Publications by authors named "Rhonda DeCook"

Objective: To determine whether plasma cholesterol concentrations in dogs with sepsis is associated with morbidity or in-hospital mortality.

Design: Retrospective cohort study from 2005-2015.

Setting: Two private referral centers.

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Neuregulin-1 (NRG1) ligand and its epidermal growth factor receptor (EGFR)/ERBB family regulate normal cellular proliferation and differentiation in many tissues including the cochlea. Aberrant NRG1 and ERBB signaling cause significant hearing impairment in mice. Dysregulation of the same signaling pathway in humans is involved in certain types of cancers such as breast cancer or non-small cell lung cancer (NSCLC).

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Second-order sensory neurons are dependent on afferents from the sense organs during a critical period in development for their survival and differentiation. Past research has mostly focused on whole populations of neurons, hampering progress in understanding the mechanisms underlying these critical phases. To move toward a better understanding of the molecular and cellular basis of afferent-dependent neuronal development, we developed a new model to study the effects of ear removal on a single identifiable cell in the hindbrain of a frog, the Mauthner cell.

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Objective: To describe the signalment, wound characteristics, and treatment of gunshot injuries in cats and dogs in urban and rural environments, and to evaluate the utility of the animal trauma triage (ATT) score as an early predictor of survival to discharge from the hospital.

Design: Retrospective case series.

Animals: 29 dogs and 8 cats.

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Sensorineural hearing loss results from damage to the hair cells of the organ of Corti and is irreversible in mammals. While hair cell regeneration may prove to be the ideal therapy after hearing loss, prevention of initial hair cell loss could provide even more benefit at a lower cost. Previous studies have shown that the deletion of Atoh1 results in embryonic loss of hair cells while the absence of Barhl1, Gfi1, and Pou4f3 leads to the progressive loss of hair cells in newborn mice.

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Due to the multisensory input into the balance system, the loss of one input, such as an ear, can generally be compensated for. However, when a mismatch or incomplete loss of inputs occurs, the ability to compensate for the stimulus misrepresentation may be compromised. The inner ear and cerebellum are important input and processing centers for balance but no genetic models have been generated to assess balance or compensation in the abnormal development of both these organs/brain areas.

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Heterosis refers to the superior performance of hybrid progeny relative to their inbred parents, but the mechanisms responsible are unknown. Hybrids between the maize inbred lines B73 and Mo17 exhibit heterosis regardless of cross direction. These reciprocal hybrids differ from each other phenotypically, and 30 to 50% of their genes are differentially expressed.

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Heterosis is the phenomenon whereby the progeny of particular inbred lines have enhanced agronomic performance relative to both parents. Although several hypotheses have been proposed to explain this fundamental biological phenomenon, the responsible molecular mechanisms have not been determined. The maize inbred lines B73 and Mo17 produce a heterotic F1 hybrid.

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The genetic control of gene expression during shoot development in Arabidopsis thaliana was analyzed by combining quantitative trait loci (QTL) and microarray analysis. Using oligonucleotide array data from 30 recombinant inbred lines derived from a cross of Columbia and Landsberg erecta ecotypes, the Arabidopsis genome was scanned for marker-by-gene linkages or so-called expression QTL (eQTL). Single-feature polymorphisms (SFPs) associated with sequence disparities between ecotypes were purged from the data.

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Arabidopsis ecotypes, Columbia (Col) and Landsberg erecta (Ler), differ in their capacity to regenerate shoots in culture, as do many other cultivars and varieties of the same plant species. Recombinant inbred (RI) lines derived from a cross of Col x Ler were scored for shoot regeneration, and the Arabidopsis genome was scanned using composite interval mapping for loci associated with shoot regeneration. Three QTL were identified--a major one on chromosome 5 in which the Col parent contributed the superior allele and two minor QTL on chromosomes 1 and 4 in which the Ler parent contributed the superior alleles.

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