Cole, Naomi A.

Objective Preparation for a career in plastic and reconstructive surgery (PRS) begins long before the residency application process. Given the challenging nature of matching into integrated PRS, the expectations for competitive applicants, including research productivity and networking at conferences, incur significant expenses. Our study is the first to detail the comprehensive costs of pursuing PRS, highlighting many hidden expenses that precede the application process. Design and Setting A branched logic survey was created to inquire about respondents' demographics, personal finances, expenses related to education and research, and opinions on the comprehensive costs of pursuing PRS. Qualitative and quantitative data were collected and analyzed using descriptive statistics. Participants The survey was distributed to PRS residency applicants in the 2023–2024 cycle and to senior members of a virtual PRS research group. The survey achieved a 28.9% response rate. Results Most respondents were fourth-year medical students (57.3%) and attended a school without a home integrated residency program (42.7%). Of students who pursued a research year (37.1%), 40.7% were unpaid, and 53.3% reported living expenses exceeding their income. Most attended more than 5 PRS conferences (29.9%), corresponding to a median total cost of $2000 to $3000. Fourth-year students typically participated in 3 away rotations (40.0%) at a cost of $6000 to $9000. The financial burden of pursuing a career in PRS, including PRS-related extracurricular activities and application-associated costs, is estimated to be $33,400–$45,479. Nearly all respondents (96.6%) believed this cost was too high or excessively high; however, 93.3% determined that it was probably or definitely worth a career in PRS. Conclusions The lofty costs associated with pursuing PRS are unsustainable for many. Additional efforts should be made to reduce financial barriers for PRS applicants. Ensuring funding to all students pursuing a research year, diversifying scholarships for conference attendance and away rotations, increasing loan forgiveness opportunities, and expanding use of lower-cost application options such as the Plastic Surgery Common Application are potential solutions to offset the cost of pursuing PRS.

Brain‐derived neurotrophic factor (BDNF) binds with high affinity to tropomyosin‐related kinase receptor subtype B (TrkB), and plays an important role in neuromuscular junction (NMJ) function (regulating neuromuscular transmission and muscle innervation). We previously showed impaired neuromuscular transmission following acute inhibition of TrkB kinase activity in TrkB F616A mice harboring a point mutation that renders the kinase domain susceptible to inhibition by 1NMPP1 treatment. Neuromuscular transmission failure is expected to predominantly affect the ability of more fatigable motor units to generate force and thus primarily impair higher force motor behaviors. Accordingly, we hypothesized that acute administration of 1NMPP1 will impair the ability of the diaphragm muscle to accomplish higher force behaviors in adult, 6‐month old TrkB F616A mice. Transdiaphragmatic pressure (Pdi) measurements were conducted across a range of motor behaviors in lightly anesthetized mice during eupnea, exposure to hypoxia (10% O 2 )/hypercapnia (5% CO 2 ), tracheal occlusion, spontaneous deep breaths (“sighs”) and during maximal activation elicited by bilateral phrenic nerve stimulation. Adult male and female TrkB F616A mice at 6 months were injected with 1NMPP1 or vehicle (DMSO) one hour prior to Pdi measurements. The Pdi generated during eupnea and hypoxia/hypercapnia was ~8 cm H 2 0 compared to ~70 cm H 2 0 during maximal stimulation. There was a significant reduction in Pdi during maximal force with bilateral phrenic nerve stimulation in the 1NMPP1 group compared to the vehicle control (p=0.01). There was no effect of 1NMPP1 on Pdi during eupnea, hypoxia/hypercapnia, tracheal occlusion, or sigh behaviors. The reduction in Pdi is generally similar to the impairment in neuromuscular transmission consistent with a predominant effect on motor units innervating fast‐twitch fatigable muscle fibers in the diaphragm muscle. Thus, impaired trophic BDNF/TrkB signaling can be expected to limit the range of motor behaviors accomplished by the diaphragm muscle and may be an important contributor to neuromuscular dysfunction. Support or Funding Information This study was supported by NIH grant R01 AG057052. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Signaling via the tropomyosin-related kinase receptor subtype B (TrkB) regulates neuromuscular transmission, and inhibition of TrkB kinase activity by 1NMPP1 in TrkB F616A mice worsens neuromuscular transmission failure (NMTF). We hypothesized that acute inhibition of TrkB kinase activity will impair the ability of the diaphragm muscle to produce maximal transdiaphragmatic pressure (Pdi) without impacting the ability to generate forces associated with ventilation, consistent with the greater susceptibility to NMTF in motor units responsible for higher-force nonventilatory behaviors. Adult male and female TrkB F616A mice were injected with 1NMPP1 ( n = 8) or vehicle (DMSO; n = 8) 1 h before Pdi measurements during eupneic breathing, hypoxia/hypercapnia (10% O 2 /5% CO 2 ), tracheal occlusion, spontaneous deep breaths (“sighs”) and during maximal activation elicited by bilateral phrenic nerve stimulation. In the vehicle-treated group, Pdi increased from ~10 cmH 2 O during eupnea and hypoxia/hypercapnia, to ~35 cmH 2 O during sighs and tracheal occlusion, and to ~65 cm H 2 O during maximal stimulation. There was no effect of acute 1NMPP1 treatment on Pdi generated during most behaviors, except during maximal stimulation (~30% reduction; P < 0.05). This reduction in maximal Pdi is generally similar to the worsening of NMTF previously reported with TrkB kinase inhibition in rodents. Accordingly, impaired TrkB signaling limits the range of motor behaviors accomplished by the diaphragm muscle and may contribute to neuromuscular dysfunction, primarily by impacting fatigable, higher force-generating motor units. NEW & NOTEWORTHY TrkB signaling plays an important role in maintaining neuromuscular function in the diaphragm muscle and may be necessary to accomplish the various motor behaviors ranging from ventilation to expulsive, behaviors requiring near-maximal forces. This study shows that inhibition of TrkB kinase activity impairs maximal pressure generation by the diaphragm muscle, but the ability to generate the lower pressures required for ventilatory behaviors is not impacted.