Preliminary Investigation of the Ground-Water Resources of Baxter, Fulton, Izard and Sharp Counties, Arkansas

One hundred and seventy-seven drillers\u27 well reports were used to investigate the groundwater resources of Baxter, Fulton, Izard, and Sharp counties. The most widely utilized aquifer zone is composed of the Cotter and Jefferson City dolomites. The well depths range from 30 to 740 ft. with a mean and median of 264 and 225 ft., respectively. The drillers\u27 yield estimates range from 1 to 50 gpm with a mean of 12.0 gpm and a median of 10 gpm. The piezometric surface has an average hydraulic gradient of 9 ft./mile with groundwater discharge occurring along the Spring and White Rivers. Overlying the Cotter-Jefferson City aquifer is the Powell Dolomite aquifer. Well depths range from 43 to 275 ft. with a mean and median of 137 and 114 ft., respectively. Driller estimated yields range from 7 to 40 gpm with a mean and median of 18 and 15 gpm, respectively. The Everton Aquifer is composed of a complex series of interfingering sandstones and carbonate layers that may act collectively or Individually as aquifers. Well depths in this aquifer range from 8 to 812 ft. with a mean of 338 ft. and a median of 500 ft. Yields range from 1 to 40 gpm with a mean and median of 11 and 7 gpm, respectively. The least productive and least utilized, but shallowest aquifer is the St. Peter Sandstone aquifer which has a depth range of 55 to 113 ft. with a mean and median of 80 and 85 ft., respectively. The yield ranges from 1 to 20 gpm with a mean and median of 9 and 5 gpm, respectively. The Spearman Rank Correlation procedure was used to compare well yields (gpm), well depth, regolith thickness, depth to water, and piezometric surface elevation of the Cotter-Jefferson City aquifer. At ∝ = 0.1, the following relationships were established: 1) greater yield at shallow well depths, 2) greater yield where the water table is closer to the surface, 3) thicker regolith in deeper wells, and thicker regolith with increased depth to water. These correlations indicate the strong control on water movement by fractures in the aquifer, and closing off of fractures at depth, and the control of regolith thickness by depth to water rather than fracture proximity

Application of residual feedback to lunar orbiter residual analysis Final report

Orbit determination of Lunar Orbiter using residual feedbac

Pharmacological And Genetic Reversal Of Age-Dependent Cognitive Deficits Attributable To Decreased Presenilin Function

Alzheimer\u27s disease (AD) is the leading cause of cognitive loss and neurodegeneration in the developed world. Although its genetic and environmental causes are not generally known, familial forms of the disease (FAD) are attributable to mutations in a single copy of the Presenilin (PS) and amyloid precursor protein genes. The dominant inheritance pattern of FAD indicates that it may be attributable to gain or change of function mutations. Studies of FAD-linked forms of presenilin (psn) in model organisms, however, indicate that they are loss of function, leading to the possibility that a reduction in PS activity might contribute to FAD and that proper psn levels are important for maintaining normal cognition throughout life. To explore this issue further, we have tested the effect of reducing psn activity during aging in Drosophila melanogaster males. We have found that flies in which the dosage of psn function is reduced by 50% display age-onset impairments in learning and memory. Treatment with metabotropic glutamate receptor (mGluR) antagonists or lithium during the aging process prevented the onset of these deficits, and treatment of aged flies reversed the age-dependent deficits. Genetic reduction of Drosophila metabotropic glutamate receptor (DmGluRA), the inositol trisphosphate receptor (InsP(3)R), or inositol polyphosphate 1-phosphatase also prevented these age-onset cognitive deficits. These findings suggest that reduced psn activity may contribute to the age-onset cognitive loss observed with FAD. They also indicate that enhanced mGluR signaling and calcium release regulated by InsP(3)R as underlying causes of the age-dependent cognitive phenotypes observed when psn activity is reduced

Social presence and dishonesty in retail

Self-service checkouts (SCOs) in retail can benefit consumers and retailers, providing control and autonomy to shoppers independent from staff, together with reduced queuing times. Recent research indicates that the absence of staff may provide the opportunity for consumers to behave dishonestly, consistent with a perceived lack of social presence. This study examined whether a social presence in the form of various instantiations of embodied, visual, humanlike SCO interface agents had an effect on opportunistic behaviour. Using a simulated SCO scenario, participants experienced various dilemmas in which they could financially benefit themselves undeservedly. We hypothesised that a humanlike social presence integrated within the checkout screen would receive more attention and result in fewer instances of dishonesty compared to a less humanlike agent. This was partially supported by the results. The findings contribute to the theoretical framework in social presence research. We concluded that companies adopting self-service technology may consider the implementation of social presence in technology applications to support ethical consumer behaviour, but that more research is required to explore the mixed findings in the current study.<br/

Cell-derived extracellular vesicles can be used as a biomarker reservoir for glioblastoma tumor subtyping

Glioblastoma (GBM) is one of the most aggressive solid tumors for which treatment options and biomarkers are limited. Small extracellular vesicles (sEVs) produced by both GBM and stromal cells are central in the inter-cellular communication that is taking place in the tumor bulk. As tumor sEVs are accessible in biofluids, recent reports have suggested that sEVs contain valuable biomarkers for GBM patient diagnosis and follow-up. The aim of the current study was to describe the protein content of sEVs produced by different GBM cell lines and patient-derived stem cells. Our results reveal that the content of the sEVs mirrors the phenotypic signature of the respective GBM cells, leading to the description of potential informative sEV-associated biomarkers for GBM subtyping, such as CD44. Overall, these data could assist future GBM in vitro studies and provide insights for the development of new diagnostic and therapeutic methods as well as personalized treatment strategies

Genotype-Phenotype Correlation in NF1: Evidence for a More Severe Phenotype Associated with Missense Mutations Affecting NF1 Codons 844–848

Neurofibromatosis type 1 (NF1), a common genetic disorder with a birth incidence of 1:2,000–3,000, is characterized by a highly variable clinical presentation. To date, only two clinically relevant intragenic genotype-phenotype correlations have been reported for NF1 missense mutations affecting p.Arg1809 and a single amino acid deletion p.Met922del. Both variants predispose to a distinct mild NF1 phenotype with neither externally visible cutaneous/plexiform neurofibromas nor other tumors. Here, we report 162 individuals (129 unrelated probands and 33 affected relatives) heterozygous for a constitutional missense mutation affecting one of five neighboring NF1 codons—Leu844, Cys845, Ala846, Leu847, and Gly848—located in the cysteine-serine-rich domain (CSRD). Collectively, these recurrent missense mutations affect ∼0.8% of unrelated NF1 mutation-positive probands in the University of Alabama at Birmingham (UAB) cohort. Major superficial plexiform neurofibromas and symptomatic spinal neurofibromas were more prevalent in these individuals compared with classic NF1-affected cohorts (both p < 0.0001). Nearly half of the individuals had symptomatic or asymptomatic optic pathway gliomas and/or skeletal abnormalities. Additionally, variants in this region seem to confer a high predisposition to develop malignancies compared with the general NF1-affected population (p = 0.0061). Our results demonstrate that these NF1 missense mutations, although located outside the GAP-related domain, may be an important risk factor for a severe presentation. A genotype-phenotype correlation at the NF1 region 844–848 exists and will be valuable in the management and genetic counseling of a significant number of individuals

Crack growth behavior of aluminum alloy 6061 T651 under uniaxial and biaxial planar testing condition

The crack growth behavior of the aluminum alloy 6061 T651 was investigated using cruciform specimens with a measurement area of 120 x 120 x 2 mm3 with two center crack configurations of the starting notch parallel to one of the loading axes and under an angle of 45°, respectively. For the case with crack direction in one of the loading axes the load ratio R = ?min / ?max as well as the force parallel to the crack direction (resulting in different T-stresses) were changed. Crack growth rate was studied under varying T-stress. Also the retardation after single overloads was determined for R = 0.1, R = 0.5 and R = 0.8. As a result a change in T-stress does not significantly affect crack growth rate on high R ratios (R = 0.5) for constant ?F loading. In case of lower R-ratios (R = 0.1) crack growth retardation was observed at presence of a static tensile load parallel to the crack growth direction due to higher influence of crack closure. Furthermore, such tensile load results in longer retardation periods after applying an overload at R = 0.1. Less pronounced overload retardation can be assumed with tensile force FX for R = 0.8 and 1.3 times overloads. Non proportional loading with a phase shift in time between the two axes of 45° and 90° results in a mixed mode situation (mode I / mode II) at the crack tip of a crack which is orientated under 45° to the loading axes. Mode I and mode II fractions change during every cycle. A phase change of 45° did not change crack growth significantly compared with proportional load. Crack branching occurred when changing from proportional loading to non-proportional 90° phase shifted loading. The two crack tips of the center crack under 45° divided in 4 crack tips under approximately 90° to the loading axes which were simultaneous propagating for more than 10 mm. Finally, two crack tips propagated faster than the remaining two. The stress intensity factors KI and KII as well as the T-stress where calculated by FEA (ABAQUS). For the 45° crack orientation and the non-proportional load case with 90° phase shift linear elastic FEA calculations show that there are time dependent rotating principal stress axes on the crack tip during one cycle. In the unnotched (uncracked) specimen there are fixed principal stress axes also in the phase shifted loading case. The configuration with 4 cracks has a significant higher ?KI than the configuration with two crack tips while ?KII is significantly lower. In addition uniaxial crack growth measurements were performed on SENB specimen in the size of 10 x 20 x 100 mm3 covering the threshold and Paris-region for loading ratios R = 0.1, 0.3, 0.5, 0.8

Transcription-coupled nucleotide excision repair is coordinated by ubiquitin and SUMO in response to ultraviolet irradiation

Cockayne Syndrome (CS) is a severe neurodegenerative and premature aging autosomal-recessive disease, caused by inherited defects in the CSA and CSB genes, leading to defects in transcription-coupled nucleotide excision repair (TC-NER) and consequently hypersensitivity to ultraviolet (UV) irradiation. TC-NER is initiated by lesion-stalled RNA polymerase II, which stabilizes the interaction with the SNF2/SWI2 ATPase CSB to facilitate recruitment of the CSA E3 Cullin ubiquitin ligase complex. However, the precise biochemical connections between CSA and CSB are unknown. The small ubiquitin-like modifier SUMO is important in the DNA damage response. We found that CSB, among an extensive set of other target proteins, is the most dynamically SUMOylated substrate in response to UV irradiation. Inhibiting SUMOylation reduced the accumulation of CSB at local sites of UV irradiation and reduced recovery of RNA synthesis. Interestingly, CSA is required for the efficient clearance of SUMOylated CSB. However, subsequent proteomic analysis of CSA-dependent ubiquitinated substrates revealed that CSA does not ubiquitinate CSB in a UV-dependent manner. Surprisingly, we found that CSA is required for the ubiquitination of the largest subunit of RNA polymerase II, RPB1. Combined, our results indicate that the CSA, CSB, RNA polymerase II triad is coordinated by ubiquitin and SUMO in response to UV irradiation. Furthermore, our work provides a resource of SUMO targets regulated in response to UV or ionizing radiation

A novel syndrome of paediatric cataract, dysmorphism, ectodermal features, and developmental delay in Australian Aboriginal family maps to 1p35.3-p36.32

Background: A novel phenotype consisting of cataract, mental retardation, erythematous skin rash and facial dysmorphism was recently described in an extended pedigree of Australian Aboriginal descent. Large scale chromosomal re-arrangements had previously been ruled out. We have conducted a genome-wide scan to map the linkage region in this family.Methods: Genome-wide linkage analysis using Single Nucleotide Polymorphism (SNP) markers on the Affymetrix 10K SNP array was conducted and analysed using MERLIN. Three positional candidate genes (ZBTB17, EPHA2 and EPHB2) were sequenced to screen for segregating mutations. Results: Under a fully penetrant, dominant model, the locus for this unique phenotype was mapped to chromosome 1p35.3-p36.32 with a maximum LOD score of 2.41. The critical region spans 48.7 cM between markers rs966321 and rs1441834 and encompasses 527 transcripts from 364 annotated genes. No coding mutations were identified in three positional candidate genes EPHA2, EPHB2 or ZBTB17. The region overlaps with a previously reported region for Volkmann cataract and the phenotype has similarity to that reported for 1p36 monosomy. Conclusions: The gene for this syndrome is located in a 25.6 Mb region on 1p35.3-p36.32. The known cataract gene in this region (EPHA2) does not harbour mutations in this family, suggesting that at least one additional gene for cataract is present in this region.Kathryn Hattersley, Kate J Laurie, Jan E Liebelt, Jozef Gecz, Shane R Durkin, Jamie E Craig and Kathryn P Burdo