A5053030917- Genetic Mapping and Diversity in Plants and Animals
- Neonatal Respiratory Health Research
- Peroxisome Proliferator-Activated Receptors
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Eosinophilic Disorders and Syndromes
- Air Quality and Health Impacts
- Respiratory Support and Mechanisms
- Genetic and phenotypic traits in livestock
- Genetic Syndromes and Imprinting
- Adipose Tissue and Metabolism
- Trypanosoma species research and implications
- Epigenetics and DNA Methylation
- Neuroscience of respiration and sleep
- Metabolism and Genetic Disorders
- RNA modifications and cancer
- Drug Transport and Resistance Mechanisms
- Lipid metabolism and biosynthesis
- Respiratory viral infections research
- Genomics, phytochemicals, and oxidative stress
- Cancer-related gene regulation
- Heme Oxygenase-1 and Carbon Monoxide
- MicroRNA in disease regulation
- Eosinophilic Esophagitis
- Trace Elements in Health
- Cancer-related molecular mechanisms research
Cincinnati Children's Hospital Medical Center
2011-2023
University of Cincinnati Medical Center
1995-2022
University of Cincinnati
2007-2020
Duke University
2009
Center for Environmental Health
2007
Ball State University
2005
Weatherford College
2004
University of Pennsylvania
2002
Environmental Health
1999
Texas A&M University
1995
Abstract Differential effects of intestinal (I‐FABP) or liver (L‐FABP) fatty acid binding proteins on uptake and esterification were examined using transfected mouse L‐cell fibroblasts. L‐FABP, but not I‐FABP, expression increased the initial rate extent cis ‐parinaric by 50 29%, respectively, compared to control cells. I‐FABP L‐FABP preferentially [ 3 H]‐oleic incorporation into triacylglycerols 5.5‐fold 3.8‐fold, respectively. While both increasedesterification ethanolamine...
Patients with mutations in the pulmonary surfactant protein C (SP-C) gene develop interstitial lung disease and exacerbations associated viral infections including respiratory syncytial virus (RSV). Pulmonary infection RSV caused more severe thickening, air space consolidation, goblet cell hyperplasia SP-C-deficient (Sftpc(-/-)) mice compared SP-C replete mice. The RSV-induced pathology resolved slowly Sftpc(-/-) inflammation persistent up to 30 days postinfection. Polymorphonuclear...
Abstract To determine the role of surfactant protein C (SP-C) in host defense, SP-C-deficient (Sftpc−/−) mice were infected with pulmonary pathogen Pseudomonas aeruginosa by intratracheal injection. Survival young, postnatal day 14 Sftpc−/− was decreased comparison to Sftpc+/+ mice. The sensitivity bacteria specific 129S6 strain mice, a that spontaneously develops interstitial lung disease-like pathology age. Pulmonary bacterial load and leukocyte infiltration increased lungs 24 h after...
Whether aged hematopoietic stem and progenitor cells (HSPCs) have impaired DNA damage repair is controversial. Using a combination of mutation indicator assays, we observe 2- to 3-fold increase in the number mutations system upon aging. Young (HSCs) (HPCs) do not show an irradiation-induced repair, young HSPCs respond very similarly with respect cell-cycle checkpoint activation apoptosis. Both DNA-damage-induced G1-S checkpoint. Induction chronic double-strand breaks by zinc-finger nucleases...
Abstract Differences in the severity of respiratory syncytial virus (RSV)‐induced lower disease infants have been attributed to multiple environmental and genetic factors. To identify factor(s) influencing RSV susceptibility, we examined infection eight inbred mouse strains. Lung titers differed significantly between strains: were 15‐fold higher AKR/J (permissive) mice compared with C57BL/6J (resistant) at 4 days after inoculation. This strain‐specific difference suggested that...
Rationale: Because acute lung injury is a sporadic disease produced by heterogeneous precipitating factors, previous genetic analyses are mainly limited to candidate gene case-control studies.Objectives: To develop genome-wide strategy in which single nucleotide polymorphism associations assessed for functional consequences survival during mice.Methods: identify genes associated with injury, 40 inbred strains were exposed acrolein and haplotype association mapping, microarray, DNA-protein...
Recent studies suggest that genetic variability can influence irritant-induced lung injury and inflammation. To begin identifying genes controlling susceptibility to inhaled irritants, seven inbred mouse strains were continuously exposed nickel sulfate (NiSO 4 ), polytetrafluoroethylene, or ozone (O 3 survival time was recorded. The A/J (A) strain sensitive, the C3H/He (C3) intermediate, C57BL/6 (B6) resistant NiSO -induced acute injury. B6AF 1 offspring also resistant. sensitivity pattern...
Section:ChooseTop of pageAbstract <<MATERIALS AND METHODSRESULTSDISCUSSIONReferencesCITING ARTICLES
Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES
The genetic basis for the underlying individual susceptibility to chlorine-induced acute lung injury is unknown. To uncover and pathophysiological processes that could provide additional homeostatic capacities during injury, 40 inbred murine strains were exposed chlorine, haplotype association mapping was performed. identified single-nucleotide polymorphism (SNP) associations evaluated through transcriptomic metabolomic profiling. Using ≥ 10% allelic frequency phenotype explained as...
Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES
Hypereosinophilic syndrome is characterized by sustained and marked eosinophilia leading to tissue damage organ dysfunction. Morbidity mortality occur primarily due cardiac thromboembolic complications. Understanding the cause mechanism of disease would aid in development targeted therapies with greater efficacy fewer side effects. We discovered a spontaneous mouse mutant our colony hypereosinophilic phenotype. Mice develop peripheral blood eosinophilia; infiltration lungs, spleen, heart...
Although fatty acid-binding proteins (FABP) differentially affect acid uptake, nothing is known regarding their role(s) in determining cellular phospholipid levels and composition. The effects of liver (L)- intestinal (I)-FABP expression on these parameters were determined using stably transfected L-cells. Expression L- I-FABP increased total mass (nmol/mg protein) 1.7- 1.3-fold relative to controls, respectively. L-FABP the masses choline glycerophospholipids (ChoGpl) 1.5-fold,...
Section:ChooseTop of pageAbstract <<Materials and MethodsResultsDiscussionReferencesCITING ARTICLES
Acute lung injury (ALI) and its most severe presentation, acute respiratory distress syndrome, represent a full spectrum of complex devastating illness, with associated mortality that still hovers around 30-40%. Even supplemental O2, routine necessary therapy for such patients, paradoxically causes injury. The detrimental effects O2 have established hyperoxic ALI (HALI) as conventional model to study neonatal adult forms syndromes in experimental animals. To confront the high problem quite...
Acute lung injury (ALI) is a devastating disease that maintains high mortality rate, despite decades of research. Hyperoxia, universal treatment for ALI and other critically ill patients, can itself cause pulmonary damage, which drastically restricts its therapeutic potential. We stipulate having the ability to use higher levels supplemental O2 longer periods would improve recovery rates. Toward this goal, mouse model was sought identify genes contributing hyperoxic (HALI) mortality....
Despite the fact that genetic imprinting, i.e., differential expression of same allele due to its different parental origins, plays a pivotal role in controlling complex traits or diseases, origin, action and transmission mode imprinted genes have still remained largely unexplored. We present new strategy for studying these properties imprinting with two-stage reciprocal F mating design, initiated two contrasting inbred lines. This maps quantitative trait loci are (i.e., iQTLs) based on...