Publications by authors named "K H Thoma"

Objectives: Objective structured clinical examinations (OSCEs) provide reliable and standardized means for assessing the performance of specific clinical skills. Our previous experience with entrustable professional activity-based multidisciplinary OSCEs suggests that this exercise offers just-in-time baseline information regarding critical intern skills. The coronavirus disease 2019 pandemic forced medical education programs to reimagine such educational experiences.

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The Serious Illness Care Program (SICP), developed in 2011 by Ariadne Labs, restructures care so that knowing and then honoring patients' wishes becomes part of routine care. 1) summarize patient perceptions of use of the Serious Illness Conversation Guide (SICG) components, 2) assess whether a serious illness conversation was documented in the electronic health record (EHR) and identify the SICG components that were included, 3) summarize clinician perceptions of use of the SICG components, and 4) assess the association of documented SICG components with the patient's perception of the SICG discussion. Clinicians at three family medicine offices were trained in serious illness conversations using the SICG.

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Advance care planning (ACP) involves patients and family members in discussions with clinicians about their values, goals, and preferences regarding future medical care. To (1) assess whether an ACP conversation using the Serious Illness Conversation (SIC) was initiated and documented; (2) assess which components of SIC were documented; (3) determine how frequently clinicians trained to use the SIC guide used ACP billing codes during the study time period, (4) determine whether there was a significant difference in mortality risk score according to documentation of each component of the SIC. Thirteen clinicians at three family medicine offices were trained in the Serious Illness Care Program and asked to document SICs in the electronic medical record (EMR).

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Autosomal dominant (AD) NFKB1 deficiency is thought to be the most common genetic etiology of common variable immunodeficiency (CVID). However, the causal link between NFKB1 variants and CVID has not been demonstrated experimentally and genetically, and there has been insufficient biochemical characterization and enrichment analysis. We show that the cotransfection of NFKB1-deficient HEK293T cells (lacking both p105 and its cleaved form p50) with a κB reporter, NFKB1/p105, and a homodimerization-defective RELA/p65 mutant results in p50:p65 heterodimer-dependent and p65:p65 homodimer-independent transcriptional activation.

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