Results of the BiPo-1 prototype for radiopurity measurements for the SuperNEMO double beta decay source foils

The development of BiPo detectors is dedicated to the measurement of extremely high radiopurity in $^{208}$Tl and $^{214}$Bi for the SuperNEMO double beta decay source foils. A modular prototype, called BiPo-1, with 0.8 $m^2$ of sensitive surface area, has been running in the Modane Underground Laboratory since February, 2008. The goal of BiPo-1 is to measure the different components of the background and in particular the surface radiopurity of the plastic scintillators that make up the detector. The first phase of data collection has been dedicated to the measurement of the radiopurity in $^{208}$Tl. After more than one year of background measurement, a surface activity of the scintillators of $\mathcal{A}$($^{208}$Tl) $=$ 1.5 $\mu$Bq/m$^2$ is reported here. Given this level of background, a larger BiPo detector having 12 m$^2$ of active surface area, is able to qualify the radiopurity of the SuperNEMO selenium double beta decay foils with the required sensitivity of $\mathcal{A}$($^{208}$Tl) $<$ 2 $\mu$Bq/kg (90% C.L.) with a six month measurement.Comment: 24 pages, submitted to N.I.M.

It’s not all academic: nursing admissions and attrition in the United States

Interest in the nursing profession is growing in the United States (US). Currently, there are more applicants for nursing school than nursing school capacities can accommodate. At the same time qualified applicants are unable to enter nursing school related to program capacities, 18% of admitted students leave nursing schools prior to graduation. The abundance of applicants should make nursing school attrition, in the US, practically nonexistent. US nursing programs must determine more effective criteria for screening applicants so that the students, most likely to succeed, are admitted to programs

Acute-Onset Optic Neuropathy in Wilson’s Disease

Wilson’s disease (WD), also known as hepatolenticular degeneration, is a rare autosomal recessive condition of excess copper accumulation that is most commonly associated with hepatic, neurologic, psychiatric, and ocular manifestations. While Kayser-Fleischer rings and sunflower cataracts are well known in WD, visual impairment is very rare. We report the case of a 20-year-old female who presented with acute liver failure and associated monocular vision loss. WD was found to be a cause of her liver disease and decreased vision

Naïve Huntington’s disease microglia mount a normal response to inflammatory stimuli but display a partially impaired development of innate immune tolerance that can be counteracted by ganglioside GM1

Abstract Chronic activation and dysfunction of microglia have been implicated in the pathogenesis and progression of many neurodegenerative disorders, including Huntington’s disease (HD). HD is a genetic condition caused by a mutation that affects the folding and function of huntingtin (HTT). Signs of microglia activation have been observed in HD patients even before the onset of symptoms. It is unclear, however, whether pro-inflammatory microglia activation in HD results from cell-autonomous expression of mutant HTT, is the response of microglia to a diseased brain environment, or both. In this study, we used primary microglia isolated from HD knock-in (Q140) and wild-type (Q7) mice to investigate their response to inflammatory conditions in vitro in the absence of confounding effects arising from brain pathology. We show that naïve Q140 microglia do not undergo spontaneous pro-inflammatory activation and respond to inflammatory triggers, including stimulation of TLR4 and TLR2 and exposure to necrotic cells, with similar kinetics of pro-inflammatory gene expression as wild-type microglia. Upon termination of the inflammatory insult, the transcription of pro-inflammatory cytokines is tapered off in Q140 and wild-type microglia with similar kinetics. However, the ability of Q140 microglia to develop tolerance in response to repeated inflammatory stimulations is partially impaired in vitro and in vivo, potentially contributing to the establishment of chronic neuroinflammation in HD. We further show that ganglioside GM1, a glycosphingolipid with anti-inflammatory effects on wild-type microglia, not only decreases the production of pro-inflammatory cytokines and nitric oxide in activated Q140 microglia, but also dramatically dampen microglia response to re-stimulation with LPS in an experimental model of tolerance. These effects are independent from the expression of interleukin 1 receptor associated kinase 3 (Irak-3), a strong modulator of LPS signaling involved in the development of innate immune tolerance and previously shown to be upregulated by immune cell treatment with gangliosides. Altogether, our data suggest that external triggers are required for HD microglia activation, but a cell-autonomous dysfunction that affects the ability of HD microglia to acquire tolerance might contribute to the establishment of neuroinflammation in HD. Administration of GM1 might be beneficial to attenuate chronic microglia activation and neuroinflammation

Peripheral nerve grafts promoting central nervous system regeneration after spinal cord injury in the primate

Partial restoration of hindlimb function in adult rats following spinal cord injury (SCI) has been demonstrated using a variety of transplantation techniques. The purpose of the present study was twofold: 1) to determine whether strategies designed to promote regeneration in the rat can yield similar results in the primate; and 2) to establish whether central nervous system (CNS) regeneration will influence voluntary grasping and locomotor function in the nonhuman primate. Ten cynomologus monkeys underwent T-11 laminectomy and resection of a 1-cm length of hemispinal cord. Five monkeys received six intercostal nerve autografts and fibrin glue containing acidic fibroblast growth factor (2.1 microg/ml) whereas controls underwent the identical laminectomy procedure but did not receive the nerve grafts. At 4 months postgrafting, the spinal cord-graft site was sectioned and immunostained for peripheral myelin proteins, biotinylated dextran amine, and tyrosine hydroxylase, whereas the midpoint of the graft was analyzed histologically for the total number of myelinated axons within and around the grafts. The animals underwent pre- and postoperative testing for changes in voluntary hindlimb grasping and gait. 1) A reproducible model of SCI in the primate was developed. 2) Spontaneous recovery of the ipsilateral hindlimb function occurred in both graft- and nongraft-treated monkeys over time without evidence of recovering the ability for voluntary tasks. 3) Regeneration of the CNS from proximal spinal axons into the peripheral nerve grafts was observed; however, the grafts did not promote regeneration beyond the lesion site. 4) The grafts significantly enhanced (p < 0.0001) the regeneration of myelinated axons into the region of the hemisected spinal cord compared with the nongrafted animals