Adam Kimple

Dr. Adam Kimple

Department of Otolaryngology, Head and Neck Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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2 January 2024 in International Forum of Allergy & Rhinology
Verified
Journal Article
Open access
Edward C KuanEdward C Kuan
Edward C Kuan
EWEric W Wang
Eric W Wang
NANithin D. Adappa
Nithin D. Adappa
DBDaniel M Beswick
Daniel M Beswick
NLNyall R. London
Nyall R. London
JPJames N. Palmer
James N. Palmer
Background: Sinonasal neoplasms, whether benign and malignant, pose a significant challenge to clinicians and represent a model area for multidisciplinary collaboration in order to optimize patient care. The International Consensus Statement on Allergy and Rhinology: Sinonasal Tumors (ICSNT) aims to summarize the best available evidence and presents 48 thematic and histopathology‐based topics spanning the field.Methods: In accordance with prior International Consensus Statement on Allergy and Rhinology documents, ICSNT assigned each topic as an Evidence‐Based Review with Recommendations, Evidence‐Based Review, and Literature Review based on the level of evidence. An international group of multidisciplinary author teams were assembled for the topic reviews using the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses format, and completed sections underwent a thorough and iterative consensus‐building process. The final document underwent rigorous synthesis and review prior to publication.Results: The ICSNT document consists of four major sections: general principles, benign neoplasms and lesions, malignant neoplasms, and quality of life and surveillance. It covers 48 conceptual and/or histopathology‐based topics relevant to sinonasal neoplasms and masses. Topics with a high level of evidence provided specific recommendations, while other areas summarized the current state of evidence. A final section highlights research opportunities and future directions, contributing to advancing knowledge and community intervention.Conclusion: As an embodiment of the multidisciplinary and collaborative model of care in sinonasal neoplasms and masses, ICSNT was designed as a comprehensive, international, and multidisciplinary collaborative endeavor. Its primary objective is to summarize the existing evidence in the field of sinonasal neoplasms and masses.

22 January 2010
Verified
Book Chapter
Open access
PDF file
SHStephanie Q. Hutsell
Stephanie Q. Hutsell
RKRandall Kimple
Randall Kimple
DSDavid Peter Siderovski
David Peter Siderovski
FWFrancis S. Willard
Francis S. Willard
Adam KimpleAdam Kimple
Adam Kimple
Surface plasmon resonance (SPR) is a highly sensitive method for the detection of molecular interactions. One interacting partner is immobilized on the sensor chip surface while the other is injected across the sensor surface. This chapter focuses on high-affinity immobilization of protein substrates for affinity and kinetic analyses using biotin/streptavidin interaction and GST/anti-GST-antibody interaction.

22 January 2010
Verified
Book Chapter
Open access
PDF file
Adam KimpleAdam Kimple
Adam Kimple
RMRobin E. Muller
Robin E. Muller
DSDavid Peter Siderovski
David Peter Siderovski
FWFrancis S. Willard
Francis S. Willard
Surface plasmon resonance (SPR) is a robust method to detect and quantify macromolecular interactions; however, to measure binding interactions, one component must be immobilized on a sensor surface. This is typically achieved using covalent immobilization via free amines or thiols, or noncovalent immobilization using high-affinity interactions such as biotin/streptavidin or antibody/antigen. In this chapter we describe a robust method to covalently immobilize His6 fusion proteins on the sensor surface for SPR analysis.

22 February 2022 in International Forum of Allergy & Rhinology
Verified
Journal Article
Open access
PDF file
Adam KimpleAdam Kimple
Adam Kimple
BSBrent A. Senior
Brent A. Senior
ENEdward T. Naureckas
Edward T. Naureckas
David A. GudisDavid A. Gudis
David A. Gudis
TMTed Meyer
Ted Meyer
SLStella E. Lee
Stella E. Lee
Background: Cystic fibrosis (CF) is a multisystem disease that often requires otolaryngology care. Individuals with CF commonly have chronic rhinosinusitis but also present with hearing loss and dysphonia. Given these manifestations of CF, otolaryngologists are frequently involved in the care of patients with CF; however, there is limited consensus on optimal management of sinonasal, otologic, and laryngologic symptoms.Methods: The Cystic Fibrosis Foundation convened a multidisciplinary team of otolaryngologists, pulmonologists, audiologists, pharmacists, a social worker, a nurse coordinator, a respiratory therapist, two adults with CF, and a caregiver of a child with CF to develop consensus recommendations. Workgroups developed draft recommendation statements based on a systematic literature review, and a ≥80% consensus was required for acceptance of each recommendation statement.Results: The committee voted on 25 statements. Eleven statements were adopted recommending a treatment or intervention, while five statements were formulated recommending against a specific treatment or intervention. The committee recommended eight statements as an option for select patients in certain circumstances, and one statement did not reach consensus.Conclusion: These multidisciplinary consensus recommendations will help providers navigate decisions related to otolaryngology consultation, medical and surgical management of CF‐CRS, hearing, and voice in individuals with CF. A collaborative and multidisciplinary approach is advocated to best care for our patients with CF. Future clinical research is needed utilizing standardized, validated outcomes with comprehensive reporting of patient outcome, effects of modulator therapies, and genetic characteristics to help continue to advance care, decrease morbidity, and improve the quality of life for individuals with CF.

3 February 2016 in The Laryngoscope
Verified
Journal Article
Closed access
PDF file
Adam KimpleAdam Kimple
Adam Kimple
SMStanley W. McClurg
Stanley W. McClurg
ASAnthony G. Del Signore
Anthony G. Del Signore
MTMohamed O. Tomoum
Mohamed O. Tomoum
FLFeng‐Chang Lin
Feng‐Chang Lin
BSBrent A. Senior
Brent A. Senior

15 September 2022 in Journal of Clinical Investigation
Verified
Journal Article
Open access
PDF file
RLRhianna E. Lee
Rhianna E. Lee
CLCatherine A. Lewis
Catherine A. Lewis
LHLihua He
Lihua He
EBEmily C. Bulik-Sullivan
Emily C. Bulik-Sullivan
SGSamuel C. Gallant
Samuel C. Gallant
SRScott Randell
Scott Randell
The vast majority of people with cystic fibrosis (CF) are now eligible for CF transmembrane regulator (CFTR) modulator therapy. The remaining individuals with CF harbor premature termination codons (PTCs) or rare CFTR variants with limited treatment options. Although the clinical modulator response can be reliably predicted using primary airway epithelial cells, primary cells carrying rare CFTR variants are scarce. To overcome this obstacle, cell lines can be created by overexpression of mouse Bmi-1 and human TERT (hTERT). Using this approach, we developed 2 non-CF and 6 CF airway epithelial cell lines, 3 of which were homozygous for the W1282X PTC variant. The Bmi-1/hTERT cell lines recapitulated primary cell morphology and ion transport function. The 2 F508del-CFTR cell lines responded robustly to CFTR modulators, which was mirrored in the parent primary cells and in the cell donors’ clinical response. Cereblon E3 ligase modulators targeting eukaryotic release factor 3a (eRF3a) rescued W1282X-CFTR function to approximately 20% of WT levels and, when paired with G418, rescued G542X-CFTR function to approximately 50% of WT levels. Intriguingly, eRF3a degraders also diminished epithelial sodium channel (ENaC) function. These studies demonstrate that Bmi-1/hTERT cell lines faithfully mirrored primary cell responses to CFTR modulators and illustrate a therapeutic approach to rescue CFTR nonsense mutations.