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Carlos Puentes

Undergraduate Major: Psychology

Future Plans: Ph.D. in clinical psychology

Carlos Puentes

Carlos was born in Havana, Cuba and moved to North Miami, Florida at the age of five. He is a psychology major with a minor in biology. His studies in psychology sparked an interest in the brain and its emergent faculties. Particularly, Carlos hopes to explore reward circuitry and how the interaction of neural circuits culminates in coherent decision making. His research interests encompass cognitive psychology and molecular biology. Carlos' interests include the neural antecedents to coherent decision making, plasticity, and the applicability of stem cells in neurodegenerative diseases. He plans to eventually attain a Ph.D. in Neurobiology.

Title: Toward Precision Medicine: A Method for Identifying Individuals who are Expected to Benefit from Antidepressants

Conducted at the University of Pennsylvania as part of the Leadership Alliance and Summer Undergraduate Internship Program (SUIP) and the UCF McNair Scholars Program.

Mentor: Nick Forand, Ph.D.

Abstract: Antidepressant medications are an effective treatment for depression; however, many who take them do not experience a response greater than they would have if they had taken a placebo. This heterogeneity of antidepressant response begets the question of what traits might predict a better response to one treatment versus another. Our study is intended to develop a predictive model with the shared intention of understanding these discrepancies and crafting a means of accurately estimating treatment outcome prior to the administration of the treatment. We developed a treatment selection algorithm that identifies whether antidepressant medications are likely to provide a benefit over that provided by placebo for any specific individual. We utilized data from 180 participants in an 8-week randomized controlled trial of antidepressant medication versus placebo to develop a predictive regression model identifying both prescriptive (variables that interact with treatment to predict response) and prognostic indices (variables that predict response irrespective of treatment) using a leave-one-out cross validation, a method that optimizes the predictive power and offers some protection against type II error. The model is used to make predictions for individuals to determine whether they would have been likely to respond to placebo, medication, both or neither.

Title: Does Cognitive Vulnerability to Sleep Loss Relate to Mood Response?

Conducted at the University of Pennsylvania as part of the Leadership Alliance and Summer Undergraduate Internship Program (SUIP) and the UCF McNair Scholars Program.

Mentor: Dr. David Dinges, University of Pennsylvania

Abstract: Prior research has suggested that chronic sleep restriction (≤ 6h a night) can produce significant neurobehavioral impairments and increase negative affect. These decrements do not affect individuals uniformly and reflect interindividual differences in susceptibility to impairment following sleep restriction. Few controlled studies have sought to observe the effects of chronic sleep restriction on mood, and examine if individual differences in neurobehavioral impairment relate to changes in affect. In the current study, N=42 healthy adults (32.6 ±9y, 20f) participated in an in-laboratory protocol involving 2 baseline nights (10h time in bed [TIB]/night), 5 sleep restriction nights (4h TIB/night) and 1 recovery night (12h TIB/night). We observed whether sleep restriction affected mood measured using the Profile of Mood States (POMS) and numerous Visual Analog Scale (VAS) items. Subjects completed the mood measures and the Psychomotor Vigilance Test (PVT) every two hours; 1000 h to 2000h test bouts were used for analysis. Vulnerability to sleep restriction was assessed using the PVT, a median split of baseline day 2 lapses (reaction time > 500 msec) subtracted from sleep restriction day 5 lapses divided subjects into vulnerable and resistant groups. Subjects experienced significant increases in the POMS confusion-bewilderment (p<.0001), and fatigue-inertia (p<.0001), and decreases in vigor-activity (p<.0001) scores after sleep restriction. Similarly, subjects exhibited significant increases on various VAS items, including anxiousness and frustration. The results indicate that sleep loss may have negative effects on mood; however, POMS subscales for depression-dejection, tension-anxiety, and anger-hostility did not significantly change. Vulnerable and resistant subjects only differed on 2 measures of mood, vigor and clear-headedness, suggesting that neurobehavioral vulnerability and subjective mood changes may be largely unrelated.