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Search Results: 1 - 10 of 228111 matches for " Barry R Davis "
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Direct Fitness Correlates and Thermal Consequences of Facultative Aggregation in a Desert Lizard
Alison R. Davis Rabosky, Ammon Corl, Heather E. M. Liwanag, Yann Surget-Groba, Barry Sinervo
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0040866
Abstract: Social aggregation is a common behavioral phenomenon thought to evolve through adaptive benefits to group living. Comparing fitness differences between aggregated and solitary individuals in nature – necessary to infer an evolutionary benefit to living in groups – has proven difficult because communally-living species tend to be obligately social and behaviorally complex. However, these differences and the mechanisms driving them are critical to understanding how solitary individuals transition to group living, as well as how and why nascent social systems change over time. Here we demonstrate that facultative aggregation in a reptile (the Desert Night Lizard, Xantusia vigilis) confers direct reproductive success and survival advantages and that thermal benefits of winter huddling disproportionately benefit small juveniles, which can favor delayed dispersal of offspring and the formation of kin groups. Using climate projection models, however, we estimate that future aggregation in night lizards could decline more than 50% due to warmer temperatures. Our results support the theory that transitions to group living arise from direct benefits to social individuals and offer a clear mechanism for the origin of kin groups through juvenile philopatry. The temperature dependence of aggregation in this and other taxa suggests that environmental variation may be a powerful but underappreciated force in the rapid transition between social and solitary behavior.
Genetic and Adverse Health Outcome Associations with Treatment Resistant Hypertension in GenHAT
Amy I. Lynch,Marguerite R. Irvin,Barry R. Davis,Charles E. Ford,John H. Eckfeldt,Donna K. Arnett
International Journal of Hypertension , 2013, DOI: 10.1155/2013/578578
Abstract: Treatment resistant hypertension (TRH) is defined as uncontrolled hypertension (HTN) despite the use of ≥3 antihypertensive medication classes or controlled HTN while treated with ≥4 antihypertensive medication classes. Risk factors for TRH include increasing age, diminished kidney function, higher body mass index, diabetes, and African American (AA) race. Importantly, previous studies suggest a genetic role in TRH, although the genetics of TRH are largely understudied. With 2203 treatment resistant cases and 2354 treatment responsive controls (36% AA) from the Genetics of Hypertension Associated Treatment Study (GenHAT), we assessed the association of 78 candidate gene polymorphisms with TRH status using logistic regression. After stratifying by race and adjusting for potential confounders, there were 2 genetic variants in the AGT gene (rs699, rs5051) statistically significantly associated with TRH among white participants. The Met allele of rs699 and the G allele of rs5051 were positively associated with TRH: ?(1.12–1.44), , and ?(1.20–1.53), , respectively. There was no similar association among AA participants (race interaction for rs699 and for rs5051). This research contributes to our understanding of the genetic basis of TRH, and further genetic studies of TRH may help reach the goal of better clinical outcomes for hypertensive patients. 1. Introduction Multidrug resistance to blood pressure (BP) lowering treatments is a growing problem in the USA [1]. In a recent report based on the National Health and Nutrition Examination Surveys (NHANES) collected in 1998–1994, 1999–2004, and 2005–2008, the percentage of treated uncontrolled patients on monotherapy fell, whereas the percentage on at least 3 medications increased over time [1]. Among those most severely affected are persons with treatment resistant hypertension (TRH) who have uncontrolled hypertension (HTN) on ≥3 antihypertensive medication classes or require ≥4 antihypertensive medications to reach their BP goals [2]. Recently, multiple studies have reported that the prevalence of TRH is 10–20% among those with HTN. However, some limitations of these estimates in the context of epidemiological studies are noted (e.g., potential misclassification due to BP measuring technique, nonadherence to medication, inadequate dosing, white-coat hypertension, and/or secondary causes of HTN) [3, 4]. Most concerning is the fact that TRH is consistently associated with increased cardiovascular disease (CVD) morbidity and mortality compared to more easily controlled HTN [3, 4]. Demonstrated risk factors for
Pharmacogenetic Associations of MMP9 and MMP12 Variants with Cardiovascular Disease in Patients with Hypertension
Rikki M. Tanner, Amy I. Lynch, Victoria H. Brophy, John H. Eckfeldt, Barry R. Davis, Charles E. Ford, Eric Boerwinkle, Donna K. Arnett
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023609
Abstract: Objectives MMP-9 and -12 function in tissue remodeling and may play roles in cardiovascular disease (CVD). We assessed associations of four MMP polymorphisms and three antihypertensive drugs with cardiovascular outcomes. Methods Hypertensives (n = 42,418) from a double-blind, randomized, clinical trial were randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin treatment (mean follow up, 4.9 years). The primary outcome was coronary heart disease (CHD). Secondary outcomes included combined CHD, all CVD outcomes combined, stroke, heart failure (HF), and mortality. Genotype-treatment interactions were tested. Results There were 38,698 participants genotyped for at least one of the polymorphisms included here. For MMP9 R668Q (rs2274756), lower hazard ratios (HRs) were found for AA subjects for most outcomes when treated with chlorthalidone versus amlodipine (eg., CCHD: GG = 1.00, GA = 1.01, AA = 0.64; P = 0.038). For MMP9 R279Q (rs17576), modest pharmacogenetic findings were observed for combined CHD and the composite CVD outcome. For MMP12 N122S (rs652438), lower HRs were observed for CHD in subjects carrying at least one G allele and being treated with chlorthalidone versus lisinopril (CHD: AA = 1.07, AG = 0.80, GG = 0.49; P = 0.005). In the lisinopril-amlodipine comparison, higher HRs were observed for participants having at least one G allele at the MMP12 N122S locus (CHD: AA = 0.94, AG = 1.19, GG = 1.93; P = 0.041). For MMP12 ?82A>G (rs2276109), no pharmacogenetic effect was found for the primary outcome, although lower HRs were observed for AA homozygotes in the chlorthalidone-amlodipine comparison for HF (P = 0.015). Conclusions We observed interactions between antihypertensive drugs and MMP9 and MMP12 for CHD and composite CVD. The data suggest that these genes may provide useful clinical information with respect to treatment decisions.
Pharmacogenetic Association of NOS3 Variants with Cardiovascular Disease in Patients with Hypertension: The GenHAT Study
Xue Zhang, Amy I. Lynch, Barry R. Davis, Charles E. Ford, Eric Boerwinkle, John H. Eckfeldt, Catherine Leiendecker-Foster, Donna K. Arnett
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034217
Abstract: Nitric oxide synthase 3 (NOS3) catalyzes production of NO in the endothelium and may play a role in cardiovascular disease (CVD). We assessed the pharmacogenetic associations of three NOS3 polymorphisms and three antihypertensive drugs with CVD outcomes. Hypertensive subjects (n = 30,280) from a multi-center, double-blind clinical trial were randomized to chlorthalidone, amlodipine, or lisinopril treatment (mean follow up, 4.9 years). Outcomes included coronary heart disease (CHD: fatal CHD and nonfatal myocardial infarction); stroke; heart failure (fatal, requiring hospitalization, or outpatient treatment); all-cause mortality; and end-stage renal disease (ESRD). Main effects of NOS3 variants on outcome and genotype-treatment interactions were tested. For NOS3 ?690 C>T (rs3918226), a higher hazard ratio (HR) was found in minor allele carriers for CHD (CC = 1.00, CT+TT = 1.12 (95% confidence interval (CI) = 1.00–1.26), P = 0.048). For NOS3 ?922 A>G (rs1800779), a higher HR was found in minor allele carriers for heart failure (AA = 1.00, AG+GG = 1.10 (CI = 1.00–1.21), P = 0.046). Significant pharmacogenetic findings were observed for stroke and all-cause mortality. For ?690 C>T, a lower HR was observed for stroke in minor allele carriers when treated with amlodipine versus lisinopril (CC = 0.85 (CI = 0.73–0.99), CT+TT = 0.49 (CI = 0.31–0.80), P = 0.04). For glu298asp G>T (rs1799983), a lower HR was observed for all-cause mortality in minor allele carriers when treated with amlodipine versus lisinopril (GG = 1.01 (CI = 0.91–1.13), GT+TT = 0.85 (CI = 0.75–0.97), P = 0.04). We observed significant associations with NOS3 variants and CHD and heart failure and significant pharmacogenetic effects for stroke and all cause mortality. This suggests that NOS3 variants may potentially provide useful clinical information with respect to treatment decisions in the future.
Transcription factor network downstream of protease activated receptors (PARs) modulating mouse bladder inflammation
Ricardo Saban, Cindy Simpson, Carole A Davis, Igor Dozmorov, Julie Maier, Ben Fowler, Michael A Ihnat, Robert E Hurst, Barry K Wershil, Marcia R Saban
BMC Immunology , 2007, DOI: 10.1186/1471-2172-8-17
Abstract: For this purpose, we used a protein/DNA combo array containing 345 different TF consensus sequences. Next, the TF selected was validated by EMSA and IHC. As mast cells seem to play a fundamental role in bladder inflammation, we determined whether c-kit receptor deficient (Kitw/Kitw-v) mice have an abrogated response to PAR stimulation. Finally, TFEB antibody was used for CHIP/Q-PCR assay and revealed up-regulation of genes known to be downstream of TFEB.TFEB, a member of the MiTF family of basic helix-loop-helix leucine zipper, was the only TF commonly up-regulated by all PAR-APs. IHC results confirm a correlation between inflammation and TFEB expression in C57BL/6 mice. In contrast, Kitw/Kitw-v mice did not exhibit inflammation in response to PAR activation. EMSA results confirmed the increased TFEB binding activity in C57BL/6 but not in Kitw/Kitw-v mice.This is the first report describing the increased expression of TFEB in bladder inflammation in response to PAR activation. As TFEB belongs to a family of TFs essential for mast cell survival, our findings suggest that this molecule may influence the participation of mast cells in PAR-mediated inflammation and that targeting TFEB/MiTF activity may be a novel approach for the treatment of bladder inflammatory disorders.Attesting to the importance of inflammation in disease, a trans-NIH Inflammation Working Group was formed recently to collect input on proposed research areas within the overarching theme of "Inflammation as a Common Mechanism of Disease" [1]. In general, inflammation plays a role in most bladder pathologies, including bladder cancer [2-5], and represents a defensive reaction to injury caused by physical damage, chemical substances, micro-organisms, or other agents [1,2]. In particular, several lines of evidence suggest that neurogenic bladder inflammation involves the participation of mast cells and sensory nerves. We previously demonstrated a key role for mast cells and their products in bladder inf
Incomplete Reporting of HIV/AIDS by Uganda’s Surveillance System and the Associated Factors  [PDF]
Denis Akankunda Bwesigye, Barry M. Loneck, Barry R. Sherman
Open Journal of Preventive Medicine (OJPM) , 2016, DOI: 10.4236/ojpm.2016.64011
Abstract: Introduction: The United States government supported Ugandan government by introducing the District Health Information Software 2 (DHIS2) in 2012 to improve HIV/AIDS surveillance. Districts have yet to fully adopt this relatively new system given a 70.2% reporting completeness achieved nationally between April-June 2013. Methods: The study examined one dependent variable of districts’ reporting completeness against four independent variables: 1) Number of client visits; 2) Number of district health units; 3) Number of NGOs delivering HIV/AIDS services; and 4) Regional location. The study employed cross-sectional study design which allowed researchers to compare many different variables at the same time. HIV/AIDS program data that were reported by districts into DHIS2 during the period of April to June 2013 were used to assess for reporting completeness. Findings: Districts with the lowest number of client visits (under 2500) achieved the highest mean reporting completeness (81.6%), whereas a range of 2501 - 5000, or over 5001client visits recorded 72.4% and 51.7% respectively. The higher the number of client visits is, the lower the reporting completeness is (p < 0.05). Those districts that were receiving support from only one and two NGO recorded 56.7% and 67.2% respectively. Districts supported by over three NGOs had the highest (80.6%) mean reporting completeness. NGOs-district support was statistically associated with reporting completeness (p < 0.05). The number of health units operated by a district was also significantly associated with reporting completeness (p < 0.05). The regional location of a district was not associated with reporting completeness (p = 0.674). Conclusion: The study results led us to recommend targeted future NGO support to districts with higher patient volume for HIV/AIDS services. Particularly, newly funded NGOs are to be established in districts operating over 40 health units. Incomplete reporting undermines identification of HIV-affected individuals and limits the ability to make evidence-based decisions regarding HIV/AIDS program planning and service delivery.
The future of HIV vasculopathy when our patients are on antiretroviral therapy
R Barry
South African Journal of Surgery , 2009,
Abstract: South Africa was one of the last countries in Africa to be affected by the HIV epidemic, but currently has one of the highest prevalences in the world. Antiretroviral therapy (ART) was recently introduced in South Africa, and as of December 2007 antiretroviral treatment coverage in this country was about 25% (UNAIDS, 2008). There is a well-documented relationship between vascular disease and HIV infection. This HIV vasculopathy may manifest as arterial aneurysms, occlusive disease or complications of hypercoagulability. The question to be asked is ‘What is the future of HIV vasculopathy when our patients are on antiretroviral therapy?’
Mixed Strategy Nash Equilibria in Signaling Games  [PDF]
Barry R. Cobb, Atin Basuchoudhary, Gregory Hartman
Theoretical Economics Letters (TEL) , 2013, DOI: 10.4236/tel.2013.31009

Signaling games are characterized by asymmetric information where the more informed player has a choice about what information to provide to its opponent. In this paper, decision trees are used to derive Nash equilibrium strategies for signaling games. We address the situation where neither player has any pure strategies at Nash equilibrium, i.e. a purely mixed strategy equilibrium. Additionally, we demonstrate that this approach can be used to determine whether certain strategies are part of a Nash equilibrium containing dominated strategies. Analyzing signaling games using a decision-theoretic approach allows the analyst to avoid testing individual strategies for equilibrium conditions and ensures a perfect Bayesian solution.

Validation of Heart Failure Events in the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) Participants Assigned to Doxazosin and Chlorthalidone
Linda B Piller, Barry R Davis, Jeffrey A Cutler, William C Cushman, Jackson T Wright, Jeff D Williamson, Frans HH Leenen, Paula T Einhorn, Otelio S Randall, John S Golden, L Julian Haywood, the ALLHAT Collaborative Research Group
Trials , 2002, DOI: 10.1186/1468-6708-3-10
Abstract: Baseline characteristics (age, race, sex, blood pressure) did not differ significantly between treatment groups (P < .05) for participants with heart failure events. Post-event pharmacologic management was similar in both groups and generally conformed to accepted heart failure therapy. Central review of a small sample of cases showed high adherence to ALLHAT heart failure criteria. Of 105 participants with quantitative ejection fraction measurements provided, (67% by echocardiogram, 31% by catheterization), 29/46 (63%) from the chlorthalidone group and 41/59 (70%) from the doxazosin group were at or below 40%. Two-year heart failure case-fatalities (22% and 19% in the doxazosin and chlorthalidone groups, respectively) were as expected and did not differ significantly (RR 0.96; 95% CI, 0.67–1.38; P = 0.83).Results of the validation process supported findings of increased heart failure in the ALLHAT doxazosin treatment arm compared to the chlorthalidone treatment arm.The Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is a randomized, two-component clinical trial sponsored by the National Heart, Lung, and Blood Institute (NHLBI). A double-blind, active-controlled hypertension component is designed to compare the rate of fatal coronary heart disease (CHD) or nonfatal myocardial infarction (MI) (the primary endpoint) in high-risk hypertensive participants, aged 55 years or older, between those randomized to treatment initiated with a diuretic (chlorthalidone) and treatment initiated with each of three alternative antihypertensive drugs: a calcium-channel blocker (amlodipine), an angiotensin-converting enzyme (ACE)-inhibitor (lisinopril), or an alpha-adrenergic blocker (doxazosin). An open-label lipid-lowering component is designed to determine if lowering LDL cholesterol with pravastatin compared to "usual care" reduces all-cause mortality in a subset of moderately hypercholesterolemic patients. Randomization to the hypertension com
Stakeholders in Social-Ecological Systems
Barry R. Noon
Ecology and Society , 2003,
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