2009 PDAC Research Symposiumpdac/index_files/PDAC2009_program_abstracts.pdf · Adrienne...

2009 PDAC Research Symposium

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Welcome!

Thank you for participating in the 2009 Postdoctoral Association of the University of Calgary (PDAC) Annual Research Symposium! We look forward to an excellent meeting, with a diverse group of postdocs from all over campus. You will find a detailed event schedule, presentation abstracts, and contact information for participants in the following pages.

PDAC is a group of postdocs at UCalgary that is interested in postdoctoral issues. We are working to make the postdoctoral experience at UCalgary a better one.

All UCalgary postdocs are PDAC members. Please consider becoming more involved by joining the PDAC executive. There are many interesting volunteer opportunities available, and we are always in need of motivated postdocs to keep our organization vibrant.

Invest in Your Success!

PDAC Executive 2009

Stuart Netherton (Chair) Heather Jamniczky (Symposium Chair)

Adrienne Benediktsson Peter Jones

Gosia Gasperowicz Julia Boughner

Eoin OʼGrady Mathieu Chansard


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Thanks to our sponsors!


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Program At-A-Glance

Time Event Location

9:00 - 10:00 Coffee and networking, poster set-up HRIC Atrium

10:00 - 11:50 Talks and career development forum Theatre 3

12:00 - 13:00 Lunch HRIC Atrium

13:00 - 15:00 Poster session HRIC Atrium


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Program Details: Talks and Forum

Time Title Presenter

10:00 - 10:10 Opening Remarks PDAC

10:10 - 10:20 Genetic screen identifies IGFBP5 as a modulator of tamoxifen resistance in breast cancer

Ahn, Bo Young

10:20 - 10:30 Perfluorocarbon aerosol and carbon dioxide: a potential treatment for acute severe asthma

El Mays, Tamer

10:30 - 10:40 Cancer attractor model and cancer cell differentiation

Wu, Wei

10:40 - 10:50 Synaptogenesis and antidepressant Xu, Fenglian

10:50 - 11:00 Quo vadis?: My research journey from PDF to Faculty

Thomas, Bejoy

11:00 - 11:40 Career Development Forum Rancourt, Derrick

Kühnel, Blanka

11:40 - 11:50 Door prizes

Career Development Forum: Invest in Your Success!

Most of you are aiming for a tenure-track position. But the success ratio is low, no more than 20%.Now is the time for you to acquire the skills you need to be competitive.Now is the time for you to carefully prepare a plan B.By discussing with Drs Blanka Kühnel and Derrick Rancourt, you will learn more about the next steps you need to take.

Dr Blanka Kühnel has an adjunct assistant professor appointment with the Department of Biochemistry and Molecular Biology at the Faculty of Medicine, University of Calgary. Blanka has research experience from both academia and industry, and has been the practicum consultant and careers course coordinator for the Master of Biomedical Technology graduate program which bridges science and business. Currently, as the BioProspects Learning Community


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coordinator, she develops programs to promote early-stage career awareness and planning amongst life science graduates.

Dr Derrick Rancourt is an Associate Professor in the Depts. of Oncology, Biochemistry & Molecular Biology and Medical Genetics, and is the establishing director of the University of Calgaryʼs Embryonic Stem Cell Facility. His research program is related to the derivation, expansion and differentiation of pluripotent stem cells. He recently stepped down as Graduate Coordinator of the Master of Biomedical Technology graduate program. Showing a keen interest in professional development for academics, he has published numerous articles on soft skills development needs for scientists and was involved in a survey on educational opportunities for science trainees through the stem cell network.


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Program Details: Posters

# Title Presenter

1 Ion Channels as New Potential Targets in Cancer Therapy

Banderali, Umberto

2 Deciphering the molecular pathways involved in directed photoreceptor differentiation

Dixit, Rajiv

3 Bullies and victims are made, not born – the proof is in the prevention.

Giesbrecht, Gerald

4 Correspondence and comparative kinetics of the ATPase and Actin Motility Velocity of Myosin Isoforms

Hoppenbrouwers, Ernst

5 Extracellular Matrix Can Drive Embryonic Stem Cells into Osteoblasts and Chondrocytes without Exogenous Growth Factors

Krawetz, Roman

6 Reperfusion Hemorrhage is an Imaging Marker for the Severity of Tissue Injury in Patients with Acute Reperfused ST-elevation Myocardial Infarction

Kumar, Andreas

7 Transport of Catalytic Particles Immersed in Fluid Media through Cylindrical Geometries under Heavy Oil Upgrading Conditions

Loria, Herbert

8 High Parity is Associated with Increased Cortical Porosity at the Distal Radius as Measured with High-Resolution pQCT

Macdonald, Heather

9 Genomic analysis of porcine circovirus type 2 isolates in Alberta pigs demonstrating clinical PCVAD

McIntyre, Leila

10 Can Arsenic Toxicity in Mammals be Reduced by Feeding Saskatchewan Grown Lentils?

Nain, Sukhbir

11 A novel system to test the pathogenesis and biomechanical consequences of tendon mineralization

OʼBrien, Etienne


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# Title Presenter

12 Interplay between quorum sensing and a LysR-type transcriptional regulator in controlling biofilm formation and virulence gene expression in Burkholderia cenocepacia

OʼGrady, Eoin

13 A novel role for the focal adhesion protein paxillin in human neutrophil transmigration

Parsons, Sean

14 Towards the Identification of Novel Regulators of TGF-β Signaling

Pot, Isabelle

15 The J protein family: implications in prion conversion Proft, Juliane

16 Neutrophil derived proteinases act as biased agonists for PAR2

Ramachandran, Rithwik

17 Effect of 6–N–propyl–2–thiouracil induced hypothyroidism in the host mouse on the development of bovine testis xenografts

Rodriguez Sosa, Jose

18 Did human fingers and toes coevolve? Rolian, Campbell

19 Development of antiviral resistancy of HIV-1 in various compartments of the gastro-intestinal tract of a patient treated with azidothymidine followed by didanosine.

Van der Meer, Frank

20 Chronic Stress Modulates Skilled Reaching and Brain Glucocorticoid Receptor Expression after Ischemia in Rats

Zucchi, Fabiola


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Abstracts

Talks

Genetic screen identifies IGFBP5 as a modulator of tamoxifen resistance in breast cancer

Ahn1, Bo Young, Adam Elwi1, Byoungchun Lee1, Diane LN Trin1, and Sung-Woo Kim1, 2, 3

Departments of Biochemistry & Molecular Biology1, University of Calgary, Clark H. Smith Brain Tumour Centre2 and Southern Alberta Cancer Research Institute3, Calgary,

Alberta, T2N 4N1, Canada

Intrinsic and acquired tamoxifen resistance in the clinic is one of the overarching challenges to the efficacious treatment of patients with estrogen receptor-positive breast cancer. Through a genome-wide RNA interference screen to discover genes responsible for tamoxifen resistance in vitro, we identified insulin-like growth factor binding protein 5 (IGFBP5) as a determinant of drug sensitivity. Specific knockdown of IGFBP5 by short hairpin RNA (shRNA) in MCF7 cells (shIGFBP5) conferred tamoxifen resistance in vitro. IGFBP5 expression was also reduced in MCF7 human breast cancer cells selected for tamoxifen resistance in culture. Both tamoxifen resistant MCF7-TAMR and shIGFBP5-infected MCF7 cells could be re-sensitized to drug by treatment with exogenous recombinant IGFBP5 protein. Treatment with recombinant IGFBP5 protein in mouse tumour xenografts reversed in vivo tamoxifen resistance of shIGFBP5-infected MCF7 cell derived tumours. Mouse tumours derived from shIGFBP5-infected MCF7 cells after tamoxifen and IGFBP5 co-treatments showed reduced levels of proliferation, which was not accompanied by changes in levels of apoptosis. IGFBP5 immunohistochemical staining in a cohort of 80 breast cancer patients demonstrated that reduced IGFBP5 expression was associated with resistance to tamoxifen therapy. Thus, IGFBP5 warrants investigation as a biomarker for patients likely to respond to tamoxifen therapy and as an agent to reverse tamoxifen resistance in the clinic.


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Perfluorocarbon Aerosol and Carbon Dioxide: a Potential Treatment for Acute Severe Asthma

El Mays1, Tamer, Parichita Choudhury1, Richard Leigh1, Emmanuel Koumoundouros2, Ken Snibson2, Francis Green1.

1- Airway inflammation group, University of Calgary, Alberta, Canada.2- Centre for Animal Biotechnology, University of Melbourne, Victoria, Australia.

Introduction: The low toxicity of perfluorocarbons (PFCs), their high affinity for respiratory gases and compatibility with lung surfactant, have made them useful candidates for treating respiratory diseases. We report promising results for treating acute allergic asthma using small volumes of PFC aerosol driven by a carbon dioxide-rich gas mixture. The carbon dioxide, which is highly soluble in PFC, was used to relax airway smooth muscle. Methods: Sheep were previously sensitized and then challenged with house dust mite (HDM) aerosols to induce early asthmatic responses (increased airway resistance). At the peak of these responses, the sheep were treated for two minutes with an aerosol of perfluoro-octylbromide (PFOB) driven by a gas mixture containing 12% CO2. Airway resistance was monitored for 20 minutes.In other sheep, a segmental bronchus was pre-contracted with methacholine and treated with PFOB/12% CO2 aerosol generated through a bronchoscope catheter. Throughout this procedure, airway opening was recorded using a digital video-camera attached to a bronchoscope.Results: Treatment with PFOB/12% CO2 for 2 minutes following HDM challenge resulted in a decrease in airway resistance. A significant (p<0.05) percent drop of airway resistance was seen immediately (53.8 ± 7.7 vs no change), at 1 to 10 minutes (52.4 ± 8.1 vs 1.9 ± 4.7) and 10 to 20 minutes (56.9 ± 8.8 vs 24.4 ± 4.2) after treatment compared with no treatment respectively.Video bronchoscopy showed an immediate (within 10 seconds) re-opening of methacholine-constricted airways following treatment with PFOB/12% CO2.Conclusions: The ability of this formulation to re-open airways obstructed by smooth muscle spasm is a unique property of this treatment. We predict that the low surface tension and reduced adhesivity of PFCs will also facilitate the penetration of mucous plugs. This will allow delivery of the relaxant carbon dioxide gas to the distally obstructed airways.


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Cancer Attractor Model and Cancer Cell Differentiation

Caide Xiao, Wu, Wei, Tarrah Hall, Hui Xu, Sui Huang, Stuart Kauffman

Institute for Biocomplexity and Informatics, Department of Bio Science, University of Calgary

Cancer is a genetic disorder and developmental disease. The heterogeneity of cancer cells may be attributed to the clonal expansion of mutated cells and /or the growing evidence of cancer stem cell hypothesis. The subpopulation of cells within tumours that is believed to drive tumour growth and recurrence, termed cancer stem cell(CSC)/tumour initiating cells, have been identified in leukemia and solid tumours. Modern research suggests that normal stem cells and cancer stem cells share several critical properties such as self-renewal, the ability to differentiation and the ability to migrate and metastasize. The CSC/TIC exhibits the capacity of recapitulating the diversity of mixed tumour population, this cell fate switching potential in tumours may occur spontaneously or ectopically with differentiation agents, for instance, all-trans retinoic acid induces acute promyelocytic leukemic cells to differentiation for therapy. This cancer cell fates as high dimensional attractor states has been proposed by Sui Huang et al. Differentiation as an attractor along with the existence of CSC provide the basis for induction of cancer (stem) cell maturation, which is differentiation therapy. Recently, few compounds with the specific inhibition or induction of CSC differentiation provide the promising for improving breast cancer treatment. We apply the cancer attractor model to screen 1500 small molecular compound library for breast cancer cells differentiation with high-throughput and high-content technology. Siteen positive hits have been identified with well-established differentiation marker on breast cancer cell line MCF-7. The cancer stem cells marker changes during the course of differentiation have been observed, further inverstigation on the global gene expression signature for cancer cell differentiation is underway.

Synaptogenesis and Antidepressant

*Xu, Fenglian, Collin Luk, Maria P. Richard, Wali Zaidi, Svetlana Farkas, Angela Getz, Arthur Lee, Jan van Minnen, and Naweed I. Syed

Hotchkiss Brain Institute, Faculty of Medicine, University of Calgary, Alberta, Canada T2N 4Z6

All animal behaviours rely critically upon precise synaptic connections that are established during early development. Therefore, aberrant neuronal connectivity often renders the nervous system dysfunctional and results in developmental disorders such as Autism spectrum disorders. Current therapeutic drugs designed to treat these disorders commonly act at the synaptic level by increasing synapse formation,


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enhancing transmitter release, and by preventing the reuptake of transmitters released into the synaptic cleft (e.g. selective serotonin reuptake inhibitor antidepressants, SSRI). However, their precise mechanisms of activity and their non-specific side effects remain elusive. In order to better understand the action of therapeutic medicines and minimize their unexpected side effects, it is crucial to first understand mechanisms underlying synapse formation and synaptic function. Our study provided the first direct evidence that synapse formation between identified Lymnaea neurons requires trophic factor-mediated concomitant electrical activity and intracellular calcium (Ca2+) oscillations on the post- but not presynaptic neurons. Blocking of trophic factor-induced electrical activity and Ca2+ oscillations on the postsynaptic cells prevents proper synapse formation. Surprisingly, we have shown that the most frequently prescribed antidepressant drug fluoxetine (Prozac) also prevents proper synapse formation by inhibiting trophic factor-induced postsynaptic Ca2+ oscillations. In addition, we provide evidence that fluoxetine induces growth cone collapse and neurite retractions by lowering growth cone Ca2+ and disturbing their cytoskeletal organizations. Our study raises serious warnings about the potentially devastating side effects of anti-depressant drugs on neurite outgrowth and synapse formation in a developing brain.(Acknowledgements: Fenglian Xu is supported by AHFMR fellowship and project is supported by CIHR)

Quo Vadis?: My research journey from PDF to Faculty

Thomas, Bejoy

Assistant Professor, Division of Psychosocial Oncology, University of Calgary and Department of Psychosocial Resources, Tom Baker Cancer Centre

In this short presentation I will highlight my research journey from building the research concept, having a supportive environment, the attaining a postdoctoral fellowship, the highs and lows of peer reviews, the need for marketing, and the gaining a ʻsoft-moneyʼ faculty position. The presentation will be intertwined with the milestones of my postdoctoral research and a glimpse of hurdles ahead. This presentation is to be seen as a case-study, with the hope that it may tweak the planning processes of my fellow postdocs.


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Abstracts

Posters

Ion Channels as New Potential Targets in Cancer Therapy

Banderali*, Umberto, Aarthi Jayanthan#, Colleen Kondo*, Aru Narendran# and Wayne R. Giles*

*Faculty of Kinesiology, University of Calgary#Department of Pediatric Oncology, Alberta Childrenʼs Hospital, Faculty of Medicine,

University of Calgary.

Ion channels are proteins localized mainly to the external membrane of cells. They perform transport (ions) between the intracellular and extracellular spaces. The activity of ion channels underlies several vital processes such as generation and propagation of electrical signals in the nervous system, absorption and secretion in epithelia and excitation-contraction coupling in muscles. In the last decade, the importance of ion channels in cellular processes relevant to cancer, e.g. cell proliferation or motility, has also been demonstrated. We have used cell lines originating from pediatric atypical teratoid/rhabdoid (AT/RT) brain tumors, a very severe form of cancer in young children and infants. We employ an electrophysiological approach to characterize the population of ion channels specifically expressed by these tumor cells. Our preliminary experiments (made on two AT/RT cell lines and on one non-tumor cell line from an AT/RT patient) indicate that a particular class of ion channels (the volume sensitive channels) is more abundant in tumor cells than in non-tumor cells. The implication of such channels in tumor cells proliferation, in apoptosis and in development of metastatic tendencies has been documented in several recent studies. Our preliminary data indicate that selected chemical compounds which can alter the normal activity of these channels interfere with cell proliferation, reducing the rate of cell culture growth. We will explore the possibility that the use of these agents in combination with conventional therapeutics will enhance treatment efficacy and help reduce side effects. While most of the current target identification approaches involve the search for molecules that are present mostly inside the cells, we will focus on regulatory agents that are at work from outside these cells. Since most of the mechanisms responsible for tumor cells resistance to drugs involve intracellular processes, a drug aimed at an extracellular target will likely reduce considerably the risks of developing such resistance.


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Deciphering the molecular pathways involved in directed photoreceptor differentiation

Dixit, Rajiv and Carol Schuurmans

Department of Biochemistry and Molecular biology Institute of Maternal and Child heath

University of CalgaryCanada

While several transcription factors have been implicated in the specification and differentiation of rod and cone photoreceptor fates, the organizational structure of the underlying transcriptional cascades has yet to be fully elucidated. We have implemented and validated an in vitro electroporation-based gain-of-function approach to test the ability of different transcription factors to specify rod and cone fates in the developing retina. Our goal was to identify a transcription factor cocktail that would efficiently bias human retinal stem cells or embryonic stem cells to differentiate into photoreceptors. To date, I have found that: 1) the bHLH transcription factor NeuroD represses the acquisition of a rod fate. However, using our electroporation assay, we have not been able to show that NeuroD is instead promoting a cone photoreceptor fate, as suggested by (Liu et al., 2008a); 2) I found that the bHLH transcription factors Ngn2, Mash1 and Math3 all have the capacity to promote rod differentiation in the developing retina, as assessed by the expression of rhodopsin; 3) I found that Ngn2 suppresses the acquisition of a cone fate, as assessed by the expression of blue opsin and peanut agglutinin; 4) I showed that Ngn2 mutant retinae prematurely express red opsin, a late onset marker for cones. Taken together with our gain-of-function analyses, this data suggests that Ngn2 is a negative regulator of a cone fate.Given my demonstration that Ngn2 function is both required and sufficient to regulate cone photoreceptor differentiation, I have now begun to examine the role of chromatin modification in this process. For this purpose, I have been using two new alleles of Ngn2 – a Ngn2VP16 allele that is an obligate transactivator and a Ngn2EnR allele that is an obligate trans-repressor. To test these alleles I have used a transient electroporation approach and I have also analyzed conditional gain-of-function transgenic lines that have been generated in the lab. I have found that the Ngn2VP16 allele promotes the generation of supernumerary S-cones, while the Ngn2EnR allele suppresses an S-cone identity. This suggests that the wild-type allele of Ngn2, which mimics the Ngn2EnR phenotype, is acting like a repressor, likely through associations with HDACs. I am following up these studies with biochemical analyses to identify Ngn2 cofactors in the retina.Taken together, my current focus on Ngn2 will reveal new insights into how a cone fate is specified in the developing retina.


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Bullies and victims are made, not born – the proof is in the prevention.

Giesbrecht1, Gerry, Bonnie Leadbeater2, and Stuart MacDonald2

1 University of Calgary; 2 University of Victoria

Multilevel modeling is used to examine within-person (aggression and emotional dysregulation) and between-person (sex, age and participation in a victimization prevention program) factors that may influence changes in peer victimization over the first three years of elementary school. Children (n=423) reported their experiences of peer victimization at entry into Grade 1 (Tb) and at the end of Grade 1 (T1), Grade 2 (T2), and Grade 3 (T3). On average, trajectories of victimization declined and individual differences in sex and age at entry into Grade 1 did not significantly influence victimization trajectories. Children who participated in the WITS® victimization prevention program showed significantly greater reduction in peer victimization than non-participants. In addition, trajectories of victimization for individual children covaried with teacher-rated emotional dysregulation and aggression: Emotional dysregulation attenuated the decline in peer victimization, while aggression resulted in increased victimization. Implications of these findings for aiding victimized children to end bully-victim relationships are discussed.

Correspondence and comparative kinetics of the ATPase and Actin Motility Velocity of Myosin Isoforms


University of Calgary

The kinetics of the actomyosin motor protein determine the maximal shortening velocity of all muscle types. Myosin isoform expression is varied according to physiological demand and pathology. Comparative studies of contractile protein kinetics are of fundamental importance to understanding muscle energetics in disease. Studies of whole muscle fibers and isolated myosin isoforms have shown that propagated velocity correlates with ATP hydrolysis. We confirmed this relationship for isoforms of cardiac actomyosin complexes and examined the nature of two, distinct actomyosin kinetics; association/dissociation of actomyosin and the ATP hydrolysis cycle. Propagated velocity of actin filaments were measured, independent of regulatory proteins, in motility assays with varying myosin isoforms. Actin-dependant ATPase activity measurements of isolated myosin sub-fragments allowed a comparison of energetics with velocity. ATPase activity and actin motility velocity of myosin isoforms derived from rat and canine cardiac and skeletal tissue were measured at temperatures of 25, 30 and 35 oC. ATPase activity plotted against motility velocity for the various myosin isoforms showed a tight linear correlation (R2 = 0.93), reflecting the often cited relationship for intact muscle first discovered by Dr. M. Barany (J Gen Physiol, 1967) across a wide range of temperatures and activities. Q10 values for the motility velocity and ATPase activity of


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all myosin types were similar. Zero-length chemical cross-linking of actomyosin complexes increased activity beyond the limit of Vmax (up to 1000 fold greater at equal [Actin]). This suggests that the association/dissociation kinetics are rate-limiting. The calculated displacement of actin filaments (D = 290 nm) per ATP hydrolyzed in our model suggest that unloaded cross-bridges may displace actin over large distances, equaling multiples of the minimal steps that can be physically made by the actomyosin interaction.

Extracellular Matrix Can Drive Embryonic Stem Cells into Osteoblasts and Chondrocytes without Exogenous Growth Factors

Krawetz, Roman, Jaymi Taiani, Yuri Elizabeth Wu, Shiying Liu, Derrick Rancourt

Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, AB, Canada, T2N 4N1

Embryonic stem cells (ESCs) are derived from the inner cell mass of a developing embryo. These cells have the potential for unlimited self-renewal as well as the ability to differentiate into all cell types that make up the adult body. Therefore, the use of ESCs for regenerative medicine has generated increased attention due to the fact that these cells can be differentiated into cell types that make up the adult skeletal system namely osteoblasts and chondrocytes. The differentiation of ESCs into osteoblasts and chondrocytes has been extensively studied within static culture systems using various chemicals and growth factors to induce differentiation. Osteogeneic differentiation medium typically contains ascorbic acid, β-glycerophosphate and either dexamethasone or vitamin D3; while chondrogenic media usually includes TGFβ-1, BMP-2, insulin and ascorbic acid. In this study we demonstrate that differentiation of ESCs into osteoblasts or chondrocytes can be induced solely by modulating the extracellular matrix (ECM) that the cells are cultured within. A collagen 1 ECM induces ESCs to become osteoblasts with some associated chondrocytes, whereas, supplementing the collagen 1 ECM with chondroitin sulphate increases the percentage of chondrocytes within the population. When collagen 1 induced osteoblasts are injected in-vivo these cells go to form bone without the appearance of teratomas. In conclusion, ESCs can be differentiated into osteoblasts and chondrocytes without the need for exogenous agents. These cells have the ability to generate adult tissues in vivo that are applicable for skeletal repair through a tissue engineering approach.


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Reperfusion Hemorrhage is an Imaging Marker for the Severity of Tissue Injury in Patients with Acute Reperfused ST-elevation Myocardial Infarction

Kumar, Andreas MD M.Sc.1, Vikram Sabhaney MD1, Stephan Poeschko MD2, JeanetteSchulz-Menger MD2, Rainer Dietz MD2, and Matthias G. Friedrich MD FESC1

1-University of Calgary, Stpehenson CMR Centre, Calgary AB Canada2-Humboldt University Berlin, Charite Franz-Volhard Klinik, Berlin Germany

BackgroundT2*-weighted cardiovascular magnetic resonance (T2*-CMR) accurately quantifies myocardial reperfusion hemorrhage in vivo. The aim of this study was to assess the relationship of hemorrhage to microvascular obstruction (MO), infarct size and functional parameters in patients with acute myocardial infarction.Methods and ResultsIn 19 patients (age 57±11), a CMR study was performed 6±1 days after reperfusion therapy for acute ST-elevation myocardial infarction. In a short axis orientation, covering the entire left ventricle (slice thickness 10mm/ 0mm), the following sequences were obtained: cine SSFP images for functional and volumetric analyses, T2*-weighted GE-EPI for hemorrhage; after injection of 0.1 mmol/kgBW early post-conrast IR-GE images were obtained for MO, and after 10 min, late gadolinium enhancement images were obtained for infarct size. Images were analyzed semi-quantitatively using a threshold-based signal detection. Myocardial infarction occurred without microvascular injury in 6 patients (group MO-), 3 patients had microvascular obstruction but no hemorrhage (group MO+H-), and hemorrhage within the microvascular obstruction zone was observed in 10 patients (group MO+H+). Hemorrhage was associated with larger infarct size (MO- 12.6±1.8g, MO+H- 14.9±5.0g, MO+H + 61.9±7.8g; p<0.01), greater amount of microvascular obstruction (MO+H- 2.2±1.2g, MO+H+ 12.2±2.2g, p<0.05), and lower LV ejection fraction (MO- 61±6%, MO+H- 63±1%, MO+H+ 35±5%; p<0.05). There was a linear relationship between infarct size and the amount of microvascular obstruction (R=0.80; figure 3), infarct size and amount of hemorrhage (R=0.77), as well as amount of microvascular obstruction and amount of hemorrhage (R=0.84). An infarct mass of 25g and microvascular obstruction of more than 5g predicted hemorrhagic infarcts with 100% accuracy.ConclusionT2*-CMR accurately quantifies hemorrhage in vivo as a novel diagnostic target in myocardial reperfusion injury. Hemorrhage may be a complication of reperfusion at an advanced stage of ischemic injury.


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Transport of Catalytic Particles Immersed in Fluid Media through Cylindrical Geometries under Heavy Oil Upgrading Conditions

Loria, Herberta,b, Pedro Pereira-Almaoa,b and Carlos E. Scottb

aDepartment of Chemical and Petroleum Engineering, Schulich School of Engineering, University of Calgary, Calgary, AB T2N 1N4

bAlberta Ingenuity Centre for In Situ Energy, University of Calgary, Calgary, AB T2N 1N4

As light oil reserves diminish, extraction and processing of heavy crude oil and bitumen become increasingly important. The use of ultradispersed catalysts is considered to be a promising way to upgrade these materials. In order to simulate such processes, mass transfer of ultradispersed particles needs to be estimated. However, an adequate mathematical expression that describes the behaviour of these particles immersed in fluid media is still missing. This work aims to study the separation and suspension of ultradispersed particles, based on their motion through diverse fluid media enclosed in cylindrical geometries. A three-dimensional convective-dispersive model that takes into account pseudo-stationary and transient cases was developed in this study. This model was also successfully experimentally validated and its results unveiled the particle and fluid media properties that are necessary to control particle deposition in order to make a better use of the particle catalytic activity. The parameters that were not considered in the models were absorbed by a single parameter: the dispersion coefficient, which served as a proportionality constant to quantify the particle concentration due to convection and dispersion. The particle agglomeration effect was also taken into account by adding to the model a function of the variation of the particle diameter with time and temperature. The application of the convective-dispersive model to practical cases was also studied in this work. These cases consisted of systems where MoO3 catalytic particles were immersed in Athabasca bitumen. The comparison of the modelʼs performance employing a constant particle diameter and considering a particle agglomeration process, for systems where Fe2O3 nanoparticles were immersed in base oil, was also part of the work for this study.

High Parity is Associated with Increased Cortical Porosity at the Distal Radius as Measured with High-Resolution pQCT

Macdonald1,2, Heather, Kyle Nishiyama1,2, Helen Buie1,2, David Hanley3, Steven Boyd1,2

1 Schulich School of Engineering, University of Calgary2 Roger Jackson Centre for Health and Wellness Research, University of Calgary

3 Department of Medicine, University of Calgary

Increased bone turnover during pregnancy and lactation leads to transient bone loss that is often reversed with weaning. However, the long-term effects of parity on bone


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microarchitecture and strength are not known. We aimed to examine these relationships in a population-based sample of women using high-resolution pQCT (HR-pQCT). We recruited participants from the Calgary cohort of the Canadian Multicentre Osteoporosis Study (CaMos) or from the general population using random-digit dialing. This analysis includes 234 women aged 40-90 yrs, 191 (82%) of whom reported 1 to 8 live births (median=2). We used HR-pQCT (XtremeCT, Scanco Medical AG) to assess trabecular and cortical bone microstructure of the distal radius and applied finite element analysis to HR-pQCT scans to estimate bone strength (ultimate stress, MPa). An automated segmentation procedure was used to quantify cortical thickness (Ct.Th) and cortical porosity (Ct.Po). We compared bone outcomes between three groups: nulliparous (no pregnancies, n=43), low parity (1-3 births, n=157) and high parity (4 or more births, n=34) using ANCOVA. Compared with nulliparous and low parity women, radius Ct.Po was 3.5-5% greater in high parity women (p<0.05) and this was mainly due to a 20% larger mean cortical pore size. In addition, radius cortical BMD was 4-5% lower in the high parity group compared with nulliparous and low parity women (p<0.05). Parameters of trabecular microarchitecture were not significantly different between groups. Our findings suggest that high parity may have a lasting negative effect on cortical bone microstructure. Further investigation is required to determine if the load-sharing capacity of the cortical compartment is compromised due to the increased porosity.

Genomic analysis of porcine circovirus type 2 isolates in Alberta pigs demonstrating clinical PCVAD

McIntyre1, Leila, Mark Chaiyakul1, Edward G. Clark2, Frank Marshall3, and Markus Czub1

1 Department of Production Animal Health, 2 Department of Veterinary Clinical and Diagnostics Sciences, 3 Swine Health Services, Clinical Associate, Faculty of Veterinary

Medicine, University of Calgary

Porcine circovirus type 2 (PCV2) is the smallest virus known to infect mammals. It is the cause of porcine circovirus associated diseases (PCVAD). PCVAD are responsible for major economical losses in the pig industries world wide. In this study 19 pigs with clinical signs of PCVAD on five Alberta pig farms were examined pathologically, including gross pathology, histopathology, and immunohistochemistry. Polymerase chain reaction (PCR) for PCV2 and sequence analysis was performed on tissue samples of 15 animals. Results showed that new strains of the porcine circovirus type 2 genogroup b were present in the majority of pigs positive for PCV2. Viruses of this genogroup have not been reported on Alberta pig farms before. Furthermore, a mixed infection with PCV2a and PCV2b occurred in the liver and lungs of one pig. Comparison of whole genome sequences showed mutations distributed over the entire genome of PCV2, however sequences enconding for immunodominant epitopes of PCV2 appear to be unaffected by these mutations.


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Can Arsenic Toxicity in Mammals be Reduced by Feeding Saskatchewan Grown Lentils?

Nain, Sukhbir, and Smits, J.E.G

Ecosystem & Public Health, Faculty of Veterinary Medicine University of Calgary

Calgary, AB

Estimates show that 100 million people worldwide are exposed to arsenic in drinking water, the majority of these being in South Asia, the primary destination for Canadian lentils. An emerging trend in global consumers of human nutrients is biofortification, or the ability to increase supply of vital nutrients through whole foods. Saskatchewan (SK) grown lentils are recognized as important sources of natural dietary folate and selenium. These SK grown lentils can provide a whole food solution to the serious global health problems from chronic arsenicosis in mammals, while at the same time, giving a strong market edge to the important lentil export industry. Initially, it is necessary to establish baseline information on the biological effects of arsenic exposure in our experimental model, laboratory rats. Hence, a study was conducted to determine the most sensitive endpoints of sub-chronic arsenic toxicity in rats. Clinical, immunological, pathological, and molecular bio-indicators were examined in rats exposed to arsenic in their drinking water. Twenty four male wistar rats (180-200g) were randomly allocated to four groups (n=6 rats/group). After one week acclimatization and socialization, rats were exposed to 0.4, 4 and 40 ppm of arsenite in drinking water, with the control group on clean drinking water. At 40ppm arsenite exposure, several biochemical variables including blood urea nitrogen, K+, Cl- and alanine aminotransferase were affected by arsenic exposure. The antibody-mediated immune response was significantly suppressed in the high dose (40ppm) groups and showed a trend to be lower even in the 4ppm group indicating the antibody response is sensitive to arsenic exposure. Several histopathological findings and biochemical indicators showed that liver function was being compromised, and one of the molecular markers demonstrated that arsenic was damaging organelle and cell membranes in a dose dependent manner. This information will provide the basis on which we are building our main, multiyear study, in which we will attempt to mitigate clinical signs and pathology from As toxicity through rats through supplementation with biofortified, lentil-based diets.


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A novel system to test the pathogenesis and biomechanical consequences of tendon mineralization

1OʼBrien, Etienne, 2Catherine Kielty, 3Duncan A. McGrouther, 1David Hart, 1Cyril Frank

1McCaig Institute for Bone and Joint Health, The University of Calgary, Canada;2Faculty of Life Sciences, The University of Manchester, Manchester, United Kingdom;

3Laboratory Medicine Academic Group, The University of Manchester, Manchester, United Kingdom

Heterotopic mineralization is reported in 7.5% of 200 asymptomatic shoulders and in 6.8% of 925 painful shoulders [1], and in 14.4 – 62 % of patients undergoing open surgical repair of the Achilles tendon [2]. It has been suggested that mineralization contributes to mechanical incompetence of affected tendons [3]. We propose to further characterise a murine model of modest injury which results in tendon mineralization in all cases [4]. Injured mice (C57BL/6 strain) will be sacrificed after 5, 10 and 15 weeks along with sham-operated and uninjured controls. Tendons will be biomechanically tested (viscoelastic and failure properties) using our custom built jig which provides data in 82% (18/22) of cases without sl ippage. With additional samples immunohistochemistry (including antibodies for collagen types II, X) will be used to localize the mineralization relative to the wound site. Finally, tissues from BALB/c mice will be used to determine possible strain specificity in tendon mineralization response. We envisage that experiments involving inhibitors of mineralization, such as siRNA against Runx2 [5], and our experimental system, will allow the influence of this process on tendon biomechanical function to be elucidated. [1] Welfing J. et al (1965) Rev Rhum 32, 325-334.[2] Ateschrang A. et al (2008) Arch Orthop Trauma Surg 128(10):1087-1092.

Interplay between quorum sensing and a LysR-type transcriptional regulator in controlling biofilm formation and virulence gene expression in Burkholderia

cenocepacia

OʼGrady, Eoin P., David T. Nguyen and Pamela A. Sokol

Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada

Burkholderia cenocepacia causes chronic and life-threatening respiratory infections in people with cystic fibrosis and chronic granulomatous disease. B. cenocepacia uses quorum sensing, a cell density-dependent communication system, to control expression of many genes important for pathogenesis. Both the CepIR and CciIR quorum sensing systems influence biofilm formation and virulence in animal infection models. We have recently identified a LysR-type transcriptional regulator (designated ShvR) that influences biofilm formation and colony morphology in B. cenocepacia. Additionally,


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shvR mutants have reduced virulence in plant and animal infection models. Transcriptome analysis, qRT-PCR and promoter::lux fusions identified a regulatory interrelationship between quorum sensing and ShvR. Expression of shvR was positively regulated by CepR and negatively regulated by CciR. ShvR negatively regulated expression of cepIR and cciIR suggesting a feedback mechanism. The CepR, CciR and ShvR regulons were examined for co-regulation or independent regulation of biofilm- and virulence-associated genes by quorum sensing and ShvR. CepR, CciR and ShvR acted as both positive and negative regulators of gene expression. ShvR controlled expression of more than 700 genes that were not regulated by either CepR or CciR suggesting independent regulation. Several gene clusters involved in exopolysaccharide biosynthesis showed altered expression in the shvR mutant but not the cepR or cciR mutants. CepR and ShvR commonly-regulated expression of 259 ORFs. Reduced biofilm formation, reduced alfalfa virulence and a shvR mutant morphotype was observed in three unique transposon mutants with insertions in an uncharacterized gene cluster. This gene cluster is positively regulated by both CepR and ShvR and negatively regulated by CciR. Phenotypic data suggest that ShvR is a major regulator of certain genes that are essential for biofilm formation and rough colony morphology. Further investigation may provide additional insights into the contribution of quorum sensing and ShvR to biofilm formation, colony morphology and virulence in plant and animal models of infection.

A novel role for the focal adhesion protein paxillin in human neutrophil transmigration

Parsons, Sean A., Dawn L. Roccamatisi, Ritu Sharma, Hong Zhang, Pina Colarusso, and Kamala D. Patel.

Department of Physiology and Biophysics and Snyder Institute for Infection, Immunity, and Inflammation, University of Calgary; Calgary, AB, Canada

Neutrophil transmigration across endothelium is important in the inflammatory response, yet it still remains poorly understood. In this study, we examine the role of the focal adhesion protein paxillin in the transmigration process, using primary human endothelial cells and neutrophils. Immunofluorescence microscopy shows that paxillin disappears from focal adhesions in areas surrounding transmigrating neutrophils, and that this disappearance is unaffected by rolling or firm adhesion alone. Down-regulation of paxillin using siRNA resulted in a decrease in neutrophil transmigration that could be rescued by the addition of exogenous paxillin; however, no effect on VE-cadherin or FAK localization, actin cytoskeletal structure, mRNA levels of E-selectin, ICAM-1, and IL-8, or overall endothelial cell appearance was observed. This suggests a specific role for the paxillin protein. Finally, using live cell imaging and confocal microscopy, we examine the effect of both down-regulating, and over-expressing paxillin on neutrophil transmigration. Together, these data help elucidate how neutrophils cross the endothelial barrier into surrounding tissues, thereby promoting inflammation.


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Towards the Identification of Novel Regulators of TGF-β Signaling

Pot, Isabelle, Lili Deng and Shirin Bonni

Southern Alberta Cancer Research Institute and Department of Biochemistry & Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta

Since abnormal cell proliferation is pivotal in tumor formation, it is critical to elucidate mechanisms that regulate cell growth. The cytokine TGF-β is a regulator of proliferation and differentiation. TGF-β stimuli are transmitted from the cell surface to the nucleus via Smad intracellular proteins. Together with transcriptional co-activators and co-repressors, the Smad proteins modulate the expression of TGF-β target genes, leading to specific cellular responses. The Smad-interacting protein SnoN is an important modulator of TGF-β signaling. Interestingly, SnoN can regulate TGF-β responses positively or negatively, depending on dosage and cell type. However, the exact molecular mechanisms by which SnoN functions are still incompletely understood. We are interested in elucidating how SnoN can elicit distinct TGF-β-mediated responses. We hypothesized that SnoN effects in TGF-β signaling may depend on the composition of the protein complex in which it resides. Using an unbiased approach involving tandem affinity purification of SnoN followed by mass spectrometry analysis, we have identified several novel SnoN-interacting proteins in TGF-β responsive epithelial cell lines. We have now validated some of the candidate interacting proteins by direct co-immunoprecipitation with SnoN, and we are performing functional studies to identify the role of these proteins in SnoN function and TGF-β-mediated responses, including inhibition of cell proliferation. This research will significantly contribute to our understanding of the mechanisms by which SnoN modulates TGF-β signaling. In addition, our results should lead to the identification of novel players in TGF-β-mediated responses. Since the TGF-β signaling pathway plays important roles in tumorigenesis, these findings may also reveal novel therapeutic targets in the treatment of cancer.

The J protein family: implications in prion conversion

Proft, Juliane, Sarah G. Gibbs, Xiaoxi Zhao and Janice E.A. Braun

Hotchkiss Brain Institute, Department of Physiology and Pharmacology, University of Calgary

The importance of the J protein family in protein folding and quality control has been recognized for many years. J proteins contain a 70 amino acid signature “J domain” comprised of four α helices with a highly conserved tripeptide of histidine, proline and aspartic acid (HPD motif) located between helices II and III. In humans, over 40 J proteins have been identified which are widely held to collectively intersect with almost every facet of cell function to maintain a fine balance between protein folding and protein triage. We have previously shown that the J proteins Rdj2 and CSPα specifically


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associate with cellular prion protein (PrPC) suggesting that they are ʻfolding catalystsʼ for PrPC and may protect against prion diseases. Prion diseases are fatal neurodegenerative disorders associated with the conversion of the cellular prion protein into an alternatively folded disease specific isoform (PrPSc). An effective treatment for prion disease remains elusive. Our discovery of PrPC/CSPα and PrPC/Rdj2 protein complexes raises a number of exciting possibilities. Does PrPC associate with multiple members of the J protein family? Does PrPC interact with the highly conserved J domain or divergent regions of these J proteins? Are J proteins involved in maintaining the normal PrPC conformation? Are J proteins involved in PrPC to PrPSc conversion? As a first step toward testing the hypothesis that J proteins may protect against prion disease, we have evaluated members of the J protein family for a possible role in PrPC to PrPSc conversion utilizing cell free conversion and pull down assays of recombinant PrPC and J proteins. We have generated a series of deletion constructs of several J proteins to establish their precise binding site to PrPC. Our results demonstrate a robust interaction between the stress inducible protein Hsp40 and recombinant mouse prion protein (rPrP-L42). The association of PrPC with Hsp40 does not occur through the highly conserved J domain and it does not block Hsp40ʼs assembly with other proteins. Hsp40, Rdj2 and CSPα do not alter the characteristic Proteinase K (PK) sensitivity of rPrP-L42, suggesting that J proteins may well be involved in maintaining normal PrPC conformation. There is no doubt that chaperones play a critical role in controlling protein misfolding and reducing the threat of neurodegeneration triggered by toxic proteins. Identifying the J protein(s) that controls normal prion conformation(s) in the cell will shed light on the mechanisms underlying the process of misfolding that leads to prion diseases.

Neutrophil derived proteinases act as biased agonists for PAR2

Ramachandran, Rithwik, Koichiro Mihara, Bernard Renaux and Morley D Hollenberg

Department of Physiology and Pharmacology, Faculty of Medicine, University of Calgary, Alberta.

Proteinase Activated Receptors (PARs) are a family of G protein coupled receptors, activated by proteinase cleavage of the receptor N-terminus to reveal a tethered receptor-activating ligand (TL). We recently reported that PAR2 receptors with mutated TL sequences could signal selectively to pathways downstream of PAR2 activation and G-protein coupling. In this study we tested the hypothesis that cleavage of the receptor N-terminus alone was sufficient to activate the receptor, without the requirement for TL binding. We exposed PAR2KNRK cells to neutrophil derived proteinases, elastase, proteinase-3 and cathepsin-G, which are known to cleave the PAR2 N-terminus at sites distinct from the R36/S37 TL exposing site. We monitored release of the receptor N-terminus using a bi-arsenical dye that binds to a tertra-cysteine motif that was engineered upstream of the PAR2 N-terminus. Cleavage and release of this N-terminal sequence was observed with all of the neutrophil derived proteinases. Following cleavage with the neutrophil derived proteinases we also observe a disarming of the


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calcium signaling response to know receptor-activating proteinases such as trypsin. We further observe that neutrophil derived elastase could activate the MAPK signaling pathway in PAR2 expressing KNRK cells. We conclude that neutrophil derived proteinases can cleave the PAR2 N-terminus at distinct sites to modulate signal trafficking downstream of PAR2. A better understanding of these neutrophil dependent biased signaling events will help us to understand the involvement of PAR2 in inflammatory diseases.

Effect of 6–N–propyl–2–thiouracil induced hypothyroidism in the host mouse on the development of bovine testis xenografts

Rodriguez-Sosa1,3, Jose R., G. M. J. Costa2, R. Rathi1, L. R. França2, I. Dobrinski1,3;

University of Pennsylvania , Philadelphia1, Federal University of Minas Gerais, Belo Horizonte, Brazil2, University of Calgary, Alberta, Canada3

In rodents, thyroid hormones inhibit Sertoli cell proliferation and promote Sertoli cell differentiation. Conversely, hypothyroidism prolongs Sertoli cell proliferation, leading to increased Sertoli cell number and testicular size. In order to evaluate whether 6–N–propyl–2–thiouracil (PTU) induced hypothyroidism in the host mouse would affect seminiferous tubule development and increase spermatogenesis in bovine testis xenografts, fragments (~1 mm3) of testes from 1–wk–old Holstein calves were transplanted ectopically to castrated immunodeficient male mice. Mice were treated with 0.1% (w/v) PTU in drinking water for 4 wk or left as control. At 5 and 7 mo grafts were analyzed by morphometry and immunohistochemistry for expression of protein gene product 9.5 (PGP 9.5) as a germ cell marker, and Muellerian inhibiting substance (MIS) and androgen receptor (AR) to assess Sertoli cell maturation. PTU treatment to the drinking water for one month suppressed thyroid hormone levels (T4) in host mice without negative systemic effects. Spermatogenesis in recovered grafts was arrested at meiosis regardless of treatment and collection time. Graft weight was lower in treated mice than in controls, but volume density of the tubular and intertubular compartments, and seminiferous epithelium was not affected by treatment. However, treatment reduced lumen density compared to controls and tubular diameter. The number of germ cells was not different between groups at any collection time. Sertoli cells showed variable MIS expression and lack of or weak AR expression regardless of treatment and collection time, indicating an immature phenotype. In conclusion, suppression of thyroid hormone levels in host mice affects seminiferous tubule development in bovine testis xenografts. However, treatment did not affect number and differentiation of germ cells. Rather, incomplete Sertoli cell maturation appears to lead to incomplete germ cell differentiation in bovine testis xenografts.


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Did human fingers and toes coevolve?

Rolian, Campbell

University of Calgary

Human hands and feet have longer, more robust first digits, and shorter lateral digits compared to African apes. These similarities are often assumed to be independently-evolved adaptations for manipulative activities and bipedalism, respectively. However, hands and feet are serially homologous structures that share virtually identical developmental blueprints, raising the possibility that digital proportions co-evolved in human hands and feet because of underlying developmental linkages that increase phenotypic covariation between them. Here we show that phenotypic covariation between serially homologous fingers and toes in Homo and Pan is not only higher than expected, it also causes these digits to evolve along highly parallel trajectories under episodes of simulated directional selection, even when selection pressures push their means in divergent directions. Further, our estimates of the selection pressures required to produce human-like fingers and toes from an African ape-like ancestor indicate that selection on the toes was substantially stronger, and likely led to parallel phenotypic changes in the hands. Our data support the hypothesis that human hands and feet coevolved, and suggest that the evolution of long robust big toes and short lateral toes for bipedalism led to changes in hominin fingers that may have facilitated the emergence of stone tool technology.

Chronic Stress Modulates Skilled Reaching and Brain Glucocorticoid Receptor Expression after Ischemia in Rats

Zucchi, Fabiola C. R., Norah F. Matthies, Noora Badr, Gerlinde A. MetzCanadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge,

AB, Canada T1K 3M4

One of the major consequences of stroke is permanent motor disturbance, such as postural imbalance and loss of skilled movement. The degree of neuronal and functional loss and subsequent recovery after stroke were shown to be influenced by high levels of stress or glucocorticoids. The purpose of the present study was to investigate the influence of chronic restraint stress on recovery and compensation of skilled reaching movement in a rat model of stroke. Furthermore, the aim was to determine if stress after stroke modulates negative feedback mechanisms by modulation of glucocorticoid receptor (GR) expression in the brain. Adult male rats were pre-trained and tested in skilled reaching task. A focal ischemic lesion was induced by devascularization of the motor cortex. Animals were assigned to daily treatment of restraint stress starting one week prior to lesion up to three weeks post-lesion. One group served as lesion only control. GR expression was accessed by immunohistochemistry. The results revealed


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that animals exposed to restraint stress had significantly lower reaching success at both pre- and post-lesion time points when compared to lesion controls. Total GR expression was decreased in the stress group, when compared to controls. In the lesion hemisphere GR expression increased when compared to non-lesion hemisphere, and the increase was statistically significant in the stress group. Such modulation of GR density can potentially alter the responsiveness to stroke treatment, and compromise recovery. The present data support the notion that chronic stress represents a major modulator of skilled movement recovery after injury. Supported by: Alberta Heritage Foundation for Medical Research, Hotchkiss Brain Institute, Norlien Foundation, Canadian Institutes of Health Research, Canadian Stroke Network, and the National Sciences and Engineering Research Council of Canada.


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Contact List

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Agrawal, Simriti

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Elwi, Adam

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O’Brien, Etienne

O’Grady, Eoin

Palacios-Derflingher, Luz

Parsons, Sean

Postodoctoral Association of the University of Calgary (PDAC)

Pot, Isabelle

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2009 PDAC Research Symposiumpdac/index_files/PDAC2009_program_abstracts.pdf · Adrienne...

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