Facility for testing ice drills

The Rapid Access Ice Drill (RAID) is designed for subsurface scientific investigations in Antarctica. Its objectives are to drill rapidly through ice, to core samples of the transition zone and bedrock, and to leave behind a borehole observatory. These objectives required the engineering and fabrication of an entirely new drilling system that included a modified mining-style coring rig, a unique fluid circulation system, a rod skid, a power unit, and a workshop with areas for the storage of supplies and consumables. An important milestone in fabrication of the RAID was the construction of a North American Test (NAT) facility where we were able to test drilling and fluid processing functions in an environment that is as close as possible to that expected in Antarctica. Our criteria for site selection was that the area should be cold during the winter months, be located in an area of low heat flow, and be at relatively high elevation. We selected a site for the facility near Bear Lake, Utah, USA. The general design of the NAT well (NAT-1) started with a 27.3 cm (10.75 in.) outer casing cemented in a 152 m deep hole. Within that casing, we hung a 14 cm (5.5 in.) casing string, and, within that casing, a column of ice was formed. The annulus between the 14 and 27.3 cm casings provided the path for circulation of a refrigerant. After in-depth study, we chose to use liquid CO2 to cool the hole. In order to minimize the likelihood of the casing splitting due to the volume increase associated with freezing water, the hole was first cooled and then ice was formed in increments from the bottom upward. First, ice cubes were placed in the inner liner and then water was added. Using this method, a column of ice was incrementally prepared for drilling tests. The drilling tests successfully demonstrated the functioning of the RAID system. Reproducing such a facility for testing of other ice drilling systems could be advantageous to other research programs in the future

Atomic-Scale Mapping and Quantification of Local Ruddlesden-Popper Phase Variations

The Ruddlesden-Popper (An+1BnO3n+1) compounds are highly tunable materials whose functional properties can be dramatically impacted by their structural phase n. The negligible differences in formation energies for different n can produce local structural variations arising from small stoichiometric deviations. Here, we present a Python analysis platform to detect, measure, and quantify the presence of different n-phases based on atomic-resolution scanning transmission electron microscopy (STEM) images. We employ image phase analysis to identify horizontal Ruddlesden-Popper faults within the lattice images and quantify the local structure. Our semiautomated technique considers effects of finite projection thickness, limited fields of view, and lateral sampling rates. This method retains real-space distribution of layer variations allowing for spatial mapping of local n-phases to enable quantification of intergrowth occurrence and qualitative description of their distribution suitable for a wide range of layered materials

Millimeter-scale freestanding superconducting infinite-layer nickelate membranes

Progress in the study of infinite-layer nickelates has always been highly linked to materials advances. In particular, the recent development of superconductivity via hole-doping was predicated on the controlled synthesis of Ni in a very high oxidation state, and subsequent topotactic reduction to a very low oxidation state, currently limited to epitaxial thin films. Here we demonstrate a process to combine these steps with a heterostructure which includes an epitaxial soluble buffer layer, enabling the release of freestanding membranes of (Nd,Sr)NiO2 encapsulated in SrTiO3, which serves as a protective layer. The membranes have comparable structural and electronic properties to that of optimized thin films, and range in lateral dimensions from millimeters to ~100 micron fragments, depending on the degree of strain released with respect to the initial substrate. The changes in the superconducting transition temperature associated with membrane release are quite similar to those reported for substrate and pressure variations, suggestive of a common underlying mechanism. These membranes structures should provide a versatile platform for a range of experimental studies and devices free from substrate constraints

Cooperativity between the preproinsulin mRNA untranslated regions Is necessary for glucose-stimulated translation

Glucose regulates proinsulin biosynthesis via stimulation of the translation of the preproinsulin mRNA in pancreatic β-cells. However, the mechanism by which this occurs has remained unclear. Using recombinant adenoviruses that express the preproinsulin mRNA with defined alterations, the untranslated regions (UTRs) of the preproinsulin mRNA were examined for elements that specifically control translation of the mRNA in rat pancreatic islets. These studies revealed that the preproinsulin 5′-UTR was necessary for glucose stimulation of preproinsulin mRNA translation, whereas the 3′-UTR appeared to suppress translation. However, together the 5′- and 3′-UTRs acted cooperatively to markedly increase glucose-induced proinsulin biosynthesis. In primary hepatocytes the presence of the preproinsulin 3′-UTR led to reduced mRNA levels compared with the presence of the SV40 3′-UTR, consistent with the presence of mRNA stability determinants in the 3′-UTR that stabilize the preproinsulin mRNA in a pancreatic β-cell-specific manner. Translation of these mRNAs in primary hepatocytes was not stimulated by glucose, indicating that regulated translation of the preproinsulin mRNA occurs in a pancreatic β-cell-specific manner. Thus, the untranslated regions of the preproinsulin mRNA play crucial roles in regulating insulin production and therefore glucose homeostasis by regulating the translation and the stability of the preproinsulin mRNA

Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis

Heterozygous coding mutations in the INS gene that encodes preproinsulin were recently shown to be an important cause of permanent neonatal diabetes. These dominantly acting mutations prevent normal folding of proinsulin, which leads to beta-cell death through endoplasmic reticulum stress and apoptosis. We now report 10 different recessive INS mutations in 15 probands with neonatal diabetes. Functional studies showed that recessive mutations resulted in diabetes because of decreased insulin biosynthesis through distinct mechanisms, including gene deletion, lack of the translation initiation signal, and altered mRNA stability because of the disruption of a polyadenylation signal. A subset of recessive mutations caused abnormal INS transcription, including the deletion of the C1 and E1 cis regulatory elements, or three different single base-pair substitutions in a CC dinucleotide sequence located between E1 and A1 elements. In keeping with an earlier and more severe beta-cell defect, patients with recessive INS mutations had a lower birth weight (-3.2 SD score vs. -2.0 SD score) and were diagnosed earlier (median 1 week vs. 10 weeks) compared to those with dominant INS mutations. Mutations in the insulin gene can therefore result in neonatal diabetes as a result of two contrasting pathogenic mechanisms. Moreover, the recessively inherited mutations provide a genetic demonstration of the essential role of multiple sequence elements that regulate the biosynthesis of insulin in man