Zoe Cohen

Interests

Teaching

I am interested in teaching Cardiovascular Physiology and Immunology to the best of my ability. I like trying new technologies, such as blogs, new learning management systems, and flipped classrooms as ways to interact with my students.

Research

I am interested in the role red blood cells might play in coagulation.

Courses

Scholarly Contributions

Journals/Publications

• Cohen, Z. (2019). Small Changes, Large Rewards: How Individualized Emails Increase Performance in an Upper Division Physiology Course. The FASEB Journal. doi:10.1096/fasebj.2019.33.1_supplement.766.22
• Farr, K. J., Cohen, Z., Nielsen, K., Rahimian, A. R., Appanaitis, I., & Hongu, N. (2016). A Palauan Healthy Lifestyle: Steps toward Tailoring Local Resources and Health Information for Non‐Communicable Disease Prevention and Intervention. The FASEB Journal, 30(S1). doi:10.1096/fasebj.30.1_supplement.901.6
• Cohen, Z., Cohen, Z. -., & Cohen, J. J. (2013). Inflammablog: peer-to-peer online learning in immunology. Immunologic research, 55(1-3).
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  Is it possible for students in different courses, at different academic levels, and at different universities to learn immunology together using the Internet? We teach a colloquium on inflammation for undergraduates at the University of Arizona and a lecture course on human immunology for graduate students and clinical and basic science fellows at the University of Colorado Anschutz Medical Campus. Students in these programs, being scattered about large campuses, have little time for student-directed discussion and peer interactions, and they never have the opportunity to meet students in the course in the other state. Instead of requiring the usual essays and term papers, we set up a blog (an online discussion group) for the two courses, and required all students to post, and comment on other posts, within and between the courses. Student writing is normally directed at a single reader, the instructor, which seems like a waste of talent; we encouraged peer exchanges. Furthermore, we were interested in observing the interactions between the Colorado students, who were older and sometimes experienced professionals, and the younger Arizonans. We used a blog because it is administratively impossible to enroll the students in two universities in a single courseware (learning management system) site. Blogging has offered insights into students' comfort with this form of social medium, and into the potential for this approach in light of the rapid adoption of blended and massively open online courses.
• Funk, J. L., Onyeagucha, B. C., Nelson, M. A., Hutchison, J., Funk, J. L., & Cohen, Z. (2013). How microRNAs influence both hereditary and inflammatory-mediated colon cancers.. Cancer genetics, 206(9-10), 309-16. doi:10.1016/j.cancergen.2013.06.005
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  MicroRNAs have emerged as important post-translational regulators of gene expression and are involved in several physiological and pathological states including the pathogenesis of human colon cancers. In regards to tumor development, microRNAs can act as oncogenes or tumor suppressors. Two hereditary predispositions (i.e., Lynch syndrome and familial adenomatous polyposis) contribute to the development of colon cancer. In addition, individuals who suffer from inflammatory bowel diseases such as Crohn's disease or ulcerative colitis have a higher risk of developing colon cancer. Here, we discuss the occurrence of the deregulated expression of microRNAs in colon cancer that arise as a result of hereditary predisposition and inflammatory bowel disease.
• Funk, J. L., Ritter, L. S., Morrison, H. W., Mcdonagh, P. F., Henry, M., Funk, J. L., Frye, J. B., Davis-gorman, G., Davidson, L., Cohen, Z., & Chandler, S. (2011). Exaggerated neutrophil-mediated reperfusion injury after ischemic stroke in a rodent model of type 2 diabetes.. Microcirculation (New York, N.Y. : 1994), 18(7), 552-61. doi:10.1111/j.1549-8719.2011.00115.x
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  We tested the hypothesis that both chronic and acute inflammatory processes contribute to worse reperfusion injury and stroke outcome in an experimental model of T2DM..Twelve- to thirteen-week-old male Zucker Diabetic Fatty (ZDF) rats vs. Zucker Lean Controls (ZLC) rats were tested at baseline and after middle cerebral artery occlusion (ischemia) and reperfusion (I-R). Neutrophil adhesion to the cerebral microcirculation, neutrophil expression of CD11b, infarction size, edema, neurologic function, sICAM, and cerebral expression of neutrophil-endothelial inflammatory genes were measured..At baseline, CD11b and sICAM were significantly increased in ZDF vs. ZLC animals (p < 0.05). After I-R, significantly more neutrophil adhesion and cell aggregates were observed in ZDF vs. ZLC (p < 0.05); infarction size, edema, and neurologic function were significantly worse in ZDF vs. ZLC (p < 0.05). CD11b and sICAM-1 remained significantly increased in ZDFs (p < 0.05), and cerebral expression of IL-1β, GRO/KC, E-selectin, and sICAM were significantly induced in ZDF, but not ZLC groups (p < 0.05) after 2.5 hours of reperfusion..Both sides of the neutrophil-endothelial interface appear to be primed prior to I-R, and remain significantly more activated during I-R in an experimental model of T2DM. Consequently, reperfusion injury appears to play a significant role in poor stroke outcome in T2DM.
• Nolan, P. E., Ritter, L. S., Nolan, P. E., Mcdonagh, P. F., Henry, M., Davidson, L., & Cohen, Z. (2009). Whole blood aggregation, coagulation, and markers of platelet activation in diet-induced diabetic C57BL/6J mice.. Diabetes research and clinical practice, 84(1), 11-8. doi:10.1016/j.diabres.2009.01.011
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  Type 2 diabetes in humans is associated with hypercoaguability; however, little is known about platelet function in mouse models of type 2 diabetes used to study this disorder. Therefore, the purpose of this study was to examine platelet aggregation, coagulation, and markers of platelet activation in a diet-induced mouse model of type 2 diabetes..Four week old, male, C57BL/6J mice were randomized to a standard chow or high fat (60% beef lard) diet for 4 months. To examine platelet function we measured ADP-induced whole blood aggregometry, whole blood coagulation by thromboelastography, tail bleeding times, platelet microparticle and platelet expression of p-selectin and platelet expression of CD61 by flow cytometry..Diabetic mice exhibited less aggregation (p
• Ritter, L. S., Mcdonagh, P. F., Davis-gorman, G., & Cohen, Z. (2008). Caspase inhibition of platelet activation.. Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis, 19(4), 305-9. doi:10.1097/mbc.0b013e3283001cf5
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  The role of caspases in platelet function is not well understood. When platelets are activated, they express phosphatidylserine on the outer plasma membrane, form platelet microparticles, and aggregate (Pag). The aims of this study were to determine if caspases play a role in the platelet activation seen in type 2 diabetes. Diabetic rats (Zucker diabetic fatty) were treated with a broad-spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone, in vivo and platelets were evaluated for phosphatidylserine expression, platelet microparticle formation, and Pag. We found a decreased phosphatidylserine exposure in zVAD-Zucker diabetic fatty rats compared to Zucker diabetic fatty-phosphate-buffered saline when activated with 20 micromol/l ADP. Zucker diabetic fatty rats treated with benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone decreased platelet microparticle numbers compared to phosphate-buffered saline control Zucker diabetic fatty rats. Further, treatment with benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethyl ketone significantly decreased Pag. These results indicate that caspases play a role in platelet activation, suggesting a unique physiologic role of these proteases and perhaps the underlying mechanisms involved in the chronic platelet activation observed in type 2 diabetes.
• Cohen, Z., Ritter, L. S., & Davidson, L. (2007). Platelet aggregation requires caspases, but is not apoptosis. The FASEB Journal. doi:10.1096/fasebj.21.6.a1126-b
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  Apoptosis utilizes three groups of proteins: death receptors, the Bcl-2 family, and caspases. Recent observations indicate that platelets contain caspases. However, the role of caspases in platelet function remains unclear. We have demonstrated in a rodent model, that there is a decrease in aggregation when platelets were treated in vitro with zVAD-fmk, a broad spectrum caspase inhibitor. There is limited research on specific caspases in platelet activation. The aim of this study was to investigate if inhibition of caspase-3, -8, or -9, attenuates ADP-induced platelet aggregation compared to aggregation with ADP alone (control). Using blood from Sprague-Dawley rats, we found that ex-vivo pre-treatment with IETD-fmk, an inhibitor specific for caspase 8, significantly attenuated platelet aggregation in ADP stimulated platelets, (Control 82.3 ± 3.9 % vs. IETD-fmk 63.8 ± 4.9 %, p ≤ 0.03). LEHD-fmk (specific for caspase 9) also significantly attenuated platelet aggregation, but to a lesser degree (LEHD-fmk 69.3 ± 4.1 %, p ≤ 0.03). DEVD-fmk, an inhibitor of caspase 3, did not significantly decrease aggregation (74.6 ± 4.0 %) when compared to control. These data suggest that caspases may play a role in platelet activation. Since the main apoptosis effector caspase (caspase 3) did not inhibit platelet aggregation, the idea that caspases work in an apoptotic-like manner in platelets is less than clear. It is clear, however, that at minimum, caspases-8 and-9 are involved in portions of platelet activation. This novel finding may lead to the development of improved agents to limit pathologic platelet activation. Supported by T32NRO7958, NIH HLB 58859, NIH NR005208.
• Stump, C. S., Sowers, J. R., Ritter, L. S., Mcdonagh, P. F., Maes, M., Davidson, L., Coull, B. M., & Cohen, Z. (2007). Exaggerated leukocyte adhesion in the cerebral microcirculation of type 2 diabetic rats after ischemic stroke and reperfusion. The FASEB Journal, 21(6).
• Mcdonagh, P. F., Gonzales, R., Davis-gorman, G., & Cohen, Z. (2006). Vitamin E reduces myocardial infarct size in type 2 diabetes. The FASEB Journal, 20(5).
• Ritter, L., Mcdonagh, P. F., Davis-gorman, G., & Cohen, Z. (2006). Caspase inhibition decreases human platelet activation. The FASEB Journal, 20(4). doi:10.1096/fasebj.20.4.a2-b
• Cohen, Z., & Cohen, J. J. (2004). Programmed Cell Death.Essays in Biochemistry, Volume 39.Edited byT G Cotter.London: Portland Press. $28.50 (paper). xx + 166 p; ill.; subject index. ISBN: 1–85578–148–4. 2003.. The Quarterly Review of Biology, 79(4), 417-417. doi:10.1086/428174
• Wilson, J., Ritter, L. S., Mcdonagh, P. F., & Cohen, Z. (2004). Caspase inhibition decreases both platelet phosphatidylserine exposure and aggregation: caspase inhibition of platelets.. Thrombosis research, 113(6), 387-93. doi:10.1016/j.thromres.2004.03.020
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  Apoptosis of nucleated cells is regulated by caspases, a group of cysteine proteases, and is characterized by phosphatidylserine expression on the outer leaflet of the plasma membrane. Reports indicate that platelets contain caspases. However, the role of caspases in platelet function is not well understood. When platelets become activated, they express phosphatidylserine (PS) on the outer leaflet of the plasma membrane. In addition, platelets aggregate when activated. The aims of this study were to determine if caspase inhibition (using the pan-caspase inhibitor zVAD-fmk): (1) decreased PS expression and (2) decreased platelet aggregation following activation. Flow cytometry was used to determine PS expression and a platelet aggregometer was used to assess aggregation. We found that platelets treated with zVAD-fmk significantly decreased both A23187-induced PS exposure (total fluorescence index, TFI: A23187=791.42+/-174; zVAD+A23187=92.97+/-57, p
• Watson, R. R., Watson, R. R., Tuttle, H. A., Mendoza, S., Mcdonagh, P. F., Gonzales, R., Davis-gorman, G., Cohen, Z., & Chen, Y. (2003). Neutrophil activation by murine retroviral infection during chronic ethanol consumption.. Alcohol and alcoholism (Oxford, Oxfordshire), 38(2), 109-14. doi:10.1093/alcalc/agg049
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  Neutrophil adhesion molecule CD11b and reactive oxygen species (ROS) are neutrophil activation markers for evaluating the functional activity of neutrophils. The aim of this study was to determine if neutrophils are activated in murine AIDS and/or chronic ethanol consumption and if neutrophil CD11b expression and ROS production vary when progressive retrovirus infection occurs..Four groups were studied: control, murine AIDS, ethanol and ethanol plus murine AIDS. Neutrophil activation was assessed by CD11b expression and ROS production using flow cytometry..We found that neutrophils lost their responsiveness to fMLP due to retrovirus or ethanol exposure. In the murine AIDS group, neutrophil CD11b expression was up-regulated along with a significant increase in ROS after 1 month of retroviral infection. After 2 months, neutrophil CD11b and ROS decreased. However, neutrophil CD11b expression further increased after 3 months. In the ethanol consumption group, neutrophil CD11b expression was down-regulated after 2 months, whereas ROS production increased in the first and third months. In the murine AIDS plus ethanol group, there were significant increases in both ROS and CD11b expression during the 3-month observation period..These findings suggest that neutrophil function is impaired by LP-BM5 retrovirus infection and/or chronic ethanol consumption. The pattern of neutrophil CD11b expression and ROS production might help to predict the stage of murine AIDS. Ethanol may further compromise neutrophil function in AIDS.
• Mcdonagh, P. F., Gonzales, R. F., Davis-gorman, G. F., Copeland, J. G., & Cohen, Z. (2002). Thrombin activity and platelet microparticle formation are increased in type 2 diabetic platelets: a potential correlation with caspase activation.. Thrombosis research, 107(5), 217-21. doi:10.1016/s0049-3848(02)00334-1
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  Diabetics suffer from many complications including a prothrombotic condition. Activated platelet membrane provides an anchor, phosphatidylserine, for the attachment of the prothrombinase complex, which allows increased thrombin formation. This study aimed to further elucidate the interrelationship between coagulation proteins and activated platelets in type 2 diabetic blood. We found that there was a significant increase (30 x) in thrombin activity in the type 2 diabetic (ZDF) blood as compared to age-matched (ZL) controls (p
• Cohen, Z., Thompson, D. R., Manning, M. C., Randolph, T. W., Falk, R. A., Meyer, J. H., Tian, B., Serravo, R., Stringer, K. A., & Ng, K. M. (1998). Alveolar macrophage cell line is not activated by exposure to polymeric microspheres. International Journal of Pharmaceutics. doi:10.1016/s0378-5173(98)00138-0
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  An in vitro cell culture model based on a rat alveolar macrophage (AM) cell line, NR8383, was used to determine if poly( l -lactide) (PLA) microspheres prepared by the precipitation with a compressed antisolvent (PCA) method can be taken up by AMs and activate AMs. To examine cellular uptake of microspheres, microspheres were labeled with rhodamine 6G. Using fluorescence microscopy, the uptake of microspheres by NR8383 cells was followed as a function of time, microsphere concentration, and susceptibility to lysosomotropic agents. To determine if microspheres can activate NR8383 cells, the oxidative burst and production of TNF- α by NR8383 cells following microsphere treatment was measured. Uptake of microspheres by NR8383 cells was dependent on microsphere concentration and appeared to occur via endocytosis, as uptake was significantly inhibited by the putative lysosomotropic agents, ammonium chloride and chloroquine. Furthermore, the microspheres do not appear to activate NR8383 cells, since microsphere exposure results in negligible oxidative burst and TNF- α production in NR8383. Microspheres prepared by the PCA method hold great potential in targeting drugs to AMs and, therefore, may be of utility for the treatment of diseases in which AMs play an important role, such as tuberculosis (TB).

Presentations

• Cohen, Z. (2018, April). Medical School Teaching Innovation. Western Group on Educational Affairs, Association of American Medical Colleges. Denver, Colorado: AAMC.

Poster Presentations

• Cohen, Z., & Parikh, T. (2023, April). A Summer Experience Prior to Starting Medical School Reduces Anxiety During the Pre-Clerkship Phase of Medicine. WGEA. Hawaii: AAMC.
• Stanescu, C. I., Cohen, Z., & Price, E. A. (2016, October). Physiology Undergraduate Curricular Changes in Response to Program Assessment. Arizona Physiological Society. Tucson, AZ: American Physiological Society.
• Cohen, Z., & Burd, G. D. (2016, October). Active Engagement in an Upper Divison Physiology of the Immune System Course: What We're Learning. Arizona Physiological Society. University of Arizona.
• Cohen, Z., & Stanescu, C. (2018, June). Small Changes, Large Rewards: How individualized emails increase performance in an upper division physiology course.. Physiology Majors Interest Group (PMIG). University of Arizona: American Physiological Society.
• Cohen, Z., & Stanescu, C. (2019, April). Small Changes, Large Rewards: How individualized emails increase performance in an upper division physiology course.. Experimental Biology. Orlando FL: American Physiological Society.
• Cohen, Z., Keen, D. A., Price, E. A., & Stanescu, C. I. (2018, Summer). Determining if Phys-MAPS is the right assessment tool for our curriculum. Physiology Majors Interest Group. Tucson, AZ.

Others

• Cohen, Z. (2018, August). How One Email From You Could Help Your Students Succeed. Chronical of Higher Education. https://www.chronicle.com/article/How-One-Email-From-You-Could/244223
• Cohen, Z. (2018, July). Small Changes, Large Rewards: How Individualized Emails Increase Classroom Performance. EVOLLLUTION. https://evolllution.com/attracting-students/retention/small-changes-large-rewards-how-individualized-emails-increase-classroom-performance/
• Cohen, Z. (2018, September). Small Ways to Help Students Succeed. Chronical of Higher Education. https://www.chronicle.com/article/Small-Ways-to-Help-Students/244515