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1,633 results on '"M. Hallett"'

151. OS2 - 166 A Novel Model of Human Lung-to-Brain Metastasis and its Application to the Identification of Essential Metastatic Regulatory Genes

Author

Naresh Murty, M Dhillon, K R Brown, D Kaplan, Branavan Manoranjan, Jason Moffat, T Tokar, Nicole McFarlane, Sujeivan Mahendram, John A. Hassell, Robin M. Hallett, Mohini Singh, Thusyanth Vijayakumar, JC Cutz, Sheila K. Singh, A Tong, I Jurisica, Maleeha Qazi, David Bakhshinyan, K Durrer, Chitra Venugopal, and Parvez Vora

Subjects
Oncology, medicine.medical_specialty, General Medicine, Biology, medicine.disease, Human lung, medicine.anatomical_structure, Neurology, Internal medicine, medicine, Cancer research, Identification (biology), Neurology (clinical), Regulator gene, Brain metastasis
Abstract

Brain Metastases (BM) represent a leading cause of cancer mortality. While metastatic lesions contain subclones derived from their primary lesion, their functional characterization has been limited by a paucity of preclinical models accurately recapitulating the stages of metastasis. This work describes the isolation of a unique subset of metastatic stem-like cells from primary human patient samples of BM, termed brain metastasis initiating cells (BMICs). Utilizing these BMICs we have established a novel patient-derived xenograft (PDX) model of BM that recapitulates the entire metastatic cascade, from primary tumor initiation to micro-metastasis and macro-metastasis formation in the brain. We then comprehensively interrogated human BM to identify genetic regulators of BMICs using in vitro and in vivo RNA interference screens, and validated hits using both our novel PDX model as well as primary clinical BM specimens. We identified SPOCK1 and TWIST2 as novel BMIC regulators, where in our model SPOCK1 regulated BMIC self-renewal and tumor initiation, and TWIST2 specifically regulated cell migration from lung to brain. A prospective cohort of primary lung cancer specimens was used to establish that SPOCK1 and TWIST2 were only expressed in patients who ultimately developed BM, thus establishing both clinical and functional utility for these gene products. This work offers the first comprehensive preclinical model of human brain metastasis for further characterization of therapeutic targets, identification of predictive biomarkers, and subsequent prophylactic treatment of patients most likely to develop BM. By blocking this process, metastatic lung cancer would effectively become a localized, more manageable disease.

Published
2016
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152. PS1 - 170 Bmi1 is a Therapeutic Target in Recurrent Childhood Medulloblastoma

Author

A. Mann, Chitra Venugopal, Thusyanth Vijayakumar, David Bakhshinyan, Sheila K. Singh, Robin M. Hallett, Branavan Manoranjan, Minomi Subapanditha, Nicole McFarlane, Mohini Singh, Maleeha Qazi, Sujeivan Mahendram, Neha Garg, Parvez Vora, and T. Davis

Subjects
Oncology, medicine.medical_specialty, Neurology, Recurrent Childhood Medulloblastoma, business.industry, BMI1, Internal medicine, Medicine, macromolecular substances, Neurology (clinical), General Medicine, business
Abstract

Medulloblastoma (MB) is the most common malignant pediatric brain tumour, and is categorized into four molecular subgroups, with Group 3 MB having the worst prognosis due to the highest rate of metastatic dissemination and relapse. In this work, we describe the epigenetic regulator Bmi1 as a novel therapeutic target for treatment of recurrent Group 3 MB. Through comparative profiling of primary and recurrent MB, we show that Bmi1 defines a treatment-refractory cell population that is uniquely targetable by a novel class of small molecule inhibitors. We have optimized an in vivo mouse-adapted therapy model that has the advantage of generating recurrent, human, treatment-refractory MBs. Our preliminary studies showed that although chemoradiotherapy administered to mice engrafted with human MB showed reduction in tumour size, Bmi1 expression was enriched in the post-treatment residual tumour. Furthermore, we found that knockdown of Bmi1 in human recurrent MB cells decreases proliferation and self-renewing capacities of MB cells in vitro as well as both tumour size and extent of spinal leptomeningeal metastases in vivo. Oral administration of a potent Bmi1 inhibitor, PTC 028, resulted in a marked reduction in tumour burden and an increased survival in treatment cohort. Bmi1 inhibitors showed high specificity for MB cells and spared normal human neural stem cells, when treated with doses relevant for MB cells. As Group 3 medulloblastoma is often metastatic and uniformly fatal at recurrence, with no current or planned trials of targeted therapy, an efficacious agent such as Bmi1 inhibitor could be rapidly transitioned to clinical trials.

Published
2016
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153. Sleep Apnea in End-Stage Renal Disease Patients on Hemodialysis and Continuous Ambulatory Peritoneal Dialysis

Author

M Hallett, Peter C. Farrell, S Burden, J Mahony, and D Stewart

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, Polysomnography, medicine.medical_treatment, Population, Biomedical Engineering, Biophysics, Bioengineering, urologic and male genital diseases, End stage renal disease, Biomaterials, Sleep Apnea Syndromes, Peritoneal Dialysis, Continuous Ambulatory, Renal Dialysis, Risk Factors, Internal medicine, medicine, Humans, education, Dialysis, Aged, education.field_of_study, medicine.diagnostic_test, business.industry, Continuous ambulatory peritoneal dialysis, Sleep apnea, General Medicine, Middle Aged, medicine.disease, Obstructive sleep apnea, Kidney Failure, Chronic, Female, Hemodialysis, business
Abstract

Fifteen unselected end-stage renal disease patients (nine hemodialysis [HD] and six continuous ambulatory peritoneal dialysis [CAPD]) were randomly selected from four Sydney metropolitan dialysis centers for sleep assessment by full polysomnography. Four of six CAPD patients and eight of nine HD patients were found to have clinically significant obstructive sleep apnea. An additional 21 unselected patients (10 CAPD and 11 HD patients) were assessed using overnight home monitoring of nasal airflow and arterial oxygen saturation. Of these, 8 of the 11 HD and 7 of the 10 CAPD patients were found to have obstructive sleep apnea. These data confirm the high incidence of obstructive sleep apnea in the end-stage renal disease population at large. Screening for obstructive sleep apnea should become a routine part of the management of these patients.

Published
1995
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154. Abstract 2680: Development and application of a novel model of human lung-to-brain metastasis: identification of TWIST2 and SPOCK1 as unique regulators of brain metastases

Author

John Hassell, Jason Moffat, Chitra Venugopal, Kathrin Durrer, Igor Jurisica, Amy Hin Yan Tong, Robin M. Hallett, David Bakhshinyan, Manvir Dhillon, Sujeivan Mahendram, Tomas Tokar, Kevin R. Brown, Nicole McFarlane, Mohini Singh, and Sheila K. Singh

Subjects
Oncology, Cancer Research, medicine.medical_specialty, education.field_of_study, business.industry, Population, Cancer, Gene signature, medicine.disease, Primary tumor, Metastasis, Cancer stem cell, Internal medicine, Medicine, business, Lung cancer, education, Brain metastasis
Abstract

Brain Metastases (BM) are the most common type of cerebral tumor in adult, occurring at a rate ten times greater than that of primary brain cancers. The inherent properties of a primary tumor cell capable of initiating a BM resemble that of a cancer stem cell (CSC). Previous work conducted in our lab identified a CSC population within lung-derived BM. We hypothesize that a subgroup of CSC-like cells, termed brain metastasis-initiating cells (BMICs), are responsible for the initiation of BM and are identifiable by an exclusive subset of genes that regulate self-renewal and metastasis. Despite the prevalence and lethality of BM, there is no clinically relevant model that fully reflects metastasis in patients. The selection of an appropriate metastatic in vivo model is crucial for the identification of genes that regulate BM formation, prognostic and/or predictive markers, and evaluation of anti-metastatic therapeutics. We recently generated a novel human-mouse xenotransplantation model of BM that allows for interrogation of each phase of the metastatic process from lung to brain, through injection of human patient-derived GFP-expressing BMICs into immunocompromised mice via three routes: 1) intracranial (IC), 2) intrathoracic (IT) and 3) intravascular/intracardiac (IV). GFP+ BMICs were harvested from the lungs and/or brains from each injection route, and RNA was submitted for microarray analysis to identify a unique metastatic and tissue-specific gene signature from BMICs isolated from IT injections. We performed RNA interference screens in vitro and in vivo on BMIC lines against 150 genes implicated in BM formation in order to identify genes involved in self-renewal, tumor initiation and metastasis. We validated two top hits, TWIST2 and SPOCK1, using our novel BM mouse model, and determined that their knockdown functionally blocked BM formation. Future work will examine the expression of these genes in primary lung FFPE samples to determine if they are predictive biomarkers of lung-to-brain metastasis in prospective cohorts of newly diagnosed lung cancer patients, and to determine their potential as therapeutic targets. Citation Format: Sheila K. Singh, Mohini Singh, Chitra Venugopal, Nicole McFarlane, David Bakhshinyan, Manvir Dhillon, Sujeivan Mahendram, Kevin Brown, Amy Tong, Kathrin Durrer, Tomas Tokar, Robin Hallett, John Hassell, Igor Jurisica, Jason Moffat. Development and application of a novel model of human lung-to-brain metastasis: identification of TWIST2 and SPOCK1 as unique regulators of brain metastases. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2680.

Published
2016
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155. Abstract 2475: Bmi1 is a therapeutic target in recurrent medulloblastoma

Author

Branavan Manornajan, Kevin Xin Wang, Chitra Venugopal, Neha Garg, Sheila K. Singh, Robin M. Hallett, Thomas P. Davis, David Bakhshinyan, Siddhartha Mitra, Michael D. Taylor, David L. Kaplan, Yoon Jae Cho, and Vijay Ramaswamy

Subjects
Oncology, Medulloblastoma, Clinical Oncology, Cancer Research, medicine.medical_specialty, education.field_of_study, Pathology, business.industry, medicine.medical_treatment, Population, Recurrent Medulloblastoma, medicine.disease, Primary tumor, Targeted therapy, Clinical trial, BMI1, Internal medicine, Medicine, business, education
Abstract

We describe the epigenetic regulator Bmi1 as a novel therapeutic target for the treatment of recurrent human Group 3 medulloblastoma, a childhood brain tumor for which there is virtually no treatment option beyond palliation. Through comparative profiling of primary and recurrent medulloblastoma, we show that Bmi1 defines a treatment-refractory cell population that is uniquely targetable by a novel class of small molecule inhibitors. When administered to mice xenografted with patient tumors, we observed significant reduction in tumor burden and increased mouse survival, without neurotoxicity. As Group 3 medulloblastoma is often metastatic and uniformly fatal at recurrence, with no current or planned trials of targeted therapy, an efficacious targeted agent would be rapidly transitioned to clinical trials. Current clinical trials for recurrent medulloblastoma patients who no longer respond to risk-adapted therapy are based on genomic profiles of primary, treatment-naïve tumors. These approaches will provide limited clinical benefit for patients since recurrent metastatic Group 3 medulloblastomas are highly genetically divergent from their primary tumor. Our experimental approach defines a tractable target, the epigenetic regulator Bmi1, which characterizes not only recurrent medulloblastoma, but many other metastatic and treatment-resistant cancers. As future clinical oncology trials will most likely begin with relapsed patients, therapeutic targets from comparative analyses in primary and matched-recurrent tumors offer the greatest clinical yield and may be readily translated to the patient bedside. Citation Format: Sheila K. Singh, Neha Garg, Branavan Manornajan, David Bakhshinyan, Chitra Venugopal, Robin Hallett, Kevin Xin Wang, Vijay Ramaswamy, Yoon-Jae Cho, Siddhartha Mitra, David Kaplan, Thomas Davis, Michael Taylor. Bmi1 is a therapeutic target in recurrent medulloblastoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2475.

Published
2016
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156. Psychogenic (functional) movement disorders: Medico-legal context

Author

M. Hallett

Subjects
medicine.medical_specialty, Movement disorders, Context (language use), medicine.disease, Factitious disorder, Sensory Systems, Neurology, Malingering, Physiology (medical), medicine, Etiology, Psychogenic disease, Neurology (clinical), medicine.symptom, Functional movement disorder, Psychology, Psychiatry, Disability insurance, Clinical psychology
Abstract

Psychogenic (or functional) movement disorders are disorders of presumed psychiatric etiology, although the pathophysiology is not completely known. Most are conversion disorders and movements are involuntary. Some patients have factitious disorder or malingering, when the movements are voluntary. Factitious disorder also has a psychiatric etiology, but malingering is goal directed behavior without psychiatric disturbance. Most authorities believe that these patients are rare, but that we cannot easily separate them from the large majority with conversion. Hence, generally all are considered to have conversion. The diagnosis of factitious and malingering could be accomplished if physicians had a good test for lying, but this is not available. Secret surveillance can be helpful, but physicians generally don’t do this. Are such patients disabled? Studies have confirmed a high level of physical and mental disability, and the patients have a poor prognosis. Hence, it would be reasonable to support disability insurance. Patients with malingering should not be entitled, but most patients are not malingerers. If a functional movement disorder arises after an accident, should they get compensation. Given that this is a real disorder and the accident triggers the disorder, the answer should be yes.

Published
2016
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157. FoxG1 interacts with Bmi1 to regulate self-renewal and tumorigenicity of medulloblastoma stem cells

Author

Cynthia Hawkins, Robin M. Hallett, Xin Wang, Colleen M. Foster, Stephen C. Mack, Branavan Manoranjan, Chitra Venugopal, Sara M. Nolte, Christopher Dunham, Nicole McFarlane, John A. Hassell, Joanna Triscott, Sandra E. Dunn, Cathy Lee, Sheila K. Singh, Katrin Scheinemann, Thorsteinn Gunnarsson, and Michael D. Taylor

Subjects
Cell, Nerve Tissue Proteins, Tumor initiation, Cell Growth Processes, Mice, SCID, Biology, Mice, Mice, Inbred NOD, Cell Line, Tumor, medicine, Transcriptional regulation, Animals, Humans, Cerebellar Neoplasms, Promoter Regions, Genetic, Medulloblastoma, Polycomb Repressive Complex 1, Wnt signaling pathway, Forkhead Transcription Factors, Cell Biology, medicine.disease, Prognosis, Phenotype, medicine.anatomical_structure, BMI1, Immunology, Cancer research, Neoplastic Stem Cells, Molecular Medicine, Stem cell, Transcriptome, Developmental Biology, Signal Transduction
Abstract

Brain tumors represent the leading cause of childhood cancer mortality, of which medulloblastoma (MB) is the most frequent malignant tumor. Recent studies have demonstrated the presence of several MB molecular subgroups, each distinct in terms of prognosis and predicted therapeutic response. Groups 1 and 2 are characterized by relatively good clinical outcomes and activation of the Wnt and Shh pathways, respectively. In contrast, groups 3 and 4 (“non-Shh/Wnt MBs”) are distinguished by metastatic disease, poor patient outcome, and lack a molecular pathway phenotype. Current gene expression platforms have not detected brain tumor-initiating cell (BTIC) self-renewal genes in groups 3 and 4 MBs as BTICs typically comprise a minority of tumor cells and may therefore go undetected on bulk tumor analyses. Since increasing BTIC frequency has been associated with increasing tumor aggressiveness and poor patient outcome, we investigated the subgroup-specific gene expression profile of candidate stem cell genes within 251 primary human MBs from four nonoverlapping MB transcriptional databases (Amsterdam, Memphis, Toronto, Boston) and 74 NanoString-subgrouped MBs (Vancouver). We assessed the functional relevance of two genes, FoxG1 and Bmi1, which were significantly enriched in non-Shh/Wnt MBs and showed these genes to mediate MB stem cell self-renewal and tumor initiation in mice. We also identified their transcriptional regulation through reciprocal promoter occupancy in CD15+ MB stem cells. Our work demonstrates the application of stem cell data gathered from genomic platforms to guide functional BTIC assays, which may then be used to develop novel BTIC self-renewal mechanisms amenable to therapeutic targeting.

Published
2012

158. A Gene Signature for Predicting Outcome in Patients with Basal-like Breast Cancer

Author

Robin M. Hallett, Anna Dvorkin-Gheva, Anita Bane, and John A. Hassell

Subjects
Oncology, CA15-3, medicine.medical_specialty, Multidisciplinary, business.industry, Gene Expression Profiling, Cancer, Breast Neoplasms, Disease, medicine.disease, Prognosis, Article, Gene expression profiling, Basal (phylogenetics), Breast cancer, Text mining, Carcinoma, Basal Cell, Recurrence, Internal medicine, medicine, Carcinoma, Humans, Female, business, Oligonucleotide Array Sequence Analysis
Abstract

Basal-like breast cancer is a molecular subtype of breast cancer with a poor prognosis. Follow-up studies of long-term outcome in these patients, demonstrates they can be separated into two clinical groups: those who succumb to their disease within the first 5 years and those expected to show excellent long term survival. Currently available clinical/histopathological variables as well as molecular signatures show little capacity to identify basal breast cancer patients with either a high or low risk of disease relapse. Using data derived from 85 basal-like breast cancer patients, we identified a 14-gene signature, which we subsequently validated on an additional 49 basal breast cancer patient set. The ability to distinguish between these two sub-groups of basal breast cancer patients at the time of initial diagnosis would permit tailoring aggressive therapeutic regimens to those patients with a poor prognosis and conversely avoid such therapy in low risk patients.

Published
2012

159. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain

Author

H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. Navon, Giovanni Antonini, K. Al Moutaery, E. Chamas, R. Schönhuber, M. Giannini, B. Debilly, I. Labatut, H. Henon, J. A. Egido, M. Baudrimont, J. N. Lorenzo, J. E. C. Bromberg, R. Antonacci, J. J. Vilchez, T. Moulin, B. Rautenstrauss, Giovanni Meola, J. Noth, S Mammi, P. Laforet, F. Lopez, C. Gehring, S. Bort, G. Rancurel, D. Decamps, S. Kostadinova, Y. Shapira, B. Neundoerfer, D. Chavrot, M. Solimena, J. P. Salier, W. Deberdt, R. Hoff-Jörgensen, A. Messina, S. Meairs, G. Rosoklija, E. Nelis, I. Bertran, C. Ertekin, J. Lohmeyer, Mitermayer Galvao dos Reis, L. Calo, E. Maccagnano, A. P. Hays, J. Verlooy, M. G. Forno, T. Blanco, L. Bail, Gabriella Silvestri, J. Montero, F. Bertrand, R. T. Ghnassia, C. Besses, T. Sereghy, F. Shalit, G. Bogliun, S. Braghi, St. Baykouchev, C. Franke, A. Lasa, L. C. Archard, J. Kriebel, S. Shaunak, M. Nocito, Alexander Tsiskaridze, E. Manfredini, T. Seigal, David G. Gadian, M. Barlas, J. D. Degos, C. Seeber, J. Caemert, J. L. Mas, R. B. Pepinsky, M. G. 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Meinardi, F. Carrara, J. Kuehnen, C. Peiro, H. Lassmann, K. Skovgaard Olsen, A. McDonald, L. Sciulli, A. Cobo, A. Monticelli, B. Conrad, J. Bagunya, J. Benitez, V. Desnizza, B. Dupont, O. Delrieu, D. Moraes, J. J. Heimans, F. Garcia Rio, M. Matsumto, A. Fernandez, R. Nermni, R. Chalmers, M. J. Marchau, F. Aguado, P. Velupillai, P. J. Martin, P. Tassan, V. Demarin, A. Engelien, T. Gerriets, Comar, J. L. Carrasco, J. P. Pruvo, A. Lopez de Munain, D. Pavitt, J. Alarcon, Chris H. Polman, B. Guldin, N. Yeni, Hartmut Brückmann, N. Wilczak, H. Szwed, R. Causaran, G. Kyriazis, M. E. Westarp, M. Gasparini, N. Pecora, J. M. Roda, E. Lang, V. Scaioli, David R. Fish, D. Caputo, O. Gratzl, R. Mercelis, A. Perretti, G. Steimetz, I. Link, C. Rigoletto, A. Catafau, G. Lucotte, M. Buti, G. Fagiolari, A. Piqueras, C. Godinot, J. C. Meurice, Erodriguez J. Dominigo, F. Lionnet, H. Grzelec, David J. Brooks, P. M. G. Munro, F. X. Weilbach, M. Maiwald, W. Split, B. Widjaja-Cramer, V. Ozturk, J. Colas, E. Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. Santoro, J. Roda, A. Bordoni, D. J. Taylor, S. Ertas, H. H. Emmen, J. Vichez, V. BesanÇon, R. E. Passingham, M. L. Malosio, A. Vérier, M. Bamberg, A. W. Hansen, E. Mostacero, G. Gaudriault, Marie Vidailhet, B. Birebent, K. Strijckmans, F. Giannini, T. Kammer, I. Araujo, J. Nowicki, E. Nikolov, A. Hutzelmann, R. Gherardi, J. Verroust, L. Austoni, A. Scheller, A. Vazquez, S. Matheron, H. Holthausen, J. M. Gerard, M. Bataillard, S. Dethy, V. H. Patterson, V. Ivanez, N. P. Hirsch, F. Ozer, M. Sutter, C. Jacomet, M. Mora, Bruno Colombo, A. Sarropoulos, T. H. Papapetropoulos, M. Schwarz, D. S. Dinner, N. Acarin, B. Iandolo, J. O. Riis, P. R. J. Barnes, F. Taroni, J. Kazenwadel, L. Torre, A. Lugaresi, I. L. Henriques, S. Pauli, S. Alfonso, Pedro Quesada, A. S. T. Planting, J. M. Castilla, Thomas Gasser, M. Van der Linden, A. Alfaro, E. Nobile-Orazio, G. Popova, W. Vaalburg, F. G. A. van der Mech, L. Williams, F. Medina, J. P. Vernant, J. Yaouanq, B. Storch-Hagenlocher, A. Potemkowski, R. Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. Bauermann, Nereo Bresolin, J. Vallée, B. C. Jacobs, A. Campos, Werner Poewe, J. A. Villanueva, A. W. Kornhuber, A. Malafosse, E. Diez-Tejedor, G. Jungreia, M. J. A. Puchner, A. Komiyama, O. Saribas, V. Volpini, L. Geremia, S. Bressi, A. Nibbio, Timothy E. Bates, T. z. Tzonev, E. Ideman, G. A. Damlacik, G. Martino, G. Crepaldi, T. Martino, Kjell Någren, E. Idiman, D. Samuel, J. M. Perez Trullen, Y. van der Graaf, J. O. Thorell, M. J. M. Dupuis, E. Sieber, R. D'Alessandro, C. Cazzaniga, J. Faiss, A. Tanguy, A. Schick, I. Hoksergen, A. Cardozo, R. Shakarishvili, G. K. Wennlng, J. L. Marti-Vilalta, J. Weissenbach, I. L. Simone, Amalia C. Bruni, Darius J. Adams, C. Weiller, A. Pietrangeli, F. Croria, C. Vigo-Pelfrey, Patricia Limousin, A. Ducros, G. Conti, O. Lindvall, E. Richter, M. Zuffi, A. Nappo, T. Riise, J. Wijdenes, M. J. Fernandez, J. Rosell, P. Vermersh, S. Servidei, M. S. C. Verdugo, F. Gouttiere, W. Solbach, M. Malbezin, I. S. Watanabe, A. Tumac, W. I. McDonald, D. A. Butterfield, P. P. Costa, F. deRino, F. Bamonti, J. M. Cesar, C. H. Lahoz, I. Mosely, M. Starck, M. H. Lemaitre, K. M. Stephan, S. Tex, R. Bokonjic, I. Mollee, L. Pastena, M. Gutierrez, F. Boiler, M. C. Martinez-Para, M. Velicogna, O. Obuz, A. Grinspan, M. Guarino, L. M. Cartier, E. Ruiz, D. Gambi, S. Messina, M. Villa, Michael G. Hanna, J. Valk, Leone Pascual, M. Clanet, Z. Argov, B. Ryniewicz, E. Magni, B. Berlanga, K. S. Wong, C. Gellera, C. Prevost, F. Gonzalez-Huix, R. Petraroli, J. E. G. Benedikz, I. Kojder, C. Bommelaer, L. Perusse, M. R. Bangioanni, Guy M. McKhann, A. Molina, C. Fresquet, E. Sindern, Florence Pasquier, M. J. Rosas, M. Altieri, O. Simoncini, M. Koutroumanidis, C. A. F. Tulleken, M. Dary-Auriol, S. Oueslati, H. Kruyer, I. Nishisho, C. R. Horning, A. Vital, G. V. Czettritz, J. Ph. Neau, B. Mihout, A. Ameri, M. Francis, S. Quasthoff, D. Taussig, S. Blunt, P. Valentin, C. Y. Gao, O. Heinzlef, H. d'Allens, C. Coudero, M. Erfas, G. Borghero, P. J. Modrego Pardo, M. C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg

Subjects
Neurology, business.industry, Media studies, Library science, Medicine, Neurology (clinical), business
Published
1994
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160. Small molecule antagonists of the Wnt/β-catenin signaling pathway target breast tumor-initiating cells in a Her2/Neu mouse model of breast cancer

Author

Andrew O. Giacomelli, John A. Hassell, Robin M. Hallett, Maria Kondratyev, Allison M.L. Nixon, Dora Ilieva, and Adele Girgis-Gabardo

Subjects
Beta-catenin, Receptor, ErbB-2, Science, Breast Neoplasms, Pyrimidinones, HER2/neu, Mice, Breast cancer, Mammary Glands, Animal, Model Organisms, Chemical Biology, medicine, Animals, skin and connective tissue diseases, Receptor, Wnt Signaling Pathway, Biology, Cells, Cultured, beta Catenin, Cell Proliferation, Multidisciplinary, biology, Cell growth, Triazines, Gene Expression Profiling, Wnt signaling pathway, Cancer, Epithelial Cells, Genomics, Animal Models, medicine.disease, Wnt Proteins, Disease Models, Animal, Chemistry, Oncology, Immunology, Cancer research, biology.protein, Neoplastic Stem Cells, Medicine, Female, Stem cell, Medicinal Chemistry, Research Article, Developmental Biology
Abstract

BackgroundRecent evidence suggests that human breast cancer is sustained by a minor subpopulation of breast tumor-initiating cells (BTIC), which confer resistance to anticancer therapies and consequently must be eradicated to achieve durable breast cancer cure.Methods/findingsTo identify signaling pathways that might be targeted to eliminate BTIC, while sparing their normal stem and progenitor cell counterparts, we performed global gene expression profiling of BTIC- and mammary epithelial stem/progenitor cell- enriched cultures derived from mouse mammary tumors and mammary glands, respectively. Such analyses suggested a role for the Wnt/Beta-catenin signaling pathway in maintaining the viability and or sustaining the self-renewal of BTICs in vitro. To determine whether the Wnt/Beta-catenin pathway played a role in BTIC processes we employed a chemical genomics approach. We found that pharmacological inhibitors of Wnt/β-catenin signaling inhibited sphere- and colony-formation by primary breast tumor cells and primary mammary epithelial cells, as well as by tumorsphere- and mammosphere-derived cells. Serial assays of self-renewal in vitro revealed that the Wnt/Beta-catenin signaling inhibitor PKF118-310 irreversibly affected BTIC, whereas it functioned reversibly to suspend the self-renewal of mammary epithelial stem/progenitor cells. Incubation of primary tumor cells in vitro with PKF118-310 eliminated their capacity to subsequently seed tumor growth after transplant into syngeneic mice. Administration of PKF118-310 to tumor-bearing mice halted tumor growth in vivo. Moreover, viable tumor cells harvested from PKF118-310 treated mice were unable to seed the growth of secondary tumors after transplant.ConclusionsThese studies demonstrate that inhibitors of Wnt/β-catenin signaling eradicated BTIC in vitro and in vivo and provide a compelling rationale for developing such antagonists for breast cancer therapy.

Published
2011

161. Identifying Mammary Epithelial Stem and Progenitor Cells

Author

John A. Hassell, Andrew O. Giacomelli, and Robin M. Hallett

Subjects
Mammary Epithelium, Amniotic epithelial cells, Myoepithelial cell, Involution (medicine), Stem cell, Progenitor cell, Biology, Fat pad, Adult stem cell, Cell biology
Abstract

The adult mouse mammary gland is composed of a branched ductal epithelium, which is embedded in a fatty stroma, termed the fat pad, comprising largely adipocytes but also fibroblasts, macrophages, and endothelial cells (Daniel and Silberstein 1987; Sakakura 1991). The various branches of the mammary tree are connected to a primary duct that terminates at the skin surface through the nipple. The mammary epithelium initially develops during embryogenesis from the ectoderm by cell migration and proliferation thus forming mammary buds, which subsequently sprout a rudimentary ductal tree that is present at birth (Sakakura 1987). Further mammary gland development is completed postnatally in defined stages (puberty, pregnancy, lactation, and involution), which are coupled to the sexual maturation and reproductive status of the animal (Fig. 12.1) (Hennighausen and Robinson 1998).

Published
2011
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162. Alteration of brain functional network at rest and in response to YMCA physical stress test in concussed athletes: RsFMRI study

Author

S.M. Slobounov, M. Gay, K. Zhang, B. Johnson, D. Pennell, W. Sebastianelli, S. Horovitz, and M. Hallett

Subjects
Adult, Male, Traumatic brain injury, Cognitive Neuroscience, Rest, Population, Poison control, Brain damage, Brain mapping, Article, Neuroimaging, medicine, Humans, education, Brain Concussion, education.field_of_study, Brain Mapping, Neuronal Plasticity, Resting state fMRI, Brain, medicine.disease, Adaptation, Physiological, Dorsolateral prefrontal cortex, medicine.anatomical_structure, Neurology, Athletic Injuries, Exercise Test, Female, medicine.symptom, Nerve Net, Psychology, Neuroscience
Abstract

There is still controversy in the literature whether a single episode of mild traumatic brain injury (mTBI) results in short- and/or long-term functional and structural deficits in the concussed brain. With the inability of traditional brain imaging techniques to properly assess the severity of brain damage induced by a concussive blow, there is hope that more advanced applications such as resting state functional magnetic resonance imaging (rsFMRI) will be more specific in accurately diagnosing mTBI. In this rsFMRI study, we examined 17 subjects 10 +/− 2 days post-sports-related mTBI and 17 age-matched normal volunteers (NVs) to investigate the possibility that the integrity of the of resting state brain network is disrupted following a single concussive blow. We hypothesized that advanced brain imaging techniques may reveal subtle alterations of functional brain connections in asymptomatic mTBI subjects. There are several findings of interest. All mTBI subjects were asymptomatic based upon clinical evaluation and neuropsychological (NP) assessments prior to the MRI session. The mTBI subjects revealed a disrupted functional network both at rest and in response to the YMCA physical stress test. Specifically, interhemispheric connectivity was significantly reduced in the primary visual cortex, hippocampal and dorsolateral prefrontal cortex networks (p

Published
2010

163. E2F1 and KIAA0191 expression predicts breast cancer patient survival

Author

Robin M. Hallett and John A. Hassell

Subjects
Medicine(all), business.industry, Biochemistry, Genetics and Molecular Biology(all), lcsh:R, lcsh:Medicine, Context (language use), Patient survival, General Medicine, Bioinformatics, medicine.disease, General Biochemistry, Genetics and Molecular Biology, Gene expression profiling, Breast cancer, Expression (architecture), lcsh:Biology (General), medicine, E2F1, Tree based, business, lcsh:Science (General), lcsh:QH301-705.5, Survival analysis, lcsh:Q1-390, Research Article
Abstract

Background Gene expression profiling of human breast tumors has uncovered several molecular signatures that can divide breast cancer patients into good and poor outcome groups. However, these signatures typically comprise many genes (~50-100), and the prognostic tests associated with identifying these signatures in patient tumor specimens require complicated methods, which are not routinely available in most hospital pathology laboratories, thus limiting their use. Hence, there is a need for more practical methods to predict patient survival. Methods We modified a feature selection algorithm and used survival analysis to derive a 2-gene signature that accurately predicts breast cancer patient survival. Results We developed a tree based decision method that segregated patients into various risk groups using KIAA0191 expression in the context of E2F1 expression levels. This approach led to highly accurate survival predictions in a large cohort of breast cancer patients using only a 2-gene signature. Conclusions Our observations suggest a possible relationship between E2F1 and KIAA0191 expression that is relevant to the pathogenesis of breast cancer. Furthermore, our findings raise the prospect that the practicality of patient prognosis methods may be improved by reducing the number of genes required for analysis. Indeed, our E2F1/KIAA0191 2-gene signature would be highly amenable for an immunohistochemistry based test, which is commonly used in hospital laboratories.

Published
2010

164. An algorithm to discover gene signatures with predictive potential

Author

Robin M. Hallett, John A. Hassell, Christine M. Gabardo, and Anna Dvorkin

Subjects
Cancer Research, Time Factors, Breast Neoplasms, Bioinformatics, lcsh:RC254-282, Metastasis, Risk groups, Text mining, Breast cancer, Predictive Value of Tests, medicine, Humans, Genetic Testing, Precision Medicine, Gene, Oligonucleotide Array Sequence Analysis, business.industry, Gene Expression Profiling, Patient Selection, Research, Reproducibility of Results, Cancer, Middle Aged, Gene signature, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, Survival Analysis, Gene Expression Regulation, Neoplastic, Gene expression profiling, Treatment Outcome, ROC Curve, Oncology, Female, business, Algorithm, Algorithms
Abstract

Background The advent of global gene expression profiling has generated unprecedented insight into our molecular understanding of cancer, including breast cancer. For example, human breast cancer patients display significant diversity in terms of their survival, recurrence, metastasis as well as response to treatment. These patient outcomes can be predicted by the transcriptional programs of their individual breast tumors. Predictive gene signatures allow us to correctly classify human breast tumors into various risk groups as well as to more accurately target therapy to ensure more durable cancer treatment. Results Here we present a novel algorithm to generate gene signatures with predictive potential. The method first classifies the expression intensity for each gene as determined by global gene expression profiling as low, average or high. The matrix containing the classified data for each gene is then used to score the expression of each gene based its individual ability to predict the patient characteristic of interest. Finally, all examined genes are ranked based on their predictive ability and the most highly ranked genes are included in the master gene signature, which is then ready for use as a predictor. This method was used to accurately predict the survival outcomes in a cohort of human breast cancer patients. Conclusions We confirmed the capacity of our algorithm to generate gene signatures with bona fide predictive ability. The simplicity of our algorithm will enable biological researchers to quickly generate valuable gene signatures without specialized software or extensive bioinformatics training.

Published
2010
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165. Clinical features of patients with blepharospasm: a report of 240 patients

Author

E L, Peckham, G, Lopez, E A, Shamim, S Pirio, Richardson, S, Sanku, R, Malkani, M, Stacy, P, Mahant, A, Crawley, A, Singleton, and M, Hallett

Subjects
Adult, Male, Dystonic Disorders, Risk Factors, Blepharospasm, Humans, Female, Age of Onset, Middle Aged, Article, Pedigree
Abstract

To characterize patients with benign essential blepharospasm (BEB) by diagnosis, environmental risk factors, and family history.Two hundred and forty patients with BEB were evaluated through a clinical examination and questionnaire. The questionnaire reviewed personal medical history, demographic factors, risk factors for the development of blepharospasm and family history of dystonia and other neurological conditions.Benign essential blepharospasm was more commonly found in women (2.8:1) and 93% of the patients were Caucasian. Fifty percent had pure BEB, 31% had BEB/Meige's syndrome, and 4% had BEB and eyelid opening apraxia (+/- Meige's syndrome). A minority of patients reported preceding photophobia (25%) or other eye conditions (22%). The majority were non-smokers, had no exposure to anti-emetic or antipsychotic agents, had a normal birth history, and had no history of head trauma. Seventy-two percent did report a stressful event immediately prior to the development of symptoms. Treatments reported included botulinum toxin (BoNT), oral medications, surgical procedures, and acupuncture. Thirty-two percent of patients reported a family history of focal dystonia, and BEB was the most commonly reported.This study confirms previous reports of usual age, sex, caffeine and tobacco use, and family history in patients with blepharospasm. New findings include a report on occupation, lower reports of preceding eye conditions and photophobia, and higher reported stressful events. Further, this study shows a change in treatment with an increase in BoNT use and decrease in surgical procedures.

Published
2010

167. Assessment: botulinum neurotoxin for the treatment of spasticity (an evidence-based review)

Author

D M, Simpson, J-M, Gracies, K, Graham, M, Hallett, J, Miyasaki, M, Naumann, B, Russman, L, Simpson, and Y, So

Subjects
Motor Neurons, Botulinum Toxins, Evidence-Based Medicine, Muscle Weakness, Neuromuscular Agents, Reflex, Abnormal, Muscle Spasticity, Outcome Assessment, Health Care, Humans, Reproducibility of Results, Muscle, Skeletal
Published
2009

168. The CDK inhibitor, R-roscovitine, promotes eosinophil apoptosis by down-regulation of Mcl-1

Author

Ana L. Alessandri, Adriano G. Rossi, Hugh J.M. Brady, John M. Hallett, Rodger Duffin, Mauro M. Teixeira, Sarah Fox, Tara A. Sheldrake, Morag C. Martin, Colette Meyer, Christopher Haslett, Andrew E. Leitch, and Ian Dransfield

Subjects
Biophysics, Down-Regulation, Inflammation, Apoptosis, Eosinophil, Biochemistry, chemistry.chemical_compound, Structural Biology, Cyclin-dependent kinase, Genetics, medicine, Roscovitine, Humans, Propidium iodide, R-roscovitine, Molecular Biology, Protein Kinase Inhibitors, Caspase, Membrane Potential, Mitochondrial, biology, Dose-Response Relationship, Drug, Kinase, Mcl-1, Cell Biology, Molecular biology, Caspase Inhibitors, Cyclin-Dependent Kinases, Mitochondria, Eosinophils, medicine.anatomical_structure, chemistry, Proto-Oncogene Proteins c-bcl-2, Purines, Caspases, biology.protein, Myeloid Cell Leukemia Sequence 1 Protein, medicine.symptom, CDK inhibitor
Abstract

Eosinophils are major players in inflammatory allergic diseases such as asthma, hay fever and eczema. Here we show that the cyclin-dependent kinase inhibitor (CDKi) R-roscovitine efficiently and rapidly induces human eosinophil apoptosis using flow cytometric analysis of annexin-V/propidium iodide staining, morphological analysis by light microscopy, transmission electron microscopy and Western immunoblotting for caspase-3 cleavage. We further dissect these observations by demonstrating that eosinophils treated with R-roscovitine lose mitochondrial membrane potential and the key survival protein Mcl-1 is down-regulated. This novel finding of efficacious induction of eosinophil apoptosis by CDKi drugs has potential as a strategy for driving resolution of eosinophilic inflammation.

Published
2009

169. Preface

Author

J. Jankovic, A. Albanese, M.Z. Atassi, J.O. Dolly, M. Hallett, and N.H. Mayer

Published
2009
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171. International Cooperative Ataxia Rating Scale for pharmacological assessment of the cerebellar syndrome. The Ataxia Neuropharmacology Committee of the World Federation of Neurology

Author

P. Trouillas, T. Takayanagi, M. Hallett, R. D. Currier, S. H. Subramony, K. Wessel, A. Bryer, H. C. Diener, S. Massaquoi, C. M. Gomez, P. Coutinho, M. B. Hamida, G. Campanella, L. Schut, D. Timann, J. Honnorat, N. Nighoghossian, B. Manyam, FILLA, ALESSANDRO, P., Trouilla, T., Takayanagi, M., Hallett, R. D., Currier, S. H., Subramony, K., Wessel, A., Bryer, H. C., Diener, S., Massaquoi, C. M., Gomez, P., Coutinho, M. B., Hamida, G., Campanella, Filla, Alessandro, L., Schut, D., Timann, J., Honnorat, N., Nighoghossian, and B., Manyam

Subjects
diagnosis/physiopathology, Gait, Cerebellar Ataxia, Movement, Posture, Walking, physiology, Oculomotor Muscle, physiology, Reference Standards, Speech Disorder, Reference Standards, Speech Disorders, physiopathology, Movement, diagnosis/physiopathology, Walking, physiopathology, Posture, Psychomotor Performance, Oculomotor Muscles, physiology, Humans, Joint, Tremor, Humans, Joints, diagnosis/physiopathology, Tremor, Gait, Psychomotor Performance
Abstract

Despite the involvement of cerebellar ataxia in a large variety of conditions and its frequent association with other neurological symptoms, the quantification of the specific core of the cerebellar syndrome is possible and useful in Neurology. Recent studies have shown that cerebellar ataxia might be sensitive to various types of pharmacological agents, but the scales used for assessment were all different. With the long-term goal of double-blind controlled trials-multicentric and international-an ad hoc Committee of the World Federation of Neurology has worked to propose a one-hundred-point semi-quantitative International Cooperative Ataxia Rating Scale (ICARS). The scale proposed involves a compartimentalized quantification of postural and stance disorders, limb ataxia, dysarthria and oculomotor disorders, in order that a subscore concerning these symptoms may be separately studied. The weight of each symptomatologic compartment has been carefully designed. The members of the Committee agreed upon precise definitions of the tests, to minimize interobserver variations. The validation of this scale is in progress.

Published
1997

172. Novel pharmacological strategies for driving inflammatory cell apoptosis and enhancing the resolution of inflammation

Author

Rodger Duffin, Andrew E. Leitch, Adriano G. Rossi, John M. Hallett, Christopher Haslett, and Nicola A. Riley

Subjects
Programmed cell death, MAP Kinase Signaling System, Anti-Inflammatory Agents, Inflammation, Apoptosis, Granulocyte, Toxicology, Inflammatory bowel disease, Pathogenesis, Phosphatidylinositol 3-Kinases, Downregulation and upregulation, Phagocytosis, medicine, Animals, Humans, Pharmacology, business.industry, medicine.disease, Cyclin-Dependent Kinases, medicine.anatomical_structure, Proto-Oncogene Proteins c-bcl-2, Rheumatoid arthritis, Immunology, medicine.symptom, business, Granulocytes, Signal Transduction
Abstract

Resolution of inflammation requires the effective downregulation of key inflammatory cells such as neutrophils and eosinophils, which normally undergo programmed cell death (apoptosis) to enable their detection and removal by phagocytes such as macrophages. Dysregulation of this process is thought to contribute to the pathogenesis and progression of chronic inflammatory disorders such as chronic obstructive pulmonary disease, asthma, rheumatoid arthritis, allergic rhinitis and inflammatory bowel disease. Importantly, knowledge of the signalling pathways responsible for the induction and execution of granulocyte apoptosis and the phagocytic removal of apoptotic cells continues to increase and, with it, the potential for incisive pharmacological intervention. In this article, we highlight pharmacological strategies that could be used to drive the resolution of inflammation by augmenting apoptosis of inflammatory cells.

Published
2007

173. Predicting Movement: When, Which and Where

Author

O. Bai, C. Bonin, and M. Hallett

Subjects
Subjective impression, medicine.diagnostic_test, Movement (music), Speech recognition, media_common.quotation_subject, Work (physics), Magnetoencephalography, Electroencephalography, Bereitschaftspotential, Perception, medicine, Psychology, Brain–computer interface, media_common, Cognitive psychology
Abstract

People have the perception that prior to making a voluntary movement, there is an intention to move. The timing of this subjective impression has been measured using Libet's clock and is on average about 300 ms prior to EMG onset. EEG and MEG show activity prior to movement, and by the voltage measurement, there is a rising negativity called the Bereitschafts potential beginning about 1.5 s prior to EMG onset. This indicates that the brain mechanisms for generating a voluntary movement begin prior to the subjective intention, that is, unconsciously. If it were possible to detect relevant EEG signals with single events in real time, then it would be possible to identify that movement is being prepared prior to, or at least simultaneously with, the subjective experience. Work in our laboratory has been making progress in identifying EEG and MEG activity indicating the intention to move and which movement will be made. Such signals could be used to drive a brain-computer interface.

Published
2007
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174. A New Research Field and A New Society, Complex Medical Engineering

Author

M. Hallett and Jinglong Wu

Subjects
Biological systems engineering, business.industry, Complex system, Medicine, Engineering ethics, Robotics, Artificial intelligence, Health systems engineering, business, Complex problems, Health informatics, Field (computer science), Interdisciplinarity
Abstract

The human neural mechanism is a complex system. The solution of many neuroscience complex problems involves highly coordinated and highly interdisciplinary research efforts between neuroscientists and biomedical engineers. The neuroscience and the biomedical engineering are melded into a new international society, known as Institute of Complex Medical Engineering (ICME). Complex Medical Engineering (CME) consists of neuroscience, neurology, biomedical robotics and biomedical informatics, using medical and engineering methods to understand the complex system of human neural mechanisms, and to apply the basic findings to technology. The goal of ICME is to establish a new forum for this interdisciplinary field of neuroscientists and biomedical engineers to discuss their investigations in same conference (symposium), and publish their research work in one periodical. The CME can bridge the gap between medicine & engineering and science & technology. The CME focuses on the complex problems in the medicine and engineering fields, and tries to solve their problems in order to find simple theories and unique tools to help us to reach new understanding and help develop better methods of improving patients' lives.

Published
2007
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176. Peripheral nerve injuries

Author

M. Hallett

Subjects
Pathology, medicine.medical_specialty, medicine.anatomical_structure, Neurology, Peripheral nerve, business.industry, Peripheral nervous system, Medicine, Neurology (clinical), business
Published
2015
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177. E.01.01 Psychogenic movement disorders

Author

M. Hallett

Subjects
Pharmacology, medicine.medical_specialty, Movement disorders, business.industry, Psychiatry and Mental health, Neurology, medicine, Psychogenic disease, Pharmacology (medical), Neurology (clinical), medicine.symptom, Psychiatry, business, Biological Psychiatry
Published
2015
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178. Expression of thyroid hormone receptor alpha (THRα) isoforms in triple negative breast cancer (TNBC)

Author

Robin M. Hallett, Katarzyna J. Jerzak, Anita Bane, Sukhbinder Dhesy-Thind, Kathleen I. Pritchard, Jessica G. Cockburn, Gregory R. Pond, and John A. Hassell

Subjects
Gene isoform, Cancer Research, business.industry, Cell growth, medicine.disease, Breast cancer, Oncology, Thyroid hormone receptor alpha, Thyroid hormones, medicine, Cancer research, business, Receptor, Triple-negative breast cancer
Abstract

e12082 Background: Thyroid hormones (THs) and their associated receptors may play a role in breast cancer progression given their promotion of cell growth and proliferation. THRα2 expression in ER ...

Published
2015
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179. MB-15 * ACTIVATED Wnt SIGNALING TARGETS Sox2+ TREATMENT-REFRACTORY Shh-DEPENDENT MEDULLOBLASTOMA STEM CELLS

Author

Sujeivan Mahendram, Branavan Manoranjan, Robin M. Hallett, Bradley W. Doble, David Bakhshinyan, Nicole McFarlane, Thusyanth Vijayakumar, Sheila K. Singh, Chitra Venugopal, John A. Hassell, and Steven Moreira

Subjects
Medulloblastoma, Cancer Research, Pathology, medicine.medical_specialty, biology, Wnt signaling pathway, medicine.disease, Oncology, SOX2, In vivo, GLI1, embryonic structures, biology.protein, Cancer research, medicine, Neurology (clinical), Sonic hedgehog, Stem cell, Signal transduction, Abstracts from the 3rd Biennial Conference on Pediatric Neuro-Oncology Basic and Translational Research
Abstract

Medulloblastoma (MB) represents the most frequent malignant pediatric brain tumor. Since MBs characterized by activated sonic hedgehog (Shh) signaling continue to pose significant challenges due to treatment resistance, we aimed to prospectively identify, characterize, and target treatment-refractory Shh-dependent MB stem cells. Using gene expression and clinical outcome data from 325 primary human MBs, we identified Sox2high patients to exclusively represent treatment-refractory Shh MB. In order to prospectively characterize Sox2+ MB stem cells, we took advantage of the CRISPR-Cas9-nickase system to knock-in a P2A-mAG sequence into the Sox2 locus. By using our Sox2 reporter we show enchanced and reduced Sox2 expression in response to small molecule Shh agonists and inhibitors, respectively. Subsequent co-enrichment of Gli1/2 and H3K4me3 at the Sox2 promoter confirmed Sox2 as a downstream target in MB. In order to establish the clinical significance of this mechanism, we treated xenografts with a modified COG ACNS0332 radio/chemo-therapy protocol and prospectively tracked the in vivo evolution of Sox2+ cells. Molecular and functional analyses following treatment yielded an increase in Sox2 expression and self-renewal potential. Given the excellent clinical outcome in Wnt-driven MB patients, we aimed to convert treatment-resistant Sox2high MB into an ostensibly benign tumor using small molecule Wnt agonists. Wnt treatment resulted in a xenograft survival advantage and complete eradication of Sox2+ MB cells. Our work demonstrates mechanistic insight into the regulation of Sox2 by the Shh pathway and the clinical importance of this interaction by identifying Sox2 as a marker of treatment-resistant Shh MB stem cells. Our treatment model has enabled us to prospectively track the evolution of Sox2+ cells in vivo and thereby target these cells upon relapse. We have futher provided evidence for a novel therapeutic approach in converting aggressive MBs into a clinically-treatable tumor, which may improve the overall survival of children with treatment-refractory Shh-dependent MB.

Published
2015
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180. Proton magnetic resonance spectroscopic imaging in cerebellar degeneration

Author

TEDESCHI, Gioacchino, A. BERTOLINO, SG MASSAQUOIUOI, G. CAMPBELL, NJ PATRONAS, BONAVITA, Simona, AS BARNETT, JR ALGER, M. HALLETT, Tedeschi, Gioacchino, A., Bertolino, Sg, Massaquoiuoi, G., Campbell, Nj, Patrona, Bonavita, Simona, As, Barnett, Jr, Alger, and M., Hallett

Published
1996

181. Pathophysiology of dystonia

Author

M, Hallett

Subjects
Dystonia, Neuronal Plasticity, Sensation, Animals, Humans, Muscle, Skeletal
Abstract

Understanding of the pathophysiology of dystonia derives primarily from studies of focal dystonias. Physiological investigations have revealed a number of abnormalities that may reflect the genetic substrate that predisposes certain individuals to develop dystonia. There is a loss of inhibition in the central nervous system, and a loss of surround inhibition specifically. Plasticity is increased, and there are sensory abnormalities. Which of these disorders is primary is uncertain.

Published
2006

182. Corticobulbar tracts

Author

M, Hallett and G, Cruccu

Subjects
Cerebral Cortex, Muscles, Neural Pathways, Cranial Nerves, Animals, Humans, Transcranial Magnetic Stimulation
Published
2006

184. Chapter 1 Corticobulbar tracts

Author

M. Hallett and Giorgio Cruccu

Subjects
business.industry, medicine.medical_treatment, Precentral gyrus, Anatomy, Masseter muscle, Pharyngeal muscles, Transcranial magnetic stimulation, medicine.anatomical_structure, Swallowing, Medicine, Evoked potential, business, Nucleus, Neuroscience, Motor cortex
Abstract

Publisher Summary This chapter reviews the cortical innervation of cranial nerve motor nuclei 5, 7, 9, 10, 11, and 12. The muscles of the 5th cranial nerve have been studied with transcranial magnetic stimulation (TMS). Responses in the masseter muscle are heavily contralateral but with some ipsilateral influence. The amplitude of the contralateral motor evoked potential (MEP) is 39% larger than the ipsilateral MEP. The cortical innervation of the 7th nerve nucleus has been carefully detailed in an anatomical study in the rhesus monkey. The corticobulbar projection is defined by injecting anterograde tracers into the face representation of each motor cortex, and in the same animals, the musculotopic organization of the facial nucleus is defined by injecting fluorescent retrograde tracers into the individual muscles of the upper and lower face. TMS studies using esophageal and pharyngeal muscle responses have demonstrated that swallowing has a bilateral but asymmetric hemispheric representation. While the cortical representation of swallowing can also be seen with positron emission tomography on the inferior precentral gyrus, this asymmetry is not as prominent.

Published
2006
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187. CTLA-4 is important in maintaining long-term survival of cardiac allografts

Author

Karen M. Hallett, Xueli Yuan, Nicholas Zavazava, Alfred J. Tector, Volkert A L Huurman, Chul-Hyun Park, Ellen Lu, Martin K. Oaks, and Anil Chandraker

Subjects
Graft Rejection, Time Factors, chemical and pharmacologic phenomena, Biology, Pharmacology, Antibodies, Immune tolerance, Mice, Antigen, Antigens, CD, Immune Tolerance, Animals, CTLA-4 Antigen, Phosphotyrosine, Transplantation, Graft Survival, CD28, hemic and immune systems, Protein-Tyrosine Kinases, Mixed lymphocyte reaction, Antigens, Differentiation, Rats, CTLA-4, Immunology, B7-1 Antigen, Phosphorylation, Heart Transplantation, Lymphocyte Culture Test, Mixed, CD80, Protein Binding
Abstract

Introduction. CTLA-4 is a negative regulatory molecule upregulated on activated T cells; however, its role in induction and maintenance of transplant tolerance is not well understood. Methods. The characteristics and effects of a novel mouse anti-rat CTLA-4 antibody (Ab) (242B58) were examined using fluorescence-activated cell sorter, mixed lymphocyte reaction, enzyme-linked immunospot, signaling studies, and a rat model of cardiac transplant tolerance induced by administration of anti-CD28 Ab and cyclosporine. Results. The anti-CTLA4 Ab was shown to bind to CTLA-4 but not prevent subsequent binding of B7 to CTLA-4. Binding to CTLA-4 did not result in phosphorylation of early cytoplasmic tyrosine kinases, suggesting that this is not a signaling Ab. However, its in vitro function was compatible with antagonization of the effects of CTLA-4, thereby increasing T-cell proliferation and interferon-gamma production in mixed lymphocyte reaction and enzyme-linked immunospot assays, respectively. Administration of 242B58 to animals treated with anti-CD28 Ab and cyclosporine either at the time of transplantation or various time-points up to 33 days posttransplantation did not result in immediate rejection, but rather caused a delayed severe acute allograft rejection at approximately 45 days posttransplant. Conclusions. Our results seem to be a reflection of the unique properties of the 242B58 Ab, which does not antagonize B7 binding to CTLA-4 and affect its ability to out-compete CD28 for B7 binding. It does, however, seem to interfere with CTLA-4 signaling, suggesting that competition for B7 may be important in induction of tolerance, but signaling through CTLA-4 is more important in maintaining a tolerant phenotype.

Published
2005

190. Small de novo duplication in the repeat region of the TATA-box-binding protein gene manifest with a phenotype similar to variant Creutzfeldt-Jakob disease

Author

A, Shatunov, E A, Fridman, F I, Pagan, J, Leib, A, Singleton, M, Hallett, and L G, Goldfarb

Subjects
Adult, Amyloid, Prions, TATA-Box Binding Protein, Creutzfeldt-Jakob Syndrome, Prion Proteins, Pedigree, Phenotype, Haplotypes, Mutation, Humans, Spinocerebellar Ataxias, Chromosomes, Human, Pair 6, Female, Protein Precursors, Trinucleotide Repeat Expansion
Abstract

A 20-year-old North American patient developed rapidly progressive cognitive decline and pronounced ataxia, a phenotype compatible with prion disease. No structural changes were found in the PRNP gene, which excludes genetic prion disease, but the patient's PRNP codon 129 Met/Met genotype is known to predispose to variant Creutzfeldt-Jakob disease (vCJD). Further studies identified an expanded allele with 55 CAG/CAA repeats in the TBP gene. The increase of trinucleotide repeat number in the coding region of the TBP gene has previously been associated with spinocerebellar ataxia type 17 (SCA17). The patient's unaffected parents and siblings show normal-size TBP alleles with 37-38 repeats. Haplotype and nucleotide sequence analyses clearly indicate that the mutation has occurred de novo on a paternal chromosome by insertion/duplication of a (CAA)(CAG)(CAA)(CAG)(15) sequence. This report presents a second fully investigated sporadic case of SCA17 occurring as a result of a DNA rearrangement within the polymorphic TBP trinucleotide repeat region. Our findings suggest that patients suspected of vCJD should undergo testing for SCA17, Huntington's disease and other neurodegenerative disorders having phenotypic similarities with vCJD.

Published
2004

194. Chapter 44 Future clinical applications of clinical neurophysiology in movement disorders

Author

G. Deuschl and M. Hallett

Subjects
Cognitive science, medicine.medical_specialty, Movement disorders, Neurology, business.industry, Disease progression, medicine, medicine.symptom, Clinical neurophysiology, business, Neuroscience
Abstract

Publisher Summary This chapter discusses the future clinical applications of clinical neurophysiology in movement disorders. This chapter formulates some expectations for future developments in this challenging application of clinical neurophysiology, knowing well that the development of neurology and clinical neurosciences is erratic, and new and promising ideas have often changed the expected developments in a favorable way. The approach in this chapter is to put together the open questions in the field of movement disorders and the possible answers that clinical neurophysiology could provide. In general, clinical neurophysiology has been strongest in the study of the pathophysiology of movement disorders. This has been helpful for understanding of the different conditions, for suggesting rational therapies and for helping with diagnosis. For the clinic, currently, clinical neurophysiology offers some help in the diagnosis of movement disorders and monitoring of disease progression and therapy.

Published
2003
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195. Symptomatic and essential palatal tremor. 2. Differences of palatal movements

Author

M. Hallett, Günther Deuschl, and Camilo Toro

Subjects
Adult, Male, Cerebellum, Electromyography, Palatal tremor, Diagnosis, Differential, stomatognathic system, Rhythmic movement disorder, Palatal Muscles, Tremor, otorhinolaryngologic diseases, medicine, Humans, Aged, Soft palate, medicine.diagnostic_test, Cranial nerves, Cranial Nerves, Anatomy, Middle Aged, medicine.disease, stomatognathic diseases, Levator veli palatini, medicine.anatomical_structure, Neurology, Female, Neurology (clinical), Palatal Muscle, Psychology, Brain Stem
Abstract

Palatal tremor, a rhythmic movement disorder of the soft palate, may be described as two separate entities: symptomatic palatal tremor (SPT) and essential palatal tremor (EPT). The symptomatic form is associated with brain stem or cerebellar disease, whereas the essential form has no known etiology. A cardinal symptom of EPT is the presence of ear clicks, which do not occur in SPT. Visual observation of the movements in the two disorders suggests that the difference in symptoms is due to the activation of different palatal muscles, the levator veli palatini in SPT and the tensor veli palatini in EPT. Electromyographic recording from the levator veli palatini muscle showed abnormal bursting activity time locked to the palatal movements in patients with SPT, but not in those with EPT. Because the two palatal muscles are innervated by different cranial nerves, SPT and EPT are likely to have separate origins.

Published
1994
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196. Reporting clinical trials: full access to all the data

Author

R N, Rosenberg, M, Aminoff, F, Boller, P S, Soerensen, R C, Griggs, M, Hallett, R T, Johnson, C, Kennard, A E, Lang, A J, Lees, R, Lisak, J, Newsom-Davis, T A, Pedley, M E, Selzer, and D, Zochodne

Subjects
Clinical Trials as Topic, Humans, Disclosure
Published
2002

197. Focal enhancement of motor cortex excitability during motor imagery: a transcranial magnetic stimulation study

Author

S, Facchini, W, Muellbacher, F, Battaglia, B, Boroojerdi, and M, Hallett

Subjects
Adult, Electrophysiology, Male, Movement, Imagination, Motor Cortex, Humans, Female, Middle Aged, Evoked Potentials, Motor, Muscle, Skeletal, Transcranial Magnetic Stimulation
Abstract

In order to learn more about the physiology of the motor cortex during motor imagery, we evaluated the changes in excitability of two different hand muscle representations in the primary motor cortex (M1) of both hemispheres during two imagery conditions.We applied focal transcranial magnetic stimulation (TMS) over each M1, recording motor evoked potentials (MEPs) from the contralateral abductor pollicis brevis (APB) and first dorsal interosseus (FDI) muscles during rest, imagery of contralateral thumb abduction (C-APB), and imagery of ipsilateral thumb abduction (I-APB). We obtained measures of motor threshold (MT), MEP recruitment curve (MEP-rc) and F waves.Motor imagery compared with rest significantly decreased the MT and increased MEPs amplitude at stimulation intensities clearly above MT in condition C-APB, but not in condition I-APB. These effects were not significantly different between right and left hemisphere. MEPs simultaneously recorded from the FDI, which was not involved in the task, did not show facilitatory effects. There were no significant changes in F wave amplitude during motor imagery compared with rest.Imagery of unilateral simple movements is associated with increased excitability only of a highly specific representation in the contralateral M1 and does not differ between hemispheres.

Published
2002

199. Evaluating Ecosystem Services Provided by Non-Native Species: An Experimental Test in California Grasslands

Author

W. Stanley Harpole, Lauren M. Hallett, Claudia Stein, and Katharine N. Suding

Subjects
Conservation of Natural Resources, Ecological Metrics, Biodiversity, lcsh:Medicine, Ecological Risk, Introduced species, Plant Science, Total human ecosystem, Biology, California, Ecosystems, Ecosystem services, Global Change Ecology, Plant-Environment Interactions, Ecosystem, lcsh:Science, Ecosystem health, Multidisciplinary, Ecology, Productivity (Ecology), business.industry, Plant Ecology, Ecology and Environmental Sciences, lcsh:R, Environmental resource management, Biology and Life Sciences, Restoration Ecology, Species diversity, Grassland, Community Ecology, Ecological Yield, Ecosystem management, lcsh:Q, business, Ecosystem Functioning, Research Article
Abstract

The concept of ecosystem services – the benefits that nature provides to human's society – has gained increasing attention over the past decade. Increasing global abiotic and biotic change, including species invasions, is threatening the secure delivery of these ecosystem services. Efficient evaluation methods of ecosystem services are urgently needed to improve our ability to determine management strategies and restoration goals in face of these new emerging ecosystems. Considering a range of multiple ecosystem functions may be a useful way to determine such strategies. We tested this framework experimentally in California grasslands, where large shifts in species composition have occurred since the late 1700's. We compared a suite of ecosystem functions within one historic native and two non-native species assemblages under different grazing intensities to address how different species assemblages vary in provisioning, regulatory and supporting ecosystem services. Forage production was reduced in one non-native assemblage (medusahead). Cultural ecosystem services, such as native species diversity, were inherently lower in both non-native assemblages, whereas most other services were maintained across grazing intensities. All systems provided similar ecosystem services under the highest grazing intensity treatment, which simulated unsustainable grazing intensity. We suggest that applying a more comprehensive ecosystem framework that considers multiple ecosystem services to evaluate new emerging ecosystems is a valuable tool to determine management goals and how to intervene in a changing ecosystem.

Published
2014
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