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    Ciliogenesis during zebra fish heart regeneration.
    (Wheaton College (Norton, Mass.), 2015) Pope, Hans William.
    Cardiac ischemic injury, a heart attack, occurs when blood flow through the coronary arteries is obstructed. As a result in humans, necrotic tissue is replaced by hard, inelastic scar tissue that impairs the heart’s ability to function. The human heart possesses little to no regenerative capacity on its own to recovery from ischemic injury. Zebrafish, however, are capable of robust cardiac regeneration after injury to the heart. Through a series of remarkable heart-localized events that mirror embryonic development, the zebrafish can replace damaged or lost heart tissue within a month. We noticed the similarity between the regeneration and development of cardiac tissue may implicate cilia are involved during regeneration. Cilia are microtubule-based organelles that serve important sensory functions during embryonic development and organ homeostasis. It is well established that sensory cilia regulate Hedgehog and Wnt signaling pathways to aid in differentiating tissues during embryogenesis. Recent studies provide evidence that cilia are present during cardiogenesis and are necessary for proper cardiomyocyte differentiation and cardiac morphology. Thus, we hypothesized cilia may play similar roles during zebrafish heart regeneration. In the current study, we tested heart tissue for the presence of cilia using immunofluorescent confocal microscopy. Our preliminary data suggest cilia are abundant in regenerating cardiac tissue 7 days after removing a portion of the ventricular apex. In addition, we began to implement the surgical procedures necessary to injure the zebrafish ventricle at Wheaton College.
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    Vision's role in the ability of cane toads to absorb landing forces.
    (Wheaton College (Norton, Mass.), 2014) Panzini, Christopher.
    In order to stick a landing, the propulsive forces and acceleration experienced during take off must be completely dissipated as the body completely decelerates. The cane toad (Bufo marinus) is an ideal model for looking at joint kinematics along with coordination upon landing, due to the fact that they control their entire landing using only their fore limbs. Since hopping is the main form of locomotion for anurans, they are frequently using this motor control in order to put together successive hops. Failure to prepare for and dissipate the large landing forces could seriously injure the toad. This study focuses o two main objectives. The first objective is to determine the normal landing force profile of the cane toad. This profile will act as the baseline for the second objective, which is to determine the role of vision in force dissipation during level hops. Both of these objectives were examined using hop experiments along with a three-dimensional force plate to collect the force profiles. I looked at both forelimb and hind limb kinematics during the landing process, along with the anticipatory muscle recruitment used by anurans to determine the motor patterns of each of the six toads used. The optic nerve of each toad was severed in order to test the necessity of vision in the ability to safely land while remaining balanced. Without vision the toads were still able to successfully control the anticipatory tuning of their muscles. Along with muscle recruitment, learning and feedback during takeoff from other sensory systems, including the vestibular and proprioceptive systems, were enough to compensate for the loss in vision.
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    A behavioral and biomechanical analysis of the effects of MeHg-induced neurotoxicity on locomotor behaviors and the protective effects of N-Acetylcysteine in adult male mice.
    (Wheaton College (Norton, Mass.), 2014) Gibson, Jennifer
    Methylmercury (MeHg) is a potent neurotoxin which humans are commonly exposed to through seafood consumption. Developmental exposure to MeHg is known to induce severe neurological deficits in the central nervous system (CNS) resulting in cognitive and locomotor impairments. However, the neurotoxic effects of MeHg in the adult nervous system are not well defined. Additionally, a number of recent studies have suggested damage to endogenous antioxidant functioning resulting in high concentrations of reactive oxygen species (ROS) as a causal factor for oxidative stress as the mechanism by which MeHg damages the CNS. Further exploration of the mechanism by which MeHg induces neurotoxicity in conjunction with an examination of the neurotoxic effects in adult behavior is necessary to provide a concrete understanding of the neurological damages associated with a developed nervous system. The present study observed adult mice administered a daily dose of 4.8 mg/kg MeHg in cookies and injections of a synthetic antioxidant N-Acetylcysteine (NAC) over the course of four weeks. A suite of behavioral tests such as inverted screen, rotor-rod, open field, and analyses of gait patterns, were conducted to measure strength, motor coordination, locomotor activity, and underlying biomechanical physiology following exposure to MeHg. Through the present investigation, quantitative deficits in the locomotor behavior of adult mice were observed through the development and application of sensitive quantitative biomechanical and behavioral measures of locomotor analysis. Furthermore, the exploration of protective effects of NAC on oxidative stress induced by MeHg revealed a positive effect on rate of survival, however, no effect on observed locomotor behaviors in mice exposed to MeHg. Further exploration of the methodologies implemented in the study may provide additional insight into the mechanism of MeHg-induced neurological deficits. This research may advance current understanding of the mechanisms by which MeHg neurological damage occurs in adults and aid in the development of treatment and protective measures.
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    Effect of methylmercury (MeHg) on DNA oxidation in the brains of adult male mice.
    (Wheaton College (Norton, Mass.), 2014) Everett, Wyll T.
    Interest in the cellular and biochemical mechanism of MeHg toxicity has stemmed from observed motor and cognitive impairments caused by this organometallic cation in adult humans and rodents. This lab group has confirmed that chronic oral MeHg exposure causes coordinated motor deficits and increased levels of oxidative stress in brain tissue. In the present study, we investigate specific neuroanatomical areas associated with motor and cognitive behaviors that are damaged by MeHg-induced oxidative stress. Adult male mice received 4.8 μg/g/day MeHg orally for 28 days. In order to assess oxidative stress, 8-hydroxy-2’-deoxyguanosine (8-OHdG) was immunohistochemically labeled and analyzed as a biomarker of MeHg-induced DNA oxidation. As hypothesized, MeHg treatment increased 8-OHdG immunoreactivity in the motor cortex. Interestingly, MeHg treatment caused no change in 8-OHdG immunoreactivity in the CA3 region of the hippocampus (CA3) and decreased 8-OHdG immunoreactivity in the magnocellular red nucleus (RMC) and accessory oculomotor nucleus (MA3). These data indicate that 8-OHdG can be used as a sensitive and reliable measure of region specific MeHg-induced oxidative stress in adults. Further investigation is necessary to confirm areas of MeHg-induced neurodegeneration, determine how MeHg-induced oxidative stress causes this degeneration, and identify how this damage produces motor and cognitive impairments.
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    The effects of dopamine pathway mutations on Drosophila melanogaster grooming and courtship behaviors.
    (Wheaton College (Norton, Mass.), 2013-09-17) Superson, Michaela R.
    The dopaminergic pathway can be manipulated in Drosophila melanogaster through a dopamine inhibitor (3-iodo-tyrosine) or a drug that rescues dopamine levels (L-DOPA). Three different fruit flies, wild-type, ebony, and catsup, were exposed to different dopamine levels. It was found that the dopamine mutants, ebony and catsup, were more affected by dopamine manipulation than wild-type flies.