Although the best psychological treatments, such as cognitive behavioral therapy, for anxiety disorders already rely on fear extinction mechanisms, these treatments underutilize principles of vicarious extinction learning. Vicarious extinction learning is a form of social safety learning that involves learning safety from the experience of others and can potentially enhance treatment potency. Social anxiety disorder (SAD), which is characterized by persistent social avoidance due to fear of negative evaluation by others, may uniquely benefit from vicarious extinction learning. Broader social contexts, like cultural norms, can also have influence on social learning and the efficacy in treatments of social anxiety. Although culture is a broad and nuanced construct, interdependent and independent self-construals have been shown to capture two of the many facets of culture. In this study, we propose that cultural factors, such as interdependent and independent self-construals, may impact vicarious extinction learning in people with high levels of social anxiety symptoms. Twenty socially anxious adults and twenty healthy controls will complete the Self-Construal Scale (SCS) and undergo a vicarious extinction task while undergoing fMRI. We expect that those with interdependent self-construals will show enhanced safety learning due to their value for seeing themselves as similar to others, as compared to those with independent self-construals. This will be evidenced by lower skin conductance responses (SCR) and greater ventromedial prefrontal cortex activation during the reinstatement phase of the task. Our results will highlight a potentially important cultural moderator of social safety learning and advance our understanding of the boundaries and clinical implications of learning safety from others.

Rejection sensitivity (RS) is a core component of social anxiety that may impact symptom severity and treatment outcomes. There may be substantial differences in both neural and behavioral responses to fear as a function of trait RS in socially anxious individuals, as reflected in altered regional brain activation patterns underlying fear and self-referential processing. Individuals with the highest levels of RS may struggle to extinguish learned social fears but it is unclear if they learn safety differently by watching another person doing so, a process called vicarious extinction learning. Recent work has highlighted the advantage of vicarious extinction learning in fear regulation over traditional extinction learning, but this has not yet been tested in socially anxious populations. Given the relevance of social learning processes in social anxiety, vicarious extinction learning may enhance the effectiveness of exposure-based therapy in this population. In this study, individuals will undergo a social fear task in which they learn to pair images of angry faces with a mild electric shock. During Phase II, participants will watch a video of another person undergoing the same task and learning safety from one of the photos previously associated with a shock. The final phase will test if participants can apply the model's safety learning to themselves. I hypothesize that high trait RS may moderate vicarious extinction learning, as seen by differential activation in the ventromedial prefrontal cortex (vmPFC). It is possible that those with higher RS might show increased vmPFC activation during extinction and might benefit more from vicarious safety learning because social signals are more salient in this population and they have more to gain from learning safety, but it is also possible that they may not benefit, or even worsen, if they are unable to empathize with the learning model and remain vigilant to cues of social rejection, as evident by decreased vmPFC activation during extinction. Regardless of the direction of the effect, trait RS may be an important variable to consider when treating socially anxious patients using extinction-based principles and may influence the development of novel interventions to target this population. 

The BVF (Boring Volcanic Field) located in the Portland Basin west of the Cascades arc, is home to a wide variety of chemically distinct basalts. These basalts resemble mid-ocean ridge basalts, ocean island basalts, and intra-plate type basalts both chemically and mineralogically. Given the small area of this field, and the availability of all sample types throughout the entire volcanically active period, the cause of this diversity remains a challenge to explain. To investigate this process, we have used a MC-ICP mass spectrometer to collect magnesium isotope ratio data. While this diversity could come from a heterogenous mantle, with each of these sample types coming from a different mantle source, we expect that there are added components which change the chemical composition of the magma. Magnesium can be used as a tracer for added contributions in igneous rocks since the isotopic ratio of this element is not changed by volcanic processes, thus the data we record is representative of the source of these samples. Additionally, magnesium is most largely fractionated by low temperature processes such as carbonate precipitation and weathering. Given this, materials such as subducted crust or sediments would leave a recognizably different magnesium ratio in any basalt produced from this interaction. By combining our magnesium data with previous major (>1 wt. %) and trace element (<0.1 wt. %) analysis, we have tested for the presence of subduction derived isotopic signatures. From these discovered influences, we will produce a more accurate model of magmatism that accounts for the variety found in the BVF.

Joubert syndrome (JS) is a neurodevelopmental disorder diagnosed by the appearance of a “molar tooth sign” on an axial brain magnetic resonance imaging (MRI). JS patients present with hypotonia (low muscle tone), abnormal eye movements, and ataxia (uncoordinated movements). Subsets of patients develop progressive medical complications. Autosomal recessive, X-linked and rare dominant causes of JS in >40 different genes can be identified by DNA sequencing in ~75% of families. Cryptic DNA variants and alternative inheritance mechanisms are thought to account for the other 25% of families. The goal of this project is to evaluate the role of non-canonical splice variants in the pathogenesis of JS. We identified candidate splice variants in MKS1 from whole genome and targeted sequencing data and prioritized using SpliceAI annotation. A synonymous variant in patient 1 and a 30 base pair intronic deletion in patient 2 were identified. For each variant, we designed two sets of primers to flank the affected splice junction. Next, we extracted RNA from patient fibroblasts. We converted RNA into complementary DNA (cDNA) and amplified using polymerase chain reaction (PCR). Using gel electrophoresis and Sanger sequencing, we compared PCR products from patients versus controls.  We identified differences in DNA band sizes between unaffected control and patient samples. Based on Sanger sequencing, we determined that exon 4 is skipped in patient 1, but we were unable to determine the specific aberrant splicing event in patient 2. We confirmed the pathogenicity of candidate splice variants, identifying the precise genetic cause. An accurate genetic diagnosis informs prognosis, avoids unnecessary work-up, and guides monitoring for associated complications. Defining all genetic causes of JS expands our knowledge of the genetic mechanisms underlying recessive Mendelian conditions, confirming a substantial role for non-canonical splice variants.