T=0 and T=1 states in the odd-odd N=Z nucleus, Br-70(35)35

Excited states in 70Br were populated in the 40Ca(32S,pn) reaction at Ebeam=80-100 MeV and the 40Ca(36Ar, αpn) reaction at Ebeam= 145 MeV. The resulting gamma decay was detected using the Gamma-sphere array triggered by a 30-element neutron detector. The cross-bombardment allowed the unambiguous assignment of levels to 70Br, comprising a total of 32 states built both on the Jπ=O+ ground state and a previously known Jπ= 9+ isomer, which is located at an excitation energy of 2293 keV by the observation of linking transitions. The structures are discussed within the context of the two-quasiparticle plus rotor model, the IBM-4 model and the cranked Nilsson-Strutinsky formalism. The nonobservation of a doublet of J = 0, T = 1 and J = 1, T = 0 states at low excitation in 70Br is indicative that T = 0 proton-neutron pairing strength is weak in comparison to T = 1 pairing

Current pathways for epidemiological research in amyotrophic lateral sclerosis

Abstract Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disease. The current status of the epidemiology, challenges to its study, and novel study design options are discussed in this paper. We focus on recent results from large-scale population based prospective studies, case-control studies and population based registries, risk factors, and neuropathologic findings in chronic traumatic encephalomyelopathy. We identify areas of interest for future research, including time-trends in the incidence and prevalence of ALS; the meaning of lifetime risk; the phenotypic description of ALS; the definition of familial versus sporadic ALS, syndromic aspects of ALS; specific risk factors such as military service, life style factors such as smoking, the use of statins, and the presence of β-N-methylamino-L-alanine (BMAA), an excitotoxic amino acid derivative possibly produced by cyanobacteria found in almost every terrestrial and aquatic habitat; the emergence and disappearance of an endemic ALS in areas of the Pacific; and gene-environment interactions in the etiology of ALS. To move the epidemiology forward, we suggest using well-characterized cohorts of newly diagnosed ALS patients to identify risk and prognostic factors; storing biological material for future studies; building on the National ALS Registry as a resource of future studies; working in multidisciplinary consortia; and addressing the possible early life etiology of ALS