Neither Realistic nor Constitutionally sound: The Problem of the FCC\u27s Community Standard for Broadcast Indecency Determinations

The Federal Communications Commission exercises the power to regulate the broadcast of constitutionally protected indecent speech under a standard upheld by the U.S. Supreme Court in its 1978 decision in FCC v. Pacifica Foundation. In the thirty years since that decision, however, the FCC has pursued an increasingly idiosyncratic application of the Pacifica test that disposes with local community standards as the legal benchmark of indecency. In doing so, the FCC\u27s approach rejects the judicial sources that originally legitimized the Pacifica indecency test, conflicts with the statutory authority by which the FCC regulates broadcasting generally, and contradicts the Court\u27s specific and more recent rulings on indecency in the context of other media. In its upcoming review of Fox Television Stations, Inc. v. FCC, the Court will have an opportunity to correct the anomalies of the FCC\u27s broadcast indecency regime. The Court should require that the FCC refer to local community standards in making its indecency determinations and bring the Commission\u27s exercise of this authority into line with governing principles of First Amendment law

OUTSIDE THE ECHO CHAMBER: A RESPONSE TO THE “CONSENSUS STATEMENT ON ABUSIVE HEAD TRAUMA IN INFANTS AND YOUNG CHILDREN”

OUTSIDE THE ECHO CHAMBER: A RESPONSE TO THE “CONSENSUS STATEMENT ON ABUSIVE HEAD TRAUMA IN INFANTS AND YOUNG CHILDREN”

Coil Condensation Detection For Humidity Control

Conditioning the air inside a building requires controlling both primary components of its enthalpy: temperature and humidity. Temperature sensors used in buildings are sufficiently reliable, durable, accurate, and precise that they can be relied on for sophisticated building control systems. Commercial resistive and capacitive humidity sensors become inaccurate near saturation and often fail permanently when exposed to liquid water. Excessive humidity can cause both occupant discomfort and permanent damage to buildings. In American climates dehumidification accounts for the vast majority of the energy used to control humidity. Therefore, a sensor which can survive and accurately measure humidity in hot, wet conditions will allow considerable savings. Simulations of the energy consumption and savings available from enthalpy economizer control and supply air temperature resets were performed for buildings in Houston, Dallas, and Philadelphia. Temperature economizers were shown to attain between 90% and 95% of the savings of an enthalpy economizer. A spreadsheet simulation of enthalpy economizer use showed that the savings available are heavily dependent on the ability to avoid its use on very hot, humid days. A newly-designed condensation sensor was developed for this project. It relies on the order-of-magnitude difference in AC reactance between humid air and liquid water. When installed on an AHU, it detects water condensing off the cooling coil as the temperature of the air drops below the dew point. Electronics were designed to provide the 0.25 V, 131 kHz current required and to obtain a 0 V output when dry and a 5 V output when wet. A field reliability test was successfully performed with the sensor passively monitoring the transitions from wet to dry at Langford Building A and the Jack E. Brown Building at Texas A&M University, College Station, TX. The sensor was shown to be able to provide the reliable state change detection needed to control an economizer. The main limitation of this sensor is slow response on dry-to-wet and wet-to-dry transitions. Most measured dry-to-wet response times were between 5 and 10 minutes, which were driven by the time required to saturate the cooling coil

Focus on the Role of D-serine and D-amino Acid Oxidase in Amyotrophic Lateral Sclerosis/Motor Neuron Disease (ALS)

Highly pathogenic avian influenza (HPAI) H5N1 virus has been circulating in Vietnam since 2003, while outbreaks of HPAI H5N6 virus are more recent, having only been reported since 2014. Although the spatial distribution of H5N1 outbreaks and risk factors for virus occurrence have been extensively studied, there have been no comparative studies for H5N6. Data collected through active surveillance of Vietnamese live-bird markets (LBMs) between 2011 and 2015 were used to explore and compare the spatio-temporal distributions of H5N1- and H5N6-positive LBMs. Conditional autoregressive models were developed to quantify spatio-temporal associations between agro-ecological factors and the two HPAI strains using the same set of predictor variables. Unlike H5N1, which exhibited a strong north-south divide, with repeated occurrence in the extreme south of a cluster of high-risk provinces, H5N6 was homogeneously distributed throughout Vietnam. Similarly, different agro-ecological factors were associated with each strain. Sample collection in the months of January and February and higher average maximum temperature were associated with higher likelihood of H5N1 positive market-day status. The likelihood of market-days being positive for H5N6 increased with decreased river density, and with successive Rounds of data collection. This study highlights marked differences in spatial patterns and risk factors for H5N1 and H5N6 in Vietnam, suggesting the need for tailored surveillance and control approaches

Metformin Treatment Has No Beneficial Effect in a Dose-Response Survival Study in the SOD1G93A Mouse Model of ALS and Is Harmful in Female Mice

Background: Amyotrophic Lateral Sclerosis (ALS) is a devastating neurological disorder characterized by selective degeneration of upper and lower motor neurons. The primary triggers for motor neuron degeneration are unknown but inflammation, oxidative stress and mitochondrial defects have been identified as potential contributing factors. Metformin is an anti-type II diabetes drug that has anti-inflammatory and anti-oxidant properties, can bring about mitochondrial biogenesis and has been shown to attenuate pathology in mouse models of Huntington’s disease and multiple sclerosis. We therefore hypothesized that it might increase survival in the SOD1G93A murine model of ALS. Methodology/Principal Findings: Treatment of male and female SOD1G93A mice (n = $6 per sex) with 2 mg/ml metformin in the drinking water from 35 days, resulted in a significant increase in motor unit survival, as measured by in vivo electrophysiology at 100 days, in male EDL muscles (24+/22 vs. 14+/22 motor units, p,0.005) and female TA muscles (21+/ 21 vs. 15+/22 motor units, P = 0.0134). We therefore continued to test the effect of 0.5, 2 and 5 mg/ml metformin in the drinking water from 35 days on disease onset and progression (identified by twice weekly determination of weight and neurological score) as well as survival in male and female SOD1G93A mice (n =$14 per sex). Results for all groups were compared using Kaplan-Meier time to event analyses. In this survival study, metformin was unable to reduce pathology at any dose and had an unexpected dose-dependent negative effect on the onset of neurological symptoms (P = 0.0236) and on disease progression (P = 0.0362) in female mice. Conclusions/Significance: This study suggests that metformin is a poor candidate for clinical trial in ALS patients and that the possibility of harmful effects of metformin in female ALS patients with type II diabetes should be investigated

Characterisation of the pathogenic effects of the in vivo expression of an ALS-linked mutation in D-amino acid oxidase: Phenotype and loss of spinal cord motor neurons

Amyotrophic lateral sclerosis (ALS) is the most common adult-onset neuromuscular disorder characterised by selective loss of motor neurons leading to fatal paralysis. Current therapeutic approaches are limited in their effectiveness. Substantial advances in understanding ALS disease mechanisms has come from the identification of pathogenic mutations in dominantly inherited familial ALS (FALS). We previously reported a coding mutation in D-amino acid oxidase (DAOR199W) associated with FALS. DAO metabolises D-serine, an essential co-agonist at the N-Methyl-D-aspartic acid glutamate receptor subtype (NMDAR). Using primary motor neuron cultures or motor neuron cell lines we demonstrated that expression of DAOR199W, promoted the formation of ubiquitinated protein aggregates, activated autophagy and increased apoptosis. The aim of this study was to characterise the effects of DAOR199W in vivo, using transgenic mice overexpressing DAOR199W. Marked abnormal motor features, e.g. kyphosis, were evident in mice expressing DAOR199W, which were associated with a significant loss (19%) of lumbar spinal cord motor neurons, analysed at 14 months. When separated by gender, this effect was greater in females (26%; p< 0.0132). In addition, we crossed the DAOR199W transgenic mouse line with the SOD1G93A mouse model of ALS to determine whether the effects of SOD1G93A were potentiated in the double transgenic line (DAOR199W/SOD1G93A). Although overall survival was not affected, onset of neurological signs was significantly earlier in female double transgenic animals than their female SOD1G93A littermates (125 days vs 131 days, P = 0.0239). In summary, some significant in vivo effects of DAOR199W on motor neuron function (i.e. kyphosis and loss of motor neurons) were detected which were most marked in females and could contribute to the earlier onset of neurological signs in double transgenic females compared to SOD1G93A littermates, highlighting the importance of recognizing gender effects present in animal models of ALS

Poloxomer 188 Has a Deleterious Effect on Dystrophic Skeletal Muscle Function

Duchenne muscular dystrophy (DMD) is an X-linked, fatal muscle wasting disease for which there is currently no cure and limited palliative treatments. Poloxomer 188 (P188) is a tri-block copolymer that has been proposed as a potential treatment for cardiomyopathy in DMD patients. Despite the reported beneficial effects of P188 on dystrophic cardiac muscle function, the effects of P188 on dystrophic skeletal muscle function are relatively unknown. Mdx mice were injected intraperitoneally with 460 mg/kg or 30 mg/kg P188 dissolved in saline, or saline alone (control). The effect of single-dose and 2-week daily treatment was assessed using a muscle function test on the Tibialis Anterior (TA) muscle in situ in anaesthetised mice. The test comprises a warm up, measurement of the force-frequency relationship and a series of eccentric contractions with a 10% stretch that have previously been shown to cause a drop in maximum force in mdx mice. After 2 weeks of P188 treatment at either 30 or 460 mg/kg/day the drop in maximum force produced following eccentric contractions was significantly greater than that seen in saline treated control mice (P = 0.0001). Two week P188 treatment at either dose did not significantly change the force-frequency relationship or maximum isometric specific force produced by the TA muscle. In conclusion P188 treatment increases susceptibility to contraction-induced injury following eccentric contractions in dystrophic skeletal muscle and hence its suitability as a potential therapeutic for DMD should be reconsidered