Interpretation of Basic Clinical Images: How Are Surgical Residents Performing Compared to Other Trainees?

BACKGROUND: During medical training students, residents, and fellows learn how to accurately interpret basic radiographic images. This skill is mostly utilized by physicians in the acute and critical care settings. It is unclear whether surgical residents' interpretation skills differ from that of other trainees. METHODS: A 30-question online quiz was developed to evaluate trainees' skills in interpreting images using various radiologic modalities. The participating cohort included (1) medical students (MS), (2) general surgery residents (GST), internal medicine residents and fellows (IMT), and radiology trainees (RT). The impact of residency specialty and level of training on performance was evaluated. RESULTS: A total of 69 postgraduate trainees and 19 MS enrolled in the online quiz. The average score was 67.6% (±16.6). GST scored higher than IMT (74.2% ± 10.7% vs. 67.9% ± 11.3%, p = 0.038); however, they were equally proficient to RT. MS had the lowest interpretation accuracy rates compared to postgraduate trainees (57.4% ± 16.8%, p < 0.001). On different radiographic modalities, junior GST performance was comparable to MS, JR-IMT, and Junior Radiology Trainees (JR-RT). On computed tomography (CT) body, GST (83.1% ± 15.7%) scored higher than IMT (70.3% ± 17.7%, p = 0.026) and MS (61.7% ± 23.4%, p < 0.001). Similar findings were demonstrated on ultrasound modality. A difference in performance was not evident for X-rays, CT head, and tubes/lines localization images. CONCLUSIONS: GST were able to correctly interpret 74.2% of basic clinical images. Although superior in the evaluation of pathologies seen on CT body and ultrasound, GST have comparable performance to other trainees in X-rays, tube/line localization images, and CT head. Integration of radiology education in surgical training may enhance performance and potentially improve patient care.

Pparg promotes differentiation and regulates mitochondrial gene expression in bladder epithelial cells.

The urothelium is an epithelial barrier lining the bladder that protects against infection, fluid exchange and damage from toxins. The nuclear receptor Pparg promotes urothelial differentiation in vitro, and Pparg mutations are associated with bladder cancer. However, the function of Pparg in the healthy urothelium is unknown. Here we show that Pparg is critical in urothelial cells for mitochondrial biogenesis, cellular differentiation and regulation of inflammation in response to urinary tract infection (UTI). Superficial cells, which are critical for maintaining the urothelial barrier, fail to mature in Pparg mutants and basal cells undergo squamous-like differentiation. Pparg mutants display persistent inflammation after UTI, and Nf-KB, which is transiently activated in response to infection in the wild type urothelium, persists for months. Our observations suggest that in addition to its known roles in adipogegnesis and macrophage differentiation, that Pparg-dependent transcription plays a role in the urothelium controlling mitochondrial function development and regeneration.

Aberrant lymphatic endothelial progenitors in lymphatic malformation development.

Lymphatic malformations (LMs) are vascular anomalies thought to arise from dysregulated lymphangiogenesis. These lesions impose a significant burden of disease on affected individuals. LM pathobiology is poorly understood, hindering the development of effective treatments. In the present studies, immunostaining of LM tissues revealed that endothelial cells lining aberrant lymphatic vessels and cells in the surrounding stroma expressed the stem cell marker, CD133, and the lymphatic endothelial protein, podoplanin. Isolated patient-derived CD133+ LM cells expressed stem cell genes (NANOG, Oct4), circulating endothelial cell precursor proteins (CD90, CD146, c-Kit, VEGFR-2), and lymphatic endothelial proteins (podoplanin, VEGFR-3). Consistent with a progenitor cell identity, CD133+ LM cells were multipotent and could be differentiated into fat, bone, smooth muscle, and lymphatic endothelial cells in vitro. CD133+ cells were compared to CD133- cells isolated from LM fluids. CD133- LM cells had lower expression of stem cell genes, but expressed circulating endothelial precursor proteins and high levels of lymphatic endothelial proteins, VE-cadherin, CD31, podoplanin, VEGFR-3 and Prox1. CD133- LM cells were not multipotent, consistent with a differentiated lymphatic endothelial cell phenotype. In a mouse xenograft model, CD133+ LM cells differentiated into lymphatic endothelial cells that formed irregularly dilated lymphatic channels, phenocopying human LMs. In vivo, CD133+ LM cells acquired expression of differentiated lymphatic endothelial cell proteins, podoplanin, LYVE1, Prox1, and VEGFR-3, comparable to expression found in LM patient tissues. Taken together, these data identify a novel LM progenitor cell population that differentiates to form the abnormal lymphatic structures characteristic of these lesions, recapitulating the human LM phenotype. This LM progenitor cell population may contribute to the clinically refractory behavior of LMs.

Retinoid signaling in progenitors controls specification and regeneration of the urothelium.

The urothelium is a multilayered epithelium that serves as a barrier between the urinary tract and blood, preventing the exchange of water and toxic substances. It consists of superficial cells specialized for synthesis and transport of uroplakins that assemble into a tough apical plaque, one or more layers of intermediate cells, and keratin 5-expressing basal cells (K5-BCs), which are considered to be progenitors in the urothelium and other specialized epithelia. Fate mapping, however, reveals that intermediate cells rather than K5-BCs are progenitors in the adult regenerating urothelium, that P cells, a transient population, are progenitors in the embryo, and that retinoids are critical in P cells and intermediate cells, respectively, for their specification during development and regeneration. These observations have important implications for tissue engineering and repair and, ultimately, may lead to treatments that prevent loss of the urothelial barrier, a major cause of voiding dysfunction and bladder pain syndrome.