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Increased bone density has been observed following physical training. However, it is not known whether the mechanical forces of muscular contraction, gravitational pull, or a combination of these forces are required to cause this adaptation. Therefore, the purpose of this study was to determine which mechanical force, muscular contraction or gravitational pull, offered the greatest contribution to increased bone mineral content observed following either swim or run training. METHODS: Female Wistar rats were randomly assigned to one of three groups: 1) Sedentary Control (SC; n = 12), 2) Run Trained (RT; 27.7 m/m, 8% incline, 2 hrs/day; n = 20), and 3) Swim Trained (ST; 2 hrs/day, 2Y/ body weight; n = 14). The animals were sacrificed after 9 weeks of training and the humeri and femurs were removed for analysis.RESULTS: Femur weight, length, diameter, and ponderal index (a measure of robustness), and bone mineral content (BMC) were not different between the three treatment groups. However, femur cortical thickness was significantly (p < 0.01) smaller in the RT when compared to ST and SC rats. The ST humeri were significantly (p < 0.05) heavier, wider, and had a greater BMC when compared with those of the RT and SC rats, while cross sectional area was unaffected by physical training. CONCLUSION: The results of this study indicate that the mechanical forces applied by the swim training protocol produced marked bone adaptation in the ST animals following 9 weeks of physical training. Whereas, the combined mechanical and gravitational forces applied during running by the RT rats produced minimal adaptation of bone following 9 weeks of physical training.

This thesis investigates possible mechanisms underlying the decreased kidney size and the development of high blood pressure in the offspring of our model of maternal iron deficiency. This study has demonstrated that a maternal iron deficient diet has no effect on gene expression of either markers of vasculogenesis/angiogenesis or regulators of apoptosis and cell proliferation in the kidneys of the offspring. The effect of maternal iron deficiency on well documented mechanisms involved in blood pressure regulation were investigated in the offspring. The data showed that neither renal sodium transport nor nephron number are involved in hypertension development in our model of maternal iron deficiency. The renin angiotensin system showed significant increase in the renal renin mRNA expression, and pulmonary ACE1 mRNA and activity levels in newborn offspring of iron deficient mothers.  These changes are unique for maternal iron deficiency as they have not been seen in the other models of nutritional programming.  However, they are also temporary and disappear by two weeks after birth and at this stage it is unknown if and how the renin angiotensin system contributes to hypertension development in the offspring of iron deficient mothers. Finally, the whole rat genome arrays were used to identify new genes and pathways affected by maternal iron deficiency in fetal kidneys.  The results of the microarray experiment suggested renal inflammation and increased collagen cross-linking leading to stiffening of vascular walls, as possible causes of hypertension in the offspring of iron deficient mothers.  Further analysis showed, however, that both mechanisms do not appear to be involved.  The microarray study also identified CD36 scavenger receptor as being significantly up-regulated in the kidneys of the fetuses of iron deficient mothers, but its expression significantly decreased in adult animals compared to controls. The data presented in this thesis indicate that the effect of an iron deficient diet on offspring blood pressure is multifactorial and complex.

The present study was designed to test for sequential effects of partial punishment training.

This study concerned the effects of short-term exposures to continuous (10 kv/meter) and pulsed 20 volts at 640 cps/100 msecs) electrostatic fields on the EEG recorded from external electrodes and hypothalamic activity recorded from implanted electrodes in rats. Each experiment lasted at least 90 minutes. The total energies of the waveforms recorded were integrated and printed out for plotting and analysis. Besides the brain activity, the ECG, respiration, and temperature of the animals were also monitored before, during,and after exposure to the electrostatic fields.

The purpose of the present study was to further investigate the effects of frustration on the reward value of a goal object. Under the assumption that animals will learn to take the shortest path to a goal and that the reward value of an object will increase as effort increases, the following hypothesis was proposed: If rats are frustrated in the short path of a single choice maze (experimental group) then the experimental group's running time for the long path will be less than that of a control group not frustrated in the short path.