The Discus Comet: C/2014 B1 (Schwartz)

Long period comet C/2014 B1 (Schwartz) exhibits a remarkable optical appearance, like that of a discus or bi-convex lens viewed edgewise. Our measurements in the four years since discovery reveal a unique elongated dust coma whose orientation is stable with respect to the projected anti-solar and orbital directions. With no tail and no trail, the limited influence of radiation pressure on the dust coma sets a lower limit to the effective particle size of 0.1 mm, while the photometry reveals a peak coma scattering cross-section 27,000 sq km (geometric albedo 0.1 assumed). From the rate of brightening of the comet we infer a dust production rate of order 10 kg/s at 10 AU heliocentric distance, presumably due to the sublimation of supervolatile ices, and perhaps triggered by the crystallization of amorphous water ice. We consider several models for the origin of the peculiar morphology. The disk-like shape is best explained by equatorial ejection of particles from a nucleus whose spin vector lies near the plane of the sky. In this interpretation, the unique appearance of C/2014 B1 is a result of a near equality between the rotation-assisted nucleus escape speed (1 to 10 m/s for a 2 to 20 kilometer-scale nucleus) and the particle ejection velocity, combined with a near-equatorial viewing perspective. To date, most other comets have been studied at heliocentric distances less than half that of C/2014 B1, where their nucleus temperatures, gas fluxes and dust ejection speeds are much higher. The throttling role of nucleus gravity is correspondingly diminished, so that the disk morphology has not before been observed.Comment: 36 Pages, 10 Figure

The neuronal pentraxin Nptx2 regulates complement activity and restrains microglia-mediated synapse loss in neurodegeneration

Complement overactivation mediates microglial synapse elimination in neurological diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but how complement activity is regulated in the brain remains largely unknown. We identified that the secreted neuronal pentraxin Nptx2 binds complement C1q and thereby regulates its activity in the brain. Nptx2-deficient mice show increased complement activity, C1q-dependent microglial synapse engulfment, and loss of excitatory synapses. In a neuroinflammation culture model and in aged TauP301S mice, adeno-associated virus (AAV)–mediated neuronal overexpression of Nptx2 was sufficient to restrain complement activity and ameliorate microglia-mediated synapse loss. Analysis of human cerebrospinal fluid (CSF) samples from a genetic FTD cohort revealed reduced concentrations of Nptx2 and Nptx2-C1q protein complexes in symptomatic patients, which correlated with elevated C1q and activated C3. Together, these results show that Nptx2 regulates complement activity and microglial synapse elimination in the brain and that diminished Nptx2 concentrations might exacerbate complement-mediated neurodegeneration in patients with FTD

Synthesis and styrene copolymerization of novel alkoxy ring-substituted octyl phenylcyanoacrylates

Novel alkoxy ring-substituted octyl phenylcyanoacrylates, RPhCH=C(CN)CO2CH2(CH2)6CH3 (where R is 2-methoxy, 3-methoxy, 4-methoxy, 2-ethoxy, 3-ethoxy, 4-ethoxy, 4-propoxy, 4-butoxy, 4-hexyloxy) were prepared and copolymerized with styrene. The acrylates were synthesized by the piperidine catalyzed Knoevenagel condensation of ring-substituted benzaldehydes and octyl cyanoacetate, and characterized by CHN analysis, IR, 1H and 13C NMR. All the acrylates were copolymerized with styrene in solution with radical initiation (ABCN) at 70C. The compositions of the copolymers were calculated from nitrogen analysis

Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer's disease.

Acknowledgements: We thank David Attwell, Siddharthan Chandran, Bart De Strooper, and James Rowland for comments on the manuscript. We thank UK DRI at UCL technical staff Elena Ghirardello and Phillip Muckett for the maintenance of animal colonies and assistance with animal experiments. We thank the Queen Square Brain Bank for Neurological Disorders for provision of human brain tissue samples. The Queen Square Brain Bank is supported by the Reta Lila Weston Institute of Neurological Studies, UCL Queen Square Institute of Neurology. We thank Tanja Kuhlmann and the University of Münster for providing the SON lentivirus. We thank Takashi Saito and Takaomi C. Saido for provision of AppNL-G-F mice. We thank Ulf Neumann and Derya Shimshek from Novartis for providing us with the BACE1 inhibitor NB-360.Funder: UK Dementia Research Institute; funder-id: http://dx.doi.org/10.13039/501100017510Funder: National Institute for Health and Care Research University College London Hospitals Biomedical Research CentreReduction of amyloid beta (Aβ) has been shown to be effective in treating Alzheimer's disease (AD), but the underlying assumption that neurons are the main source of pathogenic Aβ is untested. Here, we challenge this prevailing belief by demonstrating that oligodendrocytes are an important source of Aβ in the human brain and play a key role in promoting abnormal neuronal hyperactivity in an AD knock-in mouse model. We show that selectively suppressing oligodendrocyte Aβ production improves AD brain pathology and restores neuronal function in the mouse model in vivo. Our findings suggest that targeting oligodendrocyte Aβ production could be a promising therapeutic strategy for treating AD