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Objective: Our team set out to design and develop a low-cost 3D-printed liver transplant simulator. Design: The simulator comprises a 3D-printed recipient body cavity and the filled-fabric liver. Results: Validators perceived the model as valuable to education, noted that they would use the model at their institution and desired to integrate the model into their curriculum. In addition, the simulator was rated highly for ease of use (3.6/4), physical attributes (3.2/4) and user experience (4.4/5). Conclusion: The low-cost 3D-printed simulator for liver transplantation was highly rated in a multi-institutional validation and supports the use of simulation models in transplant surgery.

Surgical videos are commonly utilized by trainees to prepare for surgical cases. However, currently available videos tend to be of excessive length, variable quality, and exist behind paywalls or in other exclusive formats. Our objective was to create a series of videos that would address these shortcomings, and further allow for dynamic engagement between learners and experts.Our group created surgical videos using principles of microlearning, an educational strategy which deconstructs content into small units and uses social media platforms where learners and educators may actively engage. We published a library of short (3 min) videos covering various steps of abdominal transplantation operations on a YouTube channel. We leveraged Twitter to disseminate the content and engage with experts and learners from around the world.Multi-institutional.Over the period from July 2020 to January 2021, 24 microlearning videos were created, stored on a YouTube channel, and posted to Twitter weekly using a newly created account. During that time period, the videos, averaging 124 seconds in length, were viewed 4393 times and watched for a total of 127 hours. The account gained 611 followers in 37 countries and 37 US states with 312,400 impressions (defined as tweet views). Twitter users who engaged with our microlearning content (favorite, retweet, or reply) included faculty (27%), residents (21%), fellows (8%), and medical students (11%).Broad participation with the educational material and discussion on Twitter demonstrated the potential for the microlearning technique to provide educational benefit for learners internationally. The spread of the tweets shows an opportunity to augment traditional surgical education, and the willingness of faculty to discuss alternative techniques with their peers. Our group will continue to develop a library of microlearning videos for surgical operations and engage with other institutions for collaboration and expansion.

Aortic root aneurysm formation is a cardinal feature of Marfan syndrome (MFS) and likely TGF‐β driven via Smad (canonical) and ERK (non‐canonical) signalling. The current study assesses human MFS vascular smooth muscle cell (SMC) phenotype, focusing on individual contributions by Smad and ERK, with Notch3 signalling identified as a novel compensatory mechanism against TGF‐β‐driven pathology. Although significant ERK activation and mixed contractile gene expression patterns were observed by traditional analysis, this did not directly correlate with the anatomic site of the aneurysm. Smooth muscle cell phenotypic changes were TGF‐β‐dependent and opposed by ERK in vitro, implicating the canonical Smad pathway. Bulk SMC RNA sequencing after ERK inhibition showed that ERK modulates cell proliferation, apoptosis, inflammation, and Notch signalling via Notch3 in MFS. Reversing Notch3 overexpression with siRNA demonstrated that Notch3 promotes several protective remodelling pathways, including increased SMC proliferation, decreased apoptosis and reduced matrix metalloproteinase activity, in vitro. In conclusion, in human MFS aortic SMCs: (a) ERK activation is enhanced but not specific to the site of aneurysm formation; (b) ERK opposes TGF‐β‐dependent negative effects on SMC phenotype; (c) multiple distinct SMC subtypes contribute to a ‘mixed’ contractile‐synthetic phenotype in MFS aortic aneurysm; and (d) ERK drives Notch3 overexpression, a potential pathway for tissue remodelling in response to aneurysm formation.

Introduction Low-density lipoprotein cholesterol (LDL) is a known contributing factor to atherosclerotic cardiovascular disease (ASCVD) and a primary therapeutic target for medical management of ASCVD. Non-high-density lipoprotein cholesterol (non-HDL) has recently been identified as a secondary therapeutic target but is not yet widely used in vascular surgery patients. We sought to assess if vascular surgery patients were undertreated per non-HDL therapeutic guidelines. Methods This was an observational study that used a single-center database to identify a cohort of adult patients who received care from a vascular surgery provider from 01/2001 to 07/2021. ICD-9/10-CM codes were used to identify patients with a medical history of hyperlipidemia (HLD), coronary artery disease (CAD), cerebrovascular occlusive disease (CVOD), peripheral artery disease (PAD), hypertension (HTN), or diabetes mellitus (DM). Patient smoking status and medications were also identified. Lab values were obtained from the first and last patient encounter within our system. Primary outcomes were serum concentrations of LDL and non-HDL, with therapeutic thresholds defined as 70 mg/dL and 100 mg/dL, respectively. Results The cohort included 2465 patients. At first encounter, average age was 59.3 years old, 21.4% were on statins, 8.4% were on a high-intensity statin, 25.7% were diagnosed with HLD, 5.2% with CAD, 15.3% with PAD, 26.3% with DM, 18.6% with HTN, and 2.1% with CVOD. At final encounter, mean age was 64.8 years, 23.5% were on statins with 10.1% on high-intensity statin. Diagnoses frequency did not change at final encounter. At first encounter, nearly two-thirds of patients were not at an LDL Discussion Among vascular surgery patients, over half did not meet non-HDL targets. These results suggest that we may be vastly under-performing adequate medical optimization with only about one-fourth of patients on a statin at their final encounter and approximately one-tenth of patients being treated with a high-intensity statin. With recent evidence supporting non-HDL as a valuable measurement for atherosclerotic risk, there is potential to optimize medical management beyond current high-intensity statin therapy. Further investigation is needed regarding the risk of adverse events between patients treated with these varied therapeutic targets.

Background Mindstep is an app that aims to improve dementia screening by assessing cognition and risk factors. It considers important clinical risk factors, including prodromal symptoms, mental health disorders, and differential diagnoses of dementia. The 9-item Patient Health Questionnaire for depression (PHQ-9) and the 7-item Generalized Anxiety Disorder Scale (GAD-7) are widely validated and commonly used scales used in screening for depression and anxiety disorders, respectively. Shortened versions of both (PHQ-2/GAD-2) have been produced. Objective We sought to develop a method that maintained the brevity of these shorter questionnaires while maintaining the better precision of the original questionnaires. Methods Single questions were designed to encompass symptoms covered in the original questionnaires. Answers to these questions were combined with PHQ-2/GAD-2, and anonymized risk factors were collected by Mindset4Dementia from 2235 users. Machine learning models were trained to use these single questions in combination with data already collected by the app: age, response to a joke, and reporting of functional impairment to predict binary and continuous outcomes as measured using PHQ-9/GAD-7. Our model was developed with a training data set by using 10-fold cross-validation and a holdout testing data set and compared to results from using the shorter questionnaires (PHQ-2/GAD-2) alone to benchmark performance. Results We were able to achieve superior performance in predicting PHQ-9/GAD-7 screening cutoffs compared to PHQ-2 (difference in area under the curve 0.04, 95% CI 0.00-0.08, P=.02) but not GAD-2 (difference in area under the curve 0.00, 95% CI –0.02 to 0.03, P=.42). Regression models were able to accurately predict total questionnaire scores in PHQ-9 (R2=0.655, mean absolute error=2.267) and GAD-7 (R2=0.837, mean absolute error=1.780). Conclusions We app-adapted PHQ-4 by adding brief summary questions about factors normally covered in the longer questionnaires. We additionally trained machine learning models that used the wide range of additional information already collected in Mindstep to make a short app-based screening tool for affective disorders, which appears to have superior or equivalent performance to well-established methods.

Background Statins reduce aneurysm growth in mouse models of Marfan syndrome, although the mechanism is unknown. In addition to reducing cholesterol, statins block farnesylation and geranylgeranylation, which participate in membrane‐bound G‐protein signaling, including Ras. We dissected the prenylation pathway to define the effect of statins on aneurysm reduction. Methods and Results Fbn1 C1039G/+ mice were treated with (1) pravastatin (HMG‐CoA [3‐hydroxy‐3‐methylglutaryl coenzyme A] reductase inhibitor), (2) manumycin A ( MA ; FPT inhibitor), (3) perillyl alcohol ( GGPT 1 and ‐2 inhibitor), or (4) vehicle control from age 4 to 8 weeks and euthanized at 12 weeks. Histological characterization was performed. Protein analysis was completed on aortic specimens to measure ERK (extracellular signal‐regulated kinase) signaling. In vitro Fbn1 C1039G/+ aortic smooth muscle cells were utilized to measure Ras‐dependent ERK signaling and MMP (matrix metalloproteinase) activity. Pravastatin and MA significantly reduced aneurysm growth compared with vehicle control (n=8 per group). In contrast, PA did not significantly decrease aneurysm size. Histology illustrated reduced elastin breakdown in MA ‐treated mice compared with vehicle control (n=5 per group). Although elevated in control Marfan mice, both phosphorylated c‐Raf and phosphorylated ERK 1/2 were significantly reduced in MA ‐treated mice (4–5 per group). In vitro smooth muscle cell studies confirmed phosphorylated cR af and phosphorylated ERK 1/2 signaling was elevated in Fbn1 C1039G/+ smooth muscle cells (n=5 per group). Fbn1 C1039G/+ smooth muscle cell Ras‐dependent ERK signaling and MMP activity were reduced following MA treatment (n=5 per group). Corroborating in vitro findings, MMP activity was also decreased in pravastatin‐treated mice. Conclusions Aneurysm reduction in Fbn1 C1039G/+ mice following pravastatin and MA treatment was associated with a decrease in Ras‐dependent ERK signaling. MMP activity can be reduced by diminishing Ras signaling.

Saphenous vein graft aneurysms with mechanical complications should be repaired via a non-sternotomy open surgical technique.

Introduction: Enhanced TGF-β signaling drives aortic root aneurysm development in Marfan syndrome (MFS) via the non-canonical (ERK) pathway in murine models, but ERK not been studied in human tissue. Conversely, blockade of canonical (Smad) TGF-β signaling is detrimental in MFS mice. Recently, TGF-β-induced increases in smooth muscle cell (SMC) contractile genes and collagen I (COL1) expression have been proposed to lead to aortic stiffness and dilatation in MFS. Hypothesis: We hypothesized that ERK signaling is enhanced in human MFS tissue and dictates the predilection of the aortic root to develop aneurysm by altering SMC gene expression. Methods and Results: Western blot of aortic root tissue from MFS patients with root aneurysms (4.67±0.09 cm) revealed 3.1-fold increased ERK activation relative to control aortic root (p=0.03, n=8). When compared to non-dilated MFS ascending (ASC) aorta (2.94±0.14 cm), there was no difference in ERK activation between the two regions. While RT-PCR of MFS root showed increased expression of the contractile gene regulator myocardin (2.4±0.07 fold, p=0.01), and of MYH11 (3.05±0.13 fold, p=0.03) ACTA2 (2.93±0.10 fold, p Conclusions: ERK signaling is uniformly enhanced in MFS aortic root and ASC tissue, indicating that further study into aortic region-specific responses to cellular signals is needed to assess the development of focal aortic root aneurysm in MFS. Increased contractile gene expression is Smad-dependent and non-focal and thus does not clarify focal root aneurysm. COL1, while focally enhanced in the MFS root, is Smad-driven and suppressed by ERK, and may represent a compensatory response.