Project description:Throughout prehistory, human groups inhabited the Scheldt basin in northern Belgium, though few prehistoric human remains have been found there compared to the Meuse basin, where many caves contain human remains from various prehistoric phases. The limited preservation in the Scheldt basin is due to the region's high soil acidity, decalcification, and dryness, which degrade bones. The oldest known human bone is a clavicle dated to around 5790 years ago. Until recently, little effort had been made to identify human remains in the Scheldt basin. However, a recent survey identified four additional sites with prehistoric human remains. The paper aims to document these findings and explore their radiocarbon dates to better understand the region’s occupation history. The scarcity of remains before the Neolithic is attributed to taphonomic factors, and the lack of Late Neolithic remains might indicate a population decline, though flint mines and Meuse basin burials suggest otherwise. Another possibility is a shift in burial practices, with collective burials in megaliths or caves becoming common in western Europe during this time, unsuitable for the wet floodplains of the Scheldt basin. Most of the human bones discovered in the Scheldt basin were found in secondary contexts, likely displaced by fluvial activity. The bones were retrieved from former river channels and gullies, complicating interpretations of whether they originated from primary graves or were part of secondary burial practices. The absence of defleshing marks suggests the bones were not part of secondary burial rites, pointing instead to the erosion of primary graves from earlier settlements. The presence of settlement debris, including pottery and stone tools, supports this theory
Project description:OBJECTIVES: Kidney stone diseases are common in premature infants, but the underlying molecular and cellular mechanisms are not fully defined. We carried out a prospective observational study using microarray analysis to identify factors that may be crucial for the initiation and progression of stone-induced injury in the developing mouse kidney. METHODS: Mice with adenine phosphoribosyltransferase (Aprt) deficiency develop 2,8-dihydroxyadenine (DHA) nephrolithiasis. Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips. RESULTS: We observed that: (i) gene expression changes induced by Aprt deficiency are developmental stage-specific; (ii) maturation-related gene expression changes are delayed in developing Aprt-/- kidneys; and (iii) immature Aprt-deficient kidneys contain large numbers of intercalated cells blocked from terminal differentiation. CONCLUSIONS: This study presents a comprehensive picture of the transcriptional changes induced by stone injury in the developing mouse kidney. Our findings help explain growth impairment in kidneys subject to injury during the early stages of development. Total RNA were extracted from kidneys of 12 newly born and 6 adult mice (half Aprt-/- and half control). Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips.
Project description:OBJECTIVES: Kidney stone diseases are common in premature infants, but the underlying molecular and cellular mechanisms are not fully defined. We carried out a prospective observational study using microarray analysis to identify factors that may be crucial for the initiation and progression of stone-induced injury in the developing mouse kidney. METHODS: Mice with adenine phosphoribosyltransferase (Aprt) deficiency develop 2,8-dihydroxyadenine (DHA) nephrolithiasis. Gene expression changes between Aprt-/- and Aprt+/+ kidneys from newborn and adult mice were compared using Affymetrix gene chips. RESULTS: We observed that: (i) gene expression changes induced by Aprt deficiency are developmental stage-specific; (ii) maturation-related gene expression changes are delayed in developing Aprt-/- kidneys; and (iii) immature Aprt-deficient kidneys contain large numbers of intercalated cells blocked from terminal differentiation. CONCLUSIONS: This study presents a comprehensive picture of the transcriptional changes induced by stone injury in the developing mouse kidney. Our findings help explain growth impairment in kidneys subject to injury during the early stages of development.