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1. Abstract P2-03-09: Autocrine motility factor signaling pathway promotes aggressive behavior and migration in breast cancer

Author

Pamela A. Althof, AZ VanDyke, SP Thayer, D Maroni, JN Sanmann, Prosenjit Mondal, Cassie J Liu, JD Price, and JM Stevens

Subjects
Cancer Research, Autocrine Motility Factor, Breast cancer, Oncology, medicine, Cancer research, Signal transduction, Biology, medicine.disease
Abstract

Background: Autocrine motility factor (AMF) is secreted by cancer cells and acts in an autocrine or paracrine fashion to bind to its receptor, AMFR, at the cell surface of tumor cells. The AMF-AMFR pathway has been shown to promote proliferation, anti-apoptosis, motility and migration, invasion, and metastasis pathways in various cancers. However, our understanding of the AMF-AMFR pathway in breast cancer is limited. We propose that the AMF signaling pathway is an unexplored mechanism for breast cancer tumor aggression and its receptor, AMFR, may be a potential therapeutic target. Methods: Tumor tissue obtained from consented female (n = 31) and male (n = 1) patients were analyzed by the Affymetrix OncoscanTM genome-wide microarray platform and examined for somatic copy-number alterations (SCNAs) of AMFR. cBioPortal was used to investigate SCNA of AMFR and gene expression of AMF on primary breast cancer tumors from METABRIC (n = 1,784) and TCGA Pan-Cancer Atlas (n = 981) datasets. In vitro, AMF and AMFR gene expression in luminal A (MCF-7) and triple-negative breast cancer (MDA-MB-231) cell lines were assessed by qPCR. Cell migration assays were performed on MDA-MB-231 cells to investigate their migration towards AMF with AMFR present or knocked down by siRNA. Results: Microarray analysis of 32 tumors revealed that a single-copy loss of AMFR occurred 79% of the time in luminal A tumors (n = 19); 67% of the time in luminal B tumors (n = 6); 33% of the time in ER+, PR+, HER2+ tumors (n = 3); and 0% of the time in triple-negative breast cancer (TNBC) tumors (n = 4), suggesting that the loss of AMFR results in less aggressive tumors that have good overall prognosis. To extend our findings to a larger patient cohort, SCNA analysis of the METABRIC and TCGA Pan-Cancer Atlas datasets revealed that single-copy loss of AMFR occurred in 64.53% and 68.14% of luminal A tumors, 58.51% and 59.90% of luminal B tumors, 23.62% and 48.72% of HER2 overexpression tumors, and 29.80% and 39.77% of TNBC tumors, respectively. Therefore, AMFR appears most frequently deleted in the tumor genomes of good prognosis breast cancer molecular subtypes (luminal tumors). Gene expression analysis of AMF in the METABRIC (using z-scores) and TCGA Pan-Cancer Atlas (using batch-normalized numbers) datasets revealed median mRNA expressions of -0.3351 and 4862 in luminal A tumors, -0.05415 and 5841 in luminal B tumors, 0.5758 and 9390 in HER2 overexpression tumors, and 0.754 and 8798 in TNBC tumors, respectively, suggesting that the AMF-AMFR pathway is more active in aggressive breast cancers. Similarly, we observed that AMF and AMFR are transcriptionally overexpressed by 7-fold and 16-fold, respectively, in the TNBC cell line MDA-MB-231 compared to the luminal A breast cancer cell line MCF-7. When AMFR is knocked down in MDA-MB-231 cells, focused migration towards AMF is abolished. Conclusion: AMF-AMFR pathway activity correlates with aggressive cancer cell behavior and enhanced migration in breast cancer. Single-copy loss of AMFR in tumor genomes is associated with less aggressive tumors with better overall prognosis. AMFR may be an attractive therapeutic target. Citation Format: Liu C, Price JD, Maroni D, Stevens JM, VanDyke AZ, Althof PA, Mondal P, Sanmann JN, Thayer SP. Autocrine motility factor signaling pathway promotes aggressive behavior and migration in breast cancer [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P2-03-09.

Published
2019
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2. Abstract P3-01-21: Circulating tumor cells of breast cancer origin identified by fluorescence in situ hybridization and may be an early predictor of therapy failure in early breast cancer

Author

JM Stevens, AZ VanDyke, CE Grabow, JN Sanmann, JD Price, Pamela A. Althof, D Maroni, SP Thayer, and Cassie J Liu

Subjects
Cancer Research, medicine.diagnostic_test, business.industry, medicine.medical_treatment, Cancer, SCNA, medicine.disease, Primary tumor, Radiation therapy, Circulating tumor cell, Breast cancer, Oncology, Adjuvant therapy, Cancer research, medicine, business, Fluorescence in situ hybridization
Abstract

Background: Most modern methods of detecting circulating tumor cells (CTCs) involve identifying cells with epithelial markers. This approach presents challenges, as not all epithelial cells found in circulation originate from the tumor and not all CTCs express epithelial markers. We propose using a size-exclusion filtration system to enrich for CTCs in peripheral blood followed by fluorescence in situ hybridization (FISH) of the filtered cells to identify cells of tumor origin in the early-stage breast cancer patients. We further hypothesize that the presence of CTCs may be indicators of therapy failure in early-stage breast cancer patients. Methods: Patients diagnosed with breast cancer (n = 9) were consented for CTC evaluation. Primary tumor DNA was analyzed by the Affymetrix OncoscanTM genome-wide microarray platform and investigated for somatic copy-number alterations (SCNAs). For each patient, two FISH probes were then identified for two regions of gain or a region of gain and a region of loss from the microarray results. Blood samples from patients were obtained before surgery, radiation therapy, endocrine therapy, and at 6-month or 1-year follow-up visits. Blood samples were filtered using ScreenCell® Cyto V2 devices, and FISH was performed. Cells were categorized as normal (diploid for all FISH probes), suspicious (single SCNA detected by FISH), or CTC (two SCNAs detected by FISH). Patients were identified as having CTCs present in their circulation when ≥2 CTCs were observed or when one CTC and >15 suspicious cells were observed. Results: The microarray data revealed that luminal A tumors ranged from 2-43 SCNAs; luminal B tumors ranged from 15-20 SCNAs; and ER+, PR+, HER2+ tumors ranged from 46-98 SCNAs. Although a correlation appears to exist between tumor genetic complexity and molecular subtype, the degree of complexity was highly varied within each subtype. We found that neither complexity of tumor profile, molecular subtype, nor stage could predict the presence of CTCs in patients. Molecular SubtypeSCNAsCTCsSuspicious Cells OnlyLuminal A2-433/52/5Luminal B15-200/21/2ER+, PR+, HER2+46-982/20/2 In pre-surgical blood samples, we detected CTCs in 63% of patients with stage 1 disease and in 60% of patients with luminal A tumors, 0% of patients with luminal B tumors, and 100% of patients with triple-positive tumors. StageCTCsSuspicious Cells OnlyIA/B5/82/8IIA0/11/1 Although limited in number, ongoing investigation revealed that one of our patients in early follow-up with a luminal A, stage IB tumor was identified to have persistent CTCs at 1-year after starting hormonal adjuvant therapy, suggesting residual tumor burden not detected by standard clinical modalities; this finding also suggests that this patient may be at highest risk for relapse and should be considered for additional therapies. Conclusion: Size-exclusion filtration followed by FISH analysis can accurately identify CTCs in early-stage breast cancer patients. Tumor complexity, molecular subtype, and stage did not predict the presence of CTCs in circulation. Our method for CTC detection may be able to serve as a diagnostic tool for treatment failure. Citation Format: Liu C, Althof PA, Maroni D, Stevens JM, Grabow CE, VanDyke AZ, Price JD, Sanmann JN, Thayer SP. Circulating tumor cells of breast cancer origin identified by fluorescence in situ hybridization and may be an early predictor of therapy failure in early breast cancer [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P3-01-21.

Published
2019
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3. High-b-Value Diffusion MR Imaging and Basal Nuclei Apparent Diffusion Coefficient Measurements in Variant and Sporadic Creutzfeldt-Jakob Disease

Author

Hans Rolf Jäger, John Collinge, Tarek A. Yousry, JM Stevens, Harpreet Hyare, John S. Thornton, Peter Rudge, and Simon Mead

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Sensitivity and Specificity, Basal Ganglia, Creutzfeldt-Jakob Syndrome, White matter, Central nervous system disease, Young Adult, Basal (phylogenetics), Thalamus, Visual assessment, medicine, Humans, Effective diffusion coefficient, Radiology, Nuclear Medicine and imaging, Aged, Cerebral Cortex, business.industry, Water, Brain, Sporadic Creutzfeldt-Jakob disease, Middle Aged, High B-Value, medicine.disease, Mr imaging, Diffusion Magnetic Resonance Imaging, medicine.anatomical_structure, Female, Neurology (clinical), Nuclear medicine, business
Abstract

BACKGROUND AND PURPOSE: DWI using a standard b-value of 1000s/mm(2) has emerged as the most sensitive sequence for the diagnosis of CJD. The purpose of this study was to investigate whether DWI at a high b-value (b = 3000 s/mm(2)) and ADC measurements in the basal nuclei improve the diagnosis of vCJD and sCJD compared with visual assessment of DWI at a standard b-value (b = 1000 s/mm(2)). MATERIALS AND METHODS: Eight patients with vCJD, 9 patients with sCJD, and 5 healthy volunteers underwent DWI at b = 1000 s/mm(2), and 5 vCJD patients, 4 sCJD patients, and 1 growth hormone-related CJD patient underwent DWI at b = 3000 s/mm(2). Two consultant neuroradiologists performed a visual comparison of the b = 1000 and b = 3000 images. Mean MR SI and ADC values were determined for C, P, and DM thalamus ROIs bilaterally at each b-value. SI ratios for each ROI relative to white matter were calculated. RESULTS: In 9 out of 10 patients, the higher b-value images were more sensitive to SI change, particularly in cortex and thalamus, with higher SI ratios at b = 3000 in the DM thalamus. For sCJD at b = 1000, we found significantly lower ADC values in the C and P compared with controls (mean C ADC = 587.3 ± 84.7 mm(2)/s in sCJD patients versus 722.7 ± 16.6 mm(2)/s in controls; P = .007), and at b = 3000, the differences were more pronounced. In comparison, in vCJD at b = 1000, ADC values were elevated in the Pu (mean Pu ADC = 837.6 ± 33.0 mm/s(2) in vCJD patients versus 748.0 ± 17.3 mm/s(2) in controls; P < .001) but failed to reach significance at b = 3000. CONCLUSIONS: Our results demonstrate that b = 3000 DWI, being more sensitive to slowly diffusing tissue water, is more sensitive to pathology in sCJD than is conventional DWI. High-b-value DWI increases confidence in the radiologic diagnosis of human prion disease.

Published
2009
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4. Auditory temporal processing deficits in patients with insular stroke

Author

Doris-Eva Bamiou, Linda M. Luxon, Martin M. Brown, JM Stevens, I. Stow, Frank E. Musiek, Lisa Cipolotti, BAMIOU DE, MUSIECK F, STOW I, STEVENS J, CIPOLOTTI L, BROWN M, and LUXON L

Subjects
Adult, Male, medicine.medical_specialty, Auditory area, Audiology, Lesion, Audiometry, medicine, Humans, Neuropsychological assessment, Hearing Disorders, Stroke, Aged, Cerebral Cortex, Settore M-PSI/02 - Psicobiologia E Psicologia Fisiologica, medicine.diagnostic_test, Dichotic listening, Middle Aged, Tympanometry, medicine.disease, Surgery, Adult Aged Audiometry Cerebral Cortex/pathology* Female, Hearing Disorders/diagnosis, Hearing Disorders/etiology, Humans, Male, Middle Aged, Stroke/complications, Stroke/diagnosis, Female, Neurology (clinical), medicine.symptom, Psychology, Insula
Abstract

OBJECTIVE: To assess central auditory function in a series of patients with stroke of the insula and adjacent areas. METHODS: The authors recruited eight patients with stroke affecting the insula and adjacent areas and eight neurologically normal controls (matched to the patients for age, sex, handedness, and hearing thresholds). The lesion spared the adjacent auditory areas in three patients and included other auditory structures in five cases. The authors conducted pure-tone audiometry and tympanometry and a central auditory test battery, which included the dichotic digits, and three temporal tests, the duration pattern, frequency pattern, and gaps in noise tests. They collected information from the hospital notes on symptoms at presentation and neuropsychological assessment data during the acute phase. RESULTS: The central auditory tests gave normal results in all controls. The temporal tests gave abnormal results in all three cases in which other auditory areas were spared, as well as in the other five cases. Results of the gaps in noise test were abnormal contralaterally to the lesion in three and bilaterally in five cases. The central auditory deficits did not cosegregate with the presence of cognitive impairment during the acute stage. CONCLUSION: Insular lesions may affect central auditory function and, in particular, temporal resolution and sequencing, consistent with neuroimaging studies.

Published
2006
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5. Quantitative MRI measurement of superior cerebellar peduncle in progressive supranuclear palsy

Author

JM Stevens, Dominic C. Paviour, Shona L. Price, A J Lees, and Nick C. Fox

Subjects
Male, Pathology, medicine.medical_specialty, Postmortem studies, Sensitivity and Specificity, Progressive supranuclear palsy, Diagnosis, Differential, Atrophy, Cerebellum, medicine, Humans, False Positive Reactions, Prospective Studies, False Negative Reactions, Aged, business.industry, Parkinson Disease, Organ Size, Middle Aged, Multiple System Atrophy, medicine.disease, Magnetic Resonance Imaging, Volumetric measurement, eye diseases, Radiography, Volume measurements, medicine.anatomical_structure, Superior cerebellar peduncle, Cerebellar peduncle, Female, Supranuclear Palsy, Progressive, Neurology (clinical), Psychology, Nuclear medicine, business, Machado–Joseph disease
Abstract

Background: Postmortem studies have shown atrophy of the superior cerebellar peduncle (SCP) to distinguish progressive supranuclear palsy (PSP) from other neurodegenerative diseases. It is not clear whether MRI-based measurements can differentiate this relative atrophy of the SCP during life. Methods: Volumetric MRI was acquired prospectively in 53 subjects: 19 with PSP, 10 with multiple system atrophy (MSA), 12 with Parkinson disease (PD), and 12 healthy controls. SCP volume was assessed by detailed quantitative volumetric measurement and independently by blinded visual rating of SCP atrophy. Results: The mean SCP volume, corrected for total intracranial volume, was lower in patients with PSP than controls ( p p = 0.001), and patients with PD ( p = 0.003). There was an overlap between individual SCP volume measurements in the PSP subjects and the other groups. Neuroradiologic rating correctly identified PSP cases based on the presence of SCP atrophy with a sensitivity of 74% and a specificity of 94%. Conclusions: The authors propose that together with other radiologic features of progressive supranuclear palsy (PSP) such as midbrain atrophy, a visual assessment of the superior cerebellar peduncle may help increase the clinical diagnostic accuracy in PSP.

Published
2005
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6. Pathological substrate for regional distribution of increased atrophy rates in progressive supranuclear palsy

Author

Janice L. Holton, Dominic C. Paviour, JM Stevens, T Revesz, A J Lees, Jonathan M. Schott, Nick C. Fox, and Martin N. Rossor

Subjects
Male, Pathology, medicine.medical_specialty, Short Report, Autopsy, Progressive supranuclear palsy, Atrophy, Humans, Medicine, Pathological, Vertical supranuclear gaze palsy, medicine.diagnostic_test, business.industry, Cranial nerves, Brain, Magnetic resonance imaging, Middle Aged, medicine.disease, Magnetic Resonance Imaging, eye diseases, Psychiatry and Mental health, Disease Progression, Surgery, Supranuclear Palsy, Progressive, Neurology (clinical), medicine.symptom, business, Follow-Up Studies, Balance problems
Abstract

Background: Most magnetic resonance imaging (MRI) studies of progressive supranuclear palsy (PSP) are cross-sectional and lack post mortem confirmation of the diagnosis. MRI features described previously in PSP correspond to regions of pathological involvement demonstrated in separate studies, but serial MRI with pathological follow up has not been undertaken. Objective: To investigate whether regions of increased atrophy rates demonstrated in PSP during life using fluid registered serial MRI correspond with pathological findings in confirmed PSP. Methods: A 59 year old male presented with a six month history of balance problems and dysarthria. He had a symmetrical, levodopa unresponsive akinetic-rigid syndrome with a vertical supranuclear gaze palsy. A clinical diagnosis of probable PSP was made. His disease progressed relentlessly and he died five years after onset. Two serial MRI scans undertaken during life were reviewed and fluid (non-linear) registration of the images carried out. Post mortem histopathological analysis of the brain was undertaken to definitively confirm the diagnosis and compare regional pathology with the serial imaging. Results: Fluid registration demonstrated greatest rates of atrophy in the brainstem and frontal cortex, in keeping with the distribution of pathology seen at autopsy. Conclusion: Fluid registration of serial MRI allows the topography and rates of regional atrophy in PSP to be delineated in life. Atrophy patterns correlated well with regional pathological load. These observations suggest that serial MRI with registration may help differentiate PSP from clinically similar conditions and supports its use as a surrogate marker of disease progression.

Published
2004
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7. ABN Abstracts: Proceedings of the Association of British Neurologists, Cardiff City Hall, Cathays Park, 2 April-4 April 2003

Author

Martin N. Rossor, Nick C. Fox, R J L Walters, David Thomas, William R. Crum, and JM Stevens

Subjects
Cerebral atrophy, Psychiatry and Mental health, medicine.medical_specialty, Variation (linguistics), Operations research, Computer science, Internal medicine, Cardiology, medicine, Surgery, Transient (computer programming), Neurology (clinical), medicine.disease
Published
2003
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8. Alzheimer's disease due to an intronic presenilin-1 (PSEN1 intron 4) mutation

Author

Thomas B. Campbell, Nick C. Fox, JC Janssen, A. Dickinson, Richard J. Harvey, M Hall, Peter L. Lantos, Martin N. Rossor, JM Stevens, James M. Beck, John Collinge, and Lisa Cipolotti

Subjects
Apolipoprotein E, Pathology, medicine.medical_specialty, Neuropathology, Biology, medicine.disease, Gastroenterology, Central nervous system disease, Atrophy, Internal medicine, medicine, PSEN1, Neurology (clinical), medicine.symptom, Alzheimer's disease, Age of onset, Myoclonus
Abstract

We describe 21 affected individuals from a kindred with early-onset autosomal dominant familial Alzheimer's disease caused by an intronic presenilin-1 mutation (in intron 4). Mean age at onset of symptoms was 37.4 years [95% confidence interval (CI): 36.6-38.2 years], mean age at death was 44.7 years (95% CI: 43.1-46.3 years) and mean duration of illness was 7.3 years (95% CI: 5.9-8.7 years). Myoclonus and seizures were prominent features of this pedigree. In the four cases for whom neuropsychometric data were available, verbal memory impairment preceded visual memory deficits; naming was relatively preserved until late in the disease. One of these four cases underwent serial volumetric MRI scans demonstrating in vivo brain tissue loss of 3.9% (38.9 ml, annualized rate of atrophy: 1.7%) over 22 months of follow-up. The four individuals who had necropsies demonstrated the neuropathological hallmarks of Alzheimer's disease. Apolipoprotein E (APOE) status was assessed in five individuals: the case with the youngest age at onset at 33 years of age was found to be homozygous e4/e4, > 1 SD below the mean age of onset for those of known APOE genotype (36.4 ± 2.3 years, mean ± SD), and > 2 SDs below the mean age of onset for the pedigree as a whole (37.4 ± 1.7 years, mean ± SD). APOE genotype may therefore modulate age at onset in this pedigree.

Published
2000
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9. Clinicopathological features of familial Alzheimer's disease associated with the M139V mutation in the presenilin 1 gene. Pedigree but not mutation specific age at onset provides evidence for a further genetic factor

Author

John Collinge, John Hardy, JM Stevens, Peter L. Lantos, Elizabeth K. Warrington, Richard J. Harvey, P Roques, Martin N. Rossor, A. M. Kennedy, Michael Hutton, and Nick C. Fox

Subjects
Adult, Male, Apolipoprotein E, Intelligence, Neuropsychological Tests, Presenilin, Apolipoproteins E, Alzheimer Disease, Memory, medicine, Humans, Dementia, Missense mutation, Cognitive decline, Genetics, Brain, Middle Aged, medicine.disease, Pedigree, Mutation, Female, Perception, Neurology (clinical), Age of onset, Alzheimer's disease, medicine.symptom, Psychology, Myoclonus
Abstract

Sixteen affected individuals are described from two families with early onset autosomal dominant familial Alzheimer's disease. A mutation at codon 139 in the presenilin 1 gene on chromosome 14 results in a methionine to valine substitution which cosegregates with the disease in these families. Onset of dementia was before the age of 50 years in all individuals. The ages at onset within each family were tightly clustered but were significantly different between the families; this difference could not be accounted for by apolipoprotein E status and suggests the existence of a further genetic factor that modifies age at disease onset. The pattern of cognitive decline was similar in both families: early memory loss (initially selective for verbal memory in some individuals) was followed soon after by loss of arithmetic skills while naming and object perception skills were relatively preserved. A speech production deficit was observed in three members of one family but not in the other. Seizures were common and usually predated by myoclonic jerks by a number of years. Serial MRIs showed progressive cortical atrophy with periventricular white matter change appearing 3-4 years into the disease. PET revealed parieto-temporal hypometabolism in all individuals scanned. The diagnosis of Alzheimer's disease was confirmed with typical histopathology in one individual from each family.

Published
1997
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10. 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. D'Angelo, N. Baumann, S. Yorifuji, H. P. Endtz, M. A. Cassatella, R. A. C. Hughes, V. Golzi, A. Bittencourt, A. Ferreira, M. Sanson, C. Alper, M. Vermeulen, M. A. A. van Walderveen, E. Alexiou, C. H. Lucas, M. Fiorelli, Y. N. Debbink, R. Gil, S. Congia, T. Banerjee, J. M. Bouchard, A. N. Pinto, A. Ceballos-Baumann, G. Grollier, P. I. M. Schmitz, M. D. Catata, N. Lahat, N. S. Rao, P. Papathanasopoulos, J. Valls-Solé, D. Claus, G. Schroter, A. Castro, C. Videbaek, R. Martinez Dreke, A. D. Platts, M. Hermesl, A. C. PeÇanha-Martins, M. Cardoso Silva, P. Masnou, M. J. A. Tanner, Ch. Confavreux, B. Mishu, H. Rasmussen, L. Valenciano, Carlo Pozzilli, S. W. Li, V. Salzman, Y. Vashtang, Massimo Franceschi, M. Severo, G. Deuschl, S. Setien, G. Mariani, A. Protti, J. Castillo, M. J. B. Taphoorn, M. Frontali, I. Milonas, D. Decoq, J. A. Navarro, S. Castellvi-Pel, C. Ertikin, M. Urtasun, Y. Lajat, B. E. Kendall, E. Verdu, B. Gueguen, E. Boisen, R. Couderc, A Danek, JM Stevens, F. Nicoli, L. Feltri, M. L. Vazquez-Andre, J. A. Morgan-Hughes, L. D'Angelo, F. Y. Liew, L. F. Pascual, J. Patrignani Ochoa, Vittorio Martinelli, J. Cophignon, L. Zhang, S. Martin, J. F. Meder, H. C. Buschmann, L. Bertin, J. van Gijn, A. Barreiro, A. Cools, C. Leon, A. Berod, E. A. Anllo, E. Zanette, L. Petrov, R. Barona, B. Gallicchio, P. J. Cozzone, N. Diederich, G. Cancel, L. Schelosky, P. Orizaola, K. Yulug, S. Ozer, Valeria A. Sansone, B. Guiraud-Chaumeil, K. Voigt, P. Labauge, M. Eoli, J. Zhu, J. Aguirre, M. Ferrarini, B. Zyluk, E. Planas, A. Cadilha, C. Tortorella, H. Bismuth, C. E. Counsell, A. Laun, A. Ferlini, Rio J. Montalban, N. Biary, L. Becker, M. Fardeau, M. Poloni, V. M. S. de Bruin, C. Fornada, J. Barros, E. Ganzmann, E. Touze, D. Wallach, J. Peila, H. Fujimura, M. T. Iba-Zizen, G. Macchi, C. Villoslada, R. Gouider, Ph. Rondepierre, P. Grummich, P. Chiodi, C. Conte, M. Michels, P. Annunziata, G. Semana, C. Sommer, J. Vajsar, D. Zekin, J. Kulisevsky, David G. Munoz, B. Jacotot, M. Magoni, A. Luxen, T. Garcia-Silva, S. Di Cesare, Christophe Tzourio, M. Gomori, I. Picomell, L. Santoro, F. Villa, Giovanni Pennisi, T. Ribalta, J. M. Molto, L. Marzorati, P. Loiseau, F. Gemignani, A. Gironell, J. Wissel, A. Prusinski, F. Cailloux, P. Villanueva-Hemandez, P. Cozzone, T. Del Ser, J. Sans-Sabrafen, M. Zappia, P. W. A. Willems, G. Tchernia, D. Gardeur, R. Bauer, F. Palomo, H. Metz, S. Lamoureux, C. Chastang, I. Reinhard, A. Goldfarb, S. Harder, Jordi Río, C. Ozkara, E. Tekinsoy, P. Vontobell, J. De Recondo, M. Rabasa, L. Lacomblez, F. Boon, Dgt Thomas, V. Palma, Renato Mantegazza, A. Dervis, M. Nueckel, B. YalÇinerner, I. Duran, G. Dalla Volta, A. Zubimendi, J. Pinheiro, A. Marbini, Xavier Montalban, H. Wekerle, X. Pereira Monteino, F. Crespo, F. Koskas, N. Battistini, C. Ruiz, H. Offner, J. de Pommery, P. Kanovsky, J. Y. Barnett, J. Pardo, G. Tomei, R. Rene, H. M. Lokhorst, P. Thajeb, H. Bilgin, D. McGehee, R. Fahsold, L. Morgante, Katie Sidle, C. Delwaide, M. N. Diaye, P. H. Rice, A. Creange, C. Sabev, K. Stephan, K. WeilBenborn, G. Magnani, L. Grymonprez, F. Cardellach, M. Kaps, N. G. Meco, F. Vega, V. Bonifati, A. Desomer, M. Baldy-Moulinier, G. Kvale, F. J. Authier, B. Yegen, T. Ho, J. M. Rozet, E. A. Cabanis, L. Bruce, L. Ambrosoli, M. A. Petrella, M. Hernandez, P. Timmings, H. B. van der Worp, F. Mahieux, A. Urbano-Marquez, D. A. Krendel, A. A. Garcia, R. Divari, R. Michalowicz, M. R. Piedmonte, M. Bondavalli, M. Zanca, P. F. Ippel, Onofre Combarros, B. Tavitian, E. Hirsch, I. Anastasopoulos, A. Roses, A. Köhler, P. Vienna, V. Timmerman, P. Sergi, F. Cornelio, A. Di Pasquale, R. Verleger, S. Castellvirel, J. Proano, B. van Moll, F. Rubio, W. Hacke, I. Lavenu, L. Zetta, M. W. Tas, N. Bittmann, M. Bonamini, O. R. Hommes, V. Dousset, N. Afsar, S. Belal, R. R. Myers, J. Goes, Giuseppe Vita, E. Clementi, V. G. Karepov, M. Jueptner, A Vincent, P. Emmrich, Th. Heb, A. Caballo, J. Gallego, T. Mokrusch, C. Perla, L. Gebuhrer, O. Titlbach, Alessandro Prelle, A. Czlonkowska, M. Russo, D. Hadjiev, T. S. Chkhikvishvili, M. Oehlschlager, G. Becker, I. Günther, E. N. Stenager, J. Garcia Agundez, J. Casademont, J. Batlle, S. Podobnik-Sarkanji, C. Alonso-Villaverde, B. Delaguillaume, B. Genc, B. Mazoyer, A. Rodriguez-Al-barino, Ch. Hilger, B. Ferrero, R. Price, W. Grisold, L. Fuhry, D. Oulbani, D. Ewing, A. Petkov, W. Walther, A. Gokyigit, John Newsom-Davis, J. Tayot, D. Seliak, G. Pelliccioni, D. Campagne, K. Kessler, F. Boureau, D. Perani, J. P. N'Guyen, N. Tchalucova, B. A. Antin-Ozerkis, C. Lacroix, B. D. Aronovich, I. H. Jenkins, E. A. dos Reis, M. Hortells, H. M. Meinck, H. Ch. Buschmann, S. C. J. M. Jacobs, T. Wetter, P. Creissard, N. Martinez, J. Weidenfeldl, H. J. Sturenburg, G. Damlacik, V. Gracia, J. C. Turpin, A. Pou-Serradell, J. P. Vincent, T. Gagoshidze, U. Ozkutlu, M. McLeod, K. Siegfried, I. Tchaoussoglou, J. Hildebrand, S. Kowalska, M. C. Picot, G. Galardin, L. Crevits, F. Andreetta, S. Larumbe-Lobalde, G. de la Sierra, J. C. Alvarez-Cermeno, R. J. Seitz, P. L. Oey, L. Ptacek, A. M. J. Paans, A. Wirrwar, A. Schmied, J. Uilchez, H. Tounsi, D. Hipola, V. Avoledo, Y. Hirata, P. Vermersch, T. M. Aisonobe, J. Valls-SoIè, H. Staunton, J. Dichgans, R. Karabudak, I. Dones, G. Porta, E. Janssens, Maria Martinez, J. M. Fernandez-Real, R. Villagra, Y. Yoshino, C. Kabus, K. Schimrigk, I. Girard-Buttaz, F. Piccoli, F. Aichner, P. Zuchegna, S. M. Al Deeb, F. Bono, N. Busquets, A. Jobert, Patrizia Ciscato, M. Martin, L. Polman, S. Darbra, V. Le Cam-Duchez, F. Baldissera, B. Baykan-Kurt, D. Guez, M. Bratoeva, H. Matsui, M. Mila, H. Perron, L. Bjorge, G. Husby, Steven T. DeKosky, D. R. Cornblath, J. M. Gabriel, J. J. Poza, Y. Wu, A. Toscano, R. P. Kleyweg, J. Kuhnen, S. O. Confort-Gouny, A. Barcelo, A. M. Conti, C. Fiol, C. Steichen-Wiehn, J. Rodes, M. Cavenaile, C. Vedeler, M. Drlicek, C. Argentino, M. L. Peris, A. Cervello, A. Z. GinaÏ, S. Yancheva, D. Passingham, S. Aoba, D. L. Lopez, T. Rechlin, K. Sonka, L. Grazzi, V. Folnegovic-Smalc, Maurizio Moggio, S. Rivaud, F. G. I. Jennekens, C. H. Hartard, H. Meierkord, G. Stocklin, M. D. Catala, W. C. McKay, E. Salmon, C. Navarro, I. Pastor, L. Canafoglia, M. De Braekeleer, P. K. Thomas, C. Mocellini, C. Pierre-Jerome, M. C. Dalakas, P. Pollak, M. Levivier, Niall Quinn, G. E. Rivolta, Z. Tunca, H. Zeumer, J. Garcia Tena, St. Guily, P. Gaudray, Johannes Kornhuber, V. Petrunjashev, R. Montesanti, R. J. Abbott, H. Petit, G. Kiteva-Trencevska, F. Carletto, C. Ramo, I. M. Pino, P. Beau, G. F. Mennuni, F. Moschian, F. Meneghini, B. Zdziarska, B. Fontaine, C. Stephens, G. Meco, K. Reiners, G. Badlan, M. Sessa, I. Degaey, S. M. Hassan, C. Albani, F. Caroeller, M. Schroeder, G. Savettieri, A. Novelletto, R. Kurita, P. Oschmann, I. Plaza, M. Oliveres, Simone Spuler, A. Molins, M. Schwab, J. R. Kalden, C. P. Gennaula, Y. Baklan, O. Picard, J. M. Léger, B. Mokri, E. Ghidoni, M. Jacob, D. Deplanque, W. JÄnisch, C. De Andres, P. De Deyn, G. Guomundsson, B. Herron, J. Barado, J. L. Gastaut, Guglielmo Scarlato, F. Poron, Nicola Jones, H. Teisserenc, C. P. Hawkins, A. J. Steck, H. C. Chandler, S. Blanc, J. H. Faiss, Jm. Soler Insa, I. Sarova-Ponchas, M. Malberin, A. Sackmann, G. De Vuono, K. Kaiser-Rub, K. Badhia, E. Szwabowska-Orzeszko, S. Ramm, C. Jodice, G. Franck, J. Marta-Moreno, R. Sciolla, C. Fritz, A. Attaccalite, F. Weber, E. Neuman, M. Cannata, A. Rodriguez, I. Nachainkin, R. Raffaele, T. S. Yu, N. Losseff, E. Fabrizio, C. Khati, M. Keipes, M. P. Ortega, M. Ramos-Alvarez, E. Brambilla, A. Tarasov, K. H. Wollinsky, O. B. Paulson, F. Boller, G. Bozzato, H. Wagnur, R. Canton, D. Testa, E. Kutluaye, M. Calopa, D. Smadja, G. Malatesta, F. Baggi, A. Stracciari, G. Daral, G. Avanzini, J. Perret, J. Arenas, P. Boon, I. Gomes, A. Vortmeyer, P. Cesaro, S. Venz, E. Bernd Ringelstein, N. Milani, D. Laplane, P. Seibel, E. Tournier-Lasserve, Alexis Brice, L. Motti, E. Wascher, R. J. Abbot, F. Miralles, A. Turon, P. De Camilli, G. Luz, G. C. Guazzi, S. Tekin, F. Lesoin, T. Kryst, N. Lannoy, F. Gerstenbrand, S. Ballivet, H. A. M. van Diemen, J. Lopez-ArLandis, P. Bell, A. Silvani, M. A. Garcia, S. Vorstrup, D. Langdon, S. Ueno, B. Sander, V. Ozurk, C. Gurses, P. Berlit, J. M. Martinez-Lage, M. Treacy, S. O. Rodiek, S. Cherninkova, J. Grimaud, P. Marozzi, K. Hasert, S. Goldman, S. H. Ingwersen, A. Taghavy, T. Roig, R. Harper, I. Sarova-Pinchas, Anthony H.V. Schapira, R. Lebtahi, A. Vidaller, B. Stankov, D. Link, J. p. Malin, V. Petrova, Ludwig Kappos, J. L. Ochoa, T. Torbergsen, M. Carpo, M. Donato, Simon Shorvon, J. Mieszkowski, J. Perez-Serra, Raymond Voltz, G. Comi, S. Rafique, A. Perez-Sempere, N. Khalfallah, S. Bailleul, M. Borgers, S. Banfi, S. Mossman, A. Laihinen, G. Filippini, R. A. Grunewald, E. Stern, H. D. Herrmann, A. G. Droogan, P. Xue, A. Grilo, L. La Mantia, J. H. J. Wokke, S. Pizzul, Kie Kian Ang, S. Rapaport, W. Szaplyko, B. Romero, P. Brunet, A. Albanese, C. Davie, V. Crespi, F. Birklein, H. Sharif, L. Jose, D. Auer, N. Heye, Martin N. Rossor, C. E. Henderson, M. J. Koepp, J. Rubio, P. L. Baron, S. Mahal, Juha O. Rinne, J. I. Emparanza, S. E. C. Davies, Frederik Barkhof, M. Riva, R. E. Brenner, B. A. Pope, Lemaire, E. Dupont, D. Ulbricht, G. C. Pastorino, R. Retska, E. Chroni, A. Danielli, V. Malashkhia, T. Canet, J. C. Garcia-Valdecasas, J. Serena, R. A. Pfeiffer, B. Wirk, B. Muzzetto, V. Caruso, M. L. Giros, A. Ming Wang, E. L. E. Guern, F. Bille-Turg, Y. Satoh, C. H. Franke, M. Ait-Kaci-Ahmed, D. Genis, T. Pasierski, D. Riva, M. Panisset, A. Chamorro, P.A. van Doorn, S. Schellong, H. Hamer, F. Durif, P. Krauseneck, Y. Bahou, B. A. Pickut, M. Rijnites, H. Nyland, G. Jager, L. L. Serra, A. Rohl, X. P. Li, O. Arena, Hubert Kwieciński, N. Milpied, M. C. Bourdel, S. Assami, L. Law, J. Moszkowski, J. W. Thorpe, M. Aguennouz, R. Martin, D. Hoffmann, P. Morris, A. Destée, D. J. Charron, U. Senin, A. P. SempereE, M. Dreyfus, A. L. Benabid, M. Gomez, S. Heindle, M. C. Morel-Kopp, M. Hennerici, A. I. Santos, M. Djannelidze, N. Artemis, John Collinge, T. Rundek, M. Y. Voloshin, P. de Castro, Th. Wiethege, D. A. S. Compston, D. Schiffer, A. J. Hughes, D. Jimenez, V. Parlato, A. Papadimitriou, J. M. Gergaud, R. Sterzi, J. Arpa, G. de Pinieux, F. Buggle, P. Gimbergues, H. Ruottinen, R. Marzella, W. Koehler, Y. Yurekli, A. Haase, Z. Privorkin, G. K. Harvey, B. Chave, A. J. Grau, E. M. Stadlan, J. List, C. Zorzi, B.W. van Oosten, P. Derkinderen, B. Casati, J. M. Maloteaux, K. Vahedi, W. L. J. van Putten, J. C. Sabourin, D. Lorenzetti, Plenevaux, J. W. B. Moll, A. Morento Fernandez, M. Lema, M. A. Horsfleld, P. De Jongh, S. Gikova, K. Kutluk, Monique M.B. Breteler, P. Saddier, A. Berbinschi, R. E. Cull, P. Echaniz, H. Kober, C. Minault, V. Kramer, A. L. Edal, S. Passero, T. Eckardt, K. E. Davies, A. Salmaggi, R. Kaiser, A. A. Grasso, Claudio Mariani, G. Egersbach, Hakan Gurvit, O. Dereeper, C. Vital, L. Wrabetz, A. Vecino, M. Aguilar, G. Bielicki, H. Becher, J. Castro, S. Iotti, M. G. Natali-Sora, E. Berta, S. Carlomagno, L. Ayuso-Peralta, P. H. Rondepierre, I. Bonaventura, B. V. Deuren, N. Van Blercom, M. Sciaky, J. Faber, M. Alberoni, M. Nieto, F. Sellal, C. Stelmasiak, M. Takao, J. Bradley, D. Zegers de Beyl, H. Porsche, G. Goi, H. Pongratz, F. Chapon, S. Happe, Robin S. Howard, B. Weder, S. Vlaski-Jekic, J. M. Ferro, R. Nemni, A. Daif, Herbert Budka, W. Van Paesschen, B. Waldecker, F. Carceller, J. Lacau, F. Soga, J. Peres Serra, E. Timmerman, A. M. vd Vliet, J. L. Emparanza, N. Vanacore, A. Pizzuti, N. Marti, A. Davalos, N. Ayraud, U. Zettl, J. Vivancos, Z. Katsarou, H. M. Mehdorn, G. Geraud, M. Merlini, M. Schröter, A. Ebner, M. Lanteri-Minet, R. Soler, G. P. Anzola, S. L. Hauser, L. Cahalon, S. DiDonato, R. Cantello, M. Marchau, J. Gioanni, F. Heidenreich, J. Manuel Martinez Lage, P. Descoins, F. Woimant, J. F. Campo, M. H. Verdier-taillefer, M. S. F. Barkhof, G. J. Kemp, A. O. Ceballos-Baumann, J. Berciano, M. Guidi, Tarek A. Yousry, B. Chandra, A. Rapoport, P. Canhao, A. Spitzer, T. Maeda, J. M. Pereira Monteiro, V. Paquis, Th. Mokrusch, F. J. Arrieta, I. Sangla, F. Canizares-Liebana, Lang Chr, André Delacourte, V. Fetoni, P. Kovachev, D. Kidd, L. Ferini-Strambi, E. Donati, E. Idman, A. Chio, C. Queiros, D. Michaelis, S. Boyacigil, A. Rodrigo, S. M. Yelamos, B. Chassande, P. Louwen, C. Tranchant, E. Ciafalon, A. Lombardo, A. Twijnstra, A. L. Fernandez, H. Kott, A. Cannas, N. Zsurger, T. Zileli, E. Metin, P. C. Bain, G. Fromont, B. Tedesi, A. Liberani, X. Navarro, M. C. Rowbotham, V. Hachinski, F. Cavalcanti, W. Rostene, R. M. Gardiner, F. Gonzalez, B. Köster, E. A. van der Veen, J. P. Lefaucheur, C. Marescaux, D. Boucquey, E. Parati, S. Yamaguchi, A. S. Orb, R. Grant, G. D. P. Smith, P. Goethals, M. Haguenau, G. Georgiev, I. N. van Schaik, Guy A. Rouleau, E. Iceman, G. Fayet, M. G. Kaplitt, C. Baracchini, H. Magnusson, G. Meneghetti, N. Malichard, M. L. Subira, D. Mancia, A. Berenguer, D. Navarrete Palau, H. Franssen, G. Kiziltan, M. P. Lopez, J. Montalt, S. Norby, R. Piedra Crespo, T. L. Rothstein, R. Falip, B. YalÇiner, F. Chedru, I. W. Thorpe, F. W. Heatley, D. S. C. Ochoa, C. Labaune, M. Devoti, O. Lider, Jakob Korf, N. Suzuki, E. A. Maguire, A. Moulignier, J. C. van Swieten, F. Monaco, J. Cartron, A. Steck, B. Uludag, M. Alexandra, H. Reichmann, T. Rossi, L. E. Claveria, A. M. Crouzel, M. A. Mena, J. Gasnault, J. W. Kowalski, S. I. Mellgren, V. Feigin, L. Demisch, J. Montalban, J. Renato, J. Mathieu, N. Goebels, L. Bava, K. Kunre, M. Pulik, S. Di Donato, C. Tzekov, H. Veldman, S. Giménez-Roldan, B. Lechevalier, L. Redondo, B. Pillon, M. Gugenheim, E. Roullet, J. M. Valdueza, C. Gori, H. J. Friedrich, L. de Saint Martin, F. Block, E. Basart, M. Heilmann, B. Becq Giraudon, C. Rodolico, G. Stevanin, Elizabeth K. Warrington, A. T. M. Willemsen, K. Kunze, C. Ben Hamida, M. Alam, J. R. ùther, A. Battistel, G. Della Marca, Richard S. J. Frackowiak, F. Palau, T. Brandt, Chicoutimi, L. Bove, L. Callea, A. Jaspert, T. Klopstock, K. Fassbender, Alan J. Thomas, A. Ferbert, V. Nunes, Douglas Russell, P. Garancini, C. Sanz-Sebastian, O. Santiag, G. Dhaenens, G. Seidel, I. Savic, A. Florea-Strat, M. Rousseaux, N. Catala, E. O'Sullivan, M. J. Manifacier, H. Kurtel, T. Mendel, P. Chariot, M. Salas, D. Brenton, R. Lopez, J. Thorpe, Jimmy D. Bell, E. Hofmann, E. Botia, J. Pacquereau, A. Struppler, C. d'Aniello, D. Conway, A. Garcia-Merino, K. Toyooka, S. Hodgkinson, E. Ciusani, Stefano Bastianello, A. Andrade Filho, M. Zaffaroni, G. Pleiffer, F. Coria, A. Schwartz, D. Baltadjiev, I. Rother, K. Joussen, J. Touchon, K. Kutlul, P. Praamstra, H. Sirin, S. Richard, C. Mariottu, L. Frattola, S. T. Dekesky, G. Wieneke, M. Chatel, O. Godefroy, C. Desnuelle, S. OzckmekÇi, C. H. Zielinski, P. van Deventer, S. Jozwiak, I. Galan, J. M. Grau, V. Vieira, T. A. Treves, S. Ertan, A. Pujol, S. Blecic, E. M. Zanette, F. Ceriani, W. Camu, L. Aquilone, A. Benomar, F. Greco, A. Pascual-Leone Pascual, T. Yanagihara, F. A. Delfino, R. Damels, S. Merkelbach, J. Beltran, A. Barrientos, S. Brugge, B. Hildebrandt-Müller, M. H. Nascimento, M. Rocchi, F. Cervantes, E. Castelli, R. M. Pressler, S. Yeil, A. del Olmo, J. L. Herranz, L. J. Kappelle, Y. Demir, N. Inoue, R. Hershkoviz, A. Luengo, S. Bien, F. Viallet, P. Malaspina, G. De Michele, G. Nolfe, P. Adeleine, T. Liehr, G. Fenelon, H. Masson, Kailash P. Bhatia, W. Haberbosch, S. Mederer, R. S. J. Frackowiak, Tanya Stojkovic, S. Previtali, A. E. Harding, W. Kohler, N. P. Quin, T. R. Marra, J. P. Moisan, A. Melchor, M. L. Viguera, Mary G. Sweeney, G. L. Romani, J. Hezel, R. A. Dierckx, R. Torta, A. Kratzer, T. Pauwels, D. Decoo, Adriana Campi, Neil Kitchen, J. Haas, U. Neubauer, J. J. Merland, A. Yagiz, A. Antonuzzo, A. Zangaladze, J. Parra, Pablo Martinez-Lage, D. J. Brooks, S. Hauser, R. Di Pierri, M. Campero, R. Caldarelli-Stefano, A. M. Colangelo, J. L. Pozo, C. Estol, F. Picard, A. Palmieri, J. Massons, JT Phillips, G. B. Groozman, R. Pentore, L. M. Ossege, C. Bayon, Hans-Peter Hartung, R. Konyalioglu, R. Lampis, D. Ancri, M. Miletta, F. J. Claramonte, W. Retz, F. Hentges, JM Cooper, M. Cordes, M. Limburg, M. Brock, G. R. Coulton, K. Helmke, Rosa Larumbe, A. Ohly, F. Landgraf, A. M. Drewes, Claudia Trenkwalder, M. Keidel, T. Segura, C. Scholz, J. HÄgele, D. Baudoin-Martin, P. Manganelli, J. Valdueza, M. Farinotti, U. Zwiener, M. P. Schiavalla, Y. P. Young, O. Barlas, G. Hertel, E. H. Weiss, M. Eiselt, A. Lossos, M. Bartoli, L. Krolicki, W. Villafana, W. Peterson, Nicoletta Meucci, C. Agbo, R. Luksch, F. Fiacco, G. Ponsot, M. Lopez, Howard L. Weiner, M. D. Alonso, K. Petry, Sanjay M. Sisodiya, P. Giustini, S. Tyrdal, R. Poupon, J. Blanke, P. Oubary, A. A. Kruize, H. Trabucchi, R. R. C. Stewart, H. Grehl, B. M. Kulig, V. Vinhas, D. Spagnoli, B. Mahe, J. Tatay, C. Hess, M. D. Albadalejo, G. Birbamer, M. Alonso, F. Valldeoriola, J. Figols, I. Wirguin, E. Diez Tejedor, C. S. Weiller, L.H. van den Berg, P. Barreiro, L. Pianese, S. Cocozza, R. Kohnen, E. Redolfi, F. Faralli, G. Gosztonyl, A. J. Gur, A. Keyser, V. Fichter-Gagnepain, B. Wildemann, E. Omodeo-Zorini, Gregoire, J. Schopohl, F. Fraschini, G. Wunderlich, B. Jakubowska, F. P. Serra, N. B. Jensen, O. Delattre, C. Leno, A. Dario, P. Grafe, F. Graus, M. C. Vigliani, J. L. Dobato, Philip N. Hawkins, R. Marés, A. Rimola, N. Meussi, G. Aimard, W. Hospers, A. M. Robertson, C. Kaplan, W. Lamadé, Karen E. Morrison, Amadio, E. Kieffer, F. Dromer, P. Bernasconi, M. Repeto, Davide Pareyson, Jeremy Rees, A. Guarneri, P. Odin, P. Bouche, L. Nogueira, J. Munoz, L. Leocani, M. J. Arcusa, R. S. J. Frackowiack, John S. Duncan, D. Karacostas, D. Edwin, I. Costa, M. Menetrey, P. Grieb, A. M. Salvan, S. Cunha, P. Merel, P. Pfeiffer, A. Astier, F. Federico, A. Mrabet, M. G. Buzzi, L. Knudsen, I. F. Pye, L. Falqui, C. R. Hornig, C. E. Shaw, C. Brigel, T. C. Britton, R. Codoceo, T. Pampols, Vincent J. Cunningham, N. Archidiacono, G. Chazot, J. B. Posner, L. L. O. Befalo, M. Monclus, C. Cabezas, H. Moser, H. Stodal, J. Ley-Pozo, L. Brusa, R. Di Mascio, P. Giannini, J. Fernandez, R. Santiago Luis, J. Garcia Tigera, J. Wilmink, P. Pignatelli, M. El Amrani, V. Lucivero, M. Baiget, R. Lodi, P. H. Cabre, L. Grande, A. Korczyn, R. Fahlbusch, C. Milanese, W. Huber, J. Susseve, H. C. Nahser, K. Mondrup, X. O. Breakefield, J. Sarria, T. H. Vogt, A. Alessandri, M. Daffertshofer, I. Nelson, M. L. Monticelli, O. Dammann, G. G. Farnarier, G. Felisari, A. Quattrini, A. Boiardi, P. Mazetti, H. Liu, J. Duarte, M. E. Gaunt, H. Strik, N. Yulug, A. Urman, J. Posner, Aida Suarez Gonzalez, Ma. L. Giros, Z. Matkovic, D. Kompf, A. D. Korczyn, A. Steinbrecher, R. Wenzel, M. C. de Rijk, R. Doronzo, J. Julien, O. Hasegawa, M. Kramer, V. Collado-Scidel, M. Alonso de Lecinana, L. Dell'Arciprete, S. Rapuzzi, S. Bahar, H. Willison, M. T. Ramacci, J.J. Martin, Lopez-Bresnahan, C. Malapani, R. Haaxma, T. Rosenberg, J. Patrignani, R. Vichi, Martin R. Farlow, J. Roquer, L. Krols, M. Pimenta, C. Bucka, U. Klose, M. Roberts, J. Salas-Puig, R. Ghnassia, A. Mercuri, C. Maltempo, I. Tournev, P. Homeyer, D. Caparros-Lefevre, E. P. O. Sullivan, T. Vashadze, Ph. Lyrer, A. Deltoro, H. Kondo, M. Steinling, A. Graham, G. C. Miescher, A. Pace, D. Branca, G. Avello, H. H. Kornhuber, D. Fernandes, H. Friedrich, R. Chorao, H. O. Lüders, R. T. Bax, J. A. Macias, N. Yilmaz, J. Veroust, M. Miller, S. Confort-Gouny, J. L. Sastre, D. Servello, G. Boysen, S. Koeppen, V. Planté-Bordeneuve, H. Albrecht, R. H. M. King, G. Orkodashili, R. Doornbos, H. Toyooka, V. Larrue, M. Sabatelli, K. Williams, M. Stevens, V. Maria, M. Comabella, C. Lammers, R. M. L. Poublon, E. Tizzano, P. Pazzaglia, F. Zoeller, M. B. Delisle, J. P. Goument, J. M. Minderhoud, A. Sghirlanzoni, V. Meininger, M. Al Deeb, C. Bertelt, A. Cagni, A. Algra, F. Morales, K. A. Flugel, M. Maidani, M. Noya, Z. Seidl, U. Roelcke, D. Cannata, E. Katiane EmbiruÇu, E. M. Wicklein, K. Willmes, L. Hanoglu, J. F. Pellissier, Yves Agid, E. Cuadrado, S. Brock, D. Maimone, Z. G. Nadareishvili, E. Matta, S. Hilmi, V. Assuerus, F. Lomena, R. Springer, F. Cabrera-Valdivia, Oscar L. Lopez, M. Casazza, F. Vivancos, Ralf Gold, T. Crawford, B. Moulard, M. Poisson, W. l. McDonald, D. E. Grobbe, Alan Connelly, H. Ozcan, S. Abeta, H. Severo Ochoa, A. C. van Loenen, E. Libson, M. J. Marti, B. George, C. Ferrarese, B. Jacobs, L. Divano, T. Ben-Hur, A. L. Bootsma, V. Martinez, A. Conti, R. P. Maguire, B. Schmidt, D. M. Campos, D. A. Guzman, E. Meary, C. Richart, P. B. Christensen, T. Schroeder, Massimo Zeviani, K. Jensen, R. Aliaga, S. Seitz-Dertinger, J. W. Griffin, C. Fryze, H. Baas, S. Braun, A. M. Porrini, B. Yemez, M. J. Sedano, C. Creisson, A. Del Santo, A. Mainz, R. Kay, S. Livraghi, R. de Waal, D. Macgregor, H. Hefter, R. Garghentino, U. Ruotsalainen, M. Matsumoto, M. G. Beaudry, P. M. Morrison, J. C. Petit, C. Walon, Ph. Chemouilli, F. Henderson, R. Massa, A. Cruz Martinez, U. Liska, F. Hecht, Ernst Holler, V. S. de Bruin, B. B. Sheitman, S. M. Bentzen, C. Bayindir, F. Pallesta, P. E. Roland, J. Parrilla, P. Zunker, L. F. Burchinskaya, G. Mellino, S. Ben Ayed, D. Bonneau, P. Nowacki, M. Goncalves, P. Riederer, N. Mavroudakis, J. Togores, L. Rozewicz, S. Robeck, Y. Perez Gilabert, L. Rampello, A. Rogopoulos, S. Martinez, F. Schildermans, C. Radder, P. B. Hedlund, J. Cambier, M. Aabed, G. D. Jackson, P. Gasparini, P. Santacruz, J. Vandevivere, H. Dural, A. Mantel, W. Dorndorf, N. Ediboglu, A. Lofgren, J. Bogousslavsky, P. Thierauf, L. Goullard, R. Maserati, B. Moering, M. Ryba, J. Serra, G. G. Govan, A. Pascual-Leone, S. Schaeffer, M. R. Rosenfeld, A. P. Correia, K. Ray Chaudhuri, L. Campbell, R. Spreafico, B. Genetet, A. M. Tantot, R. A. G. Hughes, J. A. Vidal, G. Erkol, J. Y. Delattre, B. Yaqub, B. K. Hecht, E. Mayayo, Ph. Scheltens, J. Corral, M. Calaf, L. Henderson, C. Y. Li, U. Bogdahn, R. Sanchez-Roy, M. Navasa, J. Ballabriga, G. Broggi, T. Gudeva, C. Rose, J. Vion-Dury, J. A. Gastaut, J. Pniewski, Nicola J. Robertson, G. Kohncke, M. Billot, S. Gok, E. Castellli, F. Denktas, P. Bazzi, F. Spinelli, I. F. Moseley, C. D. Mardsen, B. Barbiroli, O. M. Koriech, A. Miller, Hiroaki Yoshikawa, F. X. Borruat, J. Zielasek, P. Le Coz, J. Pascual, A. Drouet, L. T. Giron, F. Schondube, R. Midgard, M. Alizadeh, M. Liguori, Lionel Ginsberg, L. Harms, C. Tilgner, G. Tognoni, F. Molteni, Mar Tintoré, M. Psylla, C. Goulon-Goeau, M. V. Aguilar, Massimo Filippi, K. H. Mauritz, Thomas V. Fernandez, C. Basset, S. Rossi, P. Meneses, B. Jandolo, T. Locatelli, D. Shechtcr, C. Magnani, R. Ferri, Bruno Dubois, J. M. Warier, S. Berges, F. Idiman, M. Schabet, R. R. Diehl, P. D'aurelio, M. Musior, Reinhard Hohlfeld, P. Smeyers, M. Olivé, A. Riva, C. A. Broere, N. Egund, S. Franceschetti, V. Bonavita, Nicola Canal, E. Timmermans, M. Ruiz, S. Barrandon, G. Vasilaski, B. Deweer, L. Galiano, S. F. T. M. de Bruijn, L. Masana, A. Goossens, B. Heye, K. Lauer, Heinz Gregor Wieser, Stephen R. Williams, B. Garavaglia, A. P. Sempere, F. Grigoletto, P. Poindron, R. Lopez-Pajares, I. Leite, T. A. McNell, C. Caucheteur, J. M. Giron, A. D. Collins, P. Freger, J. Sanhez Del Rio, D. A. Harn, K. Lindner, S. S. Scherer, G. Serve, M. Juncadella, X. Estivill, R. Binkhorst, M. Anderson, B. Tekinsoy, C. Sagan, T. Anastopoulos, G. Japaridze, S. Guillou, F. Erminio, Jon Sussman, P. G. Oomes, D. S. Rust, S. Mascheroni, O. Berger, M. Peresson, K. V. Toyka, T. W. Polder, M. Huberman, B. Arpaci, H. Ramtami, I. Martinez, Ph. Violon, P. P. Gazzaniga Pozzill, R. Ruda, P. Auzou, J. Parker, S. P. Morrissey, Jiahong Zhu, F. Rotondi, P. Baron, W. Schmid, P. Doneda, M. Spadaro, M. C. Nargeot, I. Banchs, J.S.P. van den Berg, R. Ferrai, M. Robotti, M. Fredj, Pedro M. Rodríguez Cruz, B. Erne, D. G. Piepgras, M. C. Arne-Bes, J. Escudero, C. Goetz, A. R. Naylor, M. Hallett, O. Abramsky, E. Bonifacio, L. E. Larsson, R. Pellikka, P. Valalentino, D. Guidetti, B. Buchwald, C. H. Lücking, D. Gauvreau, F. Pfaff, A. Ben Younes-Chennoufi, R. Kiefer, R. Massot, K. A. Hossmann, L. Werdelin, P. J. Baxter, U. Ziflo, S. Allaria, C. D. Marsden, M. Cabaret, S. P. Mueller, E. Calabrese, R. Colao, S. I. Bekkelund, M. Yilmaz, O. Oktem-Tanor, R. Gine, M. E. Scheulen, J. Beuuer, A. Melo, Z. Gulay, M. D. Have, C. Frith, D. Liberati, J. Gozlan, P. Rondot, Ch. Brunholzl, M. Pocchiari, J. Pena, L. Moiola, C. Salvadori, A. Cabello, T. Catarci, S. Webb, C. Dettmers, N. A. Gregson, Alexandra Durr, F. Iglesias, U. Knorr, L. Ferrini-Strambi, F. Kruggel, P. Allard, A. Coquerel, P. Genet, F. Vinuels, C. Oberwittler, A. Torbicki, P. Leffers, B. Renault, B. Fauser, C. Ciano, G. Uziel, J. M. Gibson, F. Anaya, C. Derouesné, C. N. Anagnostou, M. Kaido, W. Eickhoff, G. Talerico, M. L. Berthier, A. Capdevila, M. Alons, D. Rezek, E. Wondrusch, U. Kauerz, D. Mateo, M. A. Chornet, Holon, N. Pinsard, I. Doganer, E. Paoino, H. Strenge, C. Diaz, J. R. Brasic, W. Heide, I. Santilli, W. M. Korn, D. Selcuki, M. J. Barrett, D. Krieger, T. Leon, T. Houallah, M. Tournilhac, C. Nos, D. Chavot, F. Barbieri, F. J. Jimenez-Jimenez, J. Muruzabal, K. Poeck, A. Sennlaub, L. M. Iriarte, L. G. Lazzarino, C. Sanz, P. A. Fischer, S. D. Shorvon, R. Hoermann, F. Delecluse, M. Krams, O. Corabianu, F. H. Hochberg, Christopher J. Mathias, B. Debachy, C. M. Poser, L. Delodovici, A. Jimenez-Escrig, F. Baruzzi, F. Godenberg, D. Cucinotta, P. J. Garcia Ruiz, K. Maier-Hauff, P. R. Bar, R. Mezt, R. Jochens, S. Karakaneva, C. Roberti, E. Caballero, Joseph E. Parisi, M. Zamboni, T. Lacasa, B. Baklan, J. C. Gautier, J. A. Martinez-Matos, W. Pollmann, G. Thomas, L. Verze, E. Chleide, R. Alvarez Sala, I. Noel, E. Albuisson, O. Kastrup, S. I. Rapoport, H. J. Braune, H. Lörler, M. Le Merrer, A. Biraben, S. Soler, S. J. Taagholt, U. Meyding-Lamadé, K. Bleasdale-Barr, Isabella Moroni, Y. Campos, J. Matias-Guiu, G. Edan, M. G. Bousser, John B. Clark, J. Garcia de Yebenes, N. K. Olsen, P. Hitzenberger, S. Einius, Aj Thompson, Ch. J. Vecht, T. Crepin-Leblond, Klaus L. Leenders, A. Di Muzio, L. Georgieva, René Spiegel, K. Sabey, D. Ménégalli, J. Meulstee, U. Liszka, P. Giral, C. Sunol, J. M. Espadaler, A. D. Crockar, K. Varli, G. Giraud, P. J. Hülser, A. Benazzouz, A. Reggio, M. Salvatore, K. Genc, M. Kushnir, S. Barbieri, J. Ph. Azulay, M. Gianelli, N. Bathien, A. AlMemar, F. Hentati, I. Ragueneau, F. Chiarotti, R. C. F. Smits, A. K. Asbury, F. Lacruz, B. Muller, Alan J. Thompson, Gordon Smith, K. Schmidt, C. Daems Monpeun, Juergen Weber, A. Arboix, G. R. Fink, A. M. Cobo, M. Ait Kaci Ahmed, E. Gencheva, Israel-Biet, G. Schlaug, P. De Jonghe, Philip Scheltens, K. Toyka, P. Gonzalez-Porque, A. Cila, J. M. Fernandez, P. Augustin, J. Siclia, S. Medaglini, D. E. Ziogas, A. Feve, L. Kater, G. J. E. Rinkel, D. Leppert, Rüdiger J. Seitz, S. Ried, C. Turc-Carel, G. Smeyers, F. Godinho, M. Czygan, M. Rijntjes, E. Aversa, M. Frigo, Leif Østergaard, J. L. Munoz Blanco, A. Cruz-Matinez, J. De Reuck, C. Theillet, T. Barroso, V. Oikonen, Florence Lebert, M. Kilinc, C. Cordon-Cardon, G. Stoll, E. Thiery, F. Pulcinelli, J. Solski, M. Schmiegelow, L. J. Polman, P. Fernandez-Calle, C. Wikkelso, M. Ben Hamida, M. Laska, E. Kott, W. Sulkowski, C. Lucas, N. M. Bornstein, D. Schmitz, M. W. Lammers, A. de Louw, R. J. S. Wise, P. A. van Darn, C. Antozzi, P. Villanueva, P. H. E. Hilkens, C. Constantin, W. Ricart, A. Wolf, M. Gamba, P. Maguire, Alessandro Padovani, B. M. Patten, Marie Sarazin, H. Ackermann, L. Durelli, S. Timsit, Sebastian Jander, B. W. Scheithauer, G. Demir, J. P. Neau, P. Barbanti, A. Brand, N. AraÇ, V. Fischer-Gagnepain, R. Marchioli, G. Serratrice, C. Maugard-Louboutin, G. T. Spencer, D. Lücke, G. Mainardi, K. Harmant Van Rijckevorsel, G. B. Creel, R. Manzanares, Francesco Fortunato, A. May, J. Workman, K. Johkura, E. Fernandez, Carlo Colosimo, L. Calliauw, L. Bet, Félix F. Cruz-Sánchez, M. Dhib, H. 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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11. Mapping the onset and progression of atrophy in familial frontotemporal lobar degeneration

Author

Lisa Cipolotti, Jonathan M. Schott, JM Stevens, JC Janssen, Martin N. Rossor, Nick C. Fox, Keith A. Josephs, Rachael I. Scahill, JANSSEN JC, SCHOTT JM, CIPOLOTTI L, FOX NC, SCAHILL RI, JOSEPHS KA, STEVENS JM, and ROSSOR MN

Subjects
Paper, Male, Pathology, medicine.medical_specialty, Disease, Neuropsychological Tests, Asymptomatic, Brain mapping, Atrophy, Brain/pathology, Brain Mapping, Dementia/pathology, Disease Progression, Female, Follow-Up Studies, Humans, Male, Middle Aged, Neuropsychological Tests, Atrophy, mental disorders, medicine, Humans, Dementia, Brain Mapping, Settore M-PSI/02 - Psicobiologia E Psicologia Fisiologica, Neuropsychology, food and beverages, nutritional and metabolic diseases, Brain, Autosomal dominant trait, Frontotemporal lobar degeneration, Middle Aged, medicine.disease, nervous system diseases, Psychiatry and Mental health, Disease Progression, Female, Surgery, Neurology (clinical), medicine.symptom, Psychology, Follow-Up Studies
Abstract

Background: Frontotemporal lobar degeneration (FTLD) may be inherited as an autosomal dominant disease. Studying patients "at risk" for developing FTLD can provide insights into the earliest onset and evolution of the disease. Method: We carried out approximately annual clinical, MRI, and neuropsychological assessments on an asymptomatic 51 year old "at risk" family member from a family with FTLD associated with ubiquitin-positive and tau-negative inclusion bodies. We used non-linear (fluid) registration of serial MRI to determine areas undergoing significant regional atrophy at different stages of the disease. Results: Over the first 26 months of the study, the patient remained asymptomatic, but subsequently developed progressive speech production difficulties, and latterly severe orofacial dyspraxia, dyscalculia, frontal executive impairment, and limb dyspraxia. Regional atrophy was present prior to the onset of symptoms, and was initially centred on the left dorsolateral prefrontal cortex and the left middle frontal gyrus. Latterly, there was increasing asymmetric left frontal and parietal atrophy. Imaging revealed excess and increasing global atrophy throughout the study. Neuropsychological evaluation revealed mild intellectual impairment prior to the onset of these clinical symptoms; frontal executive and left parietal impairment subsequently emerged, culminating in widespread cognitive impairment. Fluid registered MRI allowed the emerging atrophy patterns to be delineated. Conclusion: We have demonstrated the onset and progressive pattern of in vivo atrophy in familial FTLD using fluid registered MRI and correlated this with the clinical features. Fluid registered MRI may be a useful technique in assessing patterns of focal atrophy in vivo and demonstrating the progression of degenerative diseases.

Published
2005

12. Cerebral achromatopsia as a presentation of Trousseau’s syndrome

Author

M. James-Galton, Martin N. Rossor, Richard W. Orrell, and JM Stevens

Subjects
Male, medicine.medical_specialty, Achromatopsia, Paraneoplastic Syndromes, Infarction, Color Vision Defects, Internal medicine, Coagulopathy, medicine, Humans, Stroke, Aged, Carcinoma, Transitional Cell, medicine.diagnostic_test, business.industry, Cerebral infarction, Magnetic resonance imaging, Cerebral Infarction, General Medicine, Disseminated Intravascular Coagulation, medicine.disease, Magnetic Resonance Imaging, eye diseases, Cerebral achromatopsia, Surgery, Urinary Bladder Neoplasms, Cardiology, Occipital lobe, business, Research Article
Abstract

Summary A 67-year-old man developed a sudden onset of achromatopsia. Magnetic resonance imaging showed occipital lobe infarction. Repeated episodes of neurological deficit referable to the posterior circulation initially suggested an embolic source, but subsequently proved to be due to a coagulopathy related to a carcinoma of the bladder. This has implications for the management of patients presenting with achromatopsia, and progressive or recurrent neurological episodes, and in particular the use of anticoagulation in this situation.

Published
1995
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13. Cerebral and cerebellar atrophy on serial magnetic resonance imaging in an initially symptom free subject at risk of familial prion disease

Author

K.F. Mekkaoui, Nick C. Fox, P.A. Freeborough, Martin N. Rossor, and JM Stevens

Subjects
Adult, Pathology, medicine.medical_specialty, Cerebellum, Ataxia, animal diseases, Prion Diseases, Central nervous system disease, Atrophy, Degenerative disease, Risk Factors, mental disorders, medicine, Humans, General Environmental Science, medicine.diagnostic_test, business.industry, General Engineering, Brain, Magnetic resonance imaging, General Medicine, medicine.disease, Magnetic Resonance Imaging, nervous system diseases, medicine.anatomical_structure, General Earth and Planetary Sciences, Cerebellar atrophy, Female, medicine.symptom, business, Myoclonus, Research Article
Abstract

Prion diseases are transmissible neurodegenerative conditions which occur in sporadic, acquired, or inherited forms. Sporadic Creutzfeldt-Jakob disease presents as a rapidly progressive dementia with myoclonus, most patients showing characteristic pseudoperiodic complexes on electroencephalography. A new variant of Creutzfeldt-Jakob is characterised by a younger age at onset, longer survival, and non-specific initial symptoms including behavioural changes, dysaesthesias, and ataxia but without the expected electroencephalographic changes.1 Some of these features are also found in 5-15% of all cases of the inherited forms of Creutzfeldt-Jakob disease and are associated with mutations in the prion protein gene.2 We report the case of a woman with a family history of prion disease in whom progressive cerebral and cerebellar atrophy was seen when two magnetic resonance scans were compared using registration. A 42 year old woman from a family with histologically confirmed prion disease entered …

Published
1997

14. Presymptomatic hippocampal atrophy in Alzheimer's disease. A longitudinal MRI study

Author

P.A. Freeborough, JM Stevens, Nick C. Fox, Päivi Hartikainen, Elizabeth K. Warrington, Martin N. Rossor, and A. M. Kennedy

Subjects
Cerebral atrophy, Male, Longitudinal study, Pathology, medicine.medical_specialty, Middle Aged, medicine.disease, Asymptomatic, Hippocampus, Magnetic Resonance Imaging, Central nervous system disease, Amyloid beta-Protein Precursor, Degenerative disease, Atrophy, Alzheimer Disease, Mutation, medicine, Dementia, Humans, Female, Neurology (clinical), medicine.symptom, Alzheimer's disease, Psychology, Aged
Abstract

The hippocampal formation (HF) is known from pathological and MRI studies to be severely atrophied in established Alzheimer's disease. However, it is unclear when the earliest changes in the HF occur. We performed a longitudinal study of asymptomatic individuals at risk of autosomal dominant familial Alzheimer's disease in order to assess presymptomatic changes in the HF. Seven at risk members of a familial Alzheimer's disease pedigree associated with the amyloid precursor protein 717 valine to glycine mutation underwent serial MR scanning and neuropsychological assessments over 3 years. These assessments were compared with results from 38 normal controls. During the study three at risk subjects became clinically affected. Volumetric measurement of the HF showed that asymmetrical atrophy developed in these subjects before the appearance of symptoms. Verbal and visual memory measures declined in parallel with hippocampal loss. A loss of up to 8% per annum of the volume of the HF occurred in the 2 years over which symptoms first appeared. These findings may have implications for early diagnosis of Alzheimer's disease.

Published
1996

15. Chromosome 14 linked familial Alzheimer's disease. A clinico-pathological study of a single pedigree

Author

Elizabeth K. Warrington, Martin N. Rossor, S Newman, A. M. Kennedy, Vincent J. Cunningham, R. S J Frackowiak, JM Stevens, P Roques, C. J. Bruton, and David Neary

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Genetic Linkage, Neurological examination, Neuropsychological Tests, Alzheimer Disease, Memory, medicine, Humans, Cerebral atrophy, Chromosomes, Human, Pair 14, Brain Diseases, medicine.diagnostic_test, Neuropsychological test, Middle Aged, medicine.disease, Magnetic Resonance Imaging, Hyperintensity, Pedigree, Glucose, Allelic heterogeneity, Female, Neurology (clinical), Alzheimer's disease, medicine.symptom, Age of onset, Psychology, Myoclonus, Tomography, Emission-Computed
Abstract

Summary The Clinical features of three affected members of a British pedigree with familial Alzheimer's disease are presented. This pedigree is one of six included in an earlier study which demonstrated linkage to chromosome 14. The individuals were investigated clinically and neuropsychologically, using both PET and MRI over a 4-year period. Further information from three deceased individuals was obtained, including histopathological confirmation of Alzheimer's disease in one case which came to autopsy. The mean age at onset for this family was 43 years. Neurological examination revealed myoclonic jerks in all cases, and one patient was documented to have seizures. Strikingly similar neuropsychological profiles were observed, characterized by an initial memory deficit with early dyscalculia and an impairment in speech production with relative absence of anomia. All individuals showed mild degrees of cerebral atrophy and two individuals had periventricular white matter lesions. PET scanning using [18F]fluorodeoxyglucose showed parieto-temporal hypometabolism in all cases and the two severely affected patients with speech production changes had additional left-sided frontal hypometabolism involving Broca's area. The least affected case initially had a more asymmetrical reduction in metabolism in the left inferior temporal and supramarginal gyri; a follow-up scan showed that this deficit had become bilateral and more severe. These clinical and neuroimaging features have not been previously reported in chromosome 14 linked pedigrees; the phenotypic variability between families suggests allelic heterogeneity at the chromosome 14 locus.

Published
1995

16. Autologous PBSCT in patients with cardiac amyloidosis

Author

D Smyth, Ruth Spearing, D Bowie, WN Patton, G Shaw, JM Stevens, D. C. Heaton, and Raymond L. Comenzo

Subjects
Transplantation, medicine.medical_specialty, Cardiac amyloidosis, business.industry, medicine, In patient, Hematology, business, Surgery
Published
2000
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17. Computed Tomography of Congenital Brain Malformations

Author

Jm Stevens

Subjects
Psychiatry and Mental health, medicine.medical_specialty, Pathology, medicine.diagnostic_test, business.industry, Book Reviews, medicine, Surgery, Computed tomography, Neurology (clinical), Radiology, business
Published
1985

18. Provisional clinical and neuroradiological criteria for the diagnosis of Pick's disease

Author

Hans Spinnler, Ulla Passant, Nigel J. Cairns, Suzie Barker, Nicola T. Lautenschlager, Elizabeth K. Warrington, R Cacabelos, Elisabet Englund, Monique M.B. Breteler, Alexander Kurz, Laura Bracco, Peter L. Lantos, Rivka Ravid, Enrico Grassi, François Boller, J. C. van Swieten, Richard J. Harvey, Florence Pasquier, Stefano F. Cappa, Hans Förstl, A Brun, Lisa Cipolotti, G. Binetti, John H. Xuereb, Florence Lebert, XA Alvarez, Paolo Forleo, Sandro Sorbi, JM Stevens, S Muggia, L Gustafson, John Collinge, John R. Hodges, and Martin N. Rossor

Subjects
medicine.medical_specialty, Neurology, business.industry, General surgery, Medicine, Pick's disease, Neurology (clinical), business, medicine.disease

20. Self-report of symptom cluster experiences in cancer patient-caregiver dyads.

Author

Kwekkeboom KL, Stevens JM, Berghoff A, and Litzelman K

Subjects
Humans, Female, Male, Middle Aged, Aged, Adult, Surveys and Questionnaires, Neoplasms psychology, Neoplasms complications, Caregivers psychology, Self Report
Abstract

Purpose: Symptom clusters have important health implications in the context of cancer, but the symptom cluster experiences of cancer caregivers and patient-caregiver dyads are not well studied. To date, most studies report statistically derived symptom clusters among patients and fail to consider the caregivers' experience. This study aimed to assess and characterize self-reported symptom cluster experiences in cancer patient-caregiver dyads., Methods: We recruited 30 patient-caregiver dyads from the outpatient oncology clinics at a Comprehensive Cancer Center in the Midwestern U.S. Participants completed web-based surveys reporting their symptom clusters at weekly intervals over 8 weeks of cancer treatment., Results: Among 48 eligible dyads, 30 (63%) agreed to participate, 29 provided data, and ≥ 80% (24 patients, 26 caregivers) completed the study. Twenty-eight patients (97%) and twenty-two caregivers (76%) reported experiencing symptoms in clusters. There was substantial variability in the symptoms reported, perceived causality, and directional relationships among symptoms, however both patients' and caregivers' frequently described symptom clusters with psychoneurologic components (co-occurring pain, fatigue, sleep disturbance, anxiety, depression, lack of appetite and/or cognitive disturbance). Symptom clusters were perceived to have a moderate impact on patients' daily lives and a mild-to-moderate impact on caregivers' daily lives., Conclusion: Dyad members experienced and successfully self-reported symptom clusters, with psychoneurologic symptom clusters prevalent among both patients and their caregivers. Self-report of symptom cluster experiences provides unique insight relevant to clinical management. Findings provide foundational support for development and testing of dyad-based interventions to mitigate symptom clusters and their negative impact on daily life among cancer-patient caregiver dyads., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Published
2024
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21. Differential role of M cells in enteroid infection by Mycobacterium avium subsp. paratuberculosis and Salmonella enterica serovar Typhimurium.

Author

Alfituri OA, Blake R, Jensen K, Mabbott NA, Hope J, and Stevens JM

Subjects
Animals, Mice, Paratuberculosis microbiology, Microbial Viability, Intestinal Mucosa microbiology, Cattle, M Cells, Mycobacterium avium subsp. paratuberculosis physiology, Salmonella typhimurium physiology, Salmonella typhimurium pathogenicity
Abstract

Infection of ruminants such as cattle with Mycobacterium avium subsp . paratuberculosis (MAP) causes Johne's disease, a disease characterized by chronic inflammation of the small intestine and diarrhoea. Infection with MAP is acquired via the faecal-to-oral route and the pathogen initially invades the epithelial lining of the small intestine. In this study we used an in vitro 3D mouse enteroid model to determine the influence of M cells in infection of the gut epithelia by MAP, in comparison with another bacterial intestinal pathogen of veterinary importance, Salmonella enterica serovar Typhimurium. The differentiation of M cells in the enteroid cultures was induced by stimulation with the cytokine receptor activator of nuclear factor-κB ligand (RANKL), and the effects on MAP and Salmonella uptake and intracellular survival were determined. The presence of M cells in the cultures correlated with increased uptake and intracellular survival of Salmonella , but had no effect on MAP. Interestingly neither pathogen was observed to preferentially accumulate within GP2-positive M cells., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Alfituri, Blake, Jensen, Mabbott, Hope and Stevens.)

Published
2024
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22. Common patient-reported sources of cancer-related distress in adults with cancer: A systematic review.

Author

Stevens JM, Montgomery K, Miller M, Saeidzadeh S, and Kwekkeboom KL

Subjects
Adult, Female, Humans, Male, Patient Reported Outcome Measures, Psychological Distress, Neoplasms psychology
Abstract

Background: Cancer-related distress (CRD) is widely experienced by people with cancer and is associated with poor outcomes. CRD screening is a recommended practice; however, CRD remains under-treated due to limited resources targeting unique sources (problems) contributing to CRD. Understanding which sources of CRD are most commonly reported will allow allocation of resources including equipping healthcare providers for intervention., Methods: We conducted a systematic review to describe the frequency of patient-reported sources of CRD and to identify relationships with CRD severity, demographics, and clinical characteristics. We included empirical studies that screened adults with cancer using the NCCN or similar problem list. Most and least common sources of CRD were identified using weighted proportions computed across studies. Relationships between sources of CRD and CRD severity, demographics, and clinical characteristics were summarized narratively., Results: Forty-eight studies were included. The most frequent sources of CRD were worry (55%), fatigue (54%), fears (45%), sadness (44%), pain (41%), and sleep disturbance (40%). Having enough food (0%), substance abuse (3%), childbearing ability (5%), fevers (5%), and spiritual concerns (5%) were infrequently reported. Sources of CRD were related to CRD severity, sex, age, race, marital status, income, education, rurality, treatment type, cancer grade, performance status, and timing of screening., Conclusions: Sources of CRD were most frequently emotional and physical, and resources should be targeted to these sources. Relationships between sources of CRD and demographic and clinical variables may suggest profiles of patient subgroups that share similar sources of CRD. Further investigation is necessary to direct intervention development and testing., (© 2024 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd.)

Published
2024
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23. Qualitative Behavioural Assessment of bonobo emotional expressivity across observer groups and zoo housing environments.

Author

Laméris DW, Salas M, Eens M, Gillespie L, Staes N, Torfs JR, Verspeek J, Vervaecke H, Ward SJ, and Stevens JM

Abstract

Human evaluation of animal emotional expressivity can inform animal welfare. Qualitative Behavioural Assessment (QBA) has been applied to domesticated and some non-domesticated animals, but its use in primates is limited despite their emotional expressivity. We aimed to develop and apply a QBA for bonobos ( Pan paniscus ) through two consecutive studies. We applied Free Choice Profiling (FCP) and the Fixed List methodology, respectively, in Study 1 and 2, and invited students and bonobo experts to rate video clips of zoo-living bonobos of different sexes and age classes, and before and after moving to a new enclosure. In Study 1, students described dimension 1 as ranging from 'quiet/calm' to 'angry/active' and dimension 2 from 'sad/anxious' to 'happy/loving'. Experts described dimension 1 ranging from 'quiet/relaxed' to 'nervous/alert' and dimension 2 from 'nervous/bored' to 'playful/happy'. Using a fixed list of descriptors, informed by findings from Study 1, students in Study 2 described dimension 1 as ranging from 'quiet/calm' to 'agitated/frustrated', and dimension 2 from 'sad/stressed' to 'happy/positively engaged'. Experts described dimension 1 as ranging from 'quiet/calm' to 'active/excited', and dimension 2 from 'sad/bored' to 'happy/positively engaged'. Students scored adults as more 'calm/quiet' and experts scored subadults as more 'happy/positively engaged'. Additionally, experts in Study 2 rated bonobos as more 'active/excited' in their new enclosure. Reliability was moderate to good for the dimensions. Additionally, animal-directed empathy of observers influenced QBA scores. This is the first time, FCP has been successfully used as a method to study primate emotional expressivity. Our findings show the promise of employing QBA in primate studies and in industry, with validation of additional metrics to enable its use for welfare-monitoring purposes., Competing Interests: None., (© The Author(s) 2024.)

Published
2024
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24. Identifying general reaction conditions by bandit optimization.

Author

Wang JY, Stevens JM, Kariofillis SK, Tom MJ, Golden DL, Li J, Tabora JE, Parasram M, Shields BJ, Primer DN, Hao B, Del Valle D, DiSomma S, Furman A, Zipp GG, Melnikov S, Paulson J, and Doyle AG

Abstract

Reaction conditions that are generally applicable to a wide variety of substrates are highly desired, especially in the pharmaceutical and chemical industries 1-6 . Although many approaches are available to evaluate the general applicability of developed conditions, a universal approach to efficiently discover these conditions during optimizations is rare. Here we report the design, implementation and application of reinforcement learning bandit optimization models 7-10 to identify generally applicable conditions by efficient condition sampling and evaluation of experimental feedback. Performance benchmarking on existing datasets statistically showed high accuracies for identifying general conditions, with up to 31% improvement over baselines that mimic state-of-the-art optimization approaches. A palladium-catalysed imidazole C-H arylation reaction, an aniline amide coupling reaction and a phenol alkylation reaction were investigated experimentally to evaluate use cases and functionalities of the bandit optimization model in practice. In all three cases, the reaction conditions that were most generally applicable yet not well studied for the respective reaction were identified after surveying less than 15% of the expert-designed reaction space., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

Published
2024
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25. Radiolucent line assessment in cemented stemmed total knee (RISK) arthroplasty: validation of a modernized classification system.

Author

Francis SL, Murphy BPDS, Elsiwy Y, Babazadeh S, Clement ND, Stoney JD, and Stevens JM

Subjects
Humans, Retrospective Studies, Reproducibility of Results, Knee Joint surgery, Tibia diagnostic imaging, Tibia surgery, Arthroplasty, Replacement, Knee, Knee Prosthesis
Abstract

Background: This study aims to implement and assess the inter- and intra-reliability of a modernized radiolucency assessment system; the Radiolucency In cemented Stemmed Knee (RISK) arthroplasty classification. Furthermore, we assessed the distribution of regions affected by radiolucency in patients undergoing stemmed cemented total knee arthroplasty., Methods: Stemmed total knee arthroplasty cases over 7-year period at a single institution were retrospectively identified and reviewed. The RISK classification system identifies five zones in the femur and five zones in the tibia in both the anteroposterior (AP) and lateral planes. Post-operative and follow-up radiographs were scored for radiolucency by four blinded reviewers at two distinct time points four weeks apart. Reliability was assessed using the kappa statistic. A heat map was generated to demonstrate the reported regions of radiolucency., Results: 29 cases (63 radiographs) of stemmed total knee arthroplasty were examined radiographically using the RISK classification system. Intra-reliability (0.83) and Inter-reliability (0.80) scores were both consistent with a strong level of agreement using the kappa scoring system. Radiolucency was more commonly associated with the tibial component (76.6%) compared to the femoral component (23.3%), and the tibial anterior-posterior (AP) region 1 (medial plateau) was the most affected (14.9%)., Conclusion: The RISK classification system is a reliable assessment tool for evaluating radiolucency around stemmed total knee arthroplasty using defined zones on both AP and lateral radiographs. Zones of radiolucency identified in this study may be relevant to implant survival and corresponded well with zones of fixation, which may help inform future research., (© 2023. The Author(s), under exclusive licence to Springer-Verlag France SAS, part of Springer Nature.)

Published
2023
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26. Psychometrics of Three Dissociation Scales: Reliability and Validity Data on the DESR, DES-II, and DESC.

Author

Arzoumanian MA, Verbeck EG, Estrellado JE, Thompson KJ, Dahlin K, Hennrich EJ, Stevens JM, and Dalenberg CJ

Subjects
Adult, Humans, Psychometrics, Reproducibility of Results, Psychiatric Status Rating Scales, Surveys and Questionnaires, Dissociative Disorders diagnosis, Stress Disorders, Post-Traumatic diagnosis
Abstract

The current study assessed the reliability and validity of three measures of dissociation. Three hundred students completed the Dissociative Experiences Scale Revised (DESR), the Dissociative Experiences Scale-II (DES-II), and the Dissociative Experiences Scale Comparison (DESC); an additional 252 community adults evaluated clarity of instructions. Findings revealed that the three dissociation measures showed acceptable test-retest reliability and Cronbach's alphas. The DESR and DES-II strongly intercorrelated, but the DESC correlated only moderately with the two remaining dissociation measures, sharing less than 10% of the variance with the original scale. Additionally, the DESR and DES-II showed stronger convergent validity (correlation with measures of alexithymia and post-traumatic stress disorder) than did the DESC. The DESC was the only measure unrelated to trauma history. Participants reported substantially greater difficulty in understanding and utilizing the metric offered by the DESC. In conclusion, evidence supports the DES-II and DESR as alternate measures, but the DESC requires more investigation.

Published
2023
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27. Analysis of the role of the QseBC two-component sensory system in epinephrine-induced motility and intracellular replication of Burkholderia pseudomallei.

Author

Meethai C, Vanaporn M, Intarak N, Lerdsittikul V, Withatanung P, Janesomboon S, Vattanaviboon P, Chareonsudjai S, Wilkinson T, Stevens MP, Stevens JM, and Korbsrisate S

Subjects
Animals, Humans, Mice, Bacterial Proteins genetics, Bacterial Proteins metabolism, Epinephrine pharmacology, Epinephrine metabolism, Flagellin metabolism, Burkholderia pseudomallei metabolism, Melioidosis
Abstract

Burkholderia pseudomallei is a facultative intracellular bacterial pathogen that causes melioidosis, a severe invasive disease of humans. We previously reported that the stress-related catecholamine hormone epinephrine enhances motility of B. pseudomallei, transcription of flagellar genes and the production of flagellin. It has been reported that the QseBC two-component sensory system regulates motility and virulence-associated genes in other Gram-negative bacteria in response to stress-related catecholamines, albeit disparities between studies exist. We constructed and whole-genome sequenced a mutant of B. pseudomallei with a deletion spanning the predicted qseBC homologues (bpsl0806 and bpsl0807). The ΔqseBC mutant exhibited significantly reduced swimming and swarming motility and reduced transcription of fliC. It also exhibited a defect in biofilm formation and net intracellular survival in J774A.1 murine macrophage-like cells. While epinephrine enhanced bacterial motility and fliC transcription, no further reduction in these phenotypes was observed with the ΔqseBC mutant in the presence of epinephrine. Plasmid-mediated expression of qseBC suppressed bacterial growth, complicating attempts to trans-complement mutant phenotypes. Our data support a role for QseBC in motility, biofilm formation and net intracellular survival of B. pseudomallei, but indicate that it is not essential for epinephrine-induced motility per se., Competing Interests: The authors declare that no competing interests exist., (Copyright: © 2023 Meethai et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Published
2023
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28. Coupling-Condensation Strategy for the Convergent Synthesis of an Imidazole-Fused 2-Aminoquinoline NLRP3 Agonist.

Author

Bi C, Chadwick J, Davies ML, DelMonte AJ, Geng P, Glace AW, Green RA, Gurak JA Jr, Haley MW, He BL, Inankur B, Jamison CR, Joe CL, Kolotuchin S, Lin D, Lou S, Nye J, Ortiz A, Purdum GE, Rosso VW, Shah M, Simmons EM, Stevens JM, Strotman NA, Tan Y, and Zhang L

Subjects
Cyclization, Acylation, NLR Family, Pyrin Domain-Containing 3 Protein, Imidazoles
Abstract

The development of a convergent route to the NLRP3 (nucleotide-binding domain and leucine-rich repeat-containing protein 3) agonist BMS-986299 is reported. The synthesis relies on a key Miyaura borylation and a tandem Suzuki-Miyaura coupling between an iodoimidazole and an o -aminochloroarene, followed by acid-mediated cyclization to afford the aminoquinoline core. The subsequent Boc cleavage and regioselective acylation afford the target compound. Two routes to the iodoimidazole intermediate are presented, along with the synthesis of the o -aminochloroarene via Negishi coupling. The convergent six-step route leads to an 80% reduction in process mass intensity compared to the linear enabling synthesis.

Published
2023
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29. A Multi-Objective Active Learning Platform and Web App for Reaction Optimization.

Author

Torres JAG, Lau SH, Anchuri P, Stevens JM, Tabora JE, Li J, Borovika A, Adams RP, and Doyle AG

Subjects
Humans, Bayes Theorem, Software, Mobile Applications
Abstract

We report the development of an open-source experimental design via Bayesian optimization platform for multi-objective reaction optimization. Using high-throughput experimentation (HTE) and virtual screening data sets containing high-dimensional continuous and discrete variables, we optimized the performance of the platform by fine-tuning the algorithm components such as reaction encodings, surrogate model parameters, and initialization techniques. Having established the framework, we applied the optimizer to real-world test scenarios for the simultaneous optimization of the reaction yield and enantioselectivity in a Ni/photoredox-catalyzed enantioselective cross-electrophile coupling of styrene oxide with two different aryl iodide substrates. Starting with no previous experimental data, the Bayesian optimizer identified reaction conditions that surpassed the previously human-driven optimization campaigns within 15 and 24 experiments, for each substrate, among 1728 possible configurations available in each optimization. To make the platform more accessible to nonexperts, we developed a graphical user interface (GUI) that can be accessed online through a web-based application and incorporated features such as condition modification on the fly and data visualization. This web application does not require software installation, removing any programming barrier to use the platform, which enables chemists to integrate Bayesian optimization routines into their everyday laboratory practices.

Published
2022
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31. Lymphostatin, a virulence factor of attaching and effacing Escherichia coli , inhibits proliferation and cytokine responses of human T cells in a manner associated with cell cycle arrest but not apoptosis or necrosis.

Author

Ruamsap N, Riyapa D, Janesomboon S, Stevens JM, Pichyangkul S, Pattanapanyasat K, Demons ST, Stevens MP, and Korbsrisate S

Subjects
Apoptosis, CD8-Positive T-Lymphocytes immunology, Cell Cycle Checkpoints immunology, Cell Division, Cell Proliferation physiology, Cytokines biosynthesis, Cytokines immunology, Enteropathogenic Escherichia coli immunology, Enteropathogenic Escherichia coli pathogenicity, Humans, Interleukin-2, Interleukin-4, Leukocytes, Mononuclear immunology, Necrosis, Virulence Factors immunology, Bacterial Toxins immunology, Escherichia coli immunology, Escherichia coli pathogenicity, Escherichia coli Infections immunology, Escherichia coli Proteins immunology, T-Lymphocytes immunology
Abstract

Lymphostatin is a virulence factor of enteropathogenic E. coli (EPEC) and non-O157 serogroup enterohaemorrhagic E. coli . Previous studies using whole-cell lysates of EPEC showed that lymphostatin inhibits the mitogen-activated proliferation of bulk human peripheral blood mononuclear cells (PBMCs) and the production of cytokines IL-2, IL-4, IL-5, and IFN-γ. Here, we used highly purified lymphostatin and PBMC-derived T cells to show that lymphostatin inhibits anti-CD3/anti-CD28-activated proliferation of human CD4 + and CD8 + T cells and blocks the synthesis of IL-2, IL-4, IL-10 and IFN-γ without affecting cell viability and in a manner dependent on an N-terminal DTD glycosyltransferase motif. Such inhibition was not observed with T cells activated by phorbol 12-myristate 13-acetate and ionomycin, implying that lymphostatin targets T cell receptor signaling. Analysis of the expression of CD69 indicated that lymphostatin suppresses T cell activation at an early stage and no impacts on apoptosis or necrosis were observed. Flow cytometric analysis of the DNA content of lymphostatin-treated CD4 + and CD8 + T cells showed a concentration- and DTD-dependent accumulation of the cells in the G0/G1 phase of the cell cycle, and corresponding reduction of the percentage of cells in S phase. Consistent with this, we found a marked reduction in the abundance of cyclins D3, E and A and loss of phosphorylated Rb over time in activated T cells from 8 donors treated with lymphostatin. Moreover, the cyclin-dependent kinase (cdk) inhibitor p27 kip1 , which inhibits progression of the cell cycle at G1 by acting on cyclin E-cdk2 or cyclin D-cdk4 complexes, was found to be accumulated in lymphostatin-treated T cells. Analysis of the abundance of phosphorylated kinases involved in signal transduction found that 30 of 39 were reduced in abundance following lymphostatin treatment of T cells from 5 donors, albeit not significantly so. Our data provide novel insights into the mode of action of lymphostatin on human T lymphocytes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Ruamsap, Riyapa, Janesomboon, Stevens, Pichyangkul, Pattanapanyasat, Demons, Stevens and Korbsrisate.)

Published
2022
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32. Patterns and Predictors of Outpatient Antibiotic Dispensation Following Total Hip and Knee Arthroplasty.

Author

Naufal E, Shadbolt C, Elsiwy Y, Thuraisingam S, Poy Lorenzo YS, Darby J, Babazadeh S, Choong PFM, Dowsey MM, and Stevens JM

Subjects
Anti-Bacterial Agents therapeutic use, Australia epidemiology, Cross-Sectional Studies, Humans, Outpatients, Postoperative Complications etiology, Risk Factors, Arthroplasty, Replacement, Hip adverse effects, Arthroplasty, Replacement, Knee adverse effects
Abstract

Background: This study aimed to evaluate the month-to-month prevalence of antibiotic dispensation in the 12 months before and after total knee arthroplasty (TKA) and total hip arthroplasty (THA) and to identify factors associated with antibiotic dispensation in the month immediately following the surgical procedure., Methods: In total, 4,115 THAs and TKAs performed between April 2013 and June 2019 from a state-wide arthroplasty referral center were analyzed. A cross-sectional study used data from an institutional arthroplasty registry, which was linked probabilistically to administrative dispensing data from the Australian Pharmaceutical Benefits Scheme. Multivariable logistic regression was carried out to identify patient and surgical risk factors for oral antibiotic dispensation., Results: Oral antibiotics were dispensed in 18.3% of patients following primary TKA and 12.0% of patients following THA in the 30 days following discharge. During the year after discharge, 66.7% of TKA patients and 58.2% of THA patients were dispensed an antibiotic at some point. Patients with poor preoperative health status were more likely to have antibiotics dispensed in the month following THA or TKA. Older age, undergoing TKA rather than THA, obesity, inflammatory arthritis, and experiencing an in-hospital wound-related or other infectious complications were associated with increased antibiotic dispensation in the 30 days following discharge., Conclusion: A high rate of antibiotic dispensation in the 30 days following THA and TKA has been observed. Although resource constraints may limit routine wound review for all patients by a surgeon, a select cohort may benefit from timely specialist review postoperatively. Several risk factors identified in this study may aid in identifying appropriate candidates for such changes to follow-up care., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Published
2022
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33. Parker Solar Probe Observations of Solar Wind Energetic Proton Beams Produced by Magnetic Reconnection in the Near-Sun Heliospheric Current Sheet.

Author

Phan TD, Verniero JL, Larson D, Lavraud B, Drake JF, Øieroset M, Eastwood JP, Bale SD, Livi R, Halekas JS, Whittlesey PL, Rahmati A, Stansby D, Pulupa M, MacDowall RJ, Szabo PA, Koval A, Desai M, Fuselier SA, Velli M, Hesse M, Pyakurel PS, Maheshwari K, Kasper JC, Stevens JM, Case AW, and Raouafi NE

Abstract

We report observations of reconnection exhausts in the Heliospheric Current Sheet (HCS) during Parker Solar Probe Encounters 08 and 07, at 16 R s and 20 R s , respectively. Heliospheric current sheet (HCS) reconnection accelerated protons to almost twice the solar wind speed and increased the proton core energy by a factor of ∼3, due to the Alfvén speed being comparable to the solar wind flow speed at these near-Sun distances. Furthermore, protons were energized to super-thermal energies. During E08, energized protons were found to have leaked out of the exhaust along separatrix field lines, appearing as field-aligned energetic proton beams in a broad region outside the HCS. Concurrent dropouts of strahl electrons, indicating disconnection from the Sun, provide further evidence for the HCS being the source of the beams. Around the HCS in E07, there were also proton beams but without electron strahl dropouts, indicating that their origin was not the local HCS reconnection exhaust., (© 2022. The Authors.)

Published
2022
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34. The influence of patellofemoral stabilisation surgery on joint congruity: an MRI surface mapping study.

Author

Stevens JM, Eldridge JD, Tortonese D, Whitehouse MR, Krishnan H, Elsiwy Y, and Clark D

Subjects
Adult, Biomechanical Phenomena, Female, Humans, Knee Joint diagnostic imaging, Knee Joint surgery, Magnetic Resonance Imaging methods, Male, Prospective Studies, Range of Motion, Articular, Patella, Patellofemoral Joint diagnostic imaging, Patellofemoral Joint surgery
Abstract

Background: In the unstable patellofemoral joint (PFJ), the patella will articulate in an abnormal manner, producing an uneven distribution of forces. It is hypothesised that incongruency of the PFJ, even without clinical instability, may lead to degenerative changes. The aim of this study was to record the change in joint contact area of the PFJ after stabilisation surgery using an established and validated MRI mapping technique., Methods: A prospective MRI imaging study of patients with a history of PFJ instability was performed. The patellofemoral joints were imaged with the use of an MRI scan during active movement from 0° through to 40° of flexion. The congruency through measurement of the contact surface area was mapped in 5-mm intervals on axial slices. Post-stabilisation surgery contact area was compared to the pre-surgery contact area., Results: In all, 26 patients were studied. The cohort included 12 male and 14 female patients with a mean age of 26 (15-43). The greatest mean differences in congruency between pre- and post-stabilised PFJs were observed at 0-10 degrees of flexion (0.54 cm 2 versus 1.18 cm 2 , p = 0.04) and between 11° and 20° flexion (1.80 cm 2 versus 3.45 cm 2 ; p = 0.01)., Conclusion: PFJ stabilisation procedures increase joint congruency. If a single axial series is to be obtained on MRI scan to compare the pre- and post-surgery joint congruity, the authors recommend 11° to 20° of tibiofemoral flexion as this was shown to have the greatest difference in contact surface area between pre- and post-operative congruency., (© 2021. The Author(s), under exclusive licence to Springer-Verlag France SAS, part of Springer Nature.)

Published
2022
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35. Tibial tuberosity-trochlear groove distance: does it measure up?

Author

Krishnan H, Eldridge JD, Clark D, Metcalfe AJ, Stevens JM, and Mandalia V

Abstract

Recognized anatomic variations that lead to patella instability include patella alta and trochlea dysplasia. Lateralization of the extensor mechanism relative to the trochlea is often considered to be a contributing factor; however, controversy remains as to the degree this contributes to instability and how this should be measured. As the tibial tuberosity-trochlear groove (TT-TG) is one of most common imaging measurements to assess lateralization of the extensor mechanism, it is important to understand its strengths and weaknesses. Care needs to be taken while interpreting the TT-TG value as it is affected by many factors. Medializing tibial tubercle osteotomy is sometimes used to correct the TT-TG, but may not truly address the underlying anatomical problem. This review set out to determine whether the TT-TG distance sufficiently summarizes the pathoanatomy, and if this assists with planning of surgery in patellar instability. Cite this article: Bone Jt Open  2022;3(3):268-274.

Published
2022
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36. Frequency, variations, and prognostic implications of chromosome 14q32 deletions in chronic lymphocytic leukemia.

Author

Harris RA, Stevens JM, Pickering DL, Althof PA, Smith LM, Sanmann JN, and Dave BJ

Subjects
Cytogenetic Analysis, Humans, In Situ Hybridization, Fluorescence, Leukemia, Lymphocytic, Chronic, B-Cell epidemiology, Leukemia, Lymphocytic, Chronic, B-Cell genetics, Prognosis, Retrospective Studies, Survival Rate, United States epidemiology, Biomarkers, Tumor genetics, Chromosome Deletion, Chromosomes, Human, Pair 14 genetics, Leukemia, Lymphocytic, Chronic, B-Cell pathology
Abstract

The clinical implications of deletions within chromosome 14q32 in CLL pathogenesis remain unclear. We examined the frequency of 14q32 deletions among CLL cases by karyotype and FISH, categorized the variation using genomic microarray, and assessed the prognostic impact by time-to-first-treatment (TTFT) analysis. A 14q32 abnormality was detected in 35 % (245/698) of cases, with the majority containing a 5' partial telomeric 14q32 deletion. These deletions within the IGH variable region (35/40) ranged from 236 kb to 1.4 Mb involving FAM30A, ADAM6, LINC00226, and LINC00221. The 214 kb minimum deleted region implicated in CLL pathogenesis encompassed LINC00221. Cases with a 14q32 deletion had a shorter median TTFT compared to cases with a sole deletion/nullisomy 13q, a good prognostic indicator, and longer than cases with a sole deletion of 11q or 17p, conferring an unfavorable prognosis. This investigation underscores the importance of comprehensive testing to apprehend the implications of 14q32 deletions in CLL., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Published
2021
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37. Detection and differentiation of Burkholderia species with pathogenic potential in environmental soil samples.

Author

Janesomboon S, Muangsombut V, Srinon V, Meethai C, Tharinjaroen CS, Amornchai P, Withatanung P, Chantratita N, Mayo M, Wuthiekanun V, Currie BJ, Stevens JM, and Korbsrisate S

Subjects
Burkholderia genetics, Burkholderia pathogenicity, Microbiota, Polymerase Chain Reaction methods, Burkholderia isolation & purification, DNA Barcoding, Taxonomic methods, Soil Microbiology
Abstract

The Burkholderia pseudomallei phylogenetic cluster includes B. pseudomallei, B. mallei, B. thailandensis, B. oklahomensis, B. humptydooensis and B. singularis. Regarded as the only pathogenic members of this group, B. pseudomallei and B. mallei cause the diseases melioidosis and glanders, respectively. Additionally, variant strains of B. pseudomallei and B. thailandensis exist that include the geographically restricted B. pseudomallei that express a B. mallei-like BimA protein (BPBM), and B. thailandensis that express a B. pseudomallei-like capsular polysaccharide (BTCV). To establish a PCR-based assay for the detection of pathogenic Burkholderia species or their variants, five PCR primers were designed to amplify species-specific sequences within the bimA (Burkholderia intracellular motility A) gene. Our multiplex PCR assay could distinguish pathogenic B. pseudomallei and BPBM from the non-pathogenic B. thailandensis and the BTCV strains. A second singleplex PCR successfully discriminated the BTCV from B. thailandensis. Apart from B. humptydooensis, specificity testing against other Burkholderia spp., as well as other Gram-negative and Gram-positive bacteria produced a negative result. The detection limit of the multiplex PCR in soil samples artificially spiked with known quantities of B. pseudomallei and B. thailandensis were 5 and 6 CFU/g soil, respectively. Furthermore, comparison between standard bacterial culture and the multiplex PCR to detect B. pseudomallei from 34 soil samples, collected from an endemic area of melioidosis, showed high sensitivity and specificity. This robust, sensitive, and specific PCR assay will be a useful tool for epidemiological study of B. pseudomallei and closely related members with pathogenic potential in soil., Competing Interests: The authors have declared that no competing interests exist.

Published
2021
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38. Bilateral distal femoral endoprosthesis for trauma.

Author

Stevens JM, Clement ND, Beckingsale T, and Patton JT

Abstract

In this paper, we describe the outcome of bilateral distal femoral endoprosthesis for the management of acute severe trauma. We also review the literature to ascertain the published functional results of distal femoral endoprosthesis for acute trauma of native knees. In severely comminuted intra-articular fractures, such as those our patient sustained, reconstruction is not always possible, and predictable outcomes can rarely be assured with conviction. Endoprosthesis is an established treatment modality for replacement after resection in limb salvage surgery. In this regard, there is a limited but vital role that endoprosthesis can play in acute complex trauma. We demonstrate a good short-term outcome when bilateral endoprostheses are utilised for complex distal femur trauma., (© The Author(s) 2020.)

Published
2020
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39. Functional redundancy of Burkholderia pseudomallei phospholipase C enzymes and their role in virulence.

Author

Srinon V, Withatanung P, Chaiwattanarungruengpaisan S, Thongdee M, Meethai C, Stevens JM, Titball RW, and Korbsrisate S

Subjects
Animals, Cell Line, Mice, Bacterial Proteins genetics, Bacterial Proteins metabolism, Burkholderia pseudomallei enzymology, Burkholderia pseudomallei genetics, Burkholderia pseudomallei pathogenicity, Melioidosis enzymology, Melioidosis genetics, Type C Phospholipases genetics, Type C Phospholipases metabolism, Virulence Factors genetics, Virulence Factors metabolism
Abstract

Phospholipase C (PLC) enzymes are key virulence factors in several pathogenic bacteria. Burkholderia pseudomallei, the causative agent of melioidosis, possesses at least three plc genes (plc1, plc2 and plc3). We found that in culture medium plc1 gene expression increased with increasing pH, whilst expression of the plc3 gene was pH (4.5 to 9.0) independent. Expression of the plc2 gene was not detected in culture medium. All three plc genes were expressed during macrophage infection by B. pseudomallei K96243. Comparing B. pseudomallei wild-type with plc mutants revealed that plc2, plc12 or plc123 mutants showed reduced intracellular survival in macrophages and reduced plaque formation in HeLa cells. However, plc1 or plc3 mutants showed no significant differences in plaque formation compared to wild-type bacteria. These findings suggest that Plc2, but not Plc1 or Plc3 are required for infection of host cells. In Galleria mellonella, plc1, plc2 or plc3 mutants were not attenuated compared to the wild-type strain, but multiple plc mutants showed reduced virulence. These findings indicate functional redundancy of the B. pseudomallei phospholipases in virulence.

Published
2020
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41. Does 24-h Activity Cycle Influence Plasma PCSK9 Concentration? A Systematic Review and Meta-Analysis.

Author

Kuo WC, Stevens JM, Ersig AL, Johnson HM, Tung TH, and Bratzke LC

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Animals, Atherosclerosis drug therapy, Exercise, Female, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors pharmacology, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Male, Mice, Middle Aged, Risk, Signal Transduction drug effects, Treatment Outcome, Young Adult, Activity Cycles physiology, Atherosclerosis blood, Proprotein Convertase 9 blood
Abstract

Purpose of Review: Higher plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) concentration has been associated with a higher risk of atherosclerotic cardiovascular disease (ASCVD). Animal and human studies have examined the relationship between 24-h activity cycles (24-HAC) and PCSK9, but conflicting results exist. Therefore, this review aimed to examine the relationship between 24-HAC and plasma PCSK9 concentration in animals and humans.Three databases (PubMed, CINAHL, and Web of Science) were searched for eligible articles. Descriptive data were summarized using network meta-analysis. The effect size was estimated using pairwise meta-analysis., Recent Findings: The interventions designed to increase moderate to vigorous physical activities (MVPA) did not significantly change plasma PCSK9 concentration (Hedges' g = 0.137; p = 0.337). However, the effect was influenced by statin therapy and intervention delivery mode. Specifically, physical activity interventions in conjunction with statin therapy significantly increased plasma PCSK9 concentration (Hedges' g = 0.275; p = 0.007). Supervised exercise training significantly increased plasma PCSK9 concentration (Hedges' g = 0.630; p = 0.001), but physical activity counseling did not (p = 0.845). The effects of MVPA on plasma PCSK9 may be moderated by statin therapy, intervention delivery mode, or other potential unknown mechanistic factors. Thus, caution should be taken when using plasma PCSK9 as an outcome indicator for physical activity interventions aimed at decreasing the risk of ASCVD. Graphical abstract.

Published
2020
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42. Identification of Burkholderia pseudomallei Genes Induced During Infection of Macrophages by Differential Fluorescence Induction.

Author

Jitprasutwit S, Jitprasutwit N, Hemsley CM, Onlamoon N, Withatanung P, Muangsombut V, Vattanaviboon P, Stevens JM, Ong C, Stevens MP, Titball RW, and Korbsrisate S

Abstract

Burkholderia pseudomallei , the causative agent of melioidosis, can survive and replicate in macrophages. Little is known about B. pseudomallei genes that are induced during macrophage infection. We constructed a B. pseudomallei K96243 promoter trap library with genomic DNA fragments fused to the 5' end of a plasmid-borne gene encoding enhanced green fluorescent protein (eGFP). Microarray analysis showed that the library spanned 88% of the B. pseudomallei genome. The recombinant plasmids were introduced into Burkholderia thailandensis E264, and promoter fusions active during in vitro culture were removed. J774A.1 murine macrophages were infected with the promoter trap library, and J774A.1 cells containing fluorescent bacteria carrying plasmids with active promoters were isolated using flow cytometric-based cell sorting. Candidate macrophage-induced B. pseudomallei genes were identified from the location of the insertions containing an active promoter activity. A proportion of the 138 genes identified in this way have been previously reported to be involved in metabolism and transport, virulence, or adaptation. Novel macrophage-induced B. pseudomallei genes were also identified. Quantitative reverse-transcription PCR analysis of 13 selected genes confirmed gene induction during macrophage infection. Deletion mutants of two macrophage-induced genes from this study were attenuated in Galleria mellonella larvae, suggesting roles in virulence. B. pseudomallei genes activated during macrophage infection may contribute to intracellular life and pathogenesis and merit further investigation toward control strategies for melioidosis., (Copyright © 2020 Jitprasutwit, Jitprasutwit, Hemsley, Onlamoon, Withatanung, Muangsombut, Vattanaviboon, Stevens, Ong, Stevens, Titball and Korbsrisate.)

Published
2020
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43. Plate and screw fixation of arthroscopically assisted tibial tuberosity osteotomy: technique and results.

Author

Stevens JM, Barton SB, Alexander M, Eldridge JD, and Clark D

Subjects
Adult, Bone Plates, Bone Screws, Cohort Studies, Female, Humans, Knee Joint physiopathology, Knee Joint surgery, Male, Middle Aged, Patient Positioning methods, Range of Motion, Articular physiology, Recovery of Function, Registries, Tibia diagnostic imaging, Treatment Outcome, United Kingdom, Arthroscopy methods, Intra-Articular Fractures surgery, Joint Instability surgery, Osteotomy methods, Tibia surgery
Abstract

Introduction: We describe a fixation technique for tibial tuberosity osteotomies (TTO) utilising a plate and screw construct which adheres to established principles of bone healing. We record and discuss the complication profile and benefits of this technique., Method: The technique is outlined, and thirty consecutive case of TTO fixed with this combination of plate and screws were analysed during a study period from January 2018 to October 2018. All patients were followed up clinically to 3 months post-operation for the purpose of identifying early complications of surgery. Radiographic series were reviewed at 2, 6 and 12 weeks post-operation for evidence of fracture, loss of position, hardware failure and union., Results: All cases went on to clinical and radiographic union by 12 weeks. We identified one case of hardware failure, one case of superficial infection and one case of stiffness requiring manipulation., Conclusion: We have found this technique of plate and screw construct to be effective in arthroscopically assisted TTO fixation leading to consistent union without loss of position with a low complication profile.

Published
2020
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44. Quantifying Mycobacterium avium subspecies paratuberculosis infection of bovine monocyte derived macrophages by confocal microscopy.

Author

Mathie HA, Jensen K, Stevens JM, Glass EJ, and Hope JC

Subjects
Animals, Cattle, Cells, Cultured, Female, Gene Expression Profiling, Staining and Labeling, Colony Count, Microbial, Macrophages microbiology, Microscopy, Confocal, Mycobacterium avium subsp. paratuberculosis pathogenicity
Abstract

Quantification of Mycobacterium avium subspecies paratuberculosis (MAP) during in vitro infection experiments is challenging due to limitations of currently utilised methods, such as colony counting. Here we describe quantifying MAP infection of bovine macrophages (Mφ) using confocal microscopy. Bovine monocyte derived macrophages were infected with MAP at a high or low dose and the number of intracellular bacteria calculated at 2 h post infection using confocal microscopy. Bacteria within simultaneously infected Mφ were quantified by colony counting in order to compare confocal microscopy results with results obtained by an established method. Confocal microscopy provided a robust alternative quantification method that allowed for assessment of the infection at the individual Mφ level. This demonstrated that MAP infection was not homogeneous, and that there were higher numbers of both infected Mφ and intracellular bacteria and bacterial aggregates at the high dose compared to the low dose, potentially impacting the Mφ response to infection. Confocal microscopy can therefore provide a level of detail regarding the infection unobtainable by other quantification methods., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Published
2020
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45. Bilateral acetabular fractures: Mechanism, fracture patterns and associated injuries.

Author

Stevens JM, Shiels S, Whitehouse MR, Ward AJ, Chesser TJ, and Acharya M

Abstract

Introduction: Acetabular fractures are uncommon and their management is often reserved for specialist pelvic and acetabular surgeons. Bilateral acetabular fractures are a particularly rare subgroup. We report the incidence, fracture pattern, mechanism of injury and outcome of patients presenting to a tertiary trauma centre with traumatic bilateral acetabular fractures., Method: Bilateral acetabular fractures were identified from a prospective database of acetabular fractures presenting to one institution over a six-year period. Patient notes and imaging studies were reviewed to identify demographics, mechanism of injury, Injury Severity Score, fracture pattern and management. Timing of operative management was explored. Patient outcomes were collected in the form of radiographs and Oxford Hip Scores at a minimum of one-year post injury., Results: Eight patients with bilateral acetabular fracture were identified from a database which contained records of 519 patients with acetabular fractures (incidence of 1.5% amongst patients with acetabular fractures). Motor vehicle accidents were the most common mechanism. Four acetabular fracture patterns were observed within the cohort. Radiographic union occurred in all cases and Oxford Hip Scores are suggestive of moderate to well functioning hip joints. Fractures were treated as single or staged procedures., Conclusion: Bilateral acetabular fractures are very rare due to the unique degree and pattern of force required to fracture both acetabula. They are associated with 4 main fracture patterns and present with Injury Severity Scores that averaged 25 (severe). They are typically observed in young males with road traffic collision being the most common mechanism of injury., (Crown Copyright © 2019 Published by Elsevier B.V. on behalf of Professor P K Surendran Memorial Education Foundation. All rights reserved.)

Published
2019
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46. Survival and functional outcome of revision total knee arthroplasty with a total stabilizer knee system: minimum 5 years of follow-up.

Author

Stevens JM, Clement ND, MacDonald D, Hamilton DF, and Burnett R

Subjects
Adult, Aged, Aged, 80 and over, Female, Follow-Up Studies, Humans, Male, Middle Aged, Patient Satisfaction, Radiography, Retrospective Studies, Arthroplasty, Replacement, Knee instrumentation, Knee Joint diagnostic imaging, Knee Joint physiopathology, Knee Prosthesis statistics & numerical data, Prosthesis Failure, Reoperation instrumentation
Abstract

Introduction: Revision knee arthroplasty surgery can range from patella resurfacing or polyethylene exchange, to staged revision and revision to a more constrained implant. Subsequently, the ability to elicit outcomes becomes difficult to obtain and hence information on functional outcome and survivorship for all modes of failure with a single revision system is valuable., Methods: We retrospectively assessed 100 consecutive revision knee replacements that were converted from a primary knee replacement to a Triathlon total stabilizer (TS) knee system (Stryker Orthopaedics, Mahwah, NJ). Inclusion criteria included failure of a primary knee replacement of any cause converted to a Stryker TS knee system. Midterm outcome of at least 5 years was required. Implants survivorship, Oxford Knee Score (OKS), Forgotten Joint Score (FJS-12), Short Form (SF-) 12, reported patient satisfaction and radiographic analysis were recorded., Results: The all-cause survival rate at 5 years was 89.0% [95% confidence interval (CI) 87.3 to 90.7]. The all-cause survival rate was generally static after the first 4 years. The mean OKS was 27 (SD 11.9, range 0 to 46), FJS was 32.3 (SD 30.4, range 0 to 100), SF-12 physical component summary was 40.6 (SD 17.6, range 23.9 to 67.1), and mental component summary was 48.3 (SD 15.5, range 23.9 to 69.1). Reported patient satisfaction in patients who were not re-revised was 82%., Conclusion: The midterm survivorship of cemented Stryker Triathlon TS knee revision for all-cause mode of failure is good to excellent; however, future follow-up is required to ensure this survivorship is observed into the long term. Despite limited functional outcome, overall patient satisfaction rates are high.

Published
2019
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47. Interleukin 10 knock-down in bovine monocyte-derived macrophages has distinct effects during infection with two divergent strains of Mycobacterium bovis.

Author

Jensen K, Stevens JM, and Glass EJ

Subjects
Animals, Cattle, Cells, Cultured, Female, Interferon-gamma metabolism, Nitric Oxide metabolism, Nitric Oxide Synthase Type II metabolism, RNA, Messenger metabolism, Tuberculosis, Bovine microbiology, Tumor Necrosis Factor-alpha metabolism, Interleukin-10 metabolism, Leukocytes, Mononuclear metabolism, Macrophages metabolism, Mycobacterium bovis metabolism, Tuberculosis, Bovine metabolism
Abstract

Mycobacterium bovis is the causative agent of bovine tuberculosis (TB), a cattle disease of global importance. M. bovis infects bovine macrophages (Mø) and subverts the host cell response to generate a suitable niche for survival and replication. We investigated the role of the anti-inflammatory cytokine interleukin (IL) 10 during in vitro infection of bovine monocyte-derived Mø (bMDM) with two divergent UK strains of M. bovis, which differentially modulate expression of IL10. The use of IL10-targeting siRNA revealed that IL10 inhibited the production of IL1B, IL6, tumour necrosis factor (TNF) and interferon gamma (IFNG) during infection of bMDM with the M. bovis strain G18. In contrast, IL10 only regulated a subset of these genes; TNF and IFNG, during infection with the M. bovis reference strain AF2122/97. Furthermore, nitric oxide (NO) production was modulated by IL10 during AF2122/97 infection, but not at the nitric oxide synthase 2 (NOS2) mRNA level, as observed during G18 infection. However, IL10 was found to promote survival of both M. bovis strains during early bMDM infection, but this effect disappeared after 24 h. The role of IL10-induced modulation of TNF, IFNG and NO production in M. bovis survival was investigated using siRNA targeting TNF, IFNG receptor 1 (IFNGR1) and NOS2. Knock-down of these genes individually did not promote survival of either M. bovis strain and therefore modulation of these genes does not account for the effect of IL10 on M. bovis survival. However, TNF knock-down was found to be detrimental to the survival of the M. bovis strain G18 during early infection. The results provide further evidence for the importance of IL10 during M. bovis infection of Mø. Furthermore, they highlight M. bovis strain specific differences in the interaction with the infected bMDM, which may influence the course of infection and progression of bovine TB., Competing Interests: The authors have declared that no competing interests exist.

Published
2019
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48. Quantitative Proteomics Reveals Differences in the Response of Neutrophils Isolated from Healthy or Diabetic Subjects to Infection with Capsule-Variant Burkholderia thailandensis.

Author

Withatanung P, Kurian D, Tangjittipokin W, Plengvidhya N, Titball RW, Korbsrisate S, and Stevens JM

Subjects
Case-Control Studies, Cell Death, Cells, Cultured, Cytokines metabolism, Diabetes Mellitus microbiology, Humans, Inflammation metabolism, Melioidosis etiology, Neutrophils metabolism, Neutrophils microbiology, Burkholderia immunology, Burkholderia Infections immunology, Diabetes Mellitus pathology, Neutrophils immunology, Proteomics
Abstract

In Thailand, diabetes mellitus is the most significant risk factor for melioidosis, a severe disease caused by Burkholderia pseudomallei. In this study, neutrophils isolated from healthy or diabetic subjects were infected with B. thailandensis E555, a variant strain with a B. pseudomallei-like capsular polysaccharide used here as a surrogate micro-organism for B. pseudomallei. At 2 h post-infection, neutrophil proteins were subjected to 4-plex iTRAQ-based comparative proteomic analysis. A total of 341 proteins were identified in two or more samples, of which several proteins involved in oxidative stress and inflammation were enriched in infected diabetic neutrophils. We validated this finding by demonstrating that infected diabetic neutrophils generated significantly elevated levels of pro-inflammatory cytokines TNFα, IL-6, IL-1β, and IL-17 compared to healthy neutrophils. Our data also revealed that infected neutrophils from healthy or diabetic individuals undergo apoptotic cell death at distinctly different rates, with infected diabetic neutrophils showing a diminished ability to delay apoptosis and an increased likelihood of undergoing a lytic form of cell death, compared to infected neutrophils from healthy individuals. Increased expression of inflammatory proteins by infected neutrophils could contribute to the increased susceptibility to infection and inflammation in diabetic patients in melioidosis-endemic areas.

Published
2019
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50. Mapping the contact area of the patellofemoral joint: the relationship between stability and joint congruence.

Author

Clark D, Stevens JM, Tortonese D, Whitehouse MR, Simpson D, and Eldridge J

Subjects
Adolescent, Adult, Case-Control Studies, Female, Humans, Joint Instability physiopathology, Male, Patellofemoral Joint physiopathology, Prospective Studies, Range of Motion, Articular, Young Adult, Body Surface Potential Mapping methods, Joint Instability diagnostic imaging, Magnetic Resonance Imaging methods, Patellofemoral Joint diagnostic imaging
Abstract

Aims: The aim of this study was to determine and compare the congruency of the articular surface contact area of the patellofemoral joint (PFJ) during both active and passive movement of the knee with the use of an MRI mapping technique in both the stable and unstable PFJ., Patients and Methods: A prospective case-control MRI imaging study of patients with a history of PFJ instability and a control group of volunteers without knee symptoms was performed. The PFJs were imaged with the use of an MRI scan during both passive and active movement from 0° through to 40° of flexion. The congruency through measurement of the contact surface area was mapped in 5-mm intervals on axial slices. In all, 40 patients were studied. The case group included 31 patients with symptomatic patellofemoral instability and the control group of nine asymptomatic volunteers. The ages were well matched between the case and control groups. The mean age was 25 years (16 to 42; sd 6.9) in the case group and 26 years (19 to 32; sd 5.1) in the control group. There were 19 female and 12 male patients in the case group., Results: The unstable PFJs were demonstrably less congruent than the stable PFJs throughout the range of knee movement. The greatest mean differences in congruency between unstable and stable PFJ's were observed between 11° and 20° flexion (1.73 cm 2 vs 4.00 cm 2 ; p < 0.005)., Conclusion: The unstable PFJ is less congruent than the stable PFJ throughout the range of knee movement studied. This approach to mapping PFJ congruency produces a measurable outcome and will allow the assessment of pre- and postoperative results following surgical intervention. This may facilitate the design of new procedures for patients with PFJ instability. If a single axial series is to be obtained on MRI scan, the authors recommend 11° to 20° of tibiofemoral flexion, as this was shown to have the greatest difference in contact surface area between the case and control groups. Cite this article: Bone Joint J 2019;101-B:552-558.

Published
2019
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