Posted by: katybug23 | April 18, 2011

March 2011

Shinozaki, Gen, Magdalena Romanowicz, Simon Kung, and David A. Mrazek. “A New Interaction between Slc6a4 Variation and Child Abuse Is Associated with Resting Heart Rate.” Depression & Anxiety 28, no. 3 (2011): 227-33.

Background: The short form of the indel promoter polymorphism (5HTTLPR) of the serotonin transporter gene (SLC6A4) and a history of child abuse have been reported to be associated with an increased risk for the development of depression. A child abuse history has also been associated with more rapid heart rate reactions. Methods: A retrospective chart review identified 282 patients with major depression who had been hospitalized and genotyped for the 5HTTLPR polymorphism. A subgroup of 185 females of European ancestry was also identified and analyzed. While hospitalized, heart rate was measured. Child abuse history was documented during the diagnostic evaluation. Analyses of the relationship between 5HTTLPR genotype, history of child abuse, and admission heart rate were conducted. Results: No main effect on heart rate from the 5HTTLPR genotype or a child abuse history was demonstrated for the entire sample or the subgroup of female patients. However, a genotype-by-abuse interaction was associated with resting heart rate on admission to the hospital (P<.05). Depressed patients, who were homozygous for the long allele and who had been abused, had a heart rate on hospital admission, which was statistically higher than patients with the same genotype but who had not been abused. These findings were consistent both for the 282 patients (7.2 bpm higher) as well as for the subgroup of 185 female patients of European ancestry (9.6 bpm higher). Conclusions: A 5HTTLPR genotype interaction of elevated heart rate with a history of child abuse was demonstrated in depressed psychiatric inpatients.

Sanford School of Medicine, Sioux Falls Campus.

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Chen, Jinghai, Gregory C. Shearer, Quanhai Chen, Chastity L. Healy, April J. Beyer, Vijaya B. Nareddy, A. Martin Gerdes, William S. Harris, Timothy D. O’Connell, and Dajun Wang. “Omega-3 Fatty Acids Prevent Pressure Overload-Induced Cardiac Fibrosis through Activation of Cyclic Gmp/Protein Kinase G Signaling in Cardiac Fibroblasts.” Circulation 123, no. 6 (2011): 584.

Background-Omega-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid) from fish oil ameliorate cardiovascular diseases. However, little is known about the effects of omega-3 polyunsaturated fatty acids on cardiac fibrosis, a major cause of diastolic dysfunction and heart failure. The present study assessed the effects of omega-3 polyunsaturated fatty acids on cardiac fibrosis.Methods and Results-We assessed left ventricular fibrosis and pathology in mice subjected to transverse aortic constriction after the consumption of a fish oil or a control diet. In control mice, 4 weeks of transverse aortic constriction induced significant cardiac dysfunction, cardiac fibrosis, and cardiac fibroblast activation (proliferation and transformation into myofibroblasts). Dietary supplementation with fish oil prevented transverse aortic constriction-induced cardiac dysfunction and cardiac fibrosis and blocked cardiac fibroblast activation. In heart tissue, transverse aortic constriction increased active transforming growth factor-beta 1 levels and phosphorylation of Smad2. In isolated adult mouse cardiac fibroblasts, transforming growth factor-beta 1 induced cardiac fibroblast transformation, proliferation, and collagen synthesis. Eicosapentaenoic acid and docosahexaenoic acid increased cyclic GMP levels and blocked cardiac fibroblast transformation, proliferation, and collagen synthesis. Eicosapentaenoic acid and docosahexaenoic acid blocked phospho-Smad2/3 nuclear translocation. DT3, a protein kinase G inhibitor, blocked the antifibrotic effects of eicosapentaenoic acid and docosahexaenoic acid. Eicosapentaenoic acid and docosahexaenoic acid increased phosphorylated endothelial nitric oxide synthase and endothelial nitric oxide synthase protein levels and nitric oxide production.Conclusion-Omega-3 fatty acids prevent cardiac fibrosis and cardiac dysfunction by blocking transforming growth factor-beta 1-induced phospho-Smad2/3 nuclear translocation through activation of the cyclic GMP/protein kinase G pathway in cardiac fibroblasts. (Circulation. 2011;123:584-593.)

Sanford School of Medicine, Sioux Falls Campus.

Kovacs, A. D., A. Saje, A. Wong, G. Szenasi, P. Kiricsi, E. Szabo, J. D. Cooper, and David A. Pearce. “Temporary Inhibition of Ampa Receptors Induces a Prolonged Improvement of Motor Performance in a Mouse Model of Juvenile Batten Disease.” Neuropharmacology 60, no. 2-3 (2011): 405-09.

Mutations in the CLN3 gene cause juvenile Batten disease, a fatal pediatric neurodegenerative disorder. The Cln3-knockout (Cln3(Delta ex1-6)) mouse model of the disease displays many pathological characteristics of the human disorder including a deficit in motor coordination. We have previously found that attenuation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-type glutamate receptor activity in one-month-old Cln3(Delta ex1-6) mice resulted in an immediate improvement of their motor skills. Here we show that at a later stage of the disease, in 6-7-month-old Cln3(Delta ex1-6) mice, acute inhibition of AMPA receptors by a single intraperitoneal injection (1 mg/kg) of the non-competitive AMPA antagonist, EGIS-8332, does not have an immediate effect. Instead, it induces a delayed but prolonged improvement of motor skills. Four days after the injection of the AMPA antagonist, Cln3(Delta ex1-6) mice reached the same motor skill level as their wild type (WT) counterparts, an improvement that persisted for an additional four days. EGIS-8332 was rapidly eliminated from the brain as measured by HPLC-MS/MS. Histological analysis performed 8 days after the drug administration revealed that EGIS-8332 did not have any impact upon glial activation or the survival of vulnerable neuron populations in 7-month-old Cln3(Delta ex1-6) mice. We propose that temporary inhibition of AMPA receptors can induce a prolonged correction of the preexisting abnormal glutamatergic neurotransmission in vivo for juvenile Batten disease. (C) 2010 Elsevier Ltd. All rights reserved.

Sanford School of Medicine, Sioux Falls Campus.

Meyers, J. E., Marie Volbrecht, B. N. Axelrod, and L. Reinsch-Boothby. “Embedded Symptom Validity Tests and Overall Neuropsychological Test Performance.” Archives of Clinical Neuropsychology 26, no. 1 (2011): 8-15.

A sample of 314 consecutive clinical and forensic referrals with mild traumatic brain injury was evaluated using the Meyers Neuropsychological Battery (MNB). A comparison was made of the test performance and performance on the embedded Symptom Validity Tests (SVTs) with a control for multicolinearity utilized. Using the nine embedded SVTs in the MNB, the incidence of poor effort fell at 26% of the total sample. Involvement in litigation was related to more failures on the individual SVTs. The correlation between failed effort measures and the Overall Test Battery Mean (OTBM) was consistently negative, regardless of litigation status, in that more failures were associated with lower OTBM scores. The correlation between the number of SVTs failed and the OTBM was -.77. Our results are similar to those presented by Green, Rohling, Lees-Haley, and Allen (2001); who reported a .73 correlation with the failure on the Word Memory Test and performance on the OTBM. The results of the current study also indicate that 50% of the variance in neuropsychological testing can be accounted by failures on internal SVTs.

Sanford School of Medicine, Sioux Falls Campus.

Yallapu, Murali M., Shadi F. Othman, Evan T. Curtis, Brij K. Gupta, Meena Jaggi, and Subhash C. Chauhan. “Multi-Functional Magnetic Nanoparticles for Magnetic Resonance Imaging and Cancer Therapy.” Biomaterials 32, no. 7 (2011): 1890-905.

We have developed a multi-layer approach for the synthesis of water-dispersible superparamagnetic iron oxide nanoparticles for hyperthermia, magnetic resonance imaging (MRI) and drug delivery applications. In this approach, iron oxide core nanoparticles were obtained by precipitation of iron salts in the presence of ammonia and provided beta-cyclodextrin and pluronic polymer (F127) coatings. This formulation (F127250) was highly water dispersible which allowed encapsulation of the anti-cancer drug(s) in beta-cyclodextrin and pluronic polymer for sustained drug release. The F127250 formulation has exhibited superior hyperthermia effects over time under alternating magnetic field compared to pure magnetic nanoparticles (MNP) and beta-cyclodextrin coated nanoparticles (CD200). Additionally, the improved MRI characteristics were also observed for the F127250 formulation in agar gel and in cisplatin resistant ovarian cancer cells (A12780CP) compared to MNP and CD200 formulations. Furthermore, the drug-loaded formulation of F127250 exhibited many folds of imaging contrast properties. Due to the internalization capacity of the F127250 formulation, its curcumin-loaded formulation (F127250-CUR) exhibited almost equivalent inhibition effects on A2780CP (ovarian), MDA-MB-231 (breast), and PC-3 (prostate) cancer cells even though curcumin release was only 40%. The improved therapeutic effects were verified by examining molecular effects using Western blotting and transmission electron microscopic (TEM) studies. F127250-CUR also exhibited haemocompatibility, suggesting a nanochemotherapuetic agent for cancer therapy. (C) 2010 Elsevier Ltd. All rights reserved.

Sanford School of Medicine, Sioux Falls Campus.

Warne, Donald. “Policy Issues in American Indian Health Governance.” Journal of Law Medicine & Ethics 39, no. 1 (2011): 42-45.

Sanford School of Medicine, Sioux Falls Campus

Elhai, Jon D., Tracey L. Biehn, Cherie Armour, Jessica J. Klopper, B. Christopher Frueh, and Patrick A. Palmieri. “Evidence for a Unique Ptsd Construct Represented by Ptsd’s D1–D3 Symptoms.” Journal of Anxiety Disorders 25, no. 3 (2011): 340-45.

Abstract: Two models of posttraumatic stress disorder (PTSD) have received the most empirical support in confirmatory factor analytic studies: Emotional Numbing model of reexperiencing, avoidance, emotional numbing and hyperarousal; and Dysphoria model of reexperiencing, avoidance, dysphoria and hyperarousal. These models only differ in placement of three PTSD symptoms: sleep problems (D1), irritability (D2), and concentration problems (D3). In the present study, we recruited 252 women victims of domestic violence and tested whether there is empirical support to separate these three PTSD symptoms into a fifth factor, while retaining the Emotional Numbing and Dysphoria models’ remaining four factors. Confirmatory factor analytic findings demonstrated that separating the three symptoms into a separate factor significantly enhanced model fit for the Emotional Numbing and Dysphoria models. These three symptoms may represent a unique latent construct. Implications are discussed.

Psychology Department.

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Engdahl, Ryan M., J. Don Richardson, Jon D. Elhai, and B. Christopher Frueh. “Comparing Posttraumatic Stress Disorder’s Symptom Structure between Deployed and Nondeployed Veterans.” Psychological Assessment 23, no. 1 (2011): 1-6.

We tested two empirically validated 4-factor models of posttraumatic stress disorder (PTSD) symptoms using the PTSD Checklist: King, Leskin, King, and Weathers’ (1998) model including reexperiencing, avoidance, emotional numbing, and hyperarousal factors, and Simms, Watson, and Doebbeling’s (2002) model including reexperiencing, avoidance, dysphoria, and hyperarousal. Our aim was to determine which fit better in two groups of military veterans: peacekeepers previously deployed to a war zone (deployed group) and those trained for peacekeeping operations who were not deployed (nondeployed group). We compared the groups using multigroup confirmatory factor analysis. Adequate model fit was demonstrated among the nondeployed group, with no significant difference between King et al.’s (1998) model (separating avoidance and numbing) and Simms et al.’s (2002) similar model involving a dysphoria factor. A better fitting factor structure consistent with Simms et al.’s (2002) model was found in the deployed group. Comprehensive measurement invariance testing demonstrated significant differences between the deployed and nondeployed groups on all structural parameters, except observed variable intercepts (thus indicating similarities only in PTSD item severity). These findings add to researchers’ understanding of PTSD’s factor structure, given the revision of PTSD that will appear in the forthcoming 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2010)-namely, that the factor structure may be quite different between groups with and without exposure to major traumatic events.

Psychology Department.

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Tsai, Tzong-Ru, Pang-Hsu Liu, and Y. L. Lio. “Optimal Maintenance Time for Imperfect Maintenance Actions on Repairable Product.” Computers & Industrial Engineering 60, no. 4 (2011): 744-49.

Abstract: This paper develops a maintenance strategy for repairable products that combines imperfect maintenance actions at pre-scheduled times and minimal repair actions for failures. Under a power law process of failures, an expected total cost is developed that involves the sum of the total cost of imperfect preventive maintenances and the expected total cost of minimal repairs. Moreover, a searching procedure is provided to determine the optimal maintenance schedule within a finite time span of warranty. When the parameters of the power law process are unknown, the accuracy of the estimated maintenance schedule is evaluated based on data through an asymptotic upper bound for the difference of the true expected total cost and its estimate. The proposed method is applied to an example regarding the maintenance of power transformers and the performance of the proposed method is investigated through a numerical study. Numerical results show that the proposed maintenance strategy could save cost whether an imperfect maintenance action or the perfect maintenance action is implemented.

Mathematics Department.

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Koodali, Ranjit T. “Photoinduced Charge Separation in Microporous and Mesoporous Materials.” Canadian Journal of Chemistry-Revue Canadienne De Chimie 89, no. 3 (2011): 257-65.

On presente une revue de la separation de charge photoinduite des molecules organiques dans des materiaux microporeux et mesoporeux. On discute particulierement des cas des N-alkylphenothiazines (PCn), de la N,N,N’,N’-tetramethylbenzidine (TMB) et de la porphyrine dans des materiaux microporeux tels les zeolites, les aluminophosphates (AlPO) et les silicoaluminophosphates (SAPO) ainsi que les materiaux mesoporeux tels le MCM-41, le MCM-48 et le SBA-15.

Chemistry Department.

Sereda, Grigoriy, and Vikul Rajpara. “Photoactivated and Photopassivated Benzylic Oxidation Catalyzed by Pristine and Oxidized Carbons.” Catalysis Communications 12, no. 7 (2011): 669-72.

The link between the structure of carbons and their performance toward catalytic benzylic oxidation by air is studied. Catalytic activity and selectivity of pristine and oxidized carbons can be enhanced, altered, or suppressed by ambient light. The photocatalytical performance of a carbonaceous material depends on the presence of defects, surface area, porosity, and surface oxidation. Adsorption of the hydroperoxide intermediate on the catalyst’s surface is suggested as a key process that links the structure of the carbonaceous material with its catalytic activity. The potential of catalysis by carbon black and photocatalysis by graphite nanofibers for greener organic synthesis has been demonstrated. (C 2010 Elsevier B.V. All rights reserved.

Chemistry Department.

Koepsell, L., L. F. Zhang, D. Neufeld, H. Fong, and Ying. Deng. “Electrospun Nanofibrous Polycaprolactone Scaffolds for Tissue Engineering of Annulus Fibrosus.” Macromolecular Bioscience 11, no. 3 (2011): 391-99.

The annulus fibrosus comprises concentric lamellae that can be damaged due to intervertebral disc degeneration; to provide permanent repair of these acquired structural defects, one solution is to fabricate scaffolds that are designed to support the growth of annulus fibrosus cells. In this study, electrospun nanofibrous scaffolds of polycaprolactone are fabricated in random, aligned, and round-end configurations. Primary porcine annulus fibrosus cells are grown on the scaffolds and evaluated for attachment, proliferation, and production of extracellular matrix. The scaffold consisting of round-end nanofibers substantially outperforms the random and aligned scaffolds on cell adhesion; additionally, the scaffold with aligned nanofibers strongly affects the orientation of cells.

Biomedical Engineering, Sioux Falls Campus.

Smith, N. L., and W. Keith. Miskimins. “Phosphorylation at Serine 482 Affects Stability of Nf90 and Its Functional Role in Mitosis.” Cell Proliferation 44, no. 2 (2011): 147-55.

NF90 is a multifunctional double-strand RNA binding protein with documented roles in transcription, mRNA stability, translation, RNA processing and transport, and mitosis. It is a phosphoprotein that interacts with, and is a substrate for, several protein kinases. The study described here was initiated to gain better understanding of specific NF90 phosphorylation sites and their relationship to mechanisms by which NF90 performs its various functions. Phosphoproteomic studies have identified NF90 serine 482 (S482) as a major phosphorylation site in vivo. Site-specific mutations were introduced at this site and the mutated proteins were expressed in MCF7 cells by transfection. Western blotting was used to examine NF90 expression, stability, and responsiveness to protein kinase activators and inhibitors. Flow cytometry was used to examine effects of NF90 mutation on cell cycle progression. Non-phosphorylatable mutant S482A was unstable compared to phosphomimetic S482E mutant. NF90-S482A expression was greatly enhanced by inhibiting proteasomal degradation or by activating PKC. Identical treatments had little effect on NF90-S482E. In contrast to WT NF90 or NF90-S482E, cells stably expressing NF90-S482A accumulated in M phase when treated with TPA. Phosphorylation at S482 is important for NF90 stability and in regulating its functional role during mitosis. Based on the sequence surrounding S482, mitotic kinase PLK1 is a strong candidate for the enzyme that phosphorylates NF90 at this site.

Basic Biomedical Sciences, Vermillion campus.

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Gomez, J. A. L., W. van Schaik, A. R. Freitas, T. M. Coque, Keith. E. Weaver, M. V. Francia, W. Witte, and G. Werner. “A Multiresistance Megaplasmid Plg1 Bearing a Hyl(Efm) Genomic Island in Hospital Enterococcus Faecium Isolates.” International Journal of Medical Microbiology 301, no. 2 (2011): 165-75.

Enterococcus faecium is considered to be a nosocomial pathogen with increasing medical importance. The putative virulence factor, hyl(Efm), encoding a putative hyaluronidase, is enriched among the hospital-associated polyclonal subpopulation of E. faecium.. The hyl(Efm) gene is described to be part of a genomic island and was recently identified to be plasmid-located. Here, we present a description of the structure, localization, and distribution of the putative pathogenicity factor hyl(Efm) and its putative island among 39 clinical isolates and elucidate the composition and host range of pLG1, a hylEfm multiresistance plasmid of approximately 281.02 kb. The hyl(Efm) gene was located within a 17,824-bp element highly similar to the putative genomic island (GI) structure that had been previously described. This genomic region was conserved among 39 hyl(Efm)-positive strains with variation in a specific region downstream of hyl(Efm) in 18 strains. The putative hyl(Efm) was located on large plasmids (150-350 kb) in 37 strains. pLG1 could be horizontally transferred into four different E. faecium recipient strains (n = 4) but not into E. faecalis (n= 3). Sequencing of pLG1 resolved putative plasmid replication, conjugation, and maintenance determinants as well as a pilin gene cluster, carbon uptake and utilization genes, heavy metal and antibiotic resistance clusters. The hylEfm transferable plasmid pLG1 bears additional putative pathogenicity factors and antibiotic resistance genes. These findings suggest horizontal gene transfer of virulence factors and antibiotic resistance gene clusters by a single genetic event (conjugative transfer) which might be triggered by heavy antibiotic use common in health care units where E. faecium is increasingly prevalent. (C) 2010 Elsevier GmbH. All rights reserved.

Basic Biomedical Sciences, Vermillion Campus.

Li, Yi-Fan, and Xuejun Wang. “The Role of the Proteasome in Heart Disease.” Biochimica et Biophysica Acta-Gene Regulatory Mechanisms 1809, no. 2, Sp. Iss. SI (2011): 141-49.

Intensive investigations into the pathophysiological significance of the proteasome in the heart did not start until the beginning of the past decade but exciting progress has been made and summarized here as two fronts. First, strong evidence continues to emerge to supports novel hypothesis that proteasome functional insufficiency represents a common pathological phenomenon in a large subset of heart disease, compromises protein quality control in heart muscle cells, and thereby acts as a major pathogenic factor promoting the progression of the subset of heart disease to congestive heart failure. This front is represented by the studies on the ubiquitin-proteasome system (UPS) in cardiac proteinopathy, which have taken advantage of a transgenic mouse model expressing a fluorescence reporter for UPS proteolytic function. Second, pharmacological inhibition of the proteasome has been explored experimentally as a potential therapeutic strategy to intervene on some forms of heart disease, such as pressure-overload cardiac hypertrophy, viral myocarditis, and myocardial ischemic injury. Not only between the two fronts but also within each one, a multitude of inconsistencies and controversies remain to be explained and clarified. At present, the controversy perhaps reflects the sophistication of cardiac proteasomes in terms of the composition, assembly, and regulation, as well as the intricacy and diversity of heart disease in terms of its etiology and pathogenesis. A definitive role of altered proteasome function in the development of various forms of heart disease remains to be established. This article is part of a Special Issue entitled The 26S Proteasome: When degradation is just not enough! (c) 2010 Elsevier B.V. All rights reserved.

Basic Biomedical Sciences, Vermillion Campus.

Tatchum-Talom, Rabelais, Kathleen M. Eyster, Curtis K. Kost, Jr., and Douglas S. Martin. “Blood Pressure and Mesenteric Vascular Reactivity in Spontaneously Hypertensive Rats 7 Months after Gonadectomy.” Journal of Cardiovascular Pharmacology 57, no. 3 (2011): 357-64.

Objective: Sexual dimorphism in the degree of high blood pressure (BP) has been observed in both animal and human hypertension. However, the mechanisms are still poorly understood. We tested the hypothesis that long-term loss of sex steroids promotes changes in mesenteric vascular reactivity that impact the maintenance of hypertension in the spontaneously hypertensive rats (SHR).Methods: Male SHR were sham operated (M-SHAM) or castrated (M-CX), and female SHR were sham-operated (F-SHAM) or ovariectomized (F-OVX) at 3 weeks of age. Seven months later, BP was measured in anesthetized rats, and vascular responsiveness was evaluated in the isolated perfused mesentery.Results: Mean arterial BP (mm Hg) was significantly greater in M-SHAM (186 +/- 6) compared with F-SHAM (159 +/- 5). Gonadectomy reduced BP in male SHR (M-CX: 160 +/- 4) but had no significant effect in female SHR (F-OVX: 153 +/- 7). Norepinephrine-induced constriction was similar in all groups. Gonadectomy attenuated serotonin-induced vasoconstriction in the mesentery. Acetylcholine (ACh)- and isoproterenol (ISO)-induced vasodilation was greater in female than male SHR. Ovariectomy of female SHR blunted ACh and ISO dilatory responses. ISO dose-response curves were shifted to the left in castrated male SHR.Conclusions: Gonadectomy exerts long-term effects on mesenteric vascular reactivity and hypertension in the SHR.

Basic Biomedical Sciences, Vermillion Campus.

Qiu, M. G., W. G. Darling, Robert J. Morecraft, C. C. Ni, J. Rajendra, and A. J. Butler. “White Matter Integrity Is a Stronger Predictor of Motor Function Than Bold Response in Patients with Stroke.” Neurorehabilitation and Neural Repair 25, no. 3 (2011): 275-84.

Objective. Neuroimaging techniques, such as diffusion tensor imaging (DTI) and blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI), provide insights into the functional reorganization of the cortical motor system after stroke. This study explores the relationship between upper extremity motor function, white matter integrity, and BOLD response of cortical motor areas. Methods. Seventeen patients met study inclusion criteria; of these 12 completed DTI assessment of white matter integrity and 9 completed fMRI assessment of motor-related activation. Primary clinical outcome measures were the Wolf Motor Function Test (WMFT) and the upper limb portion of the Fugl-Meyer (FM) motor assessment. Structural integrity of the posterior limb of the internal capsule was assessed by examining the fractional anisotropy (FA) asymmetry in the PLIC. Laterality index of motor cortical areas was measured as the BOLD response in each patient during a finger pinch task. Linear regression analyses were performed to determine whether clinical outcome was associated with structural or functional MRI measures. Results. There were strong relationships between clinical outcome measures and FA asymmetry (eg, FM score [R-2 = .655, P = .001] and WMFT asymmetry score [R-2 = .651, P < .002]) but relationships with fMRI measures were weaker. Conclusion. Clinical motor function is more closely related to the white matter integrity of the internal capsule than to BOLD response of motor areas in patients 3 to 9 months after stroke. Thus, use of DTI to assess white matter integrity in the internal capsule may provide more useful information than fMRI to interpret motor deficits following supratentorial brain injury.

Basic Biomedical Sciences, Vermillion Campus

 

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