Publications by authors named "Alec S Eidelman"

Purpose/objective: The objective of this project was to evaluate the perceptions of predental students' shadowing experiences during a pandemic and further, explore innovative solutions that can be implemented to ensure that shadowing opportunities are equitable and accessible.

Methods: Data was collected via the Web 2.0 social media platform, Instagram (owned by Meta Platforms, Inc.

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Purpose/objectives: Reflection is one of four components of the experiential learning cycle and is often the one overlooked. This practice can be used in graduate-level health care education, such as medicine and dentistry. This metacognitive practice allows students to conceptualize learning in a clinical setting and apply this knowledge to new scenarios.

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In 2012, when the National Board Dental Examination (NBDE) was changed from a numerical scoring system to pass/fail, advanced dental education programs lost a metric widely used for differentiating applicants to those programs. The American Dental Association (ADA) has developed the Advanced Dental Admission Test (ADAT) to address this issue. Implementation of the ADAT began in 2016 with a pilot program, which has not yet been widely accepted in the overall admissions process.

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Previous data obtained in our laboratory suggested that there may be constitutive signaling through the myeloid differentiation primary response gene 88 (Myd88)-dependent signaling cascade in murine mammary carcinoma. Here, we extended these findings by showing that, in the absence of an added Toll-like receptor (TLR) agonist, the myddosome complex was preformed in 4T1 tumor cells, and that Myd88 influenced cytoplasmic extracellular signal-regulated kinase (Erk)1/Erk2 levels, nuclear levels of nuclear factor-kappaB (NFκB) and signal transducer and activator of transcription 5 (STAT5), tumor-derived chemokine (C-C motif) ligand 2 (CCL2) expression, and in vitro and in vivo tumor growth. In addition, RNA-sequencing revealed that Myd88-dependent signaling enhanced the expression of genes that could contribute to breast cancer progression and genes previously associated with poor outcome for patients with breast cancer, in addition to suppressing the expression of genes capable of inhibiting breast cancer progression.

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Previously we reported that Myd88 contributed to tumor progression. To begin to decipher what may be inducing Myd88 dependent signaling we focused on proteins that could function as damage associated molecular pattern molecules (DAMPs) since DAMPs have been reported to be secreted by tumors, and certain DAMPs mediate effects through toll-like receptors. A screen of mammary carcinoma for DAMP expression showed HMGB1 and HSP60 were significantly elevated relative to normal mammary epithelium, and targeting these DAMPs, or receptors for these DAMPs influenced growth of tumor cells.

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