Attention Deficit/Hyperactivity Disorder (ADHD) is one of the most common psychiatric disorders affecting adolescents. Treatment often focuses on managing symptoms, including distractibility, poor concentration, disorganization, hyperactivity, and impulsivity. A successful transition to adulthood requires interpersonal, organizational, and planning skills, making adolescence a critical time to treat ADHD symptoms. Sibley et al. (2014) reviewed treatment literature on ADHD in adolescents and concluded that medication and behavior therapy both produce similar effects on ADHD symptoms in adolescents. This project aims to update the results of the prior review using the past ten years of research. First, an electronic database search was conducted using four categories of terms: (1) sample age, (2) disorder, (3) treatment, and (4) randomized control trial. Experts were also contacted to request additional articles published during the designated period. Inclusion criteria were then applied: (1) published between 2013-present, (2) ages 10-19, (3) ADHD diagnosis, (4) quantitative data reported for at least one ecologically valid outcome measure (e.g., ADHD symptom severity), (5) in studies where individuals not meeting age or diagnostic criteria are included, data for adolescents with ADHD must be presented separately, (6) must evaluate treatment efficacy. 20% of the studies were also randomly selected for an inter-rater reliability probe. Next, data were collected based on the type of study, methodology, and participant demographics for every included study. Effect sizes were also calculated for several outcome measures. This review is still in its preliminary stages but will provide an updated review of the most effective pharmacological and non-pharmacological treatments for ADHD in adolescents. It will demonstrate the considerable growth in the number and highlight the effectiveness of available treatments. The next step will include quantifying data to determine trends for each treatment and conclude the review by summarizing our findings.

From previous clinical cases, doctors found that children with Leigh syndrome are sensitive to volatile anesthetics. Leigh syndrome can be caused by defective Ndufs4, a subunit in complex I of the electron transportation chain. Previously, we used the Ndufs4 knockout C57Bl/6 mice to model Leigh syndrome and noticed that individuals with Ndufs4-knockout astrocytes go under anesthesia at a normal concentration, but require a lower concentration to emerge. We also found that isoflurane inhibits the effect of norepinephrine in astrocytes. Since norepinephrine is associated with individual emergence from an anesthetized state, this might help us to understand the mechanism behind our observations of the astrocyte specific Ndufs4 knockout. We furthered our study by assessing the role of gliotransmitters in the mechanism of mitochondrial disease and volatile anesthesia. Gliotransmitters are chemicals released by glial cells and used by astrocytes to modulate neuronal information processing. A pilot study was conducted in vitro in the wildtype mice assessing the release of different gliotransmitters, including cyclic adenosine monophosphate, adenosine, adenosine triphosphate, gamma-aminobutyric acid, serine, glutamine, and glutamic acid. Previously we found that the level of cAMP increased significantly after the norepinephrine treatment. Thus, we expect to see a larger acceleration in cAMP concenration in knockout mice, compared to wildtype. I am continuing this project studying the effect of the gliotransmitters in astrocyte cell cultures from the Ndufs4-knockout mice, to compare to the wildtype counterparts. Each astrocyte culture will be randomly assigned to a treatment: with or without norepinephrine. The amount of each gliotransmitter released per unit of protein is measured. I will analyze the data generated and compare to the wildtype data. Future study includes the assessment of the relationship between the metabolites within astrocytes, and the response to isoflurane and norepinephrine. This study would accelerate our understanding of the mechanism of volatile anesthesia, as well as the mitochondrial disease, which in turn will benefit numerous patients with safer and wiser treatment plans.

Attention deficit/hyperactivity disorder (ADHD) in girls had been largely under researched up until the 21st century, and still much is unknown or unclear about prevalence, symptomatology, associated impairments, longitudinal trajectories, treatment options, and treatment efficacy. In this study I attempt to characterize the ethnically diverse sample of adolescent girls (n=235) from the ADHD Teen Integrative Data Analysis Longitudinal (TIDAL) dataset (Sibley & Coxe, 2020). I investigate how different types of behavior therapy [engagement-focused (ENGAGE), comprehensive (COMP), standard (STANDARD), community-based usual care (UC), no treatment (NOTX)], medication engagement (consistent, inconsistent, negligible), clinical problem profile (simplex, internalizing, disruptive/disorganized), and family adversity predict changes in ADHD symptoms and related impairment (academic functioning, parent-teen conflict, and organizational functioning) over time. To do so I create a series of hierarchical linear regression models to examine the relationship between the predictive variables and the outcomes, and how each added variable affects the relationship using data from the ADHD TIDAL dataset. I predict an overall decline in symptoms and related impairment with the ADHD+internalizing profile predicting a greater decline than ADHD simplex and disruptive/disorganized ADHD. I also hypothesize that higher family adversity scores will predict a lesser decline in symptoms and related impairment. The results of this study will provide insight different into female presentations of ADHD. This information can then be used to optimize ADHD screening methods to reduce demographic disparities in ADHD and determine which combination of treatments are most effective for different subgroups.

As part of cellular metabolism, all organisms produce reactive oxygen species (ROS), such as (O₂^– ) and hydrogen peroxide (H₂O₂). ROS can damage multiple cellular organelles and processes, disrupting normal physiology. Proteins, lipids, and nucleic acids can be damaged by ROS molecules, resulting in cell death. Also, several human diseases have been linked to an imbalance between ROS production and antioxidant defenses. Plants' chloroplasts and mitochondria contribute a substantial amount of ROS, as they are responsible for photosynthesis and aerobic respiration. In maize, Whirly ssDNA-binding proteins help to maintain the stability of the plastid genome. We recently demonstrated that maize seedling development is accompanied by increasing oxidative stress to the demise of chloroplasts, mitochondria, and their DNA. We also showed that maize seedlings grown in the light had higher levels of oxidants and lower levels of antioxidants than dark-grown seedlings. Here, our objective is to elucidate the role of Whirly proteins in oxidative damage. We isolated organelles from maize seedlings and performed oxidant and antioxidant assays for both wild-type and whirly-mutant plants. We found a significant difference in oxidation levels between wild-type and mutant plants. Our study should provide a better understanding of the role of ssDNA-binding proteins in oxidative damage to organelles.