Threats to seabirds of northern Aotearoa New Zealand

This report aims to assess current and emerging threats to seabirds in Northern New Zealand, particularly the wider Hauraki Gulf region, and to identify knowledge gaps. In doing so, both research and conservation action can be prioritized to best mitigate threats to seabirds in the region. 1. What are current threats to seabirds in Northern New Zealand? 2. What are the knowledge gaps regarding seabird species in Northern New Zealand? 3. What are the knowledge gaps regarding threats to seabirds in Northern New Zealand? This report has been prepared by Edin Whitehead (University of Auckland), with Nigel Adams (Unitec Institute of Technology), Karen Baird (Forest & Bird/BirdLife international, NNZST), Biz Bell (Wildlife Management International Ltd.), Stephanie Borrelle (NNZST, Ocean Conservancy/University of Toronto & University of Georgia), Brendon Dunphy (University of Auckland), Chris Gaskin (NNZST), Todd Landers (Auckland Council), Matt Rayner (Auckland Museum) & James Russell (University of Auckland

Production of excited atomic hydrogen and deuterium from H2, HD and D2 photodissociation

We have measured the production of Lyman α and Balmer α fluorescence from atomic H and D for the photodissociation of H2, HD and D2 by linearly-polarized photons with energies between 22 and 64 eV. We discuss systematic uncertainties associated with ou

Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disorder. Ten percent of cases are inherited; most involve unidentified genes. We report here 13 mutations in the fused in sarcoma/translated in liposarcoma (FUS/TLS) gene on chromosome 16 that were specific for familial ALS. The FUS/TLS protein binds to RNA, functions in diverse processes, and is normally located predominantly in the nucleus. In contrast, the mutant forms of FUS/TLS accumulated in the cytoplasm of neurons, a pathology that is similar to that of the gene TAR DNA-binding protein 43 (TDP43), whose mutations also cause ALS. Neuronal cytoplasmic protein aggregation and defective RNA metabolism thus appear to be common pathogenic mechanisms involved in ALS and possibly in other neurodegenerative disorders