Jason Oliver

Overview:

Dr. Oliver is a clinical psychologist by training and is currently pursuing licensure in North Carolina. He received his graduate degree from the University of South Florida and completed his doctoral internship at Yale University School of Medicine. His research focuses on understanding of addictive behaviors, with a particular emphasis on tobacco use. His research program is heavily translational and includes both basic and clinical components. He has experience conducting human laboratory research, clinical trials and policy research. Long-term, he aims to identify new neural and behavioral markers for addiction that can serve as targets for novel interventions. 

Positions:

Assistant Professor in Psychiatry and Behavioral Sciences

Psychiatry & Behavioral Sciences, Addiction
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

Ph.D. 2015

University of South Florida

Grants:

Neurobehavioral substrates of propranolol's effects on drug cue reactivity

Administered By
Psychiatry & Behavioral Sciences
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Investigating the Effects of E-Cigarette Television Ads on Smokers

Administered By
Psychiatry & Behavioral Sciences
Awarded By
Research Triangle Institute International
Role
Principal Investigator
Start Date
End Date

Nicotine Withdrawal and Reward Processing: Connecting Neurobiology to Real-World Behavior

Administered By
Psychiatry & Behavioral Sciences, Addiction
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Clarifying the role of tobacco retail outlets on maternal smoking during pregnancy and child secondhand smoke exposure

Administered By
Psychiatry & Behavioral Sciences, Addiction
Awarded By
Virginia Commonwealth University
Role
Co Investigator
Start Date
End Date

Nicotine Withdrawal and Reward Processing: Connecting Neurobiology to Real-World Behavior

Awarded By
National Institutes of Health
Role
Mentor
Start Date
End Date

Publications:

Identifying neural signatures of tobacco retail outlet exposure: Preliminary validation of a "community neuroscience" paradigm.

An extensive epidemiological literature indicates that increased exposure to tobacco retail outlets (TROs) places never smokers at greater risk for smoking uptake and current smokers at greater risk for increased consumption and smoking relapse. Yet research into the mechanisms underlying this effect has been limited. This preliminary study represents the first effort to examine the neurobiological consequences of exposure to personally relevant TROs among both smokers (n = 17) and nonsmokers (n = 17). Individuals carried a global positioning system (GPS) tracker for 2 weeks. Traces were used to identify TROs and control outlets that fell inside and outside their ideographically defined activity space. Participants underwent functional MRI (fMRI) scanning during which they were presented with images of these storefronts, along with similar store images from a different county and rated their familiarity with these stores. The main effect of activity space was additive with a Smoking status × Store type interaction, resulting in smokers exhibiting greater neural activation to TROs falling inside activity space within the parahippocampus, precuneus, medial prefrontal cortex, and dorsal anterior insula. A similar pattern was observed for familiarity ratings. Together, these preliminary findings suggest that the otherwise distinct neural systems involved in self-orientation/self-relevance and smoking motivation may act in concert and underlie TRO influence on smoking behavior. This study also offers a novel methodological framework for evaluating the influence of community features on neural activity that can be readily adapted to study other health behaviors.
Authors
Oliver, JA; Sweitzer, MM; Engelhard, MM; Hallyburton, MB; Ribisl, KM; McClernon, FJ
MLA Citation
Oliver, Jason A., et al. “Identifying neural signatures of tobacco retail outlet exposure: Preliminary validation of a "community neuroscience" paradigm.Addict Biol, vol. 26, no. 5, Sept. 2021, p. e13029. Pubmed, doi:10.1111/adb.13029.
URI
https://scholars.duke.edu/individual/pub1475593
PMID
33663023
Source
pubmed
Published In
Addict Biol
Volume
26
Published Date
Start Page
e13029
DOI
10.1111/adb.13029

Erratum to: Pilot Randomized Controlled Trial of a Novel Smoking Cessation App Designed for Individuals With Co-Occurring Tobacco Dependence and Serious Mental Illness.

Authors
Vilardaga, R; Rizo, J; Palenski, PE; Mannelli, P; Oliver, JA; McClernon, FJ
MLA Citation
Vilardaga, Roger, et al. “Erratum to: Pilot Randomized Controlled Trial of a Novel Smoking Cessation App Designed for Individuals With Co-Occurring Tobacco Dependence and Serious Mental Illness.Nicotine Tob Res, vol. 23, no. 2, Jan. 2021, p. 411. Pubmed, doi:10.1093/ntr/ntaa125.
URI
https://scholars.duke.edu/individual/pub1453857
PMID
32761194
Source
pubmed
Published In
Nicotine Tob Res
Volume
23
Published Date
Start Page
411
DOI
10.1093/ntr/ntaa125

The effect of active site-inhibited factor VIIa on tissue factor-initiated coagulation using platelets before and after aspirin administration.

Active site-inactivated factor VIIa has potential as an antithrombotic agent. The effects of D-Phe-L-Phe-L-Arg-chloromethyl ketone-treated factor VIIa (FFR-FVIIa) were evaluated in a cell-based system mimicking in vivo initiation of coagulation. FFR-FVIIa inhibited platelet activation (as measured by expression of P-selectin) and subsequent large-scale thrombin generation in a dose-dependent manner with IC50 values of 1.4 +/- 0.8 nM (n = 8) and 0.9 +/- 0.7 nM (n = 7), respectively. Kd for factor VIIa binding to monocytes and Ki for FFR-FVIIa competing with factor VIIa were similar (11.4 +/- 0.8 pM and 10.6 +/- 1.1 pM, respectively), showing that FFR-FVIIa binds to tissue factor in the tenase complex with the same affinity as factor VIIa. Using platelets from volunteers before and after ingestion of aspirin (1.3 g), there were no significant differences in the IC50 values of FFR-FVIIa [after aspirin ingestion, the IC50 values were 1.7 +/- 0.9 nM (n = 8) for P-selectin expression, p = 0.37, and 1.4 +/- 1.3 nM (n = 7) for thrombin generation, p = 0.38]. This shows that aspirin treatment of platelets does not influence the inhibition of tissue factor-initiated coagulation by FFR-FVIIa, probably because thrombin activation of platelets is not entirely dependent upon expression of thromboxane A2.
Authors
Kjalke, M; Oliver, JA; Monroe, DM; Hoffman, M; Ezban, M; Hedner, U; Roberts, HR
MLA Citation
URI
https://scholars.duke.edu/individual/pub673840
PMID
9364985
Source
pubmed
Published In
Thrombosis and Haemostasis
Volume
78
Published Date
Start Page
1202
End Page
1208

Factors IXa and Xa play distinct roles in tissue factor-dependent initiation of coagulation.

Tissue factor is the major initiator of coagulation. Both factor IX and factor X are activated by the complex of factor VIIa and tissue factor (VIIa/TF). The goal of this study was to determine the specific roles of factors IXa and Xa in initiating coagulation. We used a model system of in vitro coagulation initiated by VIIa/TF and that included unactivated platelets and plasma concentrations of factors II, V, VIII, IX, and X, tissue factor pathway inhibitor, and antithrombin III. In some cases, factor IX and/or factor X were activated by tissue factor-bearing monocytes, but in some experiments, picomolar concentrations of preactivated factor IX or factor X were used to initiate the reactions. Timed samples were assayed for both platelet activation and thrombin activity. Factor Xa was 10 times more potent than factor IXa in initiating platelet activation, but factor IXa was much more effective in promoting thrombin generation than was factor Xa. In the presence of VIIa/TF, factor X was required for both platelet activation and thrombin generation, while factor IX was only required for thrombin generation. We conclude that VIIa/TF-activated factors IXa and Xa have distinct physiologic roles. The main role of factor Xa that is initially activated by VIIa/TF is to activate platelets by generating an initial, small amount of thrombin in the vicinity of platelets. Factor IXa, on the other hand, enhances thrombin generation by providing factor Xa on the platelet surface, leading to prothrombinase formation. Only tiny amounts of factors IX and X need to be activated by VIIa/TF to perform these distinct functions. Our experiments show that initiation of coagulation is highly dependent on activation of small amounts of factors IXa and Xa in proximity to platelet surfaces and that these factors play distinct roles in subsequent events, leading to an explosion of thrombin generation. Furthermore, the specific roles of factors IXa and Xa generated by VIIa/TF are not necessarily reflected by the kinetics of factor IXa and Xa generation.
Authors
Hoffman, M; Monroe, DM; Oliver, JA; Roberts, HR
MLA Citation
Hoffman, M., et al. “Factors IXa and Xa play distinct roles in tissue factor-dependent initiation of coagulation.Blood, vol. 86, no. 5, Sept. 1995, pp. 1794–801.
URI
https://scholars.duke.edu/individual/pub673828
PMID
7655009
Source
pubmed
Published In
Blood
Volume
86
Published Date
Start Page
1794
End Page
1801

Association Between Cigarette Smoking Frequency and Tobacco Use Disorder in U.S. Adults.

Authors
Oliver, JA; Foulds, J
MLA Citation
Oliver, Jason A., and Jonathan Foulds. “Association Between Cigarette Smoking Frequency and Tobacco Use Disorder in U.S. Adults.Am J Prev Med, vol. 60, no. 5, May 2021, pp. 726–28. Pubmed, doi:10.1016/j.amepre.2020.10.019.
URI
https://scholars.duke.edu/individual/pub1470106
PMID
33358276
Source
pubmed
Published In
Am J Prev Med
Volume
60
Published Date
Start Page
726
End Page
728
DOI
10.1016/j.amepre.2020.10.019

Research Areas:

Alcohol
Cognition
Drug addiction
Evoked potentials (Electrophysiology)
Functional Neuroimaging
Nicotine
Psychophysiology
Reward