Children in Chains: Indiscriminate Shackling of Juveniles

The U.S. Supreme Court has not yet addressed indiscriminate shackling of juveniles, but it has done so regarding adults. This Article begins by reviewing the Court‘s rulings on blanket shackling of adults in Part II. Part III reviews state appellate court decisions that have addressed the use of restraints on juveniles in court. Part IV makes the argument that indiscriminate shackling of children is unconstitutional because it violates the Fifth, Sixth, and Fourteenth Amendments (due process of law and right to counsel) to the U.S. Constitution. Part IV also examines the special characteristics of adolescents that support this argument. Part V of this Article surveys each States‘ current juvenile courtroom shackling practices and classifies those practices into four categories: (1) States that permit blanket shackling of juveniles; (2) States that do not permit blanket shackling via state legislation or regulation; (3) States that do not permit blanket shackling via written court policy; (4) States where appellate case law has prohibited indiscriminate shackling of juveniles; and (5) States that have pending legislation which will prohibit indiscriminate shackling. Florida has enacted legislation and Massachusetts has instituted a court policy, both of which address the issue of indiscriminate shackling of juveniles in court. Part VI analyzes and compares Massachusetts‘ court policy to Florida legislation

Hope : pedagogy in a despairing world

The first chapter asserts that we have exhausted our cultural repertoire, careening through both modem certainty and postmodern disorder without finding hope-the things in and for which we have been told to hope do not keep us from despair. The chapter critiques failed definitions of "hope" and proposes boundaries for this work which lead to a quest theme, and a series of questions against which to test whatever might be found in that quest. The second chapter expands the theme of cultural exhaustion, maintaining that, if one is to avoid despair, the discovery by an individual of this cultural failure must be intentional, the product of a search which involves bringing conscious awareness to what are usually automatistic behaviors. The necessary type of consciousness for that search is found to occur in an eclectic group of anthropologists, critical theorists, psychologists and iconoclasts-a group whose work generally includes a critique of modernist rationality, scientism, and control, as well as a critique of the relativism endemic in postmodernism. To render this search more generally accessible, a similar type of consciousness is sought-and found-in several Christian theologians, of a generally prophetic or liberation bent. Others, who stand against such "God talk", are acknowledged, and a path around some of their objections sought in a negative theology, requiring the sort of approach most familiar as "skillful means" in Zen practice

The Deacetylase HDAC6 Regulates Aggresome Formation and Cell Viability in Response to Misfolded Protein Stress

AbstractThe efficient clearance of cytotoxic misfolded protein aggregates is critical for cell survival. Misfolded protein aggregates are transported and removed from the cytoplasm by dynein motors via the microtubule network to a novel organelle termed the aggresome where they are processed. However, the means by which dynein motors recognize misfolded protein cargo, and the cellular factors that regulate aggresome formation, remain unknown. We have discovered that HDAC6, a microtubule-associated deacetylase, is a component of the aggresome. We demonstrate that HDAC6 has the capacity to bind both polyubiquitinated misfolded proteins and dynein motors, thereby acting to recruit misfolded protein cargo to dynein motors for transport to aggresomes. Indeed, cells deficient in HDAC6 fail to clear misfolded protein aggregates from the cytoplasm, cannot form aggresomes properly, and are hypersensitive to the accumulation of misfolded proteins. These findings identify HDAC6 as a crucial player in the cellular management of misfolded protein-induced stress

Designing Weather Insurance Contracts for Farmers in Malawi, Tanzania and Kenya: Final Report to the Commodity Risk Management Group, ARD, World Bank

This report presents project products to the Commodity Risk Management Group of the World Bank for the development and evaluation of index insurance contracts for smallholder farmers in Malawi, Tanzania, and Kenya. The development of some products we are providing was supported at no cost by the NSF-funded Center for Research on Environmental Decisions. Index insurance is a relatively new weather risk management tool. While traditional insurance insures against crop failure, index insurance insures for a specific event or risk, such as rainfall deficits. The index insurance can be more cost effective since there is no need for in-field assessment of damage because payouts are triggered by weather data directly. Index insurance addresses two problems associated with traditional crop insurance: moral hazard (incentives for a farmer to let a crop die in order to get an insurance payout) and adverse selection (in which insurance is priced based on the risks of the entire population but only the most vulnerable farmers purchase insurance). However, index insurance only provides partial protection and is therefore only one part of a complete risk management package. It is critical that the client have a comprehensive understanding of exactly what risks are covered (and what risks are not covered) by the index product so that clients can effectively use the insurance as a part of their risk management system. Products must be transparent and completely understandable to the client or they will not be able to play their proper role

Ocular Itch Relief with Alcaftadine 0.25% Versus Olopatadine 0.2% in Allergic Conjunctivitis: Pooled Analysis of Two Multicenter Randomized Clinical Trials

Introduction: The efficacy and safety of the once-daily topical ophthalmic solutions, alcaftadine 0.25% and olopatadine 0.2%, in preventing ocular itching associated with allergic conjunctivitis were evaluated. Methods: Pooled analysis was conducted of two double-masked, multicenter, active- and placebo-controlled studies using the conjunctival allergen challenge (CAC) model of allergic conjunctivitis. Subjects were randomized 1:1:1 to receive alcaftadine 0.25%, olopatadine 0.2%, or placebo. The primary efficacy measure was subject-evaluated mean ocular itching at 3 min post-CAC and 16 h after treatment instillation. Secondary measures included ocular itching at 5 and 7 min post-CAC. Ocular itch was determined over all time points measured (3, 5, and 7 min) post-CAC and the proportion of subjects with minimal itch (itch score <1) and zero itch (itch score = 0) was also assessed. Results: A total of 284 subjects were enrolled in the two studies. At 3 min post-CAC and 16 h after treatment instillation, alcaftadine 0.25% achieved a significantly lower mean itch score compared with olopatadine 0.2% (0.50 vs. 0.87, respectively; P = 0.0006). Alcaftadine demonstrated a significantly lower mean itch score over all time points compared with olopatadine (0.68 vs. 0.92, respectively; P = 0.0390); both alcaftadine- and olopatadine-treated subjects achieved significantly lower overall mean ocular itching scores compared with placebo (2.10; P < 0.0001 for both actives). Minimal itch over all time points was reported by 76.1% of alcaftadine-treated subjects compared with 58.1% of olopatadine-treated subjects (P = 0.0121). Treatment with alcaftadine 0.25% and olopatadine 0.2% was safe and well tolerated; no serious adverse events were reported. Conclusion: Once-daily alcaftadine 0.25% ophthalmic solution demonstrated greater efficacy in prevention of ocular itching compared with olopatadine 0.2% at 3 min post-CAC (primary endpoint), and over all time points, 16 h post-treatment instillation. Alcaftadine and olopatadine both provided effective relief compared with placebo and were generally well tolerated. Electronic supplementary material The online version of this article (doi:10.1007/s12325-014-0155-3) contains supplementary material, which is available to authorized users

Dimerization of the transmembrane domain of amyloid precursor proteins and familial Alzheimer's disease mutants

<p>Abstract</p> <p>Background</p> <p>Amyloid precursor protein (APP) is enzymatically cleaved by γ-secretase to form two peptide products, either Aβ40 or the more neurotoxic Aβ42. The Aβ42/40 ratio is increased in many cases of familial Alzheimer's disease (FAD). The transmembrane domain (TM) of APP contains the known dimerization motif GXXXA. We have investigated the dimerization of both wild type and FAD mutant APP transmembrane domains.</p> <p>Results</p> <p>Using synthetic peptides derived from the APP-TM domain, we show that this segment is capable of forming stable transmembrane dimers. A model of a dimeric APP-TM domain reveals a putative dimerization interface, and interestingly, majority of FAD mutations in APP are localized to this interface region. We find that FAD-APP mutations destabilize the APP-TM dimer and increase the population of APP peptide monomers.</p> <p>Conclusion</p> <p>The dissociation constants are correlated to both the Aβ42/Aβ40 ratio and the mean age of disease onset in AD patients. We also show that these TM-peptides reduce Aβ production and Aβ42/Aβ40 ratios when added to HEK293 cells overexpressing the Swedish FAD mutation and γ-secretase components, potentially revealing a new class of γ-secretase inhibitors.</p

Molecular-beam epitaxy of p-type m-plane GaN

We report on the plasma-assisted molecular-beam epitaxy of Mg-doped (10 (1) over bar0) GaN on (10 (1) over bar0) 6H-SiC. Secondary ion mass spectroscopy measurements show the incorporation of Mg into the GaN films with an enhanced Mg incorporation under N-rich conditions relative to Ga-rich growth. Transport measurements of Mg-doped layers grown under Ga-rich conditions show hole concentrations in the range of p=1x10(18) to p=7x10(18) cm(-3) and a dependence between hole concentration and Mg beam equivalent pressure. An anisotropy in in-plane hole mobilities was observed, with the hole mobility parallel to [11 (2) over bar0] being higher than that parallel to [0001] for the same hole concentration. Mobilities parallel to [11 (2) over bar0] were as high as similar to 11.5 cm(2)/Vs (at p similar to 1.8 x 10(18) cm(-3)). (c) 2005 American Institute of Physics

Neurodevelopmental Processes in the Prefrontal Cortex Derailed by Chronic HIV-1 Viral Protein Exposure

Due to the widespread access to, and implementation of, combination antiretroviral therapy, individuals perinatally infected with human immunodeficiency virus type 1 (HIV-1) are living into adolescence and adulthood. Perinatally infected adolescents living with HIV-1 (pALHIV) are plagued by progressive, chronic neurocognitive impairments; the pathophysiological mechanisms underlying these deficits, however, remain understudied. A longitudinal experimental design from postnatal day (PD) 30 to PD 180 was utilized to establish the development of pyramidal neurons, and associated dendritic spines, from layers II-III of the medial prefrontal cortex (mPFC) in HIV-1 transgenic (Tg) and control animals. Three putative neuroinflammatory markers (i.e., IL-1β, IL-6, and TNF-α) were evaluated early in development (i.e., PD 30) as a potential mechanism underlying synaptic dysfunction in the mPFC. Constitutive expression of HIV-1 viral proteins induced prominent neurodevelopmental alterations and progressive synaptodendritic dysfunction, independent of biological sex, in pyramidal neurons from layers II-III of the mPFC. From a neurodevelopmental perspective, HIV-1 Tg rats exhibited prominent deficits in dendritic and synaptic pruning. With regards to progressive synaptodendritic dysfunction, HIV-1 Tg animals exhibited an age-related population shift towards dendritic spines with decreased volume, increased backbone length, and decreased head diameter; parameters associated with a more immature dendritic spine phenotype. There was no compelling evidence for neuroinflammation in the mPFC during early development. Collectively, progressive neuronal and dendritic spine dysmorphology herald synaptodendritic dysfunction as a key neural mechanism underlying chronic neurocognitive impairments in pALHIV