Validating a New Surgical Gouge for Autogenous Ear Reconstruction During Simulated Microtia Workshops.

Autologous ear reconstruction remains a gold standard surgical technique for the treatment of external ear deformities. This highly technical procedure requires experience, an understanding of aesthetic principles, and a surgical approach that can consistently produce optimal results. As an experienced microtia surgeon having trained under Dr Satoru Nagata, the senior author has emphasized the importance of appropriate surgical tools during this procedure. Here, we present results of a novel surgical handle and gouge meant to optimize complex cartilage carving. The senior author regularly holds microtia workshops to help train individuals around the United States. During 2 of such workshops held in 2022, participants were given access to both the standard, commercially available surgical gouge as well as a prototype of a novel surgical gouge developed by the authors. Participants were then given a Likert-scale survey to assess their subjective feedback for both tools. Twenty-seven total participants completed the postworkshop survey. Cumulatively, the results demonstrated that participants rated the custom gouge significantly higher than its counterpart (4.2 versus 3.2, P<0.001). They also had a significantly higher likelihood of using the custom gouge again (4.1 versus 3.2, P=0.023). The custom gouge designed by the senior author demonstrated higher subjective ratings when compared with what is currently available on the market. This serves as a primary validation study that demonstrates feasibility for further assessment in a true operative setting.

Assessing the Current State of Microtia Reconstruction in the United States.

OBJECTIVE: Microtia is a congenital ear deformity with variability in surgical techniques and tools across surgeons pursuing an autologous reconstruction. Different techniques have emerged over time, and surgeons opt for various tools to aid in creating the complex three-dimensional cartilaginous ear framework. The purpose of this study was to understand the current state of microtia reconstruction in the United States. METHODS: Microtia surgeons affiliated with the nonprofit, Ear Community, were invited to complete a 20-item survey. Data were collected on demographic information regarding surgeons, considerations when approaching microtia repair in patients, and techniques and comfort levels. Additional data were collected on materials, tools, flaps, and skin grafts used for reconstruction. RESULTS: Twenty-two surgeons responded to the survey reporting 3 different techniques learned and utilized in practice including the Brent, Nagata, and Firmin techniques. About two-thirds of surgeons were "extremely comfortable" with their techniques and one-third were "extremely uncomfortable" or "somewhat uncomfortable." Most respondents reported using a tunneled temporoparietal fascial flap or a posterior fascial flap along with a full-thickness skin graft for the second stage (ear elevation). Most surgeons utilized a combination of scalpels and gouges when carving the ear framework along with sutures or wire. CONCLUSIONS: This study highlights the current state of autogenous microtia reconstruction underscoring the variability in approaches and preferences. These data may guide future directions that aim to improve patient outcomes. Surgeons may gain insight into different practices and choose to adopt different aspects to enhance their surgical approach.

The Familial α-Synuclein A53E Mutation Enhances Cell Death in Response to Environmental Toxins Due to a Larger Population of Oligomers.

Amyloid formation of α-synuclein (α-Syn) and its familial mutations are directly linked with Parkinson's disease (PD) pathogenesis. Recently, a new familial α-Syn mutation (A53E) was discovered, associated with an early onset aggressive form of PD, which delays α-Syn aggregation. When we overexpressed wild-type (WT) and A53E proteins in cells, showed neither toxicity nor aggregate formation, suggesting merely overexpression may not recapitulate the PD phenotype in cell models. We hypothesized that cells expressing the A53E mutant might possess enhanced susceptibility to PD-associated toxicants compared to that of the WT. When cells were treated with PD toxicants (dopamine and rotenone), cells expressing A53E showed more susceptibility to cell death along with compromised mitochondrial potential and an increased production of reactive oxygen species. The higher toxicity of A53E could be due to more oligomers being formed in cells as confirmed by a dot blot assay using amyloid specific OC and A11 antibody and using an  in vitro aggregation study. The cellular model presented here suggests that along with familial mutation, environmental and other cellular factors might play a crucial role in dictating PD pathogenesis.