Jeffrey Everitt

Positions:

Professor in Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

D.V.M. 1977

Cornell University

Adjunct Professor of Pathology, College of Veterinary Medicine,, Department Of Pathology

North Carolina State University

Grants:

Molecular Genetics of BBS

Administered By
Institutes and Centers
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Advanced Technologies for Reducing Decompression Obligation and Risk

Administered By
Anesthesiology, General, Vascular, High Risk Transplant & Critical Care
Awarded By
Creare, Inc.
Role
Co Investigator
Start Date
End Date

Combatting Bladder Cancer by Inducing Epithelial Turnover

Administered By
Pathology
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Stable therapy in Pompe disease through genome editing

Administered By
Pediatrics, Medical Genetics
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Publications:

Ex Vivo MR Histology and Cytometric Feature Mapping Connect Three-dimensional in Vivo MR Images to Two-dimensional Histopathologic Images of Murine Sarcomas.

Purpose To establish a platform for quantitative tissue-based interpretation of cytoarchitecture features from tumor MRI measurements. Materials and Methods In a pilot preclinical study, multicontrast in vivo MRI of murine soft-tissue sarcomas in 10 mice, followed by ex vivo MRI of fixed tissues (termed MR histology), was performed. Paraffin-embedded limb cross-sections were stained with hematoxylin-eosin, digitized, and registered with MRI. Registration was assessed by using binarized tumor maps and Dice similarity coefficients (DSCs). Quantitative cytometric feature maps from histologic slides were derived by using nuclear segmentation and compared with registered MRI, including apparent diffusion coefficients and transverse relaxation times as affected by magnetic field heterogeneity (T2* maps). Cytometric features were compared with each MR image individually by using simple linear regression analysis to identify the features of interest, and the goodness of fit was assessed on the basis of R2 values. Results Registration of MR images to histopathologic slide images resulted in mean DSCs of 0.912 for ex vivo MR histology and 0.881 for in vivo MRI. Triplicate repeats showed high registration repeatability (mean DSC, >0.9). Whole-slide nuclear segmentations were automated to detect nuclei on histopathologic slides (DSC = 0.8), and feature maps were generated for correlative analysis with MR images. Notable trends were observed between cell density and in vivo apparent diffusion coefficients (best line fit: R2 = 0.96, P < .001). Multiple cytoarchitectural features exhibited linear relationships with in vivo T2* maps, including nuclear circularity (best line fit: R2 = 0.99, P < .001) and variance in nuclear circularity (best line fit: R2 = 0.98, P < .001). Conclusion An infrastructure for registering and quantitatively comparing in vivo tumor MRI with traditional histologic analysis was successfully implemented in a preclinical pilot study of soft-tissue sarcomas. Keywords: MRI, Pathology, Animal Studies, Tissue Characterization Supplemental material is available for this article. © RSNA, 2021.
Authors
Blocker, SJ; Cook, J; Mowery, YM; Everitt, JI; Qi, Y; Hornburg, KJ; Cofer, GP; Zapata, F; Bassil, AM; Badea, CT; Kirsch, DG; Johnson, GA
MLA Citation
Blocker, Stephanie J., et al. “Ex Vivo MR Histology and Cytometric Feature Mapping Connect Three-dimensional in Vivo MR Images to Two-dimensional Histopathologic Images of Murine Sarcomas.Radiol Imaging Cancer, vol. 3, no. 3, May 2021, p. e200103. Pubmed, doi:10.1148/rycan.2021200103.
URI
https://scholars.duke.edu/individual/pub1483145
PMID
34018846
Source
pubmed
Published In
Radiol Imaging Cancer
Volume
3
Published Date
Start Page
e200103
DOI
10.1148/rycan.2021200103

Infectious diseases of the upper respiratory tract: implications for toxicology studies.

Authors
Everitt, JI; Richter, CB
MLA Citation
Everitt, J. I., and C. B. Richter. “Infectious diseases of the upper respiratory tract: implications for toxicology studies.Environmental Health Perspectives, vol. 85, Environmental Health Perspectives, Apr. 1990, pp. 239–47. Crossref, doi:10.1289/ehp.85-1568352.
URI
https://scholars.duke.edu/individual/pub1483719
Source
crossref
Published In
Environmental Health Perspectives
Volume
85
Published Date
Start Page
239
End Page
247
DOI
10.1289/ehp.85-1568352

Polymer-assisted intratumoral delivery of ethanol: Preclinical investigation of safety and efficacy in a murine breast cancer model.

Focal tumor ablation with ethanol could provide benefits in low-resource settings because of its low overall cost, minimal imaging technology requirements, and acceptable clinical outcomes. Unfortunately, ethanol ablation is not commonly utilized because of a lack of predictability of the ablation zone, caused by inefficient retention of ethanol at the injection site. To create a predictable zone of ablation, we have developed a polymer-assisted ablation method using ethyl cellulose (EC) mixed with ethanol. EC is ethanol-soluble and water-insoluble, allowing for EC-ethanol to be injected as a liquid and precipitate into a solid, occluding the leakage of ethanol upon contact with tissue. The aims of this study were to compare the 1) safety, 2) release kinetics, 3) spatial distribution, 4) necrotic volume, and 5) overall survival of EC-ethanol to conventional ethanol ablation in a murine breast tumor model. Non-target tissue damage was monitored through localized adverse events recording, ethanol release kinetics with Raman spectroscopy, injectate distribution with in vivo imaging, target-tissue necrosis with NADH-diaphorase staining, and overall survival by proxy of tumor growth. EC-ethanol exhibited decreased localized adverse events, a slowing of the release rate of ethanol, more compact injection zones, 5-fold increase in target-tissue necrosis, and longer overall survival rates compared to the same volume of pure ethanol. A single 150 μL dose of 6% EC-ethanol achieved a similar survival probability rates to six daily 50 μL doses of pure ethanol used to simulate a slow-release of ethanol over 6 days. Taken together, these results demonstrate that EC-ethanol is safer and more effective than ethanol alone for ablating tumors.
Authors
Nief, C; Morhard, R; Chelales, E; Adrianzen Alvarez, D; Bourla Bs, I; Lam, CT; Sag, AA; Crouch, BT; Mueller, JL; Katz, D; Dewhirst, MW; Everitt, JI; Ramanujam, N
MLA Citation
Nief, Corrine, et al. “Polymer-assisted intratumoral delivery of ethanol: Preclinical investigation of safety and efficacy in a murine breast cancer model.Plos One, vol. 16, no. 1, 2021, p. e0234535. Pubmed, doi:10.1371/journal.pone.0234535.
URI
https://scholars.duke.edu/individual/pub1472908
PMID
33507942
Source
pubmed
Published In
Plos One
Volume
16
Published Date
Start Page
e0234535
DOI
10.1371/journal.pone.0234535

Coagulopathy Characterized by Rotational Thromboelastometry in a Porcine Pediatric ECMO Model.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is used to support patients with reversible cardiopulmonary insufficiency. Although it is a lifesaving technology, bleeding, inflammation, and thrombosis are well-described complications of ECMO. Adult porcine models of ECMO have been used to recapitulate the physiology and hemostatic consequences of ECMO cannulation in adults. However, these models lack the unique physiology and persistence of fetal forms of coagulation factors and fibrinogen as in human infants. We aimed to describe physiologic and coagulation parameters of piglets cannulated and supported with VA-ECMO. Four healthy piglets (5.7-6.4 kg) were cannulated via jugular vein and carotid artery by cutdown and supported for a maximum of 20 hours. Heparin was used with a goal activated clotting time of 180-220 seconds. Arterial blood gas (ABG) was performed hourly, and blood was transfused from an adult donor to maintain hematocrit (Hct) > 24%. Rotational thromboelastometry (ROTEM) was performed at seven time points. All animals achieved adequate flow with a patent circuit throughout the run (pre- and post-oxygenator pressure gradient <10 mmHg). There was slow but significant hemorrhage at cannulation, arterial line, and bladder catheter sites. All animals required the maximum blood transfusion volume available. All animals became anemic after exhaustion of blood for transfusion. ABG showed progressively declining Hct and adequate oxygenation. ROTEM demonstrated decreasing fibrin-only ROTEM (FIBTEM) clot firmness. Histology was overall unremarkable. Pediatric swine are an important model for the study of pediatric ECMO. We have demonstrated the feasibility of such a model while providing descriptions of physiologic, hematologic, and coagulation parameters throughout. Weak whole-blood clot firmness by ROTEM suggested defects in fibrinogen, and there was a clinical bleeding tendency in all animals studied. This model serves as an important means to study the complex derangements in hemostasis during ECMO.
Authors
Reed, CR; Bonadonna, D; Everitt, J; Robinson, V; Otto, J; Tracy, ET
MLA Citation
Reed, Christopher R., et al. “Coagulopathy Characterized by Rotational Thromboelastometry in a Porcine Pediatric ECMO Model.J Extra Corpor Technol, vol. 52, no. 3, Sept. 2020, pp. 203–11. Pubmed, doi:10.1182/ject-2000011.
URI
https://scholars.duke.edu/individual/pub1462678
PMID
32981958
Source
pubmed
Published In
Journal of Extra Corporeal Technology
Volume
52
Published Date
Start Page
203
End Page
211
DOI
10.1182/ject-2000011

Promotion by sodium barbital induces early development but does not increase the multiplicity of hereditary renal tumors in Eker rats

Authors
Wolf, DC; Goldsworthy, TL; Janszen, DB; Harden, R; Donner, EM; David, CS; Everitt, JI
MLA Citation
Wolf, D. C., et al. “Promotion by sodium barbital induces early development but does not increase the multiplicity of hereditary renal tumors in Eker rats.” Carcinogenesis, vol. 21, no. 8, Oxford University Press (OUP), Aug. 2000, pp. 1553–58. Crossref, doi:10.1093/carcin/21.5.553.
URI
https://scholars.duke.edu/individual/pub1483716
Source
crossref
Published In
Carcinogenesis
Volume
21
Published Date
Start Page
1553
End Page
1558
DOI
10.1093/carcin/21.5.553