OBJECTIVE:The objective of this study was to quantify the weight gain of freshmen during their first 12 weeks at Cornell University. In addition, students completed questionnaires that revealed particular behaviors and activities that were associated with weight gain. DESIGN: Serial, correlational study. SUBJECTS: A total of 68 freshmen from Cornell University. MEASUREMENT: A total of 60 students were weighed during the first week of the semester, then again 12 weeks later. They were also given a questionnaire to complete concerning their behavior during the previous 12 weeks. RESULTS: After adjusting for clothing weights, the mean weight gain of the freshmen was 1.972.4 kg, a value significantly different from 0. Two regression models generated from the questionnaire were fitted to the weight gain. The first linear regression model (Model 1) accounted for 58% of the variance and indicated that eating in the 'all-you-can-eat' dining halls accounted for 20% of the variance in weight gain. Snacking and eating high-fat 'junk food' accounted for anther 20%. When initial weight was used as a covariate (Model 2), the consumption of junk foods, meal frequency and number of snacks accounted for 47% of the variance. CONCLUSION:The study clearly demonstrated that significant weight gain during first semester college is a real phenomenon and can be attributed to tangible environmental stimuli. The weight gain is considerably greater than that observed in the population and may be useful as a model to test various techniques that may reduce or reverse the 'epidemic' of obesity observed in the general population.

The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the ‘obesity epidemic’ – the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models – the general intake model and the dual intervention point model – that address this issue and might offer better ways to understand how body fatness is controlled.

Background: The Tissue Monitoring System (TMS) is an algorithm that estimates changes in body tissue from a series of daily weight measures. It is intended to provide people with a feedback of changes in their tissue weight so they may have a basis for estimating how much they would have to change their intake or expenditure to maintain their weight at a prescribed level. We tested the effectiveness of the TMS to prevent freshmen from gaining weight during their first semester in college. Methods: In two similar but independent studies (Fall 2002(Fall , 2003, female freshmen college students were given analog bathroom scales and instructed to weigh themselves each morning immediately after rising from bed, then e-mail their weight to our staff. After 7 days, a linear function was performed on the most recent 7 days of the weight-day function for each participant. In the first study, the slope of this function was e-mailed back to the participants. In the second study, the difference between last point and the original weight was determined, using linear regression techniques, converted to calories, and the information was e-mailed back to the participants. Control participants in both studies were weighed at the beginning and the end of the semester. Results: The untreated controls gained 3.170.51 kg and 2.070.65 kg, respectively (Po0.01 for both studies), whereas weight gain of the experimental groups was 0.170.99 kg and À0.8270.56 kg, values that were not significantly different than zero. Conclusions: The TMS appears to be an effective technique to help female college freshmen resist gaining weight in an environment that is conducive to weight gain. These results suggest that the TMS may be a useful method to help curb the slow increase in the prevalence of overweight and obesity that is characteristic of all industrialized societies.

In addition to mental retardation, individuals with Down syndrome (DS) also develop the neuropathological changes typical of Alzheimer’s disease (AD) and the majority of these individuals become demented. The Ts65Dn mouse model of DS exhibits key features of these disorders, including early degeneration of cholinergic basal forebrain (CBF) neurons and impairments in functions dependent on the two CBF projection systems; namely, attention and explicit memory. Herein, we demonstrate that supplementing the maternal diet with excess choline during pregnancy and lactation dramatically improved attentional function of the adult trisomic offspring. Specifically, the adult offspring of choline-supplemented Ts65Dn dams performed significantly better than unsupplemented Ts65Dn mice on a series of five visual attention tasks, and in fact, on some tasks did not differ from the normosomic (2N) controls. A second area of dysfunction in the trisomic animals, heightened reactivity to committing an error, was partially normalized by the early choline supplementation. The 2N littermates also benefited from increased maternal choline intake on one attention task. These findings collectively suggest that perinatal choline supplementation might significantly lessen cognitive dysfunction in DS and reduce cognitive decline in related neurodegenerative disorders such as AD.

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Fragile X syndrome (FXS) is the most common inherited form of mental retardation, occurring in roughly 1/4000 males and 1/8000 females. An abnormal expansion of a trinucleotide CGG repeat sequence in the fmr1 gene results in transcriptional silencing of this gene, which codes for the Fragile X Mental Retardation Protein (FMRP). The loss of FMRP, directly and/or indirectly, gives rise to the FXS phenotype, which includes a characteristic set of anatomic and cognitive/behavioral features. The present studies were designed to test the hallmark areas of dysfunction (i.e. attention, inhibitory control, hyperarousal, and emotional regulation) seen in human FXS and further characterize spared and impaired functions in fmr1 KO mice. The performance of F1 hybrid fmr1 KO mice (a C57BL/6J x FVB/NJ cross) and wild-type (WT) littermate controls were evaluated on a series of tasks designed to assess inhibitory control and various aspects of attention, Reversal Learning Task, and Associate Learning Task. Regulation of arousal and emotion, two domains affected in FXS, was also evaluated in these tasks by examining the animals' reaction to the unexpected presentation of potent olfactory distractors (in the Distraction task), as well as their reaction to committing an error on the previous trial.The present studies provided the first evidence that the hallmark deficits in human FXS --impaired attention, inhibitory control, and arousal regulation -are also impaired in the fmr1 mouse model of FXS. In addition, these findings demonstrate that attentional dysfunction and impaired inhibitory control are most prominent when task contingencies change and when the animal has just committed an errorsituations that arouse or disturb the mice. Analysis of videotapes further demonstrates that arousal regulation is impaired in the fmr1 KO mice. Additionally, the fmr1 KO mice were not impaired in associative learning, transfer of learning, or reversal Jisook's stidies in New Generation stimulated her desire for a deeper and moe systematic understanding of the neural mechanisms of human brain. She was accepted into the Department of Psychology at Yonsei University, which is considered one of the best programs in Korea. This allowed her the unique combination of being able to study at Yonsei University and to work part time for New Generation C&C. Working and studying at the same time allowed her many opportunities to apply academic knowledge to real-world situations.To the end, Jisook assisted Dr. Kang in her lab, the Cognitive Neuroscience and Medical Physics Lab at the Seoul National University Hospital. There, she conducted studies on memory and learning in normal human conditions, as well as abnormal states of perception such as epilepsy and dementia. Through cutting-edge imaging methods (i.e. fMRI, PET, and MRI) coupled with some behavioral tests, she furthered her knowledge of functional and structural workings of the human brain iv during learning, memorizing, and recognizing. She also ganed insight into how the activity of the brain dif...