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The aim of the project is to examine how autobiographical connection to climate change messages (displayed via personalized billboard messages) increases people’s concerns and mitigation intentions regarding climate change.

Advanced undergraduate class project that aims to replicate a previously published research study about the relationship between dissociation and different components of participants' happiest and saddest memories (Duman & Tekcan, 2022).

Advanced undergraduate class replication project of Stone, Guan, LaBarbera, Ceren, Garcia, Huie, Stump, & Wang (2022).

The current study hopes to closely replicate the findings of Duman and Teckcan (2022), given the implications of their results on how personality impacts autobiographical memory. The study of susceptibility to unstable or inaccurate memories is of particular interest to researchers, given the importance of understanding these phenomena in real-world contexts like therapy settings (Dalenberg, 1996). Replication is vital to ensure that the nature of psychological research is self-correcting, reliable, and generalizable (Schie & Leer, 2019).

Template for participating labs in the Finkel RRR. Participating labs should Fork this template to create their own project page.

This study examines whether cohabitation prior to and/or relocation as a consequence of getting married influences the memory of the wedding event and/or how that event is integrated into the life story.

This study will replicate and extend the five experiments reported by Bransford & Johnson (1972) examining the influence of context on comprehension and recall of ambiguous texts. We will use the exact stimuli reported in the original where possible, but expand each experiment to include full context and partial context conditions before and after text presentation in addition to a no context control (with single and repeated presentation).

β-Adrenergic receptor (βAR)-mediated transactivation of epidermal growth factor receptor (EGFR) has beenshown to relay pro-survival effects via unknown mechanisms. We hypothesized that acute βAR-mediatedEGFR transactivation in the heart promotes differential subcellular activation of ERK1/2 and Akt, promotingcell survival through modulation of apoptosis. C57BL/6 mice underwent acute i.p. injection with isoproterenol(ISO)±AG 1478 (EGFR antagonist) to assess the impact of βAR-mediated EGFR transactivation on the phosphorylationof ERK1/2 (P-ERK1/2) and Akt (P-Akt) in distinct cardiac subcellular fractions. Increased P-ERK1/2 andP-Akt were observed in cytosolic, plasma membrane and nuclear fractions following ISO stimulation. Whereasthe P-ERK1/2 response was EGFR-sensitive in all fractions, the P-Akt response was EGFR-sensitive only in theplasma membrane and nucleus, results confirmed in primary rat neonatal cardiomyocytes (RNCM). βARmediatedEGFR-transactivation also decreased apoptosis in serum-depleted RNCM, as measured via TUNEL aswell as caspase 3 activity/cleavage, which were sensitive to the inhibition of either ERK1/2 (PD184352) or Akt(LY-294002) signaling. Caspase 3 activity/cleavage was also sensitive to the inhibition of transcription, which,with an increase in nuclear P-ERK1/2 and P-Akt in response to ISO, suggested that βAR-mediated EGFRtransactivation may regulate apoptotic gene transcription. An Apoptosis PCR Array identified tnfsf10 (TRAIL) tobe altered by ISO in an EGFR-sensitive manner, results confirmed via RT-PCR and ELISA measurement of bothmembrane-bound and soluble cardiomyocyte TRAIL levels. βAR-mediated EGFR transactivation induces differentialsubcellular activation of ERK1/2 and Akt leading to increased cell survival through themodulation of caspase3 activity and apoptotic gene expression in cardiomyocytes.

Chronic stimulationof -adrenergic receptors ( AR) can promote survival signalingvia transactivation of epidermal growth factor receptor (EGFR)but ultimately alters cardiac structure and contractility over time, inpart via enhanced cytokine signaling. We hypothesized that chroniccatecholamine signaling will have a temporal impact on cardiactranscript expression in vivo, in particular cytokines, and that EGFRtransactivation plays a role in this process. C57BL/6 mice underwentinfusion with vehicle or isoproterenol (Iso) gefitinib (Gef) for 1 or2 wk. Cardiac contractility decreased following 2 wk of Iso treatment,while cardiac hypertrophy, fibrosis, and apoptosis were enhanced atboth timepoints. Inclusion of Gef preserved contractility, blockedIso-induced apoptosis, and prevented hypertrophy at the 2-wk timepoint,but caused fibrosis on its own. RNAseq analysis revealedhundreds of cardiac transcripts altered by Iso at each timepoint withsubsequent RT-quantitative PCR validation confirming distinct temporalpatterns of transcript regulation, including those involved incardiac remodeling and survival signaling, as well as numerouscytokines. Although Gef infusion alone did not significantly altercytokine expression, it abrogated the Iso-mediated changes in amajority of the AR-sensitive cytokines, including CCL2 and TNF- .Additionally, the impact of AR-dependent EGFR transactivation onthe acute regulation of cytokine transcript expression was assessed inisolated cardiomyocytes and in cardiac fibroblasts, where the majorityof Iso-dependent, and EGFR-sensitive, changes in cytokines occurred.Overall, coincident with changes in cardiac structure and contractility, AR stimulation dynamically alters cardiac transcript expression overtime, including numerous cytokines that are regulated via EGFRdependentsignaling.