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Academic medicine as a practice model provides unique benefits to society. Clinical care remains an important part of the academic mission; however, equally important are the educational and research missions. More specifically, the sustainability of health care in the United States relies on an educated and expertly trained physician workforce directly provided by academic medicine models. Similarly, the research charge to deliver innovation and discovery to improve health care and to cure disease is key to academic missions. Therefore, to support and promote the growth and sustainability of academic medicine, attracting and engaging top talent from fellows in training and early career faculty is of vital importance. However, as the health care needs of the nation have risen, clinicians have experienced unprecedented demand, and individual wellness and burnout have been examined more closely. Here, we provide a close look at the unique drivers of burnout in academic cardiovascular medicine and propose system-level and personal interventions to support individual wellness in this model.

[Image: see text] Central Picture Legend: Ethical standards for global health initiatives.

Background The introduction of integrated 6-year cardiothoracic surgery (CTS) residency programs has shifted recruitment efforts to encompass not only general surgery (GS) residents, but also medical students. Objective The aim of this paper is to assess medical student and GS resident clinical exposure to CTS. Design Data from the Association of American Medical Colleges Visiting Student Application Service and the Accreditation Council for Graduate Medical Education Case Log Reports were collected from 2010 to 2017 and 2010 to 2018, respectively. The data extracted included medical students who applied and received an offer for elective rotations and the cases performed as a GS resident. Results A mean of 95 ± 28.5 medical students applied for CTS rotations annually and the applicants for CTS rotations increased by an average of 11.8% per year. However, significantly less students received an offer compared to other specialties (53.4% CTS vs 74.1% GS, 79.3% plastic surgery, 86.3% urology, 85.7% otolaryngology, 88.6% neurological surgery, and 89.6% orthopedic surgery) (p GS residents performed a mean of 39.3 ± 0.8 CTS procedures during residency: 32.9 ± 1.0 performed as a junior resident and 6.3 ± 0.7 as a chief resident. Out of all CTS procedures, 7.3% were cardiac procedures, with rates increasing from 5.6% to 8.4% during the study period (p = 0.001). Conclusions Elective rotation opportunities in CTS are high in demand for medical students while GS residents receive limited CTS exposure, especially cardiac cases. Increasing clinical opportunities in both groups will aid in recruiting young talent to the field.

Sustained inflammation and matrix metalloproteinase (MMP) activation contribute to vascular occlusive/proliferative disorders. Interleukin-17 (IL-17) is a proinflammatory cytokine that signals mainly via TRAF3 Interacting Protein 2 (TRAF3IP2), an upstream regulator of various critical transcription factors, including AP-1 and NF-κB. Reversion inducing cysteine rich protein with kazal motifs (RECK) is a membrane-anchored MMP inhibitor. Here we investigated whether IL-17A/TRAF3IP2 signaling promotes MMP-13-dependent human aortic smooth muscle cell (SMC) proliferation and migration, and determined whether RECK overexpression blunts these responses. Indeed, IL-17A treatment induced (a) JNK, p38 MAPK, AP-1, NF-κB, and CREB activation, (b) miR-21 induction, (c) miR-27b and miR-320 inhibition, (d) MMP-13 expression and activation, (e) RECK suppression, and (f) SMC migration and proliferation, all in a TRAF3IP2-dependent manner. In fact, gain of TRAG3IP2 function, by itself, induced MMP-13 expression and activation, and RECK suppression. Furthermore, treatment with recombinant MMP-13 stimulated SMC migration in part via ERK activation. Importantly, RECK gain-of-function attenuated MMP-13 activity without affecting its mRNA or protein levels, and inhibited IL-17A- and MMP-13-induced SMC migration. These results indicate that increased MMP-13 and decreased RECK contribute to IL-17A-induced TRAF3IP2-dependent SMC migration and proliferation, and suggest that TRAF3IP2 inhibitors or RECK inducers have the potential to block the progression of neointimal thickening in hyperplastic vascular diseases.

Minocycline, an FDA-approved second-generation semisynthetic tetracycline, exerts antioxidant, anti-apoptotic and anti-inflammatory effects, independent of its antimicrobial properties. Interleukin (IL)-17A is an immune and inflammatory mediator, and its sustained induction is associated with various cardiovascular diseases. Here we investigated (i) whether IL-17A induces cardiomyocyte contractile depression and death, (ii) whether minocycline reverses IL-17A’s negative inotropic effects and (iii) investigated the underlying molecular mechanisms. Indeed, treatment with recombinant mouse IL-17A impaired adult cardiomyocyte contractility as evidenced by a 34% inhibition in maximal velocity of shortening and relengthening after 4 h (P

Proximal tubular epithelial cells (PTEC) in the S1 segment of the kidney abundantly express sodium-glucose co-transporters (SGLT) that play a critical role in whole body glucose homeostasis. We recently reported suppression of RECK ( Re version Inducing C ysteine Rich Protein with K azal Motifs), a membrane anchored endogenous MMP inhibitor and anti-fibrotic mediator, in the kidneys of db/db mice, a model of diabetic kidney disease (DKD), as well as in high glucose (HG) treated human kidney proximal tubule cells (HK−2). We further demonstrated that empagliflozin (EMPA), an SGLT2 inhibitor, reversed these effects. Little is known regarding the mechanisms underlying RECK suppression under hyperglycemic conditions, and its rescue by EMPA. Consistent with our previous studies, HG (25 mM) suppressed RECK expression in HK-2 cells. Further mechanistic investigations revealed that HG induced superoxide and hydrogen peroxide generation, oxidative stress-dependent TRAF3IP2 upregulation, NF-κB and p38 MAPK activation, inflammatory cytokine expression (IL-1β, IL-6, TNF-α, and MCP-1), miR-21 induction, MMP2 activation, and RECK suppression. Moreover, RECK gain-of-function inhibited HG-induced MMP2 activation and HK-2 cell migration. Similar to HG, advanced glycation end products (AGE) induced TRAF3IP2 and suppressed RECK, effects that were inhibited by EMPA. Importantly, EMPA treatment ameliorated all of these deleterious effects, and inhibited epithelial-to-mesenchymal transition (EMT) and HK-2 cell migration. Collectively, these findings indicate that hyperglycemia and associated AGE suppress RECK expression via oxidative stress/TRAF3IP2/NF-κB and p38 MAPK/miR-21 induction. Furthermore, these results suggest that interventions aimed at restoring RECK or inhibiting SGLT2 have the potential to treat kidney inflammatory response/fibrosis and nephropathy under chronic hyperglycemic conditions, such as DKD.

Hyperglycemia-induced production of endothelin (ET)-1 is a hallmark of endothelial dysfunction in diabetes. Although the detrimental vascular effects of increased ET-1 are well known, the molecular mechanisms regulating endothelial synthesis of ET-1 in the setting of diabetes remain largely unidentified. Here, we show that adapter molecule TRAF3 interacting protein 2 (TRAF3IP2) mediates high glucose-induced ET-1 production in endothelial cells and ET-1-mediated endothelial cell inflammation. Specifically, we found that high glucose upregulated TRAF3IP2 in human aortic endothelial cells, which subsequently led to activation of JNK and IKKβ. shRNA-mediated silencing of TRAF3IP2, JNK1, or IKKβ abrogated high-glucose-induced ET-converting enzyme 1 expression and ET-1 production. Likewise, overexpression of TRAF3IP2, in the absence of high glucose, led to activation of JNK and IKKβ as well as increased ET-1 production. Furthermore, ET-1 transcriptionally upregulated TRAF3IP2, and this upregulation was prevented by pharmacological inhibition of ET-1 receptor B using BQ-788, or inhibition of NADPH oxidase-derived reactive oxygen species using gp91ds-tat and GKT137831. Notably, we found that knockdown of TRAF3IP2 abolished ET-1-induced proinflammatory and adhesion molecule (IL-1β, TNF-α, monocyte chemoattractant protein 1, ICAM-1, VCAM-1, and E-selectin) expression and monocyte adhesion to endothelial cells. Finally, we report that TRAF3IP2 is upregulated and colocalized with CD31, an endothelial marker, in the aorta of diabetic mice. Collectively, findings from the present study identify endothelial TRAF3IP2 as a potential new therapeutic target to suppress ET-1 production and associated vascular complications in diabetes. NEW & NOTEWORTHY This study provides the first evidence that the adapter molecule TRAF3 interacting protein 2 mediates high glucose-induced production of endothelin-1 by endothelial cells as well as endothelin-1-mediated endothelial cell inflammation. The findings presented herein suggest that TRAF3 interacting protein 2 may be an important therapeutic target in diabetic vasculopathy characterized by excess endothelin-1 production.

Human beings have evolved their modes of communication continually through the ages. Over the last decade, social media in their various forms have become the preferred mode among younger generations, and their use has increased among older generations as well. Worldwide users of social media are expected by 2021 to number over 3 billion, which is approximately a third of the world’s population.1 The region with the highest penetration rate of social networks is North America, wherein around 60% of the population has more than one social media account, and 78% of the US population has a social networking profile.2 Social media offer enormous potential benefits for both care providers and patients, as the platform allows for the dissemination and gathering of information and has the innate ability to network globally. In fact, in a recent survey, 70% of surgeons indicated that they believe social media benefited professional development, while 22% preferred social media as their primary modality of networking and communication with colleagues.3 In using social media, care providers, particularly physicians and surgeons, must pay close attention to professionalism, specifically within the framework of professional ethics.

The overall goals of this study were to investigate whether metformin exerts anti-fibrotic effects in aldosterone (Aldo)+salt-treated wild type mouse hearts, and determine the underlying molecular mechanisms in isolated adult cardiac fibroblasts (CF). In vitro, Aldo induced CF activation, migration, and proliferation, and these effects were inhibited by metformin. Further, Aldo induced PPM1A (Protein Phosphatase Magnesium Dependent 1A) activation and inhibited AMPK phosphorylation. At a pharmacologically relevant concentration, metformin restored AMPK activation, and inhibited Aldo-induced Nox4/H2O2-dependent TRAF3IP2 induction, pro-inflammatory cytokine expression, and CF migration and proliferation. Further, metformin potentiated the inhibitory effects of spironolactone, a mineralocorticoid receptor antagonist, on Aldo-induced collagen expression, and CF migration and proliferation. These results were recapitulated in vivo, where metformin reversed Aldo+salt-induced oxidative stress, suppression of AMPK activation, TRAF3IP2 induction, pro-inflammatory cytokine expression, and cardiac fibrosis, without significantly modulating systolic blood pressure. These in vitro and in vivo data indicate that metformin has the potential to reduce adverse cardiac remodeling in hypertensive heart disease.

Background Arterial stiffness is emerging as an independent risk factor for the development of chronic kidney disease. The sodium glucose co-transporter 2 (SGLT2) inhibitors, which lower serum glucose by inhibiting SGLT2-mediated glucose reabsorption in renal proximal tubules, have shown promise in reducing arterial stiffness and the risk of cardiovascular and kidney disease in individuals with type 2 diabetes mellitus. Since hyperglycemia contributes to arterial stiffness, we hypothesized that the SGLT2 inhibitor empagliflozin (EMPA) would improve endothelial function, reduce aortic stiffness, and attenuate kidney disease by lowering hyperglycemia in type 2 diabetic female mice (db/db). Materials/methods Ten-week-old female wild-type control (C57BLKS/J) and db/db (BKS.Cg-Dock7m+/+Leprdb/J) mice were divided into three groups: lean untreated controls (CkC, n = 17), untreated db/db (DbC, n = 19) and EMPA-treated db/db mice (DbE, n = 19). EMPA was mixed with normal mouse chow at a concentration to deliver 10 mg kg−1 day−1, and fed for 5 weeks, initiated at 11 weeks of age. Results Compared to CkC, DbC showed increased glucose levels, blood pressure, aortic and endothelial cell stiffness, and impaired endothelium-dependent vasorelaxation. Furthermore, DbC exhibited impaired activation of endothelial nitric oxide synthase, increased renal resistivity and pulsatility indexes, enhanced renal expression of advanced glycation end products, and periarterial and tubulointerstitial fibrosis. EMPA promoted glycosuria and blunted these vascular and renal impairments, without affecting increases in blood pressure. In addition, expression of “reversion inducing cysteine rich protein with Kazal motifs” (RECK), an anti-fibrotic mediator, was significantly suppressed in DbC kidneys and partially restored by EMPA. Confirming the in vivo data, EMPA reversed high glucose-induced RECK suppression in human proximal tubule cells. Conclusions Empagliflozin ameliorates kidney injury in type 2 diabetic female mice by promoting glycosuria, and possibly by reducing systemic and renal artery stiffness, and reversing RECK suppression.

Persistent inflammation promotes development and progression of heart failure (HF). TWEAK (TNF-Related WEAK Inducer Of Apoptosis), a NF-κB- and/or AP-1-responsive proinflammatory cytokine that signals via TWEAK receptor (TWEAKR), is expressed at high levels in human and preclinical models of HF. Since the adapter molecule TRAF3IP2 (TRAF3 Interacting Protein 2) is an upstream regulator of various proinflammatory pathways, including those activated by NF-κB and AP-1, we hypothesized that targeting TRAF3IP2 inhibits TWEAK-induced proinflammatory and pro-fibrotic responses in vitro and in vivo. Consistent with the hypothesis, forced expression of TRAF3IP2 upregulated TWEAK and its receptor expression in cultured adult mouse cardiac fibroblasts (CF). Further, exogenous TWEAK upregulated TRAF3IP2 expression in a time- and dose-dependent manner, suggesting a positive-feedback regulation of TRAF3IP2 and TWEAK. TWEAK also promoted TRAF3IP2 nuclear translocation. Confirming its critical role in TWEAK signaling, silencing TRAF3IP2 inhibited TWEAK autoregulation, TWEAKR upregulation, p38 MAPK, NF-κB and AP-1 activation, inflammatory cytokine expression, MMP and TIMP1 activation, collagen expression and secretion, and importantly, proliferation and migration. Recapitulating these in vitro results, continuous infusion of TWEAK for 7 days increased systolic blood pressure (SBP), upregulated TRAF3IP2 expression, activated p38 MAPK, NF-κB and AP-1, induced the expression of multiple proinflammatory and pro-fibrotic mediators, and interstitial fibrosis in hearts of wild type mice. These proinflammatory and pro-fibrotic changes occurred in conjunction with myocardial hypertrophy and contractile dysfunction. Importantly, genetic ablation of TRAF3IP2 inhibited these TWEAK-induced adverse cardiac changes independent of increases in SBP, indicating that TRAF3IP2 plays a causal role, and thus a therapeutic target, in chronic inflammatory and fibro-proliferative diseases.

Objectives In an effort to stimulate residents and trainers to increase their use of simulation training and the Thoracic Surgery Curriculum, a gamification strategy was developed in a friendly but competitive environment. Methods "Top Gun." Low-fidelity simulators distributed annually were used for the technical competition. Baseline and final video assessments were performed, and 5 finalists were invited to compete in a live setting from 2013 to 2015. "Jeopardy." A screening examination was devised to test knowledge contained in the Thoracic Surgery Curriculum. The top 6 2-member teams were invited to compete in a live setting structured around the popular game show Jeopardy . Results "Top Gun." Over 3 years, there were 43 baseline and 34 final submissions. In all areas of assessment, there was demonstrable improvement. There was increasing evidence of simulation as seen by practice and ritualistic behavior. "Jeopardy." Sixty-eight individuals completed the screening examination, and 30 teams were formed. The largest representation came from the second-year residents in traditional programs. Contestants reported an average in-training examination percentile of 72.9. Finalists reported increased use of the Thoracic Surgery Curriculum by an average of 10 hours per week in preparation. The live competition was friendly, engaging, and spirited. Conclusions This gamification approach focused on technical and cognitive skills, has been successfully implemented, and has encouraged the use of simulators and the Thoracic Surgery Curriculum. This framework may capitalize on the competitive nature of our trainees and can provide recognition of their achievements.

The legacy of Nina Starr Braunwald lives on in her innovations, clearing a path for women in cardiothoracic surgery, and in the lives of those she has trained or supported. As one of the early pioneers in cardiac surgery, she represents what is excellent in our profession. The Braunwald family has donated to The Thoracic Surgery Foundation in the form of Research Awards, and a survey was conducted to determine the career paths of recipients since the first award in 1993.

Cardiopulmonary bypass (CPB) stimulates systemic and pulmonary inflammation. Modified ultrafiltration (MUF) mitigates deleterious CPB effects by unclear mechanisms. We evaluated pulmonary inflammation in piglets undergoing CPB followed by MUF. Twenty-four piglets underwent 60 min of hypothermic CPB. MUF subjects (n=12) underwent hemoconcentration postCPB to the target hematocrit. Pulmonary vascular resistance (PVR), proinflammatory cytokine concentrations, and transpulmonary thromboxane gradients were determined at baseline, following CPB, and at end of the study (EOS) in MUF and control (n=12) groups. PVR significantly increased postCPB in both groups but decreased after MUF. MUF and control groups were similar in regards to systemic cytokine concentrations. Bronchoalveolar lavage concentrations of IL-6 and IL-8 significantly increased in controls throughout the study. Alveolar IL-6 and IL-8 were unchanged at EOS in MUF subjects, and IL-6 concentrations were significantly less than controls at EOS (P=0.015). Similarly, transpulmonary thromboxane gradient was significantly less at EOS in MUF subjects compared with controls (P=0.04). MUF removed circulating inflammatory mediators, lessened pulmonary hypertension, and reduced pulmonary-derived inflammatory markers, providing further evidence that MUF ameliorates pulmonary-based inflammation. These findings lend insight into mechanisms behind salutary clinical benefits of MUF after CPB.

Background There has been much focus on factors influencing medical students' career choice, prompted by such concerns as a sufficient future surgical workforce, declining applicant pool, changing gender composition, and a cultural shift in values and priorities. Once in a surgical residency, there are little data on factors influencing general surgery (GS) residents' final specialty choice. Study Design A survey instrument was developed and content validated in conjunction with the Association of American Medical Colleges Center for Workforce Studies. The final instrument was distributed electronically between March 24 and May 2, 2008, through 251 GS program directors to all ACGME-accredited GS residents (n = 7,508). Results Response rate was 29% (2,153 residents; 89% programs). Half of GS residents remained undecided about specialty choice through the 2nd year, declining to 2% by year 5. Of the two-thirds who decided on a specialty, 16.5% chose to remain in GS, 14.6% chose plastics, 9.3% cardiothoracic, and 8.5% vascular. The specialty choice factors most likely to be very important were type of procedures and techniques, exposure to positive role model, and ability to balance work and personal life. Relative importance of factors in specialty choice varied by gender and chosen specialty. Mentors play a key role in specialty choice (66% decided had mentors versus 47% undecided). Work schedule was the most frequently selected shortcoming in every specialty except plastics. Cardiothoracic surgery followed by GS had the highest shortcomings. Conclusions The majority of GS residents plan to subspecialize. Three factors dominate specialty choice. Faculty need to understand their impact potential to modify or change perceptions of their specialty.

Tricuspid stenosis in the setting of endocardial pacing leads is a rare entity, attributed to infection or lead malposition. We report the case of a 37-year-old man without these risk factors, who presented with new onset severe tricuspid stenosis in the setting of multiple chronic pacing leads. (PACE 2010; e49–e52)

Background Applications to cardiothoracic surgery (CTS) training programs have declined precipitously. The viewpoints of potential applicants, general surgery residents, have not yet been assessed. Their perceptions are crucial to understanding the cause and formulating appropriate changes in our educational system. Methods An initial survey instrument was content-validated, and the final instrument was distributed electronically between March 24 and May 2, 2008 through 251 general surgery program directors to all Accreditation Council for Graduate Medical Education-accredited general surgery residents (7,508). Results The response rate was 29% (2153 residents; 89% programs). Respondent's demographics matched existing data; 6% were committed to CTS, and 26% reported prior or current interest in CTS. Interest waned after postgraduate year 3. Interest correlated with CTS rotation duration. Of the respondents committed to CTS, 76% had mentors (71% were cardiothoracic surgeons). CTS had the most shortcomings among 9 subspecialties. Job security and availability accounted for 46% of reported shortcomings (3 to 14 times higher than other subspecialties). Work schedule accounted for 25%. Length of training was not a very important factor, although it was identified as an option to increase interest in CTS. Residents who were undecided or uninterested in CTS were twice as likely to cite the ability to balance work and personal life as important than residents who chose CTS. Conclusions The dominant concern documented in the survey is job security and availability. The importance of mentorship and exposure to CTS faculty in promoting interest was also evident. Decision makers should consider these findings when planning changes in education and the specialty.

Diagnosis of thoracic injury begins with a history of events and examination of the patient. Appropriate radiographic studies will be dictated by the findings on history and physical. Procedural examinations, such as endoscopy or angiography, may also be needed for accurate diagnosis.

Rationale: One of the limitations associated with lung transplantation is the lack of available organs. Objective: To determine whether a lung donor–management protocol could increase the number of lungs for transplantation without affecting the survival rates of the recipients. Methods: We implemented the San Antonio Lung Transplant protocol for managing potential lung donors according to modifications of standard criteria for donor selection and strategies for donor management. We then compared information gathered during a 4-yr period, during which the protocol was used with information gathered during a 4-yr period before protocol implementation. Primary outcome measures were the procurement rate of lungs and the 30-d and 1-yr survival rates of recipients. Main Results: We reviewed data from 711 potential lung donors. The mean rate of lung procurement was significantly higher (p 0.0001) during the protocol period (25.5%) than during the preprotocol period (11.5%), with an estimated risk ratio of 2.2 in favor of the protocol period. More patients received transplants during the protocol period (n 121) than during the pre-protocol period (n 53; p 0.0001). Of 98 actual lung donors during the protocol period, 53 (54%) had initially been considered poor donors; these donors provided 64 (53%) of the 121 lung transplants. The type of donor was not associated with significant differences in recipients’ 30-d and 1-yr survival rates or any clinical measures of adequate graft function. Conclusions: The protocol was associated with a significant increase in the number of lung donors and transplant procedures without compromising pulmonary function, length of stay, or survival of the recipients.

Surgical simulators are gaining rapid acceptance as training tools for early learners and for retraining experienced surgeons with new techniques. Because the robotic system intervenes between the surgeon and the “tactile” sense of surgery, robotics offers a unique opportunity to provide very high fidelity simulation of the surgical experience. Surgeons will be able to learn and practice component parts of complex operations prior to taking the technique to the operating theatre with live patients.

Using petrographic, weak-acid extraction inductively coupled plasma spectrometry, and experimental analyses, this study illustrates that the Classic period ( ad 200–800) potters of prehispanic Ejutla (Oaxaca, Mexico) made a diverse array of ceramic products. Ancient Ejutla potters modified the handling and firing of local clay to make fine and coarse wares as well as reduced and oxidized vessels. Our analyses indicate that these different production strategies had distinct effects on compositional signatures. Yet, by employing a multidimensional analytical tack, we are able to associate an assortment of ceramic varieties with the Ejutla producers and their local clay.