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Establishing the biogenicity of sedimentary surface textures with unresolved microbial origin is critical to any environmental and geobiological interpretation of clastic settings. Here, some Ediacaran wrinkle structures and associated carbonaceous greywacke samples containing mat fragments rich in 'bacteriomorph acritarchs' are investigated. Their biogenicity was evaluated with transmitted light and scanning electron microscopy, epifluorescence and Raman spectroscopy, and confirmed by the presence of distinct cyanobacterial biomarkers. The comparison of results yielded by these techniques validates the use of Raman spectroscopy on Neoproterozoic kerogen (organic‐walled microfossils and amorphous organic material) under low metamorphic conditions. Raman spectrographs also allowed recognition of associated rare‐earth element‐rich phosphate (monazite) and subsidiary metal sulphide concentrations, and interpreted as a result of biosorption and/or mat trapping under normal oxic conditions. These microbial mat features represent cyanobacterial bloom‐forming Bavlinella acritarchs, which characterise eutrophic episodes in a semi‐enclosed retroarc basin sandwiched between an active Cadomian arc and West Gondwana. [ABSTRACT FROM AUTHOR]

Background: Metachromatic Leukodystrophy (MLD, OMIM 250100) is a neurodegenerative disease caused by mutations in the ARSA gene (OMIM 607574) that lead to deficiency in Arylsulfatase A (ASA). ASA pseudodeficiency (PD‐ASA) is a biochemical condition that substantially diminishes ASA activity but is not associated with clinical manifestations. PD‐ASA is associated with the c.1055A>G (p.Asn352Ser) (rs2071421) and c.*96A>G (rs6151429) variants, which have an estimated frequency of 2% in the population. Objective: To determine the activity of Arylsulfatase A and to identify variants and haplotypes in the ARSA gene in Mexican individuals with pseudodeficiency. Methods: Two‐hundred apparently healthy individuals were included to determine the enzymatic activity of ASA in leukocytes by spectrophotometric analysis, and identification of the PD‐ASA alleles was performed by PCR‐RFLP assays. Genotypes were confirmed by semi‐automated Sanger sequencing. Haplotypes were constructed using Arlequin v.10.04, and linkage disequilibrium analysis was performed with Cube X. Results: The enzymatic activity of ASA was determined to be 1.74–2.09 nmol/mg protein/min and later correlated with genotypes and haplotypes. For the (p.Asn352Ser) variant, we found 126 (0.63) individuals with the AA genotype, 62 with AG (0.31) and 12 with GG (0.06); the frequency of the polymorphic allele was 0.215 (86 alleles, 21.5%), and the variant was in HWE (p =.2484). The variant c.*96A>G was also in HWE (p =.2105): 185 individuals (0.925) with the AA genotype, 14 (0.07) with AG, and 1 (0.005) with (GG), with a frequency of 0.04 (4%) for the polymorphic allele. The inference of haplotypes resulted in 312 (0.78) AA, 72 (0.18) GA, and 16 (0.04) GG haplotypes. The AG haplotype was not found. The variants were found to be in linkage disequilibrium (D' = 1). Of the nine possible diplotypes, AA/AG, AA/GG, and AG/GG were not found, in concordance with the hypothesis that the G allele of c.*96A>G does not occur in the absence of the G allele of c.1055A>G. We found a slight correlation between ASA biochemical activity and variants, mainly due to the G allele of c.*96A>G in either genotypes or haplotypes. Conclusions: In Northwestern Mexico, the presence of PD‐ASA alleles was biochemically and molecularly determined, and the frequencies were found to be in HWE. The frequency of PD‐ASA for the North Western Mexican mestizo is 8%. [ABSTRACT FROM AUTHOR]

This paper presents a detailed geological and geomorphological analysis of the so‐called givoni (low‐relief, mainly gravelly landforms subparallel to the coastline) associated with the MIS 5 terrace in the northern Gulf of Taranto (southern Italy). These landforms can be interpreted as former beach ridges, swash/drift‐aligned spits, or swash/drift‐aligned barriers (BSBs); thus, givoni are palaeoshoreline indicators. In the study area, recognizing the classic landforms associated with marine terraces, that is, surfaces and scarps, is difficult, as the givoni are often associated and variably combined with surfaces and scarps. Thus, we reconstruct the formation and evolution processes of the MIS 5 marine terrace, including the formation of surfaces, scarps, and BSBs (and the resulting composite landforms), in an overall evolutionary framework based on eustatic oscillations. Then, we reconstruct a complete set of situations in which BSBs form on loose or semiconsolidated substrates in response to eustatic oscillations: (a) BSBs can form during a highstand of a warm stage on previously consolidated sediment; (b) BSBs may represent coastlines formed during sea‐level standstills in the context of a general regressive phase following the highstand peak that created a relict sea cliff; (c) BSBs may represent coastlines formed during a new relative highstand in a warm substage on previously unconsolidated deposits formed during the same stage; and (d) BSBs may be formed by a process similar to that of the previous case, except that the sea level stopped rising against a pre‐existing BSB. [ABSTRACT FROM AUTHOR]

Of the five mammalian muscarinic acetylcholine (ACh) receptors, M5 is the only subtype expressed in midbrain dopaminergic neurons, where it functions to potentiate dopamine release. We have identified a direct physical interaction between M5 and the AP-3 adaptor complex regulator AGAP1. This interaction was specific with regard to muscarinic receptor (MR) and AGAP subtypes, and mediated the binding of AP-3 to M5. Interaction with AGAP1 and activity of AP-3 were required for the endocytic recycling of M5 in neurons, the lack of which resulted in the downregulation of cell surface receptor density after sustained receptor stimulation. The elimination of AP-3 or abrogation of AGAP1–M5 interaction in vivo decreased the magnitude of presynaptic M5-mediated dopamine release potentiation in the striatum. Our study argues for the presence of a previously unknown receptor-recycling pathway that may underlie mechanisms of G-protein-coupled receptor (GPCR) homeostasis. These results also suggest a novel therapeutic target for the treatment of dopaminergic dysfunction. [ABSTRACT FROM AUTHOR]