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These datasets provide sedimentological data partly at annual resolution and an age model for the lateglacial part of (1) the ICDP sediment core 5017-1-A retrieved from the deep northern Dead Sea basin in 2010/11, and (2) for the Masada outcrop located at the southwestern shore of the Dead Sea sampled in 2018. The here investigated two sediment sections cover the last glacial-interglacial transition (ca. 17-11.5 ka BP) in the hydroclimatically sensitive Levant, when the water level of Lake Lisan – the precursor of the Dead Sea – dropped dramatically from its glacial high-stand to the Holocene low levels. Here, we analyze the interval between the last two gypsum units – the Upper Gypsum Unit (UGU) and the Additional Gypsum Unit (AGU) – which were also used to correlate the two sites. In the ICDP core this section is located between ~101 and 88.5 m sediment depth below lake floor and at Masada it encompasses the uppermost ~3.8 m sediments of the Lisan Formation, which form the terminal deposit at this site. Due to the lake level decline, the complete transition into the Holocene is only recorded in the ICDP core, while sedimentation at Masada terminates earlier. The microfacies was investigated by continuous thin section microscopy, while additional macroscopic information is provided from over- and underlying sediment sections. A revised chronology using age modelling in OxCal (Ramsey 2008; Ramsey 2009; Ramsey and Lee 2013) was developed for the ICDP core and a floating varve chronology was constructed at Masada. Using these new microfacies data from marginal (Masada) and deep-water (ICDP core) sediments, the hydroclimatic variability during the final stage of Lake Lisan can be reconstructed, which could provide important insights into the development of human sedentism in the region at this time.

This dataset provides lithological data from ICDP core 5017-1-A, retrieved from the deep northern Dead Sea basin in 2010/11, for the last glacial-interglacial transition (ca. 17-11.5 ka BP). The microfacies of the Lisan Formation was investigated between ~101 and 88.5 m sediment depth below lake floor by continuous thin section microscopy, while additional macroscopic information is provided from core catchers, as well as from over- and underlying sediment sections. Thin sections were prepared following the standard procedure by Brauer and Casanova (2001) that was adjusted for salty sediments. Thin section analyses were performed on overlapping large-scale thin sections using a Zeiss Axiolab pol microscope at magnifications of 50-400x.

This dataset provides annually resolved microfacies data from ICDP core 5017-1-A, retrieved from the deep northern Dead Sea basin in 2010/11, for the last glacial-interglacial transition (ca. 17-11.5 ka BP). Sediments of the Lisan Formation were investigated between ~101 and 88.5 m sediment depth below lake floor by continuous thin section microscopy, while additional macroscopic information is provided from core catchers, as well as from over- and underlying sediment sections. Thin sections were prepared following the standard procedure by Brauer and Casanova (2001) that was adjusted for salty sediments. Thin section analyses were performed on overlapping large-scale thin sections using a Zeiss Axiolab pol microscope at magnifications of 50-400x. Microfacies analyses included varve counting and measurements of varve and sublayer thickness.

This dataset provides the results from Bayesian age depth modelling in OxCal for ICDP core 5017-1-A, retrieved from the deep northern Dead Sea basin in 2010/11, for the last glacial-interglacial transition between ~101 and 88.5 m sediment depth below lake floor (ca. 17-11.5 ka BP). The model was performed in OxCal v.4.4 using a P_Sequence (1,1,C(-2,2)) (Ramsey 2008; Ramsey 2009; Ramsey and Lee 2013) and includes three tephrochronological ages from Neugebauer et al. (2021) and three radiocarbon ages from Kitagawa et al. (2017).

This dataset provides microfacies data from the sediment profile at Masada (MAS), located at the southwestern shore of the Dead Sea for the last glacial-interglacial transition (ca. 17-11.5 ka BP). The uppermost ~3.8 m sediments of the Lisan Formation were analyzed, which form the terminal deposit at this site. About 1.37 m from the uppermost UGU to the lowermost AGU were sampled continuously for thin section analyses, while macroscopic information is provided for most of the gypsum units. Sampling was performed in 2018 and followed the subsequent procedure: after smoothing the outcrop surface with a sharp knife, stainless steel boxes (~34 cm x 5 cm) with removable side walls were pressed into the sediment along a vertical profile. The boxes were overlapping by several centimeters and a battery-operated dovetail saw was used to cut the hard gypsum sections. At the GFZ in Potsdam, the sediments were carefully transferred into aluminum boxes and impregnated with epoxy resin. Thin sections (10x2 cm) with 2 cm overlap were prepared subsequently. Thin section analyses were performed using a Zeiss Axiolab pol microscope at magnifications of 50-400x. A floating varve chronology was established between the UGU and AGU and anchored at the bottom of the AGU using the transferred age from the new OxCal age model from the ICDP core. Uncertainties are derived from the age model and varve counting. Microfacies analyses included varve counting and measurements of varve and sublayer thickness.

This dataset provides annually resolved microfacies data from ICDP core 5017-1-A, retrieved from the deep northern Dead Sea basin in 2010/11, for the last glacial-interglacial transition (ca. 14-13 ka BP). Sediments of the Lisan Formation were investigated between ~94.7 and 91.8 m sediment depth below lake floor (lithozone C2) by continuous thin section microscopy. Thin sections were prepared following the standard procedure by Brauer and Casanova (2001) that was adjusted for salty sediments. Thin section analyses were performed on overlapping large-scale thin sections using a Zeiss Axiolab pol microscope at magnifications of 50-400x. Microfacies analyses included varve counting and measurements of varve and sublayer thickness. The amount of varves in erosional gaps was interpolated and the position of mass flow deposits (MFD) is marked.

BACKGROUND: The pancreatic β cell, as the sole source of the vital hormone insulin, has been under intensive study for more than a century. Given the potential of newly created insulin-producing cells as a treatment or even cure of type 1 diabetes (T1D) and possibly in severe cases of type 2 diabetes (T2D), multiple academic and commercial laboratories are working to derive surrogate glucose-responsive, insulin-producing cells. SCOPE OF REVIEW: The recent development of advanced phenotyping technologies, including molecular, epigenomic, histological, or functional, have greatly improved our understanding of the critical properties of human β cells. Using this information, here we summarize the salient features of normal, fully functional adult human β cells, and propose minimal criteria for what should rightfully be termed 'β cells' as opposed to insulin-producing but not fully-functional surrogates that we propose should be referred to as 'β-like' cells or insulin-producing cells. MAJOR CONCLUSIONS: Clear criteria can be established to differentiate fully functional, mature β cells from 'β-like' surrogates. In addition, we outline important knowledge gaps that must be addressed to enable a greater understanding of the β cell.

As a result of deprivation of oxygen (hypoxia) and nutrients, the growth and viability of cells is reduced. Hypoxia-inducible factor (HIF)-1alpha helps to restore oxygen homeostasis by inducing glycolysis, erythropoiesis and angiogenesis. Here we show that hypoxia and hypoglycaemia reduce proliferation and increase apoptosis in wild-type (HIF-1alpha+/+) embryonic stem (ES) cells, but not in ES cells with inactivated HIF-1alpha genes (HIF-1alpha-/-); however, a deficiency of HIF-1alpha does not affect apoptosis induced by cytokines. We find that hypoxia/hypoglycaemia-regulated genes involved in controlling the cell cycle are either HIF-1alpha-dependent (those encoding the proteins p53, p21, Bcl-2) or HIF-1alpha-independent (p27, GADD153), suggesting that there are at least two different adaptive responses to being deprived of oxygen and nutrients. Loss of HIF-1alpha reduces hypoxia-induced expression of vascular endothelial growth factor, prevents formation of large vessels in ES-derived tumours, and impairs vascular function, resulting in hypoxic microenvironments within the tumour mass. However, growth of HIF-1alpha tumours was not retarded but was accelerated, owing to decreased hypoxia-induced apoptosis and increased stress-induced proliferation. As hypoxic stress contributes to many (patho)biological disorders, this new role for HIF-1alpha in hypoxic control of cell growth and death may be of general pathophysiological importance.