A review of analytical methods for assessing preservation in waterlogged archaeological wood and their application in practice

Waterlogged archaeological wood can present management challenges due to its vulnerability to chemical and biological decay, both during burial and post-excavation. Decay processes also often leave it severely weakened and therefore susceptible to mechanical damage. Quantifying preservation and understanding active decay mechanisms is therefore critical in informing the management of this unique cultural resource. It is critical that assessments of preservation are robust, and sensitive enough to allow changes over time to be detected. A wide range of analytical methods can be applied to assess the state of preservation of waterlogged archaeological wood, and determining which of these is most appropriate to the circumstances can be challenging. This review summarises some of the most commonly reported methods suitable for the analysis of waterlogged archaeological wood, ranging from widely used ‘low-tech’ methods, to assessment using advanced analytical instrumentation. Methods are evaluated in terms of the information gained weighed up against their cost, logistical considerations, and time investments, with the aim of supporting the development of an analytical strategy. We conclude that although an analytical strategy must be informed by the aims of assessment as well as any external restrictions, the best available analytical techniques should be employed in order to supply an accurate baseline against which future change can be measured. Critically, a multi-analytical approach is vital in obtaining a clear picture of the present state of decay, as no single technique gives the best assessment

Correction to : A review of analytical methods for assessing preservation in waterlogged archaeological wood and their application in practice (Heritage Science, (2020), 8, 1, (83), 10.1186/s40494-020-00422-y)

Following publication of the original article [1], it was reported that the caption for Fig. 4a erroneously stated that it showed soft rot decay. In fact, the image shows decay by erosion bacteria. The caption for Fig. 4a has been amended and the original article has been updated

Lessons from Star Carr on the vulnerability of organic archaeological remains to environmental change

Examples of wetland deposits can be found across the globe and are known for preserving organic archaeological and environmental remains that are vitally important to our understanding of past human–environment interactions. The Mesolithic site of Star Carr (Yorkshire, United Kingdom) represents one of the most influential archives of human response to the changing climate at the end of the last glacial in Northern Europe. A hallmark of the site since its discovery in 1948 has been the exceptional preservation of its organic remains. Disturbingly, recent excavations have suggested that the geochemistry of the site is no longer conducive to such remarkable survival of organic archaeological and environmental materials. Microcosm (laboratory-based) burial experiments have been undertaken, alongside analysis of artifacts excavated from the site, to assess the effect of these geochemical changes on the remaining archaeological material. By applying a suite of macroscopic and molecular analyses, we demonstrate that the geochemical changes at Star Carr are contributing to the inexorable and rapid loss of valuable archaeological and paleoenvironmental information. Our findings have global implications for other wetland sites, particularly archaeological sites preserved in situ

Human PDE4A8, a novel brain-expressed PDE4 cAMP-specific phosphodiesterase that has undergone rapid evolutionary change

We have isolated cDNAs encoding PDE4A8 (phosphodiesterase 4 isoform A8), a new human cAMP-specific PDE4 isoform encoded by the PDE4A gene. PDE4A8 has a novel N-terminal region of 85 amino acids that differs from those of the related ‘long’ PDE4A4, PDE4A10 and PDE4A11 isoforms. The human PDE4A8 N-terminal region has diverged substantially from the corresponding isoforms in the rat and other mammals, consistent with rapid evolutionary change in this region of the protein. When expressed in COS-7 cells, PDE4A8 localized predominantly in the cytosol, but approx. 20% of the enzyme was associated with membrane fractions. Cytosolic PDE4A8 was exquisitely sensitive to inhibition by the prototypical PDE4 inhibitor rolipram (IC<sub>50</sub> of 11±1 nM compared with 1600 nM for PDE4A4), but was less sensitive to inhibition by cilomilast (IC<sub>50</sub> of 101±7 nM compared with 61 nM for PDE4A4). PDE4A8 mRNA was found to be expressed predominantly in skeletal muscle and brain, a pattern that differs from the tissue expression of other human PDE4 isoforms and also from that of rat PDE4A8. Immunohistochemical analysis showed that PDE4A8 could be detected in discrete regions of human brain, including the cerebellum, spinal cord and cerebral cortex. The unique tissue distribution of PDE4A8, combined with the evolutionary divergence of its N-terminus, suggest that this isoform may have a specific function in regulating cAMP levels in human skeletal muscle and brain

Correction to: An autosomal dominant neurological disorder caused by de novo variants in FAR1 resulting in uncontrolled synthesis of ether lipids (Genetics in Medicine, (2021), 23, 4, (740-750), 10.1038/s41436-020-01027-3)

In the original author list, Seth Perlman’s degrees were listed as MD, PhD. Dr Perlman’s degree is MD. The original version has been corrected

An autosomal dominant neurological disorder caused by de novo variants in FAR1 resulting in uncontrolled synthesis of ether lipids

Purpose: In this study we investigate the disease etiology in 12 patients with de novo variants in FAR1 all resulting in an amino acid change at position 480 (p.Arg480Cys/His/Leu). Methods: Following next-generation sequencing and clinical phenotyping, functional characterization was performed in patients’ fibroblasts using FAR1 enzyme analysis, FAR1 immunoblotting/immunofluorescence, and lipidomics. Results: All patients had spastic paraparesis and bilateral congenital/juvenile cataracts, in most combined with speech and gross motor developmental delay and truncal hypotonia. FAR1 deficiency caused by biallelic variants results in defective ether lipid synthesis and plasmalogen deficiency. In contrast, patients’ fibroblasts with the de novo FAR1 variants showed elevated plasmalogen levels. Further functional studies in fibroblasts showed that these variants cause a disruption of the plasmalogen-dependent feedback regulation of FAR1 protein levels leading to uncontrolled ether lipid production. Conclusion: Heterozygous de novo variants affecting the Arg480 residue of FAR1 lead to an autosomal dominant disorder with a different disease mechanism than that of recessive FAR1 deficiency and a diametrically opposed biochemical phenotype. Our findings show that for patients with spastic paraparesis and bilateral cataracts, FAR1 should be considered as a candidate gene and added to gene panels for hereditary spastic paraplegia, cerebral palsy, and juvenile cataracts