding athletes for their online interactions

Innovations in Practice: The Relationship Between Sleep Disturbances, Depression, and Interpersonal Functioning in Treatment for Adolescent Depression

Sleep disturbance is frequently comorbid with depression and sleep complaints are the most common residual symptoms after treatment among adolescents with depression. The present analyses investigated the effect of sleep disturbance in depressed adolescents treated with interpersonal psychotherapy for adolescents (IPT-A) versus treatment as usual (TAU) in school-based mental health clinics

Foreground Subtraction in Intensity Mapping with the SKA

21cm intensity mapping experiments aim to observe the diffuse neutral hydrogen (HI) distribution on large scales which traces the Cosmic structure. The Square Kilometre Array (SKA) will have the capacity to measure the 21cm signal over a large fraction of the sky. However, the redshifted 21cm signal in the respective frequencies is faint compared to the Galactic foregrounds produced by synchrotron and free-free electron emission. In this article, we review selected foreground subtraction methods suggested to effectively separate the 21cm signal from the foregrounds with intensity mapping simulations or data. We simulate an intensity mapping experiment feasible with SKA phase 1 including extragalactic and Galactic foregrounds. We give an example of the residuals of the foreground subtraction with a independent component analysis and show that the angular power spectrum is recovered within the statistical errors on most scales. Additionally, the scale of the Baryon Acoustic Oscillations is shown to be unaffected by foreground subtraction.Comment: This article is part of the 'SKA Cosmology Chapter, Advancing Astrophysics with the SKA (AASKA14), Conference, Giardini Naxos (Italy), June 9th-13th 2014

The teaching practice of Building on MOSTs

This research report is based on work supported by the U.S. National Science Foundation (NSF) under Grant Nos. DRL-1720410, DRL-1720566, and DRL-1720613

A de novo dominant mutation in KIF1A associated with axonal neuropathy, spasticity and autism spectrum disorder

Mutations in the kinesin family member 1A (KIF1A) gene have been associated with a wide range of phenotypes including recessive mutations causing hereditary sensory neuropathy and hereditary spastic paraplegia and de novo dominant mutations causing a more complex neurological disorder affecting both the central and peripheral nervous system. We identified by exome sequencing a de novo dominant missense variant, (c.38G>A, p.R13H), within an ATP binding site of the kinesin motor domain in a patient manifesting a complex phenotype characterized by autism spectrum disorder (ASD), spastic paraplegia and axonal neuropathy. The presence of ASD distinguishes this case from previously reported patients with de novo dominant mutations in KIF1A

Hyperoxia Causes Mitochondrial Fragmentation in Pulmonary Endothelial Cells by Increasing Expression of Pro-Fission Proteins

Objective—We explored mechanisms that alter mitochondrial structure and function in pulmonary endothelial cells (PEC) function after hyperoxia. Approach and Results—Mitochondrial structures of PECs exposed to hyperoxia or normoxia were visualized and mitochondrial fragmentation quantified. Expression of pro-fission or fusion proteins or autophagy-related proteins were assessed by Western blot. Mitochondrial oxidative state was determined using mito-roGFP. Tetramethylrhodamine methyl ester estimated mitochondrial polarization in treatment groups. The role of mitochondrially derived reactive oxygen species in mt-fragmentation was investigated with mito-TEMPOL and mitochondrial DNA (mtDNA) damage studied by using ENDO III (mt-tat-endonuclease III), a protein that repairs mDNA damage. Drp-1 (dynamin-related protein 1) was overexpressed or silenced to test the role of this protein in cell survival or transwell resistance. Hyperoxia increased fragmentation of PEC mitochondria in a time-dependent manner through 48 hours of exposure. Hyperoxic PECs exhibited increased phosphorylation of Drp-1 (serine 616), decreases in Mfn1 (mitofusion protein 1), but increases in OPA-1 (optic atrophy 1). Pro-autophagy proteins p62 (LC3 adapter–binding protein SQSTM1/p62), PINK-1 (PTEN-induced putative kinase 1), and LC3B (microtubule-associated protein 1A/1B-light chain 3) were increased. Returning cells to normoxia for 24 hours reversed the increased mt-fragmentation and changes in expression of pro-fission proteins. Hyperoxia-induced changes in mitochondrial structure or cell survival were mitigated by antioxidants mito-TEMPOL, Drp-1 silencing, or inhibition or protection by the mitochondrial endonuclease ENDO III. Hyperoxia induced oxidation and mitochondrial depolarization and impaired transwell resistance. Decrease in resistance was mitigated by mito-TEMPOL or ENDO III and reproduced by overexpression of Drp-1. Conclusions—Because hyperoxia evoked mt-fragmentation, cell survival and transwell resistance are prevented by ENDO III and mito-TEMPOL and Drp-1 silencing, and these data link hyperoxia-induced mt-DNA damage, Drp-1 expression, mt-fragmentation, and PEC dysfunction