Texas STATEMAP Program Summary, FY19 (2019–2020)

Five geologic maps have been completed at a 1:24,000 scale in four project areas with support from STATEMAP and the Bureau of Economic Geology's State of Texas Advanced Resource Recovery program (STARR). Three of these maps were on the Texas Coastal Plain, including one (the Lake Stephenson quadrangle) on the upper Texas Coastal Plain in the Galveston Bay area and two (the Bloomington and Olivia quadrangles) on the middle Texas Coastal Plain in the Matagorda Bay area. These maps continue efforts to: 1. Better understand the evolution of the coastal plain in response to sea-level changes associated with numerous Quaternary glacial and interglacial cycles. 2. Develop more effective methods to map low-relief coastal deposits using high-resolution topographic maps produced from airborne lidar data and near-surface geophysical methods. High-resolution topography and geophysical methods both aid in the identification of stratal units and their distribution in areas where exposures are poor or nonexistent. Mineral-resource mapping produced one map (the Katemcy quadrangle) to extend recent mapping of an industrial sand resource area in central Texas. This map facilitates the development of mineral resources of the state, emphasizing those that will help meet the demand for industrial sand for hydraulic fracturing and construction. The detailed map can be used to evaluate and explore the mineral-resource potential of the area. Mapping in the central Texas urban growth corridor northeast of Austin produced one map (the Taylor quadrangle) that extends previous mapping in this critical urban growth and transportation corridor. This map addresses the ongoing need for planning and managing groundwater, surface water, land use, and construction projects where rapid population growth and suburban development have caused an increased demand for water and earth resources.Bureau of Economic Geolog

Age of onset and cumulative risk of mental disorders:a cross-national analysis of population surveys from 29 countries

Background: Information on the frequency and timing of mental disorder onsets across the lifespan is of fundamental importance for public health planning. Broad, cross-national estimates of this information from coordinated general population surveys were last updated in 2007. We aimed to provide updated and improved estimates of age-of-onset distributions, lifetime prevalence, and morbid risk. Methods: In this cross-national analysis, we analysed data from respondents aged 18 years or older to the World Mental Health surveys, a coordinated series of cross-sectional, face-to-face community epidemiological surveys administered between 2001 and 2022. In the surveys, the WHO Composite International Diagnostic Interview, a fully structured psychiatric diagnostic interview, was used to assess age of onset, lifetime prevalence, and morbid risk of 13 DSM-IV mental disorders until age 75 years across surveys by sex. We did not assess ethnicity. The surveys were geographically clustered and weighted to adjust for selection probability, and standard errors of incidence rates and cumulative incidence curves were calculated using the jackknife repeated replications simulation method, taking weighting and geographical clustering of data into account. Findings: We included 156 331 respondents from 32 surveys in 29 countries, including 12 low-income and middle-income countries and 17 high-income countries, and including 85 308 (54·5%) female respondents and 71 023 (45·4%) male respondents. The lifetime prevalence of any mental disorder was 28·6% (95% CI 27·9–29·2) for male respondents and 29·8% (29·2–30·3) for female respondents. Morbid risk of any mental disorder by age 75 years was 46·4% (44·9–47·8) for male respondents and 53·1% (51·9–54·3) for female respondents. Conditional probabilities of first onset peaked at approximately age 15 years, with a median age of onset of 19 years (IQR 14–32) for male respondents and 20 years (12–36) for female respondents. The two most prevalent disorders were alcohol use disorder and major depressive disorder for male respondents and major depressive disorder and specific phobia for female respondents. Interpretation: By age 75 years, approximately half the population can expect to develop one or more of the 13 mental disorders considered in this Article. These disorders typically first emerge in childhood, adolescence, or young adulthood. Services should have the capacity to detect and treat common mental disorders promptly and to optimise care that suits people at these crucial parts of the life course. Funding: None.</p

Ancillary human health benefits of improved air quality resulting from climate change mitigation

<p>Abstract</p> <p>Background</p> <p>Greenhouse gas (GHG) mitigation policies can provide ancillary benefits in terms of short-term improvements in air quality and associated health benefits. Several studies have analyzed the ancillary impacts of GHG policies for a variety of locations, pollutants, and policies. In this paper we review the existing evidence on ancillary health benefits relating to air pollution from various GHG strategies and provide a framework for such analysis.</p> <p>Methods</p> <p>We evaluate techniques used in different stages of such research for estimation of: (1) changes in air pollutant concentrations; (2) avoided adverse health endpoints; and (3) economic valuation of health consequences. The limitations and merits of various methods are examined. Finally, we conclude with recommendations for ancillary benefits analysis and related research gaps in the relevant disciplines.</p> <p>Results</p> <p>We found that to date most assessments have focused their analysis more heavily on one aspect of the framework (e.g., economic analysis). While a wide range of methods was applied to various policies and regions, results from multiple studies provide strong evidence that the short-term public health and economic benefits of ancillary benefits related to GHG mitigation strategies are substantial. Further, results of these analyses are likely to be underestimates because there are a number of important unquantified health and economic endpoints.</p> <p>Conclusion</p> <p>Remaining challenges include integrating the understanding of the relative toxicity of particulate matter by components or sources, developing better estimates of public health and environmental impacts on selected sub-populations, and devising new methods for evaluating heretofore unquantified and non-monetized benefits.</p

Solid-phase arsenic speciation in aquifer sediments: A micro-X-ray absorption spectroscopy approach for quantifying trace-level speciation

Arsenic (As) is a geogenic contaminant affecting groundwater in geologically diverse systems globally. Arsenic release from aquifer sediments to groundwater is favored when biogeochemical conditions, especially oxidation-reduction (redox) potential, in aquifers fluctuate. The specific objective of this research is to identify the solid-phase sources and geochemical mechanisms of release of As in aquifers of the Des Moines Lobe glacial advance. The overarching concept is that conditions present at the aquifer-aquitard interfaces promote a suite of geochemical reactions leading to mineral alteration and release of As to groundwater. A microprobe X-ray absorption spectroscopy (μXAS) approach is developed and applied to rotosonic drill core samples to identify the solid-phase speciation of As in aquifer, aquitard, and aquifer-aquitard interface sediments. This approach addresses the low solid-phase As concentrations, as well as the fine-scale physical and chemical heterogeneity of the sediments. The spectroscopy data are analyzed using novel cosine-distance and correlation-distance hierarchical clustering for Fe 1s and As 1s μXAS datasets. The solid-phase Fe and As speciation is then interpreted using sediment and well-water chemical data to propose solid-phase As reservoirs and release mechanisms. The results confirm that in two of the three locations studied, the glacial sediment forming the aquitard is the source of As to the aquifer sediments. The results are consistent with three different As release mechanisms: (1) desorption from Fe (oxyhydr)oxides, (2) reductive dissolution of Fe (oxyhydr)oxides, and (3) oxidative dissolution of Fe sulfides. The findings confirm that glacial sediments at the interface between aquifer and aquitard are geochemically active zones for As. The diversity of As release mechanisms is consistent with the geographic heterogeneity observed in the distribution of elevated-As wells

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Long-Term Outcomes and the Post-Intensive Care Syndrome in Critically Ill Children: A North American Perspective

Advances in medical and surgical care for children in the pediatric intensive care unit (PICU) have led to vast reductions in mortality, but survivors often leave with newly acquired or worsened morbidity. Emerging evidence reveals that survivors of pediatric critical illness may experience a constellation of physical, emotional, cognitive, and social impairments, collectively known as the “post-intensive care syndrome in pediatrics” (PICs-P). The spectrum of PICs-P manifestations within each domain are heterogeneous. This is attributed to the wide age and developmental diversity of children admitted to PICUs and the high prevalence of chronic complex conditions. PICs-P recovery follows variable trajectories based on numerous patient, family, and environmental factors. Those who improve tend to do so within less than a year of discharge. A small proportion, however, may actually worsen over time. There are many gaps in our current understanding of PICs-P. A unified approach to screening, preventing, and treating PICs-P-related morbidity has been hindered by disparate research methodology. Initiatives are underway to harmonize clinical and research priorities, validate new and existing epidemiologic and patient-specific tools for the prediction or monitoring of outcomes, and define research priorities for investigators interested in long-term outcomes

Sirtuins and Immuno-Metabolism of Sepsis

Sepsis and septic shock are the leading causes of death in non-coronary intensive care units worldwide. During sepsis-associated immune dysfunction, the early/hyper-inflammatory phase transitions to a late/hypo-inflammatory phase as sepsis progresses. The majority of sepsis-related deaths occur during the hypo-inflammatory phase. There are no phase-specific therapies currently available for clinical use in sepsis. Metabolic rewiring directs the transition from hyper-inflammatory to hypo-inflammatory immune responses to protect homeostasis during sepsis inflammation, but the mechanisms underlying this immuno-metabolic network are unclear. Here, we review the roles of NAD+ sensing Sirtuin (SIRT) family members in controlling immunometabolic rewiring during the acute systemic inflammatory response associated with sepsis. We discuss individual contributions among family members SIRT 1, 2, 3, 4 and 6 in regulating the metabolic switch between carbohydrate-fueled hyper-inflammation to lipid-fueled hypo-inflammation. We further highlight the role of SIRT1 and SIRT2 as potential &ldquo;druggable&rdquo; targets for promoting immunometabolic homeostasis and increasing sepsis survival