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Dating agricultural artefacts such as field walls and clearance cairns using radiocarbon can be challenging, especially since the association with datable material may be poor. Rock surface burial dating using luminescence offers an alternative. Here we report on the luminescence dating of a medieval circular stone-walled enclosure at Sønnebøe, northern Scania, Sweden, using both buried rocks and sediments. Luminescence burial profiles from IRSL signals measured at 50 °C (IR 50) indicated significant prior light exposure in 7 of the 8 samples tested (5 granite, 2 felsic gneiss), in some cases multiple exposure burial cycles were indicated. These rock surfaces had apparently been exposed for sufficient time to allow accurate IRSL ages for the most recent burial event. In contrasts, no useful post-IR IRSL profiles were obtained indicating that this signal was not sufficiently reset to allow accurate determination of the burial dose on any of these rocks. IR 50 fading corrections (typically ∼50%) were derived by comparing field saturation with that induced in the laboratory. Quartz extracted from sediments surrounding the rocks gave an average measured to given dose ratio of 1.03 ± 0.01 (n = 90), and these sediment samples were then dated using multigrain aliquots; the corresponding feldspar dose recovery ratio obtained using rock samples was 0.98 ± 0.05 (n = 28). A total of 15 ages were derived; 8 quartz OSL ages from the disturbed coarse grained sediments surrounding the structure, and 7 fading corrected IR 50 ages from the surfaces of rocks (2–3 mm chips, ∼1 mm thick) used in the construction of the structure itself. The exposure events preserved by the ring enclosure stones unequivocally show wall building taking place at the site between 800 and 300 years ago. • Direct dating of stone walled structures. • Rock surface burial dating using IR 50 luminescence bleaching profiles. • Comparison of dating results obtained from sand sized sedimentary grains and granitic rocks. • Application of improved modelling of infinite matrix beta and gamma dose rates in rocks. [ABSTRACT FROM AUTHOR]

Autosomal-dominant ataxia with sensory and autonomic neuropathy is a highly specific combined phenotype that we described in two Swedish kindreds in 2014; its genetic cause had remained unknown. Here, we report the discovery of exonic GGC trinucleotide repeat expansions, encoding poly-glycine, in zinc finger homeobox 3 (ZFHX3) in these families. The expansions were identified in whole-genome datasets within genomic segments that all affected family members shared. Non-expanded alleles carried one or more interruptions within the repeat. We also found ZFHX3 repeat expansions in three additional families, all from the region of Skåne in southern Sweden. Individuals with expanded repeats developed balance and gait disturbances at 15 to 60 years of age and had sensory neuropathy and slow saccades. Anticipation was observed in all families and correlated with different repeat lengths determined through long-read sequencing in two family members. The most severely affected individuals had marked autonomic dysfunction, with severe orthostatism as the most disabling clinical feature. Neuropathology revealed p62-positive intracytoplasmic and intranuclear inclusions in neurons of the central and enteric nervous system, as well as alpha-synuclein positivity. ZFHX3 is located within the 16q22 locus, to which spinocerebellar ataxia type 4 (SCA4) repeatedly had been mapped; the clinical phenotype in our families corresponded well with the unique phenotype described in SCA4, and the original SCA4 kindred originated from Sweden. ZFHX3 has known functions in neuronal development and differentiation n both the central and peripheral nervous system. Our findings demonstrate that SCA4 is caused by repeat expansions in ZFHX3. [Display omitted] In five families from Skåne region in Sweden, expanded repeat expansions in ZFHX3 were identified as the cause for spinocerebellar ataxia type 4, SCA4. SCA4 is an autosomal-dominant disorder with progressive gait and balance disturbance and dyscoordination of movements. SCA4 might compromise nerves controlling automatic bodily functions. [ABSTRACT FROM AUTHOR]