An Archaeological Survey of the Proposed Fannin County Bridge Study Areas Fannin County, Texas

North Texas Municipal Water District (NTMWD) is proposing to construct the Lower Bois d’Arc Creek Reservoir in northeast Fannin County, Texas. Due to the proposed inundation, nine bridge/culvert locations will be inundated, and new bridges/culverts will be constructed. White Hawk, which is handling the engineering for the project, contracted with AR Consultants, Inc. to evaluate the proposed bridge locations to determine if significant cultural resources are within the study areas. Prior to and during the cultural resources survey, it was thought that 11 locations would be impacted and 11 were surveyed. After the survey was complete, it was determined that locations 4A and 8 would not be impacted by this project. Even so, the survey results for these two locations is included in this report. All road improvements and new construction will take place within a study area that can vary from 140 to 300 feet wide. In total, 112.11 acres were surveyed. The routes were surveyed on August 29-31, 2016, January 30-February 2, and May 11 2017. During the survey, four historic sites (41FN253, 41FN255, 41FN256 and 41FN257) and one site (41FN254) with historic and prehistoric components were recorded. No historic artifacts were collected; prehistoric artifacts and notes from these sites will be curated at the Texas Archeological Research Laboratory at the University of Texas in Austin. As land access on private land was only granted within the easement, the sites on private land could only be fully defined, recorded, and evaluated within these corridors. Sites found on land owned by NTMWD were recorded fully. Because of this, site 41FN257, which sits on private land, was not fully recorded. Therefore, only the portion of the site within the project area can be evaluated, and site 41FN257 is recommended not eligible for inclusion on the National Register of Historic Places or as a State Antiquities Landmark. Sites 41FN253, 41FN254, 41FN255, and 41FN256, which were recorded fully, are also recommended not eligible for inclusion on the National Register of Historic Places or as State Antiquities Landmark. Given the results of this survey, AR Consultants, Inc. recommends that further cultural resource investigations are unnecessary for this project, and requests that the Texas Historical Commission concur with this recommendation

Lessons From the Pandemic: Engaging Wicked Problems With Transdisciplinary Deliberation

Some crises, such as those brought on or exposed by the COVID-19 pandemic, are wicked problems—large, complex problems with no immediate answer. As such, they make rich centerpieces for learning with respect to public deliberation and issue-based dialogue. This essay reflects on an experimental, transdisciplinary health and science communication course entitled Comprehending COVID-19. The course represents a collaborative effort among 14 faculty representing 10 different academic departments to create a resource for teaching students how to deliberate the pandemic, despite its attending, oversaturated, fake-news-infused, infodemic. We offer transdisciplinary deliberation as a pedagogical framework to expand communication repertoires in ways useful for sifting through the messiness of an infodemic while also developing key deliberation skills for productively engaging participatory decision-making with concern to wicked problems

Transcriptomic analysis of field-droughted sorghum from seedling to maturity reveals biotic and metabolic responses.

Drought is the most important environmental stress limiting crop yields. The C4 cereal sorghum [Sorghum bicolor (L.) Moench] is a critical food, forage, and emerging bioenergy crop that is notably drought-tolerant. We conducted a large-scale field experiment, imposing preflowering and postflowering drought stress on 2 genotypes of sorghum across a tightly resolved time series, from plant emergence to postanthesis, resulting in a dataset of nearly 400 transcriptomes. We observed a fast and global transcriptomic response in leaf and root tissues with clear temporal patterns, including modulation of well-known drought pathways. We also identified genotypic differences in core photosynthesis and reactive oxygen species scavenging pathways, highlighting possible mechanisms of drought tolerance and of the delayed senescence, characteristic of the stay-green phenotype. Finally, we discovered a large-scale depletion in the expression of genes critical to arbuscular mycorrhizal (AM) symbiosis, with a corresponding drop in AM fungal mass in the plants' roots

A VLT spectroscopic survey of RX J0152.7-1357, a forming cluster of galaxies at z=0.837

We present the results of an extensive spectroscopic survey of RX J0152.7-1357, one of the most massive distant clusters of galaxies known. Multi-object spectroscopy, carried out with FORS1 and FORS2 on the ESO Very Large Telescope (VLT), has allowed us to measure more than 200 redshifts in the cluster field and to confirm 102 galaxies as cluster members. The mean redshift of the cluster is $z=0.837 \pm 0.001$ and we estimate the velocity dispersion of the overall cluster galaxy distribution to be $\sim 1600 \mathrm{km \ s^{-1}}$. The distribution of cluster members is clearly irregular, with two main clumps that follow the X-ray cluster emission mapped by Chandra. A third clump of galaxies to the east of the central structure and at the cluster redshift has also been identified. The two main clumps have velocity dispersions of$\sim919$and$\sim737 \mathrm{km s^{-1}}$respectively, and the peculiar velocity of the two clumps suggests that they will merge into a single more massive cluster. A segregation in the star formation activity of the member galaxies is observed. All star forming galaxies are located outside the high-density peaks, which are populated only by passive galaxies. A population of red galaxies (belonging to the cluster red sequence) with clear post-starburst spectral features and [OII] ($\lambda$3727) emission lines is observed in the outskirts of the cluster. Two AGNs, which were previously confused with the diffuse X-ray emission from the intracluster medium in ROSAT and BeppoSAX observations, are found to be cluster members.Comment: 16 pages. 13 figures. Accepted for publication in Astronomy & Astrophysics. Tables 4 and 5 available in printed version. Corrected typos and missing reference

Clinical impairment in premanifest and early Huntington's disease is associated with regionally specific atrophy.

TRACK-HD is a multicentre longitudinal observational study investigating the use of clinical assessments and 3-Tesla magnetic resonance imaging as potential biomarkers for future therapeutic trials in Huntington's disease (HD). The cross-sectional data from this large well-characterized dataset provide the opportunity to improve our knowledge of how the underlying neuropathology of HD may contribute to the clinical manifestations of the disease across the spectrum of premanifest (PreHD) and early HD. Two hundred and thirty nine gene-positive subjects (120 PreHD and 119 early HD) from the TRACK-HD study were included. Using voxel-based morphometry (VBM), grey and white matter volumes were correlated with performance in four domains: quantitative motor (tongue force, metronome tapping, and gait); oculomotor [anti-saccade error rate (ASE)]; cognition (negative emotion recognition, spot the change and the University of Pennsylvania smell identification test) and neuropsychiatric measures (apathy, affect and irritability). After adjusting for estimated disease severity, regionally specific associations between structural loss and task performance were found (familywise error corrected, P < 0.05); impairment in tongue force, metronome tapping and ASE were all associated with striatal loss. Additionally, tongue force deficits and ASE were associated with volume reduction in the occipital lobe. Impaired recognition of negative emotions was associated with volumetric reductions in the precuneus and cuneus. Our study reveals specific associations between atrophy and decline in a range of clinical modalities, demonstrating the utility of VBM correlation analysis for investigating these relationships in HD

Detection of motor changes in huntington's disease using dynamic causal modeling

Deficits in motor functioning are one of the hallmarks of Huntington's disease (HD), a genetically caused neurodegenerative disorder. We applied functional magnetic resonance imaging (fMRI) and dynamic causal modeling (DCM) to assess changes that occur with disease progression in the neural circuitry of key areas associated with executive and cognitive aspects of motor control. Seventy-seven healthy controls, 62 pre-symptomatic HD gene carriers (preHD), and 16 patients with manifest HD symptoms (earlyHD) performed a motor finger-tapping fMRI task with systematically varying speed and complexity. DCM was used to assess the causal interactions among seven pre-defined regions of interest, comprising primary motor cortex, supplementary motor area (SMA), dorsal premotor cortex, and superior parietal cortex. To capture heterogeneity among HD gene carriers, DCM parameters were entered into a hierarchical cluster analysis using Ward's method and squared Euclidian distance as a measure of similarity. After applying Bonferroni correction for the number of tests, DCM analysis revealed a group difference that was not present in the conventional fMRI analysis. We found an inhibitory effect of complexity on the connection from parietal to premotor areas in preHD, which became excitatory in earlyHD and correlated with putamen atrophy. While speed of finger movements did not modulate the connection from caudal to pre-SMA in controls and preHD, this connection became strongly negative in earlyHD. This second effect did not survive correction for multiple comparisons. Hierarchical clustering separated the gene mutation carriers into three clusters that also differed significantly between these two connections and thereby confirmed their relevance. DCM proved useful in identifying group differences that would have remained undetected by standard analyses and may aid in the investigation of between-subject heterogeneity

Experience of, awareness of and help-seeking for potential cancer symptoms in smokers and non-smokers: A cross-sectional study

Background Presenting to primary care with potential cancer symptoms is contingent on one’s ability to recognize potentially serious symptoms. We investigated differences between smokers and non-smokers in symptoms experienced, awareness and consulting of potential respiratory, head and neck cancer symptoms. Methods Smokers and non-smokers aged over 50 from Yorkshire general practice lists were sent a postal questionnaire asking about symptoms, consulting and awareness of cancer symptoms. Data were analysed using STATA14. Results Response rate after one reminder was 30.5% (1205/3954). Smoking status was associated with experience of cough (p<0.001), breathlessness (p = 0.002) and tiredness (p = 0.004) with smokers (25.8% of population) more likely than never-smokers (53.6% of population) to experience all three symptoms (cough OR = 2.56;95%CI[1.75–3.75], breathlessness OR = 2.39;95%CI[1.43–4.00], tiredness OR = 1.57;95%CI[1.12–2.19]). Smoking status was associated with awareness of breathlessness as a potential cancer symptom (p = 0.035) and consulting for cough (p = 0.011) with smokers less likely to consult than never-smokers (OR = 0.37;95% CI[0.17–0.80]). Conclusion Our findings suggest that current smokers are more likely to experience cough, breathlessness and tiredness, but are less likely to consult for cough than never-smokers. To increase cancer awareness and promote consulting among smokers, innovative interventions improving symptom recognition and empowering smokers to seek help are required

Intellectual enrichment and genetic modifiers of cognition and brain volume in Huntington's disease

An important step towards the development of treatments for cognitive impairment in ageing and neurodegenerative diseases is to identify genetic and environmental modifiers of cognitive function and understand the mechanism by which they exert an effect. In Huntington’s disease, the most common autosomal dominant dementia, a small number of studies have identified intellectual enrichment, i.e. a cognitively stimulating lifestyle and genetic polymorphisms as potential modifiers of cognitive function. The aim of our study was to further investigate the relationship and interaction between genetic factors and intellectual enrichment on cognitive function and brain atrophy in Huntington’s disease. For this purpose, we analysed data from Track-HD, a multi-centre longitudinal study in Huntington’s disease gene carriers and focused on the role of intellectual enrichment (estimated at baseline) and the genes FAN1, MSH3, BDNF, COMT and MAPT in predicting cognitive decline and brain atrophy. We found that carrying the 3a allele in the MSH3 gene had a positive effect on global cognitive function and brain atrophy in multiple cortical regions, such that 3a allele carriers had a slower rate of cognitive decline and atrophy compared with non-carriers, in agreement with its role in somatic instability. No other genetic predictor had a significant effect on cognitive function and the effect of MSH3 was independent of intellectual enrichment. Intellectual enrichment also had a positive effect on cognitive function; participants with higher intellectual enrichment, i.e. those who were better educated, had higher verbal intelligence and performed an occupation that was intellectually engaging, had better cognitive function overall, in agreement with previous studies in Huntington’s disease and other dementias. We also found that intellectual enrichment interacted with the BDNF gene, such that the positive effect of intellectual enrichment was greater in Met66 allele carriers than non-carriers. A similar relationship was also identified for changes in whole brain and caudate volume; the positive effect of intellectual enrichment was greater for Met66 allele carriers, rather than for non-carriers. In summary, our study provides additional evidence for the beneficial role of intellectual enrichment and carrying the 3a allele in MSH3 in cognitive function in Huntington’s disease and their effect on brain structure

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease