Enhanced Fusion-Evaporation Cross Sections in Neutron-Rich 132^{132}Sn on 64^{64}Ni

Evaporation residue cross sections have been measured with neutron-rich radioactive $^{132}$Sn beams on $^{64}$Ni in the vicinity of the Coulomb barrier. The average beam intensity was $2\times 10^{4}$ particles per second and the smallest cross section measured was less than 5 mb. Large subbarrier fusion enhancement was observed. Coupled-channels calculations taking into account inelastic excitation and neutron transfer underpredict the measured cross sections below the barrier.Comment: 4 pages including 1 table and 3 figure

Dental caries experience, care index and restorative index in children with learning disabilities and children without learning disabilities; a systematic review and meta-analysis

Background Children with learning disabilities (CLD) have worse health outcomes than children with no learning disabilities (CNLD). This systematic review compared caries experience and met dental care need for CLD to CNLD using Decayed, Missing, Filled Permanent Teeth (DMFT) and decayed, missing/extracted, filled primary teeth (dmft/deft), care index (CI), and restorative index (RI) values. Methods Without date or language restrictions four databases were searched for; cross-sectional studies comparing caries experience and CI/ RI in CLD matched to groups of CNLD. Screening and data extraction were carried out independently and in duplicate. Risk of bias was assessed using the Newcastle-Ottawa Scale. Meta-analyses were carried out (random effects model). Results There were 25 articles with 3976 children (1 to 18 years old), from 18 countries, fitting the inclusion criteria. Children with; Down syndrome were investigated in 11 studies, autism in 8 and mixed learning disabilities in 6. The overall mean DMFT for CLD was 2.31 (standard deviation±1.97; range 0.22 to 7.2) and for CNLD was 2.51 (±2.14; 0.37 to 4.76). Using standardised mean difference (SMD), meta-analysis showed no evidence of a difference between CLD and CNLD (n = 16 studies) for caries experience (SMD = -0.43; 95%CI = -0.91 to 0.05). This was similar for sub-groups of children with autism (SMD = -0.28; 95%CI = 1.31 to 0.75) and mixed disabilities (SMD = 0.26; 95%CI = -0.94 to 1.47). However, for children with Down syndrome, caries experience was lower for CLD than CNLD (SMD = -0.73; 95%CI = -1.28 to − 0.18). For primary teeth, mean dmft/deft was 2.24 for CLD and 2.48 for CNLD (n = 8 studies). Meta-analyses showed no evidence of a difference between CLD and CNLD for caries experience across all disability groups (SMD = 0.41; 95% CI = -0.14 to 0.96), or in sub-groups: Down syndrome (SMD = 0.55; 95%CI- = − 0.40 to 1.52), autism (SMD = 0.43; 95%CI = -0.53 to 2.39) and mixed disabilities (SMD = -0.10; 95%CI = -0.34 to 0.14). The studies’ risk of bias were medium to high. Conclusion There was no evidence of a difference in caries levels in primary or permanent dentitions for CLD and CNLD. This was similar for learning disability sub-groups, except for Down syndrome where dental caries levels in permanent teeth was lower. Data on met need for dental caries was inconclusive

Microbial interactions with phosphorus containing glasses representative of vitrified radioactive waste

The presence of phosphorus in borosilicate glass (at 0.1 – 1.3 mol% P2O5) and in iron-phosphate glass (at 53 mol% P2O5) stimulated the growth and metabolic activity of anaerobic bacteria in model systems. Dissolution of these phosphorus containing glasses was either inhibited or accelerated by microbial metabolic activity, depending on the solution chemistry and the glass composition. The breakdown of organic carbon to volatile fatty acids increased glass dissolution. The interaction of microbially reduced Fe(II) with phosphorus-containing glass under anoxic conditions decreased dissolution rates, whereas the interaction of Fe(III) with phosphorus-containing glass under oxic conditions increased glass dissolution. Phosphorus addition to borosilicate glasses did not significantly affect the microbial species present, however, the diversity of the microbial community was enhanced on the surface of the iron phosphate glass. Results demonstrate the potential for microbes to influence the geochemistry of radioactive waste disposal environments with implication for wasteform durability

The differential diagnosis of chronic daily headaches: an algorithm-based approach

Chronic daily headaches (CDHs) refers to primary headaches that happen on at least 15 days per month, for 4 or more hours per day, for at least three consecutive months. The differential diagnosis of CDHs is challenging and should proceed in an orderly fashion. The approach begins with a search for “red flags” that suggest the possibility of a secondary headache. If secondary headaches that mimic CDHs are excluded, either on clinical grounds or through investigation, the next step is to classify the headaches based on the duration of attacks. If the attacks last less than 4 hours per day, a trigeminal autonomic cephalalgia (TAC) is likely. TACs include episodic and chronic cluster headache, episodic and chronic paroxysmal hemicrania, SUNCT, and hypnic headache. If the duration is ≥4 h, a CDH is likely and the differential diagnosis encompasses chronic migraine, chronic tension-type headache, new daily persistent headache and hemicrania continua. The clinical approach to diagnosing CDH is the scope of this review

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

Diving into the vertical dimension of elasmobranch movement ecology

Knowledge of the three-dimensional movement patterns of elasmobranchs is vital to understand their ecological roles and exposure to anthropogenic pressures. To date, comparative studies among species at global scales have mostly focused on horizontal movements. Our study addresses the knowledge gap of vertical movements by compiling the first global synthesis of vertical habitat use by elasmobranchs from data obtained by deployment of 989 biotelemetry tags on 38 elasmobranch species. Elasmobranchs displayed high intra- and interspecific variability in vertical movement patterns. Substantial vertical overlap was observed for many epipelagic elasmobranchs, indicating an increased likelihood to display spatial overlap, biologically interact, and share similar risk to anthropogenic threats that vary on a vertical gradient. We highlight the critical next steps toward incorporating vertical movement into global management and monitoring strategies for elasmobranchs, emphasizing the need to address geographic and taxonomic biases in deployments and to concurrently consider both horizontal and vertical movements