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The Aesthetic Surgery Education and Research Foundation

Award Winners and Funded Projects
Study of the Pathophysiology of Filler-induced Blindness Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Kihyun Cho, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $8,390

Project Name: Study of the Pathophysiology of Filler-induced Blindness

Project Summary: Although rare, blindness following soft tissue filler injection can and does occur.(1) We propose a retrograde arterial embolism of filler as the responsible mechanism for filler-induced blindness. Many authors have proposed this mechanism in their publications.(2,3) However, no previous human study has been done to prove this proposed mechanism. Also, the intravascular volume and injection pressure needed to create emboli by hyaluronic acid filler in the ophthalmic artery and internal carotid artery is unknown.

The aim of this study is to investigate the pathophysiology of filler-induced blindness. We plan to do this using a fresh cadaver perfusion technique. The measurement of injection pressure and filler volume needed to embolize the ophthalmic artery and internal carotid artery will also be determined. We aim to provide an evidence-based safe guidelines for soft tissue filler injection.

 
Establishing Competency-Based Education in Plastic Surgery Residency Training Using A Novel Surgical Simulation Environment Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Mirko Gilardino, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $12,800

Project Name: Establishing Competency-Based Education in Plastic Surgery Residency Training Using A Novel Surgical Simulation Environment

Project Summary: The purpose of this study is to develop the groundwork for Competency-Based Education (CBE) in Plastic Surgery residency training. Using a pilot Plastic Surgery procedure, this project will define the essential competencies for that procedure, develop a surgical simulator to assist the teaching and evaluation of the identified competencies in the pre­clinical stage, and finally to determine an evaluation strategy to transition this learning modality to the clinical teaching realm. The information gleaned from this Pilot procedure can then be applied to other areas/procedures within Plastic Surgery training.

Clinical Relevance: The introduction and implementation of CBE in residency training is an emerging necessity and will likely be the standard of surgical teaching across North America in the future. This project will provide important groundwork on how surgical competencies in Plastic Surgery can be developed, taught and evaluated. Furthermore, the project's second aim to develop a prototype teaching surgical simulator for Plastic Surgery will provide an important tool on which to gauge early levels of competence in residency education and provide a platform to assist the teaching of technical skills. The summative goal is to use the data gleaned from this work is to identify, standardize and objectify Plastic Surgery competencies for all procedures we must teach, thus improving and standardizing the quality of Plastic Surgery resident education and competence of our graduates. Lastly, in the emerging reality of numerous surgical specialties encroaching upon various traditional domains of Plastic Surgery (ex. Aesthetic Surgery, Microsurgery, etc), it is essential that our specialty lead the field in surgical education and maintain our stronghold on these areas of expertise. This project will be one step towards establishing our specialties' ongoing leadership in Plastic Surgery education.

 
Defining the extent and limitations of the SMAS-platysma unit Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Charlies Thorne, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $11,650

Project Name: Defining the extent and limitations of the SMAS-platysma unit

Project Summary: We believe there are several nuances related to the SMAS-platysma that are currently under-appreciated and the source of much of the current controversy in aesthetic facial rejuvenation. The goal of this study is to elucidate and define comprehensively the SMAS-platysma unit. Specifically, we will: 1) define the exact anatomic relationships of the platysma with key anatomic structures, including the modiolus 2) demonstrate the differences in viscoelastic properties of the SMAS-platysma unit with various surgical techniques 3) delineate the ramifications in the lower neck as a result of various manipulations to the  SMAS-platystma unit

 
Genomic Profiling to Understand the Pathogenesis of BIA-ALCL Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Nandu Nairn, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $ 10,000

Project Name: Genomic Profiling to Understand the Pathogenesis of BIA-ALCL

Project Summary:

Hypothesis:
We hypothesize that micro and nano-silica nanoparticles with polyurethane may differentially affect the induction of new biomarkers that can potentially influence the pathogenesis of BIA-ALCL.

Accordingly, we propose following specific aim:  

Specific Aim:
To study the comparative effect of nano, micro, and macro silica gel in combination with the polyurethane on global mRNA profiling in T-Cell. Hypothesis: a) silica and polyurethane is the basic implant materials; b) comparison of different sizes will reveal their physiological implications; c) The mRNA profiling will reveal novel yet unidentified molecular factors associated with the implant materials; d) identification of novel molecular markers specific to implant constituents may lead to better treatment approach in BIA-ALCL.

Significance:
Currently more than 11 million women worldwide have breast implants and this number is continuously increasing. Recent reports of BIA-ALCL can be a significant health concern for women with implants. As such, examination of the molecular basis of BIA-ALCL may reveal specific biomarkers leading to better therapeutic approach.

 
Pathogenesis of BIA-ALCL Print

The ASERF Scientific Research Committee and Board of Directors are pleased to announce the following grant award:

Researcher: Marshall Kadin, MD

Grant Award: ASERF Interim Grant

Amount Awarded: $ 193,110

Project Name: Pathogenesis  of BIA-ALCL

Project Summary: Hypothesis: Anaplastic cells in BIA-ALCL produce cytokines that shape the tumor microenvironment (Figure 1). Our preliminary results indicate that anaplastic cells in culture produce IL-13 which induces immunoglobulin heavy chain class switch of plasma cells to produce IgE. We found IgE bound to the surface of mast cells and antigen presenting cells (APC) within involved tissues. Mast cells produce prostaglandin D2 (PGD2) which recruits Th2 cells and eosinophils prominent in BIA-ALCL lesions. A possible source of IgE is plasma cells in tumors and regional lymph nodes. Neither IL-13, IgE nor PGD2 has been quantified in malignant seromas before nor after treatment or compared to benign seromas. Whether IgE binds to bacteria or tumor associated antigens also has not been explored. IL-13 can be produced by effector T cells and innate lymphoid cells (ILCs) which will be addressed in this proposal. We hypothesize there will be different clinical presentations according to the cellular origin and functional polarization of anaplastic cells, specifically the Th1/ILC1 phenotype may associated with clinically indolent behavior and the Th3/ILC3 phenotype with invasive tumors.

To address our hypothesis our specific aims are:

Aim 1- Determine the significance of cytokine, prostaglandin D2 and IgE levels in benign and malignant seroma fluids and blood at clinical presentation and after treatment.

Aim 2- Determine if anaplastic cells are derived from effector T cells or innate lymphoid cells.

   Subaim 1- Determine which subset anaplastic cells belong to- Th1/1LC1, Th2/ILC2, or Th3/ILC3.

   Subaim 2- Is there a difference in subsets between in situ and invasive disease?

   Subaim 3- Can Th3/ILC3 anaplastic cells be repolarized to Th1/ILC1?

Aim 3- Identify precursors of BIA-ALCL with a similar phenotype in capsules, seroma fluids and regional lymph nodes.

AIM 4- Determine if IgE binds to bacterial and/or tumor associated antigens

 
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