Relativistic Chiral Mean Field Model for Finite Nuclei

We present a relativistic chiral mean field (RCMF) model, which is a method for the proper treatment of pion-exchange interaction in the nuclear many-body problem. There the dominant term of the pionic correlation is expressed in two-particle two-hole (2p-2h) states with particle-holes having pionic quantum number, J^{pi}. The charge-and-parity-projected relativistic mean field (CPPRMF) model developed so far treats surface properties of pionic correlation in 2p-2h states with J^{pi} = 0^{-} (spherical ansatz). We extend the CPPRMF model by taking 2p-2h states with higher spin quantum numbers, J^{pi} = 1^{+}, 2^{-}, 3^{+}, ... to describe the full strength of the pionic correlation in the intermediate range (r > 0.5 fm). We apply the RCMF model to the ^{4}He nucleus as a pilot calculation for the study of medium and heavy nuclei. We study the behavior of energy convergence with the pionic quantum number, J^{pi}, and find convergence around J^{pi}_{max} = 6^{-}. We include further the effect of the short-range repulsion in terms of the unitary correlation operator method (UCOM) for the central part of the pion-exchange interaction. The energy contribution of about 50% of the net two-body interaction comes from the tensor part and 20% comes from the spin-spin central part of the pion-exchange interaction.Comment: 22 pages, 12 figure

To Eat or Not To Eat: Contributions of Dorsal Hippocampal Neurons and Memory to Meal Onset

There is extensive research regarding the neural mechanisms that control satiety and meal termination; in contrast, there is very limited understanding of how the central nervous system regulates meal onset and thus the duration of the postprandial intermeal interval (ppIMI) and meal frequency. Based on emerging evidence, we hypothesize that dorsal hippocampal neurons, which are critical for episodic memory, form a memory of a meal and inhibit meal onset during the ppIMI. To test whether hippocampal neurons form a memory of a meal, we first determined that ingesting sucrose or isopreferred concentrations of the non-caloric sweetener saccharin increased the expression of the plasticity-related immediate early gene activity-regulated cytoskeleton-associated protein (Arc) in dorsal CA1 hippocampal (dCA1) neurons in Sprague-Dawley rats. Furthermore, repeated exposure to the sucrose meal attenuated the ability of the sucrose to induce Arc expression. Together, these data indicate that orosensory stimulation produced by a sweet taste is sufficient to induce synaptic plasticity in dCA1 neurons in an experience-dependent manner. Second, we showed that reversibly inactivating dorsal hippocampal neurons with infusions of the GABAA agonist muscimol after the end of a sucrose meal accelerated the onset of the next meal, indicating that dorsal hippocampal neurons inhibit meal onset. Lastly, using a clinically-relevant animal model of early life inflammatory injury, we found that neonatal injury (1) impairs hippocampal-dependent memory, (2) decreases the ppIMI and increases sucrose intake, (3) increases body mass, (4) attenuates sucrose-induced Arc expression in dCA1 neurons, and that (5) blocking inflammatory pain with morphine at the time of injury reverses the effects of injury on memory, energy intake and Arc expression. Collectively, the findings of this dissertation support the overarching hypothesis that dorsal hippocampal neurons inhibit meal onset during the ppIMI and suggest that dorsal hippocampal dysfunction may contribute to the development and/or maintenance of diet-induced obesity

The Effects of Nicotine Conditioned Place Preference in D2 Primed Adolescent Rats: Age-Related and Gender Effects.

This study investigated nicotine conditioned place preference (CPP) in two different ages of adolescence using a rodent model of schizophrenia. Both 2- and 3-chambered CPP apparatuses were used to test whether the CPP was due to an aversion to the white chamber. Animals were neontally treated with the dopamine D2/D3 agonist, quinpirole, or saline and raised to either early postweanling age (P 22) or adolescence (P 29). Rats were conditioned to prefer the white chamber using nicotine. Results showed that nicotine induced CPP and appeared to alleviate an increased stress response in D2 primed animals, which appeared to diminish over time. Additionally, adult D2 and non-D2 primed rats were tested on the elevated T-maze. Results revealed that D2 primed rats demonstrated a significant increase in unconditioned fear. This study showed that nicotine induced CPP in D2 and non-D2 primed rats regardless of age, and D2 primed rats appear to demonstrate an increase in stress levels that was alleviated by nicotine

Novel elucidation and treatment of pancreatic chronic graft-versus-host disease in mice

Chronic graft-versus-host disease (cGVHD) is a severe complication of allogeneic haematopoietic stem cell transplantation. There is a growing understanding of cGVHD, and several effective therapies for cGVHD have been reported. However, pancreatic cGVHD is a potentially untapped study field. Our thought-provoking study using a mouse model of cGVHD suggested that the pancreas could be impaired by cGVHD-induced inflammation and fibrosis and that endoplasmic reticulum (ER) stress was augmented in the pancreas affected by cGVHD. These findings urged us to treat pancreatic cGVHD through reduction of ER stress, and we used 4-phenylbutyric acid (PBA) as an ER stress reducer. A series of experiments have indicated that PBA can suppress cGVHD-elicited ER stress in the pancreas and accordingly alleviate pancreatic cGVHD. Furthermore, we focused on a correlation between epithelial to mesenchymal transition (EMT) and fibrosis in the cGVHD-affected pancreas, because EMT was conceivably implicated in various fibrosis-associated diseases. Our investigation has suggested that the expression of EMT markers was increased in the cGVHD-disordered pancreas and that it could be reduced by PBA. Taken together, we have provided a clue to elucidate the pathogenic process of pancreatic cGVHD and created a potentially effective treatment of this disease using the ER stress alleviator PBA