Curry College

Understanding the relationship between the structure and function of biological molecules (carbohydrates, lipids, proteins, and nucleic acids) is a fundamental concept covered in an undergraduate introductory biology course with which students often struggle. Students at this level often feel intimidated when asked to recall and differentiate between the specifics of each macromolecule including monomers, polymers, types of bonds or functional groups present, and the function of each. Demonstrating a deeper understanding of the material such as the relationship between structure and function is even more challenging since this requires higher-level conceptualization and synthesis skills. While lecturing can deliver an abundance of facts, providing students with hands-on opportunities to discover information themselves and practice putting together complex ideas often results in an increase in engagement and ultimately student satisfaction and confidence in the sciences. We developed a student-designed 3D modeling project in order to provide our students a hands-on approach to learning about biological macromolecules. The project begins with several low-stakes active learning activities and culminates with model design and peer teaching of an assigned macromolecule. Our observations and evaluations collected over the past twelve semesters of implementation in a small introductory biology course for science majors suggest that students who fully participate in this project show an increase in their perceived understanding of this material and engagement in the course. In this lesson we provide a detailed description of our activity including supporting materials and suggested adaptations for online or large classrooms. <em>Primary Image:</em>&nbsp;3D printed phospholipids. Individual phospholipids were 3D printed and colored using permanent marker. Magnets were added after printing to represent intermolecular forces that allow phospholipid head groups to interact within the phospholipid bilayer of cells. Image credit: Emily M. Nowicki, picture taken in-house.

Review Update (2016) https://doi.org/10.1002/14651858.CD003519.pub4 Review Update (2012) https://doi.org/10.1002/14651858.CD003519.pub3 Review Update (2007) https://doi.org/10.1002/14651858.CD003519.pub2 Original review (2003) https://doi.org/10.1002/14651858.CD003519 Protocol (2002) DOI unavailable.

Given the rapid growth of the Latino population in the United States, criminological research has begun to explore the ways in which pathways to crime may depend on different social statuses such as race and ethnicity. Incorporating cultural factors into the study of general strain theory (GST) among Latino youth can help elucidate which cultural factors protect these adolescents from engaging in criminal activity and provide recommendations for relevant crime prevention policy. Using data from the Dating Violence among Latino Adolescents study, the current research seeks to develop a more nuanced, culturally sensitive understanding of the victimization–delinquency overlap among Latino youth using a GST framework. Overall, results from this study both support and raise questions about the generalizability of GST to the Latino population. The results provide partial support for the role of culturally relevant variables in the GST process. In addition, results from this study show anger is the key construct mediating the victimization–delinquency overlap among Latino youth. Findings from this research expand our knowledge of how GST applies to an expanding, yet understudied population.

We previously theorized that Attention-Deficit Hyperactivity Disorder (ADHD) may increase susceptibility to narcolepsy and hypersomnia, potentially sharing genomic and pathophysiological features with addictive behaviours linked to Reward Deficiency Syndrome (RDS). We further suggested that the emergence of narcolepsy in individuals with underlying ADHD or RDS may place additional stress on the dopaminergic reward system. To explore this, we conducted comprehensive data mining using GWAS catalog databases focused on ADHD and narcolepsy, identifying three relevant datasets. These were individually analyzed in GWAS meta-analyses, followed by a combined GWAS meta-meta-analysis. From this, we derived a Primary Gene List (PGL) of 512 genes and a Secondary Gene List (SGL) of 42 genes, which were further examined through in-depth silico, systems biology, and pharmacogenomic (PGx) approaches. Our findings revealed a fully connected protein–protein interaction (PPI) network between ADHD and narcolepsy, with FOXP2 and RBFOX1 emerging as shared genes. We also identified schizophrenia as a potential endophenotype linking ADHD and narcolepsy. PGx analysis revealed pharmacogenomic relevance for seven genes from the SGL. To further investigate PGx–PPI relationships, we incorporated ten GARS family genes along with eight identified pharmacogenes in PGx-PPIs, and included FOXP2, RBFOX1, and GRIN2A, despite the absence of PGx data for the latter three. This analysis highlighted DRD2 and NRXN1 as central components of the dopaminergic [Genetic Addiction Risk Severity (GARS)] pathway, forming critical connections in the ADHD–schizophrenia–narcolepsy axis. These results support our initial hypothesis of a shared genetic basis between ADHD and narcolepsy. Additionally, we identified potentially overlapping genes with schizophrenia and highlighted dopaminergic regulatory variants of FOXP2, RBFOX1, and GRIN2A as promising diagnostic markers and therapeutic targets for future research.

Artificially increasing dopamine transmission is the common mechanism by which substances with addictive potential lead to addiction. A key area of research in neurobiology is the role of dopamine. Significant advancements have been made in uncovering the intracellular signaling pathways that mediate both dopamine's immediate effects and its long-term influence on brain function. Recent discoveries have also highlighted specific molecules that could serve as potential therapeutic targets for neurological and psychiatric disorders. While understanding several important caveats, we believe dopamine acts as a master regulator of brain circuitry across major chromosomes mapping the mental health genome. This view may have important clinical relevance, emphasizing the critical role of dopaminergic activity across the genome. Importantly, we are cognizant that dopamine does not work in insolation, and its finite actions are due to a highly interactive network (known as the brain reward cascade), involving at least seven other major neurotransmitters.

Overdose involving opioids is the black heart of the addiction crisis. "Pre-addiction," as an encouraging concept by NIDA and NIAAA, seems best captured with the construct of dopamine dysregulation. Referring to the abundant publications on "Reward Deficiency Syndrome" (RDS), Genetic Addiction Risk Score (GARS) test, RDSQ29, and KB220, Pre-addiction can be referred to as "reward dysregulation" as a suitable suggestion. The hypothesis is that the true phenotype is RDS, and other behavioral disorders are endophenotypes where the genetic variants play important roles, specifically in the Brain Reward Cascade (BRC). This study tested the pharmacogenomics of the GARS panel by a multi-model in silico investigation in four layers: 1) Protein-Protein Interactions (PPIs); 2) Gene Regulatory Networks (GRNs); 3) Disease, drugs and chemicals (DDCs); and 4) Gene Coexpression Networks (GCNs). All in silico findings were combined in an Enrichment Analysis for 59 refined genes, which represented highly significant associations of dopamine pathways in the BRC and supported our hypothesis. This paper provides scientific evidence for the importance of incorporating GARS as a predictive test to identify Pre-addiction, introduce unique therapeutic targets assisting in the treatment of pain, drug dosing of prescription pharmaceuticals, and identify the risk for subsequent addiction early in -life.