Cross-Section Measurement of Virtual Photoproduction of Iso-Triplet Three-Body Hypernucleus, ⋀nn

Missing-mass spectroscopy with the 3H(e, e′K+) reaction was carried out at Jefferson Lab’s (JLab) Hall A in Oct–Nov, 2018. The differential cross section for the 3H(γ∗, K+)Λnn was deduced at ω = Ee − Ee′ = 2.102 GeV and at the forward K+-scattering angle (0° ≤ θγ∗K ≤ 5°) in the laboratory frame. Given typical predicted energies and decay widths, which are (BΛ, Γ) = (−0.25, 0.8) and (−0.55, 4.7) MeV, the cross sections were found to be 11.2 ± 4.8(stat.)+4.1−2.1(sys.) and 18.1 ± 6.8(stat.)+4.2−2.9(sys.) nb/sr, respectively. The obtained result would impose a constraint for interaction models particularly between Λ and neutron by comparing to theoretical calculations

Clinical and molecular characterisation of KCNT1-related severe early onset epilepsy

Objective: To characterise the phenotypic spectrum, molecular genetic findings and functional consequences of pathogenic variants in early onset KCNT1-epilepsy. Methods: We identified a cohort of 31 patients with epilepsy of infancy with migrating focal seizures (EIMFS) and screened for variants in KCNT1 using direct Sanger sequencing, a multiple gene next generation sequencing panel and whole exome sequencing. Additional patients with non-EIMFS early onset epilepsy in whom we identified KCNT1 variants on local diagnostic multiple gene panel testing were also included. Where possible, we performed homology modelling to predict putative effects of variants on protein structure and function. We undertook electrophysiological assessment of mutant KCNT1 channels in a Xenopus oocyte model system. Results: We identified pathogenic variants in KCNT1 in 12 patients, four of which are novel. Most variants occurred de novo. Ten had a clinical diagnosis of EIMFS and the other two presented with early onset severe nocturnal frontal lobe seizures. Three patients had a trial of quinidine with good clinical response in one. Computational modelling analysis implicates abnormal pore function (F346L) and impaired tetramer formation (F502V) as putative disease mechanisms. All evaluated KCNT1 variants resulted in marked gain-of-function, with significantly increased channel amplitude and variable blockade by quinidine. Conclusions: Gain-of-function KCNT1 pathogenic variants cause a spectrum of severe focal epilepsies with onset in early infancy. Currently, genotype-phenotype correlations are unclear, though clinical outcome is poor for the majority of cases. Further elucidation of disease mechanisms may facilitate the development of targeted treatments, much needed for this pharmacoresistant genetic epilepsy

Appropriate bleaching technique for coconut fiber

Recipes for bleaching of coconut fiber at both ambient and elevated temperature were investigated using appropriate statistical design of experiments using hydrogen peroxide with essential bleaching assisting auxiliaries. The statistical tool is also being utilized to suggest optimized recipe for the treatments considering mainly whiteness index, yellowness index, and tenacity. Statistical computation affirmed need of higher amount of bleaching chemicals in elevated temperature than ambient bleaching. Both the bleaching treatments were resulting in small mass loss essentially of noncellulosic nature including lignin and thus result in improved mechanical properties. The change in whiteness and yellowness index of the bleached fiber under the shed storage condition for duration of 2 years was found to be negligible