Secondary Natural Gas Recovery: Targeted Technology Applications for Infield Reserve Growth in Fluvial Reservoirs, Stratton Field, South Texas

Integrated evaluations of geology, geophysics, reservoir engineering, and petrophysics were conducted for mid-Oligocene-age fluvial reservoirs in Stratton field as part of this study. Located in South Texas within the Frio Fluvial-Deltaic Sandstone along the Vicksburg Fault Zone play (FR-4), Stratton field represents a mature gas field with significant opportunities for natural gas reserve appreciation. These fluvial reservoirs exhibit heterogeneity and often contain multiple compartments. The study identifies a considerable potential for reserve appreciation, with documented opportunities for a 100 percent increase in reserves within a large contiguous area of Stratton field, despite 40 years of prior development. Remaining natural gas reserves can be accessed through recompletion of existing wells that have bypassed reservoir compartments or by drilling infield wells to target compartments not effectively drained at current well spacing. Exploration efforts to discover new reservoirs, identify incompletely drained compartments, or tap bypassed gas zones in old fields can benefit from detailed geological studies integrating engineering, petrophysical, and geophysical methodologies. Various geophysical techniques, including 3-D surface seismic, vertical seismic profiling, amplitude versus offset, and 2-D seismic inversion, were utilized to visualize subtle changes in reservoir topology and compartment boundaries at depths as low as 6,800 ft. The study delineates three classes of compartment sizes based on analysis of ten groups of Frio reservoirs. Forward stochastic modeling of maximum gas recovery suggests that well spacings of 340, 200, and 60 acres (or less) offer optimal gas-contact efficiency in large, medium, and small compartment size reservoirs, respectively.Bureau of Economic Geolog

Governance in Large Nonprofit Health Systems: Current Profile and Emerging Patterns

From the foreword: Nonprofit healthcare organizations are not exempt from good governance. In fact, more today than ever, the hospitals and health care systems of this country must have the discipline and commitment to organize their governance structures and practices to provide forward-thinking leadership and stand up to scrutiny from any type of evaluation and review. As we move from “sick care” organizations to “health care” organizations with accountability for the health of the population of our communities from birth to end-of-life, the role of governance becomes even more critical. Fourteen of the largest and most notable health care systems in this country have been included in a research study to examine their governance structures and practices in relation to nine benchmarks. The CEOs and board members of these organizations were interviewed about their structures, processes and cultures, and then compared to national best practices. The study also included close review of pertinent system documents. This report is a must read for hospital and health care system CEOs and boards. It provides evidence-based outcomes that will assist an organization in advancing its governance practices. This study outlines critical success factors for governance structure and performance. It answers many questions that boards may be struggling with today and provides advancing actions. The research methodology is thorough and reliable with specific outcomes that provide high-performance opportunities. Each CEO who participated in the research study has written about a best practice in his or her respective organization that advances governance responsibility. These insights add a personal dimension to this report.https://uknowledge.uky.edu/hsm_book/1000/thumbnail.jp

Governance in Nonprofit Community Health Systems: An Initial Report on CEO Perspectives

Compares the structures, compositions, practices, processes, and cultures of nonprofit healthcare governing boards with selected benchmarks of good governance. Presents survey data from 123 community health systems and includes recommendations

Characteristics of vertebrate-dispersed fruits in Hong Kong

Hong Kong has a native angiosperm flora of approximately 1800 species, of which 27% (482 spp) bear fleshy, presumably vertebrate-dispersed fruits, including 76% of the 337 tree and shrub species and 70% of the 103 climber species. Morphological characteristics were determined for 255 species and nutritional characteristics of the fruit pulp for 153 species. Most fruit species were black (45 1%) or red (24.3%) and 85.9% had a mean diameter <13 mm Nutritional characteristics varied widely between species with ranges and median values as follows: pulp percentage (range 10.0-99 2%, median 69 2%), water content of pulp (11 1-94 0%, 78%), lipid (0-84 0%, 2 0%), soluble carbohydrate (4-88%, 53%), nitrogen (0.2-3.4%, 0.86%), neutral detergent fibre (1-44%, 14.3%) Fruit development time (50-360 d, 156 d) showed a negative correlation with lipid content, but no significant correlation with fruit or seed size. Principal components analysis of fruit characteristics was dominated by a trend from single-seeded fruits with a thin, lipid-rich pulp layer to multiple-seeded fruits with much, watery, carbohydrate-rich pulp. Bird-dispersed species cover the full range of fruit characteristics except those too large to swallow and too hard to peck bits from. Mammals (bats, civets and/or macaques) are known or suspected to consume most of the fruits too large for birds as well as many bird fruits but none with high-lipid content Summer fruits (May-September) were significantly larger and had significantly higher seed size and carbohydrate content than winter fruits (November-March) Winter fruits took more than twice as long to develop as summer fruits.published_or_final_versio

Effect of a reduction in glomerular filtration rate after nephrectomy on arterial stiffness and central hemodynamics: rationale and design of the EARNEST study

Background: There is strong evidence of an association between chronic kidney disease (CKD) and cardiovascular disease. To date, however, proof that a reduction in glomerular filtration rate (GFR) is a causative factor in cardiovascular disease is lacking. Kidney donors comprise a highly screened population without risk factors such as diabetes and inflammation, which invariably confound the association between CKD and cardiovascular disease. There is strong evidence that increased arterial stiffness and left ventricular hypertrophy and fibrosis, rather than atherosclerotic disease, mediate the adverse cardiovascular effects of CKD. The expanding practice of live kidney donation provides a unique opportunity to study the cardiovascular effects of an isolated reduction in GFR in a prospective fashion. At the same time, the proposed study will address ongoing safety concerns that persist because most longitudinal outcome studies have been undertaken at single centers and compared donor cohorts with an inappropriately selected control group.&lt;p&gt;&lt;/p&gt; Hypotheses: The reduction in GFR accompanying uninephrectomy causes (1) a pressure-independent increase in aortic stiffness (aortic pulse wave velocity) and (2) an increase in peripheral and central blood pressure.&lt;p&gt;&lt;/p&gt; Methods: This is a prospective, multicenter, longitudinal, parallel group study of 440 living kidney donors and 440 healthy controls. All controls will be eligible for living kidney donation using current UK transplant criteria. Investigations will be performed at baseline and repeated at 12 months in the first instance. These include measurement of arterial stiffness using applanation tonometry to determine pulse wave velocity and pulse wave analysis, office blood pressure, 24-hour ambulatory blood pressure monitoring, and a series of biomarkers for cardiovascular and bone mineral disease.&lt;p&gt;&lt;/p&gt; Conclusions: These data will prove valuable by characterizing the direction of causality between cardiovascular and renal disease. This should help inform whether targeting reduced GFR alongside more traditional cardiovascular risk factors is warranted. In addition, this study will contribute important safety data on living kidney donors by providing a longitudinal assessment of well-validated surrogate markers of cardiovascular disease, namely, blood pressure and arterial stiffness. If any adverse effects are detected, these may be potentially reversed with the early introduction of targeted therapy. This should ensure that kidney donors do not come to long-term harm and thereby preserve the ongoing expansion of the living donor transplant program.&lt;p&gt;&lt;/p&gt

The severity of acute kidney injury predicts progression to chronic kidney disease

Acute kidney injury (AKI) is associated with progression to advanced chronic kidney disease (CKD). We tested whether patients who survive AKI and are at higher risk for CKD progression can be identified during their hospital admission, thus providing opportunities to intervene. This was assessed in patients in the Department of Veterans Affairs Healthcare System hospitalized with a primary diagnosis indicating AKI (ICD9 codes 584.xx). In the exploratory phase, three multivariate prediction models for progression to stage 4 CKD were developed. In the confirmatory phase, the models were validated in 11,589 patients admitted for myocardial infarction or pneumonia during the same time frame that had RIFLE codes R, I, or F and complete data for all predictor variables. Of the 5351 patients in the AKI group, 728 entered stage 4 CKD after hospitalization. Models 1, 2, and 3 were all significant with ‘c' statistics of 0.82, 0.81, and 0.77, respectively. In model validation, all three were highly significant when tested in the confirmatory patients, with moderate to large effect sizes and good predictive accuracy (‘c' 0.81–0.82). Patients with AKI who required dialysis and then recovered were at especially high risk for progression to CKD. Hence, the severity of AKI is a robust predictor of progression to CKD

Establishing race-, gender- and age-specific reference intervals for pyridoxal 5’-phosphate in the NHANES population to better identify adult hypophosphatasia

Introduction Bisphosphonate treatment in adults with hypophosphatasia (HPP) may increase fracture risk. PLP is a useful marker in biochemically differentiating HPP from osteoporosis in adults. In order to identify elevated PLP, robust reference intervals are needed which are calculated in a large, representative sample population. Methods Complete data from 9069 individuals (ages 20–80, 50.6% female) from two years of the NHANES Survey (2007–2008 and 2009–2010) were investigated. Differences in PLP in the presence of four factors; inflammation (CRP ≥5.0 mg/L), low ALP (<36 IU/L), chronic kidney disease (eGFR <60 mL/min/1.732), and daily vitamin B6 supplementation, were investigated. Race, gender and age differences in PLP were then investigated; 95% reference intervals were calculated that reflected these differences. Results Inflammation and chronic kidney disease were associated with lower PLP (p < .0001 and p = .0005 respectively), while low ALP and vitamin B6 supplementation were associated with higher PLP (both p < .0001). Individuals were excluded based on the presence of these factors; a reference interval population (n = 4463) was established. There were significant differences in PLP depending on race and gender (p < .0001) Increasing age was correlated with decreasing PLP (spearman's rho −0.204, p < .0001). Race- and gender-specific 95% reference intervals were calculated. In male patients, these were also calculated according to age groups: young and older adults (ages 20–49 years and ≥50 years respectively). Conclusions In order to identify adult hypophosphatasia based on elevated PLP, considerations must be made depending on the race, gender and age of the individual. Factors associated with significant differences in PLP must also be considered when assessing biochemical measurements

Large-scale proteomic analysis of human brain identifies proteins associated with cognitive trajectory in advanced age

In advanced age, some individuals maintain a stable cognitive trajectory while others experience a rapid decline. Such variation in cognitive trajectory is only partially explained by traditional neurodegenerative pathologies. Hence, to identify new processes underlying variation in cognitive trajectory, we perform an unbiased proteome-wide association study of cognitive trajectory in a discovery (n = 104) and replication cohort (n = 39) of initially cognitively unimpaired, longitudinally assessed older-adult brain donors. We find 579 proteins associated with cognitive trajectory after meta-analysis. Notably, we present evidence for increased neuronal mitochondrial activities in cognitive stability regardless of the burden of traditional neuropathologies. Furthermore, we provide additional evidence for increased synaptic abundance and decreased inflammation and apoptosis in cognitive stability. Importantly, we nominate proteins associated with cognitive trajectory, particularly the 38 proteins that act independently of neuropathologies and are also hub proteins of protein co-expression networks, as promising targets for future mechanistic studies of cognitive trajectory.Accelerating Medicine Partnership for AD [U01AG046161, U01 AG061357]; Emory Alzheimer's Disease Research Center [P50 AG025688]; NINDS Emory Neuroscience Core [P30 NS055077]; intramural program of the National Institute on Aging (NIA); Alzheimer's Association; Alzheimer's Research UK; Michael J. Fox Foundation for Parkinson's Research; Weston Brain Institute Biomarkers Across Neurodegenerative Diseases Grant [11060]; National Institute of Neurological Disorders and Stroke [U24 NS072026]; National Institute on Aging [P30 AG19610]; Arizona Department of Health Services [211002]; Arizona Biomedical Research Commission [4001, 0011, 05-901, 1001]; [R01 AG056533]; [R01 AG053960]; [U01 MH115484]; [I01 BX003853]; [IK2 BX001820]; [R01 AG061800]; [R01 AG057911]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Defining Anuran Malformations in the Context of a Developmental Problem

This paper summarizes terminology and general concepts involved in animal development for the purpose of providing background for the study and understanding of frog malformations. The results of our radiographic investigation of rear limb malformations in Rana pipiens provide evidence that frog malformations are the product of early developmental errors. Although bacteria, parasites and viruses were identified in these metamorphosed frogs, the relevant window to look for the teratogenic affect of these agents is in the early tadpole stage during limb development. As a result, our microbiological findings must be regarded as inconclusive relative to determining their contribution to malformations because we conducted our examinations on metamorphosed frogs not tadpoles. Future studies need to look at teratogenic agents (chemical, microbial, physical or mechanical) that are present in the embryo, tadpole, and their environments at stages of development that are relevant for the malformation type. The impact of these teratogenic agents then needs to be assessed in appropriate animal models using studies that are designed to mimic field conditions. The results of these laboratory tests should then be analyzed in such a way that will allow comparison with the findings in the wild-caught tadpoles and frogs

International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci.

The risk of posttraumatic stress disorder (PTSD) following trauma is heritable, but robust common variants have yet to be identified. In a multi-ethnic cohort including over 30,000 PTSD cases and 170,000 controls we conduct a genome-wide association study of PTSD. We demonstrate SNP-based heritability estimates of 5-20%, varying by sex. Three genome-wide significant loci are identified, 2 in European and 1 in African-ancestry analyses. Analyses stratified by sex implicate 3 additional loci in men. Along with other novel genes and non-coding RNAs, a Parkinson's disease gene involved in dopamine regulation, PARK2, is associated with PTSD. Finally, we demonstrate that polygenic risk for PTSD is significantly predictive of re-experiencing symptoms in the Million Veteran Program dataset, although specific loci did not replicate. These results demonstrate the role of genetic variation in the biology of risk for PTSD and highlight the necessity of conducting sex-stratified analyses and expanding GWAS beyond European ancestry populations