In Defense of Property

This Article responds to an emerging view, in scholarship and popular society, that it is normatively undesirable to employ property law as a means of protecting indigenous cultural heritage. Recent critiques suggest that propertizing culture impedes the free flow of ideas, speech, and perhaps culture itself. In our view, these critiques arise largely because commentators associate property with a narrow model of individual ownership that reflects neither the substance of indigenous cultural property claims nor major theoretical developments in the broader field of property law. Thus, departing from the individual rights paradigm, our Article situates indigenous cultural property claims, particularly those of American Indians, in the interests of peoples rather than persons, arguing that such cultural properties are integral to indigenous group identity or peoplehood, and deserve particular legal protection. Further, we observe that whereas individual rights are overwhelmingly advanced by property law\u27s dominant ownership model, which consolidates control in the title-holder, indigenous peoples often seek to fulfill an ongoing duty of care toward cultural resources in the absence of title. To capture this distinction, we offer a stewardship model of property to explain and justify indigenous peoples\u27 cultural property claims in terms of non-owners\u27 fiduciary obligations toward cultural resources. We posit that re-envisioning cultural property law in terms of peoplehood and stewardship more fully illuminates both the particular nature of indigenous claims and the potential for property law itself to embrace a broader and more flexible set of interests

MAP7 regulates axon morphogenesis by recruiting kinesin-1 to microtubules and modulating organelle transport.

Neuronal cell morphogenesis depends on proper regulation of microtubule-based transport, but the underlying mechanisms are not well understood. Here, we report our study of MAP7, a unique microtubule-associated protein that interacts with both microtubules and the motor protein kinesin-1. Structure-function analysis in rat embryonic sensory neurons shows that the kinesin-1 interacting domain in MAP7 is required for axon and branch growth but not for branch formation. Also, two unique microtubule binding sites are found in MAP7 that have distinct dissociation kinetics and are both required for branch formation. Furthermore, MAP7 recruits kinesin-1 dynamically to microtubules, leading to alterations in organelle transport behaviors, particularly pause/speed switching. As MAP7 is localized to branch sites, our results suggest a novel mechanism mediated by the dual interactions of MAP7 with microtubules and kinesin-1 in the precise control of microtubule-based transport during axon morphogenesis

Optimizing Guideline-Recommended Antibiotic Doses for Pediatric Infective Endocarditis

The American Heart Association recently published an updated scientific statement on the management of infective endocarditis in childhood. The recommendations included for vancomycin, aminoglycoside, and β-lactam dosing and monitoring are based primarily on expert opinion and do not consider available evidence for dose optimization based on pharmacokinetic and pharmacodynamic principles in pediatric patients. This is concerning because even when clinically necessary, some practitioners may be hesitant to deviate from guideline-recommended doses. In this perspective, we highlight potential areas for improvement in the statement-recommended doses and summarize evidence supporting antibiotic dosing optimization. The addition of a pediatric clinical pharmacist with expertise in antibiotic dosing to the panel would be beneficial for future updates

Genesis in Hyperreality: Legitimizing Disingenuous Controversy at the Creation Museum

This essay analyzes the argumentative structure of the Answers in Genesis ministry\u27s Creation Museum in Petersburg, Kentucky. Founded by a $27 million grant, the 70,000 square-foot museum appropriates the stylistic and authoritative signifiers of natural history museums, complete with technically proficient hyperreal displays and modern curatorial techniques. In this essay, we argue that the museum provides a culturally authoritative space in which Young Earth Creationists can visually craft the appearance that there is an ongoing scientific controversy over matters long settled in the scientific community (evolution), or what scholars call a disingenuous or manufactured controversy. We analyze the displays and layout as argumentative texts to explain how the museum negotiates its own purported status as a museum with its ideological mission to promulgate biblical literalism. The Creation Museum provides an exemplary case study in how the rhetoric of controversy is used to undermine existing scientific knowledge and legitimize pseudoscientific beliefs. This essay contributes to argumentation studies by explaining how religious fundamentalists simulate the structure of a contentious argument by adopting the material signifiers of expert authority to ground their claims

Rituximab induced pulmonary edema managed with extracorporeal life support

Though rare, rituximab has been reported to induce severe pulmonary edema. We describe the first report of ECLS utilization for this indication. A 31-year-old female with severe thrombotic thrombocytopenic purpura developed florid pulmonary edema after rituximab infusion. Despite advanced ventilatory settings, she developed severe respiratory acidosis and remained hypoxemic with a significant vasopressor requirement. Since her pulmonary insult was likely transient, ECLS was considered. Due to combined cardiorespiratory failure, she received support with peripheral venoarterial ECLS. During her ECLS course, she received daily plasmapheresis and high dose steroids. Her pulmonary function recovered and she was decannulated after 8 days. She was discharged after 23 days without residual sequelae

Understanding Current Signals Induced by Drifting Electrons

Consider an electron drifting in a gas toward a collection electrode. A common misconception is that the electron produces a detectable signal only upon arrival at the electrode. In fact, the situation is quite the opposite. The electron induces a detectable current in the electrode as soon as it starts moving through the gas. This induced current vanishes when the electron arrives at the plate. To illustrate this phenomenon experimentally, we use a gas-filled parallel plate ionization chamber and a collimated $^{241}$Am alpha source, which produces a track of a fixed number of ionization electrons at a constant distance from the collection electrode. We find that the detected signal from the ionization chamber grows with the electron drift distance, as predicted by the model of charge induction, and in conflict with the idea that electrons are detectable upon arrival at the collection plate.Comment: 21 pages, 12 figure

Blunted Cystine–Glutamate Antiporter Function in the Nucleus Accumbens Promotes Cocaine-induced Drug Seeking

Repeated cocaine alters glutamate neurotransmission, in part, by reducing cystine–glutamate exchange via system xc−, which maintains glutamate levels and receptor stimulation in the extrasynaptic compartment. In the present study, we undertook two approaches to determine the significance of plasticity involving system xc−. First, we examined whether the cysteine prodrug N-acetylcysteine attenuates cocaine-primed reinstatement by targeting system xc−. Rats were trained to self-administer cocaine (1 mg/kg/200 μl, i.v.) under extended access conditions (6 h/day). After extinction training, cocaine (10 mg/kg, i.p.) primed reinstatement was assessed in rats pretreated with N-acetylcysteine (0–60 mg/kg, i.p.) in the presence or absence of the system xc− inhibitor (S)-4-carboxyphenylglycine (CPG; 0.5 μM; infused into the nucleus accumbens). N-acetylcysteine attenuated cocaine-primed reinstatement, and this effect was reversed by co-administration of CPG. Secondly, we examined whether reduced system xc− activity is necessary for cocaine-primed reinstatement. To do this, we administered N-acetylcysteine (0 or 90 mg/kg, i.p.) prior to 12 daily self-administration sessions (1 mg/kg/200 μl, i.v.; 6 h/day) since this procedure has previously been shown to prevent reduced activity of system xc−. On the reinstatement test day, we then acutely impaired system xc− in some of the rats by infusing CPG (0.5 μM) into the nucleus accumbens. Rats that had received N-acetylcysteine prior to daily self-administration sessions exhibited diminished cocaine-primed reinstatement; this effect was reversed by infusing the cystine–glutamate exchange inhibitor CPG into the nucleus accumbens. Collectively these data establish system xc− in the nucleus accumbens as a key mechanism contributing to cocaine-primed reinstatement

Trends and Variation in End-of-Life Care for Medicare Beneficiaries With Severe Chronic Illness

Provides an updated analysis of regional and hospital variations in end-of-life care for Medicare beneficiaries with chronic illnesses, including percentage of hospital deaths, days in intensive care units, and physician labor per patient

The SUMO Ligase Protein Inhibitor of Activated STAT 1 (PIAS1) is a constituent PML-NB protein that contributes to the intrinsic antiviral immune response to herpes simplex virus 1 (HSV-1)

Aspects of intrinsic antiviral immunity are mediated by promyelocytic leukaemia (PML)-nuclear body (PML-NB) constituent proteins. During herpesvirus infection, these antiviral proteins are independently recruited to nuclear domains that contain infecting viral genomes to cooperatively promote viral genome silencing. Central to the execution of this particular antiviral response is the small ubiquitin-like modifier (SUMO) signalling pathway. However, the participating SUMOylation enzymes are not fully characterized. We identify the SUMO ligase Protein Inhibitor of Activated STAT1 (PIAS1) as a constituent PML-NB protein. We show that PIAS1 localizes at PML-NBs in a SUMO interaction motif (SIM)-dependent manner that requires SUMOylated or SUMOylation competent PML. Following infection with herpes simplex virus 1 (HSV-1), PIAS1 is recruited to nuclear sites associated with viral genome entry in a SIM-dependent manner, consistent with the SIM-dependent recruitment mechanisms of other well characterized PML-NB proteins. In contrast to Daxx and Sp100, however, the recruitment of PIAS1 is enhanced by PML. PIAS1 promotes the stable accumulation of SUMO1 at nuclear sites associated with HSV-1 genome entry, whereas the accumulation of other evaluated PML-NB proteins occurs independently of PIAS1. We show that PIAS1 cooperatively contributes to HSV-1 restriction through mechanisms that are additive to those of PML and cooperative with those of PIAS4. The antiviral mechanisms of PIAS1 are counteracted by ICP0, the HSV-1 SUMO-targeted ubiquitin ligase, which disrupts the recruitment of PIAS1 to nuclear domains that contain infecting HSV-1 genomes through mechanisms that do not directly result in PIAS1 degradation

Consanguinity and rare mutations outside of MCCC genes underlie nonspecific phenotypes of MCCD.

Purpose3-Methylcrotonyl-CoA carboxylase deficiency (MCCD) is an autosomal recessive disorder of leucine catabolism that has a highly variable clinical phenotype, ranging from acute metabolic acidosis to nonspecific symptoms such as developmental delay, failure to thrive, hemiparesis, muscular hypotonia, and multiple sclerosis. Implementation of newborn screening for MCCD has resulted in broadening the range of phenotypic expression to include asymptomatic adults. The purpose of this study was to identify factors underlying the varying phenotypes of MCCD.MethodsWe performed exome sequencing on DNA from 33 cases and 108 healthy controls. We examined these data for associations between either MCC mutational status, genetic ancestry, or consanguinity and the absence or presence/specificity of clinical symptoms in MCCD cases.ResultsWe determined that individuals with nonspecific clinical phenotypes are highly inbred compared with cases that are asymptomatic and healthy controls. For 5 of these 10 individuals, we discovered a homozygous damaging mutation in a disease gene that is likely to underlie their nonspecific clinical phenotypes previously attributed to MCCD.ConclusionOur study shows that nonspecific phenotypes attributed to MCCD are associated with consanguinity and are likely not due to mutations in the MCC enzyme but result from rare homozygous mutations in other disease genes.Genet Med 17 8, 660-667