175 results on '"B. Winer"'
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2. Editorial Practice, Symbols, Manuscripts, and Abbreviations
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
3. Table Talk Recorded by Henry Nelson Coleridge
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
4. Chronological Table 1772-1834
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
5. Table Talk Recorded by John Taylor Coleridge
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
6. Appendix C. Manuscript F
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
7. Appendix A. Abbreviations in the Manuscripts of H. N. Coleridge Expanded in the Present Edition
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
8. Acknowledgements
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
9. Appendix E. Table-Talk by William Wordsworth
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
10. Appendix D. The Confessional
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
11. Appendix B. Manuscript E
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
12. Appendix F. Reports of Conversations with Coleridge on Subjects in Table Talk
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
13. List of Illustrations
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
14. Appendix G. Collation Table
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
15. Contents
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
16. Title Page, Epigraph, Copyright, Dedication
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Samuel Taylor Coleridge, Kathleen Coburn, and B. Winer
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- 2019
17. Bollingen Series: Table Talk, Part I
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Samuel Taylor Coleridge, Kathleen Coburn, B. Winer
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- 2019
18. An Update in Guillain-Barré Syndrome
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J. B. Winer
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Guillain-Barré syndrome (GBS) was first described in 1916 (Guillain G, 1916) and is approaching its 100th anniversary. Our knowledge of the syndrome has hugely expanded since that time. Once originally considered to be only demyelinating in pathology we now recognise both axonal and demyelinating subtypes. Numerous triggering or antecedent events including infections are recognised and GBS is considered an immunological response to these. GBS is now considered to be a clinical syndrome of an acute inflammatory neuropathy encompassing a number of subtypes with evidence of different immunological mechanisms. Some of these are clearly understood while others remain to be fully elucidated. Complement fixing antibodies against peripheral nerve gangliosides alone and in combination are increasingly recognised as an important mechanism of nerve damage. New antibodies against other nerve antigens such as neurofascin have been recently described. Research databases have been set up to look at factors associated with prognosis and the influence of intravenous immunoglobulin (IvIg) pharmacokinetics in therapy. Exciting new studies are in progress to examine a possible role for complement inhibition in the treatment of the syndrome.
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- 2014
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19. Hyponatraemia in Guillain-Barré syndrome revisited
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John B. Winer, Yusuf A. Rajabally, and Fu Liong Hiew
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Adult ,Male ,medicine.medical_specialty ,Vital capacity ,endocrine system diseases ,medicine.medical_treatment ,Neuromuscular weakness ,Guillain-Barre Syndrome ,Independent predictor ,Malignancy ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Humans ,Medicine ,In patient ,030212 general & internal medicine ,Aged ,Retrospective Studies ,Guillain-Barre syndrome ,business.industry ,nutritional and metabolic diseases ,General Medicine ,Middle Aged ,Prognosis ,medicine.disease ,nervous system diseases ,Surgery ,Neurology ,Muscle strength ,Female ,Neurology (clinical) ,Diuretic ,business ,030217 neurology & neurosurgery ,Hyponatremia - Abstract
The objective of this study was to determine the relevance of hyponatraemia in the prognosis of Guillain-Barré syndrome (GBS).We retrospectively analysed records of 48 consecutive patients with GBS and performed a systematic literature review on frequency/correlates of hyponatraemia in GBS.Hyponatraemia133 mmol/l was detected in 18/48 of our patients with GBS (37.5%). In 10/18 (55.5%), hyponatraemia occurred post-immunoglobulin therapy. Hyponatraemia correlated with age50 years (P = 0.011), concurrent malignancy (P = 0.039), diuretic use (P0.001), preceding diarrhoea (P = 0.042) and Medical Research Council (MRC) sum score at discharge (MRCSSD) (P = 0.026). Only concurrent malignancy (P0.001) and diuretic use (P0.001) were independently associated with hyponatraemia. MRCSSD also correlated with MRC sum score on admission (MRCSSA) (P0.001), length of hospital stay (P0.001), summated compound muscle action potential (P = 0.034) and lowest forced vital capacity (P = 0.001). Only MRCSSA (P = 0.004) and length of hospital stay (P0.001) independently predicted MRCSSD. Combining our findings with previous literature indicates comparable frequencies of hyponatraemia in GBS in four of five studies and association with mortality in three of four studies, with an independent link in one. Independent association of hyponatraemia with muscle strength is not demonstrated.Hyponatraemia appears of comparable frequency in GBS to that in other diseased cohorts suggesting it is common but non-specific. Hyponatraemia has otherwise been shown to be an independent predictor of death in other disorders and available data indicate the same is also likely in GBS, although this may vary in patient subgroups. Hyponatraemia is, however, not an independent prognostic indicator of neuromuscular weakness severity in GBS.
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- 2015
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20. Concurrent Oral 1 - Therapy of rheumatic disease: OP4. Effectiveness of Rituximab in Rheumatoid Arthritis: Results from the British Society for Rheumatology Biologics Register (BSRBR)
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Anthony Sebba, Kimme L. Hyrich, N. Schlesinger, Juan J. Scali, Andrea Rubbert-Roth, A. Pikhlak, R. Cartwright, Deborah P M Symmons, E. Weisbarth-Riedel, K Chakravarty, B. Bodalia, E. Incera, I. Kone-Paut, Darren M. Ashcroft, A. E. Yücel, Sarah Mapplebeck, R. Preiss, Katalin Dankó, David A. Isenberg, Patrick Gordon, Alexander So, M. Gattorno, Moetaza M. Soliman, John B Winer, U. Arulmani, Bryan Lecky, V. Murphy, G. Krammer, P. Quartier, K. Leslie, E. Ramos, E. Hachulla, Kath D. Watson, F. Zulian, Ernest Choy, George D. Kitas, Dimitrios Christidis, David Scott, I. Foeldvari, Bhaskar Dasgupta, Mark Lunt, Ronald F van Vollenhoven, D. Richard, Beverley White-Alao, J. Hoyer, M. De Meulemeester, H. J. Lachmann, L. Lepore, J. Kerrane, P. N. Hawkins, Nada Hassan, Emma Vernon, Anna Kowalczyk, Fowzia Ibrahim, Moshe Zilberstein, Robert G. Cooper, Alan Hakim, Mark C. Genovese, P. Sallstig, Bridget Griffiths, and J. B. Kuemmerle-Deschner
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musculoskeletal diseases ,medicine.medical_specialty ,Tumor necrosis factors ,business.industry ,Rheumatic disease ,Physical function ,medicine.disease ,Rheumatology ,Antirheumatic Agents ,Patient Self-Report ,Rheumatoid arthritis ,Internal medicine ,medicine ,Physical therapy ,Pharmacology (medical) ,Rituximab ,business ,skin and connective tissue diseases ,medicine.drug - Abstract
Background: Rituximab (RTX) in combination with methotrexate (MTX) has been licensed since 2006 for the management of severe active rheumatoid arthritis (RA) in patients who have failed at least one anti-tumour necrosis factor (anti-TNF) therapy. Published clinical trials have demonstrated the efficacy of RTX in improving both clinical symptoms and patients' physical function. This study aimed to assess the effectiveness of RTX in RA patients treated in routine clinical practice by examining clinical and patient reported outcomes six months after receiving a first course of RTX. Methods: The analysis involved 550 RA patients registered with the BSRBR, who were starting RTX and were followed up for at least 6 months. Change in Disease Activity Score (DAS28) and European League Against Rheumatism (EULAR) response were used to assess the clinical response while change in Health Assessment Questionnaire (HAQ) score was used to assess the physical function of the patients 6 months after starting RTX. The change in DAS28 and HAQ was compared between seronegative and seropositive patients and anti-TNF naïve patients versus anti-TNF failures. The response was also compared between patients receiving RTX in combination with MTX, other non-biologic disease modifying anti-rheumatic drugs (nbDMARDs) or no nbDMARDs. Results: The mean (s.d.) age of the cohort was 59 (12) years and 78% of the patients were females. The patients had a mean (s.d.) of 15 (10) years of disease duration. 16% were biologic naïve while 84% were anti-TNF failures. 32% of the patients were seronegative and 68% were seropositive. The mean (95% CI) DAS28 at baseline was 6.2 (6.1, 6.3) which decreased to 4.8 (4.7, 4.9) at 6 months of follow up. 16% were EULAR good responders, 43% were moderate responders and 41% were non responders. The mean (95% CI) change in HAQ was −0.1 (−0.2, −0.1) (Table 1). The mean change in DAS28 was similar in seropositive and seronegative patients (p = 0.18) while the anti-TNF naïve patients showed a greater reduction in DAS28 scores than anti-TNF failures (p = 0.05). Patients receiving RTX in combination with MTX showed similar changes in DAS28 and HAQ compared to patients receiving RTX alone or with other nbDMARDs. Conclusions: RTX has proven to be effective in the routine clinical practice. Anti-TNF naïve patients seem to benefit more from RTX treatment than anti-TNF failures. Disclosure statement: The authors have declared no conflicts of interest
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- 2017
21. Influence of timing on electrodiagnosis of Guillain–Barré syndrome in the first six weeks: A retrospective study
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John B. Winer, Yusuf A. Rajabally, and Fu Liong Hiew
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Adult ,Male ,medicine.medical_specialty ,Pediatrics ,Time Factors ,Electrodiagnosis ,Specific time ,Guillain-Barre Syndrome ,Time frame ,medicine ,Humans ,In patient ,Aged ,Retrospective Studies ,Guillain-Barre syndrome ,medicine.diagnostic_test ,business.industry ,Retrospective cohort study ,Middle Aged ,medicine.disease ,Surgery ,Neurology ,Acute Inflammatory Demyelinating Polyneuropathy ,Cohort ,Female ,Neurology (clinical) ,business - Abstract
The effect of timing is uncertain on the electrophysiology of Guillain-Barré syndrome (GBS). On this may however depend the usefulness of systematic serial studies performed at specific time intervals. We retrospectively analyzed records of 118 consecutive patients with GBS from Birmingham, U.K. (2001-2012), studied between 0-14days, or, 15-42days post-onset using new criteria which we recently proposed [4]. Rates of acute inflammatory demyelinating polyneuropathy (AIDP) (p=0.45), axonal GBS (p=0.32) and equivocal forms (p=0.46) were similar for both timings. Similarly, no significant differences between timings were observed using Hadden et al.'s criteria. Proportions were comparable to published serial studies for both timings, for AIDP (p=0.25; p=0.10) and axonal GBS (p=0.73; p=0.56) but were higher than with serial studies for equivocal forms in patients studied on days 0-14 (p=0.012), although not in those studied on days 15-42 (p=0.17). This suggests that over the initial 6weeks post-onset, timing fails to influence subtype proportions in a large GBS cohort, irrespective of criteria used. Repeat studies appear therefore unlikely to be helpful when systematically performed within this time frame, except in equivocal cases. The benefit of repeat studies remains possible at other times but may need to be individualized, and requires future prospective evaluation.
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- 2015
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22. ANO5Gene Analysis in a Large Cohort of Patients with Anoctaminopathy: Confirmation of Male Prevalence and High Occurrence of the Common Exon 5 Gene Mutation
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Russell Lane, Isabelle Pénisson-Besnier, Wojtek Rakowicz, Charlotte K. Brierley, Cheryl Longman, Fiona Norwood, Andrew P. Jackson, Dieter Gläser, Matt Parton, Rumaisa Bashir, David Hilton-Jones, Debbie Hicks, Benedikt Schoser, Marcus Deschauer, Paul Maddison, John Nixon, Laura E. Rufibach, Meriel McEntagart, Isabel Illa, John McConville, Rita Barresi, John B Winer, Herbert Schreiber, Grainne S. Gorman, Laurence A. Bindoff, Christopher J Price, Hanns Lochmüller, Partha Ray, Simon Hammans, David Cottrell, Mark Roberts, Anthony H.V. Schapira, J. Hudson, Francesco Muntoni, Elizabeth Harris, Jay Panicker, Richard Walters, Ali Al-Memar, Robert G. Cooper, Esther Hwang, Sabine Krause, Pamela J. Shaw, Robert J. Swingler, Michelle Eagle, Bertold Schrank, Anna Sarkozy, Andrew W. Gibson, Maggie C. Walter, Richard E. Petty, Michael G. Hanna, Kathryn R. Wagner, Chris Turner, Peter Van den Bergh, Aijaz Khan, Geraldine Bailey, Michela Guglieri, NP Davies, Kate Bushby, Volker Straub, Jürgen Seeger, Liesbeth De Waele, Steve Laval, Douglass M. Turnbull, UCL - SSS/IONS/NEUR - Clinical Neuroscience, and UCL - (SLuc) Service de neurologie
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muscular dystrophy ,Adult ,Male ,medicine.medical_specialty ,Anoctamins ,Gene mutation ,Biology ,ANO5 ,medicine.disease_cause ,Exon ,Sex Factors ,Chloride Channels ,Internal medicine ,Prevalence ,Genetics ,medicine ,Muscular dystrophy ,Humans ,Allele ,Myopathy ,Genetics (clinical) ,Retrospective Studies ,Aged ,LGMD2L ,Mutation ,Clinical pathology ,Gender ,Genetic Variation ,Middle Aged ,medicine.disease ,Europe ,Phenotype ,Muscular Dystrophies, Limb-Girdle ,Female ,medicine.symptom ,Limb-girdle muscular dystrophy - Abstract
Limb girdle muscular dystrophy type 2L or anoctaminopathy is a condition mainly characterized by adult onset proximal lower limb muscular weakness and raised CK values, due to recessive ANO5 gene mutations. An exon 5 founder mutation (c.191dupA) has been identified in most of the British and German LGMD2L patients so far reported. We aimed to further investigate the prevalence and spectrum of ANO5 gene mutations and related clinical phenotypes, by screening 205 undiagnosed patients referred to our molecular service with a clinical suspicion of anoctaminopathy. A total of 42 unrelated patients had two ANO5 mutations (21%), whereas 14 carried a single change. We identified 34 pathogenic changes, 15 of which are novel. The c.191dupA mutation represents 61% of mutated alleles and appears to be less prevalent in non-Northern European populations. Retrospective clinical analysis corroborates the prevalently proximal lower limb phenotype, the male predominance and absence of major cardiac or respiratory involvement. Identification of cases with isolated hyperCKaemia and very late symptomatic male and female subjects confirms the extension of the phenotypic spectrum of the disease. Anoctaminopathy appears to be one of the most common adult muscular dystrophies in Northern Europe, with a prevalence of about 20%-25% in unselected undiagnosed cases. © 2013 WILEY PERIODICALS, INC.
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- 2013
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23. Titin founder mutation is a common cause of myofibrillar myopathy with early respiratory failure
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Patrick F. Chinnery, John B Winer, Kate Bushby, Hanns Lochmüller, Helen Griffin, Aravind V Ramesh, Gerald Pfeffer, Anna Sarkozy, Mark Busby, Maria Elena Farrugia, Volker Straub, Ian J. Wilson, Rita Barresi, J. Hudson, Steven A. Hardy, Hedley C. A. Emsley, Hannah R Elliott, Ashok Raman, Sujit S. Vaidya, Aleksandar Radunovic, Rita Horvath, Chris Everett, and Alec Ming
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Adult ,Male ,Gerontology ,Neuromuscular disease ,Disease ,medicine.disease_cause ,Polymerase Chain Reaction ,Article ,03 medical and health sciences ,symbols.namesake ,0302 clinical medicine ,Muscular Diseases ,medicine ,Humans ,Connectin ,Muscular dystrophy ,Muscle, Skeletal ,Myopathy ,Aged ,030304 developmental biology ,Sanger sequencing ,Genetics ,0303 health sciences ,Mutation ,biology ,business.industry ,Genetic Diseases, Inborn ,Middle Aged ,medicine.disease ,Magnetic Resonance Imaging ,Founder Effect ,Pedigree ,3. Good health ,Psychiatry and Mental health ,Haplotypes ,biology.protein ,symbols ,Female ,Surgery ,Titin ,Neurology (clinical) ,medicine.symptom ,Respiratory Insufficiency ,business ,030217 neurology & neurosurgery ,Founder effect - Abstract
Objective Titin gene (TTN) mutations have been described in eight families with hereditary myopathy with early respiratory failure (HMERF). Some of the original patients had features resembling myofibrillar myopathy (MFM), arguing that TTN mutations could be a much more common cause of inherited muscle disease, especially in presence of early respiratory involvement. Methods We studied 127 undiagnosed patients with clinical presentation compatible with MFM. Sanger sequencing for the two previously described TTN mutations in HMERF (p.C30071R in the 119th fibronectin-3 (FN3) domain, and p.R32450W in the kinase domain) was performed in all patients. Patients with mutations had detailed review of their clinical records, muscle MRI findings and muscle pathology. Results We identified five new families with the p.C30071R mutation who were clinically similar to previously reported cases, and muscle pathology demonstrated diagnostic features of MFM. Two further families had novel variants in the 119th FN3 domain (p.P30091L and p.N30145K). No patients were identified with mutations at position p.32450. Conclusions Mutations in TTN are a cause of MFM, and titinopathy is more common than previously thought. The finding of the p.C30071R mutation in 3.9% of our study population is likely due to a British founder effect. The occurrence of novel FN3 domain variants, although still of uncertain pathogenicity, suggests that other mutations in this domain may cause MFM, and that the disease is likely to be globally distributed. We suggest that HMERF due to mutations in the TTN gene be nosologically classified as MFM-titinopathy.
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- 2013
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24. Authors' reply to BioMarin Europe
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Jacqueline Palace, John B Winer, David Nicholl, and David Hilton-Jones
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medicine.medical_specialty ,Amifampridine ,business.industry ,General Engineering ,General Medicine ,medicine.disease ,Orphan drug ,Family medicine ,General Earth and Planetary Sciences ,Medicine ,business ,Lambert-Eaton myasthenic syndrome ,General Environmental Science ,medicine.drug - Abstract
BioMarin Europe feels that our letter on the costs of orphan drugs such as amifampridine (Firdapse) for Lambert Eaton myasthenic syndrome (LEMS) and the safety of existing unlicensed treatments, such as 3,4-diaminopyridine base (3,4-DAP), contained inaccuracies.1 2 The Department of Health has confirmed that the additional cost of amifampridine in England is £9 768 668 (€11 400 035; $15 294 803) (excluding …
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- 2016
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25. Effects of essential hypertension on short latency human somatosensory-evoked potentials
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Louisa Edwards, John B. Winer, Una Martin, David McIntyre, and Christopher Ring
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Adult ,Male ,Cognitive Neuroscience ,Neural Conduction ,Blood Pressure ,Experimental and Cognitive Psychology ,Stimulation ,Essential hypertension ,Somatosensory system ,Developmental Neuroscience ,Evoked Potentials, Somatosensory ,medicine ,Humans ,Peripheral Nerves ,Biological Psychiatry ,Endocrine and Autonomic Systems ,General Neuroscience ,Electroencephalography ,medicine.disease ,Electric Stimulation ,Median nerve ,Median Nerve ,Neuropsychology and Physiological Psychology ,medicine.anatomical_structure ,Blood pressure ,Neurology ,Somatosensory evoked potential ,Data Interpretation, Statistical ,Peripheral nervous system ,Hypertension ,Female ,Psychology ,Neuroscience ,Sensory nerve - Abstract
Reduced perception of somatosensory stimulation in patients with essential hypertension may be due to deficits in the ascending somatosensory pathway. Function in the ascending somatosensory pathway was assessed by measuring N9, N13, and N20 somatosensory-evoked potentials in 14 unmedicated essential hypertensives and 22 normotensives. N9 amplitudes were smaller and N13 amplitudes marginally smaller in hypertensives than normotensives. N9 amplitudes were inversely associated with blood pressure. N20 amplitudes and N9, N13, and N20 latencies did not differ between groups. In addition, plexus-to-cord, cord-to-cortex, and plexus-to-cortex conduction times were not different between groups. These data suggest that hypertension affects the peripheral nervous system by reducing the number of active sensory nerve fibers without affecting myelination. However, hypertension does not seem to affect the afferent somatosensory pathway within the brain.
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- 2010
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26. When the Guillain-Barre patient fails to respond to treatment
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John B. Winer
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medicine.medical_specialty ,Guillain-Barre syndrome ,business.industry ,Disease progression ,Drug Resistance ,Immunoglobulins, Intravenous ,Plasmapheresis ,General Medicine ,Disease ,Guillain-Barre Syndrome ,medicine.disease ,Drug Administration Schedule ,Surgery ,Diagnosis, Differential ,Natural history ,Recurrence ,Disease Progression ,medicine ,Humans ,Neurology (clinical) ,Diagnostic Errors ,Intensive care medicine ,business ,After treatment - Abstract
Most patients with Guillain-Barré syndrome (GBS) respond to treatment with intravenous immunoglobulin, but it is not uncommon for some to continue to deteriorate for a period after treatment has been started. This may reflect the natural history of the disease, or an error in diagnosis. This article reflects my own view of what to do in this situation, with a review of what few data there are to guide decision making.
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- 2009
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27. Thymoma mimicking pulmonary stenosis
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John B. Winer, Hassan Douis, and Mariam Jafri
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medicine.medical_specialty ,Thymoma ,business.industry ,medicine.disease ,Myasthenia gravis ,Stenosis ,hemic and lymphatic diseases ,medicine.artery ,Pulmonary artery ,medicine ,Radiology, Nuclear Medicine and imaging ,Pulmonary Trunk ,In patient ,Radiology ,business - Abstract
Thymomas are rare tumours that are usually diagnosed in patients with myasthenia gravis or as an incidental finding. We describe a case of a thymoma mimicking pulmonary stenosis due to external compression of the pulmonary artery. To our knowledge this has only been described in two previous cases in the literature.
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- 2008
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28. New mutations, genotype phenotype studies and manifesting carriers in giant axonal neuropathy
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Tracey Willis, M Groves, Henry Houlden, John B Winer, Gaynor Cole, Helen Roper, Mary M. Reilly, and Zosia Miedzybrodzka
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Adult ,Male ,Pathology ,medicine.medical_specialty ,Adolescent ,Genotype ,Biopsy ,DNA Mutational Analysis ,Short Report ,Genetic Carrier Screening ,Genes, Recessive ,Biology ,medicine.disease_cause ,Compound heterozygosity ,Nerve Fibers, Myelinated ,Sural Nerve ,medicine ,Humans ,Child ,Giant axonal neuropathy ,Chromosome Aberrations ,Neurologic Examination ,Genetics ,Mutation ,Nerve biopsy ,medicine.diagnostic_test ,Homozygote ,Gigaxonin ,Brain ,medicine.disease ,Phenotype ,Axons ,Cytoskeletal Proteins ,Microscopy, Electron ,Psychiatry and Mental health ,Child, Preschool ,Female ,Surgery ,Neurology (clinical) ,Nervous System Diseases ,Chromosomes, Human, Pair 16 - Abstract
Giant axonal neuropathy (GAN; MIM 256850) is a severe childhood onset autosomal recessive sensorimotor neuropathy affecting both the peripheral nerves and the central nervous system. Bomont and colleagues identified a novel ubiquitously expressed gene they named Gigaxonin on chromosome 16q24 as the cause of GAN in a number of families. We analysed five families with GAN for mutations in the Gigaxonin gene and mutations were found in four families; three families had homozygous mutations, one had two compound heterozygous mutations and one family had no mutation identified. All families had the typical clinical features, kinky hair and nerve biopsy. We report some unusual clinical features associated with GAN and Gigaxonin mutations as well as confirm the heterogeneity in GAN and the identification of two families with manifesting carriers.
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- 2007
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29. Observation of D-0-(D)over-bar(0) Mixing Using the CDF II Detector
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T. Aaltonen, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Antos, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanskas, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, T. Bae, A. Barbaro Galtieri, V. Barnes, B. Barnett, P. Barria, P. Bartos, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretvas, A. Bhatti, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, P. Butti, A. Buzatu, A. Calamba, S. Camarda, M. Campanelli, F. Canelli, B. Carls, D. Carlsmith, R. Carosi, S. Carrillo, B. Casal, M. Casarsa, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, K. Cho, D. Chokheli, A. Clark, C. Clarke, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, M. Cremonesi, D. Cruz, J. Cuevas, R. Culbertson, N. d’Ascenzo, M. Datta, P. de Barbaro, L. Demortier, M. D’Errico, F. Devoto, A. Di Canto, B. Di Ruzza, J. Dittmann, S. Donati, M. D’Onofrio, M. Dorigo, A. Driutti, K. Ebina, R. Edgar, A. Elagin, R. Erbacher, S. Errede, B. Esham, S. Farrington, J. Fernández Ramos, R. Field, G. Flanagan, R. Forrest, M. Franklin, J. Freeman, H. Frisch, Y. Funakoshi, C. Galloni, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, S. Giagu, V. Giakoumopoulou, K. Gibson, C. Ginsburg, N. Giokaris, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, A. Golossanov, G. Gomez, G. Gomez Ceballos, M. Goncharov, O. González López, I. Gorelov, A. Goshaw, K. Goulianos, E. Gramellini, S. Grinstein, C. Grosso Pilcher, R. Group, J. Guimaraes da Costa, S. Hahn, J. Han, F. Happacher, K. Hara, M. Hare, R. Harr, T. Harrington Taber, K. Hatakeyama, C. Hays, J. Heinrich, M. Herndon, A. Hocker, Z. Hong, W. Hopkins, S. Hou, R. Hughes, U. Husemann, M. Hussein, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. James, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, M. Jones, K. Joo, S. Jun, T. Junk, M. Kambeitz, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Kreps, J. Kroll, M. Kruse, T. Kuhr, N. Kulkarni, M. Kurata, A. Laasanen, S. Lammel, M. Lancaster, K. Lannon, G. Latino, H. Lee, J. Lee, S. Leo, S. Leone, J. Lewis, A. Limosani, E. Lipeles, A. Lister, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, A. Lucà, J. Lueck, P. Lujan, P. Lukens, G. Lungu, J. Lys, R. Lysak, R. Madrak, P. Maestro, S. Malik, G. Manca, A. Manousakis Katsikakis, L. Marchese, F. Margaroli, P. Marino, M. Martínez, K. Matera, M. Mattson, A. Mazzacane, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, C. Moon, R. Moore, M. Morello, A. Mukherjee, T.h. Muller, P. Murat, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. 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Vellidi, C. Vernieri, M. Vidal, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wallny, S. Wang, D. Water, W. Wester, D. Whiteson, A. Wicklund, S. Wilbur, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, A. Zanetti, Y. Zeng, C. Zhou, and S. Zucchelli
- Subjects
D0-D0bar mixing ,CDF ,CONSTRAINTS ,TEVATRON - Abstract
We measure the time dependence of the ratio of decay rates for D-0 -> K+ pi(-) to the Cabibbo- favored decay D-0 -> K- pi(+). The charge conjugate decays are included. A signal of 3: 3 x 10(4) D*(+) -> pi D-+(0), D-0 -> K+ pi(-) decays is obtained with D-0 proper decay times between 0.75 and 10 mean D-0 lifetimes. The data were recorded with the CDF II detector at the Fermilab Tevatron and correspond to an integrated luminosity of 9: 6 fb(-1) for p (p) over bar collisions at root s = 1: 96 TeV. Assuming CP conservation, we search for D-0-(D) over bar (0) mixing and measure the mixing parameters to be R-D = (3: 51 +/- 0: 35) x 10(-3), y' = (4: 3 +/- 4: 3) x 10(-3), and x'(2) = (0: 08 +/- 0: 18) x 10(-3). We report Bayesian probability intervals in the x'(2)- y' plane and find that the significance of excluding the no- mixing hypothesis is equivalent to 6.1 Gaussian standard deviations, providing the second observation of D-0-(D) over bar (0) mixing from a single experiment.
- Published
- 2013
30. Search for B0s→μ+μ− and B0→μ+μ− decays with the full CDF Run II data set
- Author
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T. Aaltonen, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Antos, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanskas, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, T. Bae, A. Barbaro Galtieri, V. Barnes, B. Barnett, P. Barria, P. Bartos, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretvas, A. Bhatti, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, P. Butti, A. Buzatu, A. Calamba, S. Camarda, M. Campanelli, F. Canelli, B. Carls, D. Carlsmith, R. Carosi, S. Carrillo, B. Casal, M. Casarsa, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, K. Cho, D. Chokheli, M. Ciocci, A. Clark, C. Clarke, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, M. Cremonesi, D. Cruz, J. Cuevas, R. Culbertson, N. d’Ascenzo, M. Datta, P. De Barbaro, L. Demortier, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, M. Dorigo, A. Driutti, K. Ebina, R. Edgar, A. Elagin, R. Erbacher, S. Errede, B. Esham, R. Eusebi, S. Farrington, J. Fernández Ramos, R. Field, G. Flanagan, R. Forrest, M. Franklin, J. Freeman, H. Frisch, Y. Funakoshi, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, S. Giagu, V. Giakoumopoulou, K. Gibson, C. Ginsburg, N. Giokaris, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, A. Golossanov, G. Gomez, G. Gomez Ceballos, M. Goncharov, O. González López, I. Gorelov, A. Goshaw, K. Goulianos, E. Gramellini, S. Grinstein, C. Grosso Pilcher, R. Group, J. Guimaraes da Costa, S. Hahn, J. Han, F. Happacher, K. Hara, M. Hare, R. Harr, T. Harrington Taber, K. Hatakeyama, C. Hays, J. Heinrich, M. Herndon, A. Hocker, Z. Hong, W. Hopkins, S. Hou, R. Hughes, U. Husemann, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. James, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, M. Jones, K. Joo, S. Jun, T. Junk, M. Kambeitz, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Kreps, J. Kroll, M. Kruse, T. Kuhr, M. Kurata, A. Laasanen, S. Lammel, M. Lancaster, K. Lannon, G. Latino, H. Lee, J. Lee, S. Leo, S. Leone, J. Lewis, A. Limosani, E. Lipeles, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Lukens, G. Lungu, J. Lys, R. Lysak, R. Madrak, P. Maestro, S. Malik, G. Manca, A. Manousakis Katsikakis, F. Margaroli, P. Marino, M. Martínez, K. Matera, M. Mattson, A. Mazzacane, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, C. Moon, R. Moore, M. Morello, A. Mukherjee, T.h. Muller, P. Murat, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, T. Nigmanov, L. Nodulman, S. Noh, O. Norniella, L. Oakes, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, C. Pagliarone, E. Palencia, P. Palni, V. Papadimitriou, W. Parker, G. Pauletta, M. Paulini, C. Paus, T. Phillips, G. Piacentino, E. Pianori, J. Pilot, K. Pitts, C. Plager, L. Pondrom, S. Poprocki, K. Potamianos, F. Prokoshin, A. Pranko, F. Ptohos, G. Punzi, N. Ranjan, I. Redondo Fernández, P. Renton, M. Rescigno, T. Riddick, L. Ristori, A. Robson, T. Rodriguez, S. Rolli, M. Ronzani, R. Roser, J. Rosner, F. Ruffini, A. Ruiz, J. Russ, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy Navarro, P. Schlabach, E. Schmidt, T. Schwarz, L. Scodellaro, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shears, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber Tecker, A. Simonenko, P. Sinervo, K. Sliwa, J. Smith, F. Snider, V. Sorin, H. Song, D. Sperka, M. Stancari, R. Denis, B. Stelzer, O. Stelzer Chilton, D. Stentz, J. Strologas, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, E. Thomson, V. Thukral, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, F. Ukegawa, S. Uozumi, F. Vázquez, G. Velev, C. Vellidis, C. Vernieri, M. Vidal, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wallny, S. Wang, A. Warburton, D. Waters, W. Wester, D. Whiteson, A. Wicklund, S. Wilbur, H. Williams, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolbers, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W. M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, A. Zanetti, Y. Zeng, C. Zhou, BRIGLIADORI, LUCA, CASTRO, ANDREA, DENINNO, MARIA MADDALENA, MAZZANTI, PAOLO, MOGGI, NICCOLO', MUSSINI, MANUEL, RIMONDI, FRANCO, ZUCCHELLI, STEFANO, T. Aaltonen, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Anto, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanska, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, T. Bae, A. Barbaro-Galtieri, V. Barne, B. Barnett, P. Barria, P. Barto, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretva, A. Bhatti, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, L. Brigliadori, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, P. Butti, A. Buzatu, A. Calamba, S. Camarda, M. Campanelli, F. Canelli, B. Carl, D. Carlsmith, R. Carosi, S. Carrillo, B. Casal, M. Casarsa, A. Castro, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli-Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, K. Cho, D. Chokheli, M. Ciocci, A. Clark, C. Clarke, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, M. Cremonesi, D. Cruz, J. Cueva, R. Culbertson, N. d’Ascenzo, M. Datta, P. De Barbaro, L. Demortier, M. Deninno, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, M. Dorigo, A. Driutti, K. Ebina, R. Edgar, A. Elagin, R. Erbacher, S. Errede, B. Esham, R. Eusebi, S. Farrington, J. Fernández Ramo, R. Field, G. Flanagan, R. Forrest, M. Franklin, J. Freeman, H. Frisch, Y. Funakoshi, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, S. Giagu, V. Giakoumopoulou, K. Gibson, C. Ginsburg, N. Giokari, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, A. Golossanov, G. Gomez, G. Gomez-Ceballo, M. Goncharov, O. González López, I. Gorelov, A. Goshaw, K. Gouliano, E. Gramellini, S. Grinstein, C. Grosso-Pilcher, R. Group, J. Guimaraes da Costa, S. Hahn, J. Han, F. Happacher, K. Hara, M. Hare, R. Harr, T. Harrington-Taber, K. Hatakeyama, C. Hay, J. Heinrich, M. Herndon, A. Hocker, Z. Hong, W. Hopkin, S. Hou, R. Hughe, U. Husemann, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. Jame, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, M. Jone, K. Joo, S. Jun, T. Junk, M. Kambeitz, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Krep, J. Kroll, M. Kruse, T. Kuhr, M. Kurata, A. Laasanen, S. Lammel, M. Lancaster, K. Lannon, G. Latino, H. Lee, J. Lee, S. Leo, S. Leone, J. Lewi, A. Limosani, E. Lipele, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Luken, G. Lungu, J. Ly, R. Lysak, R. Madrak, P. Maestro, S. Malik, G. Manca, A. Manousakis-Katsikaki, F. Margaroli, P. Marino, M. Martínez, K. Matera, M. Mattson, A. Mazzacane, P. Mazzanti, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, N. Moggi, C. Moon, R. Moore, M. Morello, A. Mukherjee, Th. Muller, P. Murat, M. Mussini, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, T. Nigmanov, L. Nodulman, S. Noh, O. Norniella, L. Oake, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, C. Pagliarone, E. Palencia, P. Palni, V. Papadimitriou, W. Parker, G. Pauletta, M. Paulini, C. Pau, T. Phillip, G. Piacentino, E. Pianori, J. Pilot, K. Pitt, C. Plager, L. Pondrom, S. Poprocki, K. Potamiano, F. Prokoshin, A. Pranko, F. Ptoho, G. Punzi, N. Ranjan, I. Redondo Fernández, P. Renton, M. Rescigno, T. Riddick, F. Rimondi, L. Ristori, A. Robson, T. Rodriguez, S. Rolli, M. Ronzani, R. Roser, J. Rosner, F. Ruffini, A. Ruiz, J. Ru, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy-Navarro, P. Schlabach, E. Schmidt, T. Schwarz, L. Scodellaro, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shear, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber-Tecker, A. Simonenko, P. Sinervo, K. Sliwa, J. Smith, F. Snider, V. Sorin, H. Song, D. Sperka, M. Stancari, R. Deni, B. Stelzer, O. Stelzer-Chilton, D. Stentz, J. Strologa, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, E. Thomson, V. Thukral, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, F. Ukegawa, S. Uozumi, F. Vázquez, G. Velev, C. Vellidi, C. Vernieri, M. Vidal, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wallny, S. Wang, A. Warburton, D. Water, W. Wester, D. Whiteson, A. Wicklund, S. Wilbur, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, A. Zanetti, Y. Zeng, C. Zhou, and S. Zucchelli
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B0S ,CDF ,TEVATRON - Abstract
We report on a search for B0s→μ+μ− and B0→μ+μ− decays using proton-antiproton collision data at s√=1.96 TeV corresponding to 10 fb−1 of integrated luminosity collected by the CDF II detector at the Fermilab Tevatron collider. The observed number of B0 candidates is consistent with background-only expectations and yields an upper limit on the branching fraction of B(B0→μ+μ−)
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- 2013
31. A proposed dosing algorithm for the individualized dosing of human immunoglobulin in chronic inflammatory neuropathies
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Lauren Ellis, Yusuf A. Rajabally, Robert D M Hadden, Mary M. Reilly, Michael P. Lunn, and John B Winer
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0301 basic medicine ,Adult ,Male ,medicine.medical_specialty ,Individualized dosing ,Human immunoglobulin ,03 medical and health sciences ,Polyneuropathies ,0302 clinical medicine ,Medicine ,Humans ,Dosing ,Aged ,biology ,Dosing algorithm ,business.industry ,General Neuroscience ,Immunoglobulins, Intravenous ,Polyradiculoneuropathy ,Middle Aged ,medicine.disease ,Surgery ,030104 developmental biology ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Anesthesia ,biology.protein ,Female ,Neurology (clinical) ,Antibody ,business ,Inflammatory neuropathy ,030217 neurology & neurosurgery ,Algorithms ,Multifocal motor neuropathy - Abstract
Dosing guidelines for immunoglobulin (Ig) treatment in neurological disorders do not consider variations in Ig half-life or between patients. Individualization of therapy could optimize clinical outcomes and help control costs. We developed an algorithm to optimize Ig dose based on patient's response and present this here as an example of how dosing might be individualized in a pharmacokinetically rational way and how this achieves potential dose and cost savings. Patients are "normalized" with no more than two initial doses of 2 g/kg, identifying responders. A third dose is not administered until the patient's condition deteriorates, allowing a "dose interval" to be set. The dose is then reduced until relapse allowing dose optimization. Using this algorithm, we have individualized Ig doses for 71 chronic inflammatory neuropathy patients. The majority of patients had chronic inflammatory demyelinating polyradiculoneuropathy (n = 39) or multifocal motor neuropathy (n = 24). The mean (standard deviation) dose of Ig administered was 1.4 (0.6) g/kg, with a mean dosing interval of 4.3 weeks (median 4 weeks, range 0.5-10). Use of our standardized algorithm has allowed us to quickly optimize Ig dosing.
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- 2015
32. Guillain–Barré syndrome and its treatment
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John B. Winer and Michael R. Douglas
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Background information ,Weakness ,Pediatrics ,medicine.medical_specialty ,biology ,Guillain-Barre syndrome ,business.industry ,General Neuroscience ,Disease ,Guillain-Barre Syndrome ,medicine.disease ,biology.organism_classification ,Campylobacter jejuni ,Enteritis ,Serology ,Immunology ,medicine ,biology.protein ,Humans ,Pharmacology (medical) ,Neurology (clinical) ,medicine.symptom ,business ,Antiganglioside antibodies - Abstract
Guillain-Barré syndrome typically presents with an acute ascending areflexic weakness, progressing over 4 weeks or less. The most common form of the disease is an acute inflammatory demyelinating polyneuropathy, but other forms with primarily axonal pathologies are well documented. The association of Guillain-Barré syndrome with a range of antecedent infections, particularly Campylobacter jejuni enteritis, is also established. A range of serological and neurophysiological investigations can assist in making an accurate diagnosis. Background information about the syndrome and the evidence base for such treatments are discussed herein.
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- 2006
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33. Paraneoplastic Neurological Antibodies: A Laboratory Experience
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Abid Karim, Arthur R. Bradwell, John B Winer, Richard G. Hughes, and Adrian C. Williams
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Pathology ,medicine.medical_specialty ,Anti-nuclear antibody ,Antibodies, Neoplasm ,Blotting, Western ,Immunofluorescence ,General Biochemistry, Genetics and Molecular Biology ,History and Philosophy of Science ,Western blot ,Cerebellum ,Prevalence ,Humans ,Medicine ,Fluorescent Antibody Technique, Indirect ,Autoantibodies ,Retrospective Studies ,Neurons ,medicine.diagnostic_test ,biology ,Clinical Laboratory Techniques ,business.industry ,General Neuroscience ,Autoantibody ,Immunohistochemistry ,United Kingdom ,Blot ,Antibodies, Antinuclear ,Immunology ,Etiology ,biology.protein ,Fluorescein ,Antibody ,business ,Paraneoplastic Syndromes, Nervous System - Abstract
Antineuronal antibodies are associated with rare paraneoplastic neurological syndromes, and their identification alerts clinicians to examine for the presence of a tumor. Presented here is laboratory experience (prevalence, difficulties, and procedures) and several interesting but inconclusive results. A total of 1045 samples were screened over a 2-year period; 91 showed a degree of binding of antibodies to the cerebellum, and 22 of these 91 were confirmed, by Western blot, to have specific antineuronal antibodies. Thirteen of 22 were Hu-positive, and 6 of these also had antinuclear antibodies. Six were Yo-positive, 2 had anti-Ma antibodies, and 1 was Tr-positive. An additional 27 of 91 patients had cerebellar antibodies giving recognized staining patterns (Hu, Yo, and Ma). However, Western blot did not confirm these specificities, and hence they were reported as atypical. Six of 27 of these patients had neoplasms; 3 of the 6 gave nucleolar patterns (not Ma). Two appeared similar to Yo, and 1 similar to Hu. Antineuronal antibodies are rare, and in the absence of a specific etiology patients should be examined further for the possible presence of an underlying tumor. Methodical classification of the antibodies must be conducted to avoid incorrect reporting. Further criteria on the typing/reporting of atypical results may aid diagnosis of paraneoplastic neurological syndromes.
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- 2005
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34. Measurement of the branching fraction B(Λ_{b}^{0}→Λ_{c}^{+}π^{-}π^{+}π^{-}) at CDF
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T. Aaltonen, B. Álvarez González, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Antos, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanskas, B. Auerbach, A. Aurisano, F. Azfar, P. Azzurri, W. Badgett, T. Bae, A. Barbaro Galtieri, V. Barnes, B. Barnett, P. Barria, P. Bartos, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretvas, A. Bhatti, M. Binkley, D. Bisello, I. Bizjak, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, A. Buzatu, A. Calamba, C. Calancha, S. Camarda, M. Campanelli, M. Campbell, F. Canelli, B. Carls, D. Carlsmith, R. Carosi, S. Carrillo, S. Carron, B. Casal, M. Casarsa, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, F. Chlebana, K. Cho, D. Chokheli, W. Chung, Y. Chung, M. Ciocci, A. Clark, C. Clarke, G. Compostella, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, F. Crescioli, J. Cuevas, R. Culbertson, D. Dagenhart, N. d’Ascenzo, M. Datta, P. de Barbaro, M. Dell’Orso, L. Demortier, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, P. Dong, M. Dorigo, T. Dorigo, K. Ebina, A. Elagin, A. Eppig, R. Erbacher, S. Errede, N. Ershaidat, R. Eusebi, H. Fang, S. Farrington, M. Feindt, J. Fernandez, R. Field, G. Flanagan, R. Forrest, M. Frank, M. Franklin, J. Freeman, Y. Funakoshi, I. Furic, M. Gallinaro, J. Garcia, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, V. Giakoumopoulou, P. Giannetti, K. Gibson, C. Ginsburg, N. Giokaris, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, N. Goldschmidt, A. Golossanov, G. Gomez, G. Gomez Ceballos, M. Goncharov, O. González, I. Gorelov, A. Goshaw, K. Goulianos, S. Grinstein, C. Grosso Pilcher, R. Group, J. Guimaraes da Costa, Z. Gunay Unalan, C. Haber, S. Hahn, E. Halkiadakis, A. Hamaguchi, J. Han, F. Happacher, K. Hara, D. Hare, M. Hare, R. Harr, K. Hatakeyama, C. Hays, M. Heck, J. Heinrich, M. Herndon, S. Hewamanage, A. Hocker, W. Hopkins, D. Horn, S. Hou, R. Hughes, M. Hurwitz, U. Husemann, N. Hussain, M. Hussein, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. James, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, W. Johnson, M. Jones, K. Joo, S. Jun, T. Junk, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, V. Khotilovich, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Kreps, J. Kroll, D. Krop, M. Kruse, V. Krutelyov, T. Kuhr, M. Kurata, S. Kwang, A. Laasanen, S. Lami, S. Lammel, M. Lancaster, R. Lander, K. Lannon, A. Lath, G. Latino, T. LeCompte, E. Lee, H. Lee, J. Lee, S. Lee, S. Leo, S. Leone, J. Lewis, A. Limosani, C. J. Lin, J. Linacre, M. Lindgren, E. Lipeles, A. Lister, D. Litvintsev, C. Liu, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Lukens, G. Lungu, J. Lys, R. Lysak, R. Madrak, K. Maeshima, P. Maestro, S. Malik, G. Manca, A. Manousakis Katsikakis, F. Margaroli, C. Marino, M. Martínez, K. Matera, M. Mattson, A. Mazzacane, K. McFarland, P. McIntyre, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, M. Mondragon, C. Moon, R. Moore, M. Morello, J. Morlock, P. Movilla Fernandez, A. Mukherjee, T.h. Muller, P. Murat, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, M. Neubauer, J. Nielsen, L. Nodulman, S. Noh, O. Norniella, L. Oakes, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, S. Pagan Griso, C. Pagliarone, E. Palencia, V. Papadimitriou, A. Paramonov, J. Patrick, G. Pauletta, M. Paulini, C. Paus, D. Pellett, A. Penzo, T. Phillips, G. Piacentino, E. Pianori, J. Pilot, K. Pitts, C. Plager, L. Pondrom, S. Poprocki, K. Potamianos, O. Poukhov, F. Prokoshin, A. Pranko, F. Ptohos, G. Punzi, A. Rahaman, V. Ramakrishnan, N. Ranjan, I. Redondo, P. Renton, M. Rescigno, T. Riddick, L. Ristori, A. Robson, T. Rodrigo, T. Rodriguez, E. Rogers, S. Rolli, R. Roser, F. Ruffini, A. Ruiz, J. Russ, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy Navarro, P. Schlabach, A. Schmidt, E. Schmidt, M. Schmidt, T. Schwarz, L. Scodellaro, A. Scribano, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shears, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber Tecker, A. Simonenko, P. Sinervo, A. Sissakian, K. Sliwa, J. Smith, F. Snider, A. Soha, V. Sorin, P. Squillacioti, M. Stancari, R. S.t. Denis, B. Stelzer, O. Stelzer Chilton, D. Stentz, J. Strologas, G. Strycker, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, J. Thome, G. Thompson, E. Thomson, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, Y. Tu, F. Ukegawa, S. Uozumi, A. Varganov, E. Vataga, F. Vázquez, G. Velev, C. Vellidis, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, A. Warburton, D. Waters, W. Wester, D. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. Williams, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolbers, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W. M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, S. Yu, J. Yun, A. Zanetti, Y. Zeng, BRIGLIADORI, LUCA, CASTRO, ANDREA, DENINNO, MARIA MADDALENA, MAZZANTI, PAOLO, MOGGI, NICCOLO', MUSSINI, MANUEL, RIMONDI, FRANCO, ZUCCHELLI, STEFANO, T. Aaltonen, B. Álvarez González, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. Anto, G. Apollinari, J. Appel, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanska, B. Auerbach, A. Aurisano, F. Azfar, P. Azzurri, W. Badgett, T. Bae, A. Barbaro-Galtieri, V. Barne, B. Barnett, P. Barria, P. Barto, M. Bauce, F. Bedeschi, S. Behari, G. Bellettini, J. Bellinger, D. Benjamin, A. Beretva, A. Bhatti, M. Binkley, D. Bisello, I. Bizjak, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, L. Brigliadori, C. Bromberg, E. Brucken, J. Budagov, H. Budd, K. Burkett, G. Busetto, P. Bussey, A. Buzatu, A. Calamba, C. Calancha, S. Camarda, M. Campanelli, M. Campbell, F. Canelli, B. Carl, D. Carlsmith, R. Carosi, S. Carrillo, S. Carron, B. Casal, M. Casarsa, A. Castro, P. Catastini, D. Cauz, V. Cavaliere, M. Cavalli-Sforza, A. Cerri, L. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, F. Chlebana, K. Cho, D. Chokheli, W. Chung, Y. Chung, M. Ciocci, A. Clark, C. Clarke, G. Compostella, M. Convery, J. Conway, M. Corbo, M. Cordelli, C. Cox, D. Cox, F. Crescioli, J. Cueva, R. Culbertson, D. Dagenhart, N. d’Ascenzo, M. Datta, P. de Barbaro, M. Dell’Orso, L. Demortier, M. Deninno, F. Devoto, M. d’Errico, A. Di Canto, B. Di Ruzza, J. Dittmann, M. D’Onofrio, S. Donati, P. Dong, M. Dorigo, T. Dorigo, K. Ebina, A. Elagin, A. Eppig, R. Erbacher, S. Errede, N. Ershaidat, R. Eusebi, H. Fang, S. Farrington, M. Feindt, J. Fernandez, R. Field, G. Flanagan, R. Forrest, M. Frank, M. Franklin, J. Freeman, Y. Funakoshi, I. Furic, M. Gallinaro, J. Garcia, A. Garfinkel, P. Garosi, H. Gerberich, E. Gerchtein, V. Giakoumopoulou, P. Giannetti, K. Gibson, C. Ginsburg, N. Giokari, P. Giromini, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, N. Goldschmidt, A. Golossanov, G. Gomez, G. Gomez-Ceballo, M. Goncharov, O. González, I. Gorelov, A. Goshaw, K. Gouliano, S. Grinstein, C. Grosso-Pilcher, R. Group, J. Guimaraes da Costa, Z. Gunay-Unalan, C. Haber, S. Hahn, E. Halkiadaki, A. Hamaguchi, J. Han, F. Happacher, K. Hara, D. Hare, M. Hare, R. Harr, K. Hatakeyama, C. Hay, M. Heck, J. Heinrich, M. Herndon, S. Hewamanage, A. Hocker, W. Hopkin, D. Horn, S. Hou, R. Hughe, M. Hurwitz, U. Husemann, N. Hussain, M. Hussein, J. Huston, G. Introzzi, M. Iori, A. Ivanov, E. Jame, D. Jang, B. Jayatilaka, E. Jeon, S. Jindariani, W. Johnson, M. Jone, K. Joo, S. Jun, T. Junk, T. Kamon, P. Karchin, A. Kasmi, Y. Kato, W. Ketchum, J. Keung, V. Khotilovich, B. Kilminster, D. Kim, H. Kim, J. Kim, M. Kim, S. Kim, Y. Kim, N. Kimura, M. Kirby, K. Knoepfel, K. Kondo, D. Kong, J. Konigsberg, A. Kotwal, M. Krep, J. Kroll, D. Krop, M. Kruse, V. Krutelyov, T. Kuhr, M. Kurata, S. Kwang, A. Laasanen, S. Lami, S. Lammel, M. Lancaster, R. Lander, K. Lannon, A. Lath, G. Latino, T. LeCompte, E. Lee, H. Lee, J. Lee, S. Lee, S. Leo, S. Leone, J. Lewi, A. Limosani, C.-J. Lin, J. Linacre, M. Lindgren, E. Lipele, A. Lister, D. Litvintsev, C. Liu, H. Liu, Q. Liu, T. Liu, S. Lockwitz, A. Loginov, D. Lucchesi, J. Lueck, P. Lujan, P. Luken, G. Lungu, J. Ly, R. Lysak, R. Madrak, K. Maeshima, P. Maestro, S. Malik, G. Manca, A. Manousakis-Katsikaki, F. Margaroli, C. Marino, M. Martínez, K. Matera, M. Mattson, A. Mazzacane, P. Mazzanti, K. McFarland, P. McIntyre, R. McNulty, A. Mehta, P. Mehtala, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, N. Moggi, M. Mondragon, C. Moon, R. Moore, M. Morello, J. Morlock, P. Movilla Fernandez, A. Mukherjee, Th. Muller, P. Murat, M. Mussini, J. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, M. Neubauer, J. Nielsen, L. Nodulman, S. Noh, O. Norniella, L. Oake, S. Oh, Y. Oh, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, S. Pagan Griso, C. Pagliarone, E. Palencia, V. Papadimitriou, A. Paramonov, J. Patrick, G. Pauletta, M. Paulini, C. Pau, D. Pellett, A. Penzo, T. Phillip, G. Piacentino, E. Pianori, J. Pilot, K. Pitt, C. Plager, L. Pondrom, S. Poprocki, K. Potamiano, O. Poukhov, F. Prokoshin, A. Pranko, F. Ptoho, G. Punzi, A. Rahaman, V. Ramakrishnan, N. Ranjan, I. Redondo, P. Renton, M. Rescigno, T. Riddick, F. Rimondi, L. Ristori, A. Robson, T. Rodrigo, T. Rodriguez, E. Roger, S. Rolli, R. Roser, F. Ruffini, A. Ruiz, J. Ru, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Santi, K. Sato, V. Saveliev, A. Savoy-Navarro, P. Schlabach, A. Schmidt, E. Schmidt, M. Schmidt, T. Schwarz, L. Scodellaro, A. Scribano, F. Scuri, S. Seidel, Y. Seiya, A. Semenov, F. Sforza, S. Shalhout, T. Shear, P. Shepard, M. Shimojima, M. Shochet, I. Shreyber-Tecker, A. Simonenko, P. Sinervo, A. Sissakian, K. Sliwa, J. Smith, F. Snider, A. Soha, V. Sorin, P. Squillacioti, M. Stancari, R. St. Deni, B. Stelzer, O. Stelzer-Chilton, D. Stentz, J. Strologa, G. Strycker, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. Thom, J. Thome, G. Thompson, E. Thomson, D. Toback, S. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, P. Totaro, M. Trovato, Y. Tu, F. Ukegawa, S. Uozumi, A. Varganov, E. Vataga, F. Vázquez, G. Velev, C. Vellidi, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, A. Warburton, D. Water, W. Wester, D. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. William, J. Wilson, P. Wilson, B. Winer, P. Wittich, S. Wolber, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, D. Yamato, T. Yang, U. Yang, Y. Yang, W.-M. Yao, G. Yeh, K. Yi, J. Yoh, K. Yorita, T. Yoshida, G. Yu, I. Yu, S. Yu, J. Yun, A. Zanetti, Y. Zeng, and S. Zucchelli
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CDF ,+Lambda%2Fc%2B+pi%2B+2pi-+|+Lambda%2Fb0+-->+Lambda%2Fc%2B+pi-+|+1960+GeV-cms%22">Lambda/b0: branching ratio: measured | CDF | Batavia TEVATRON Coll | anti-p p: interaction | Lambda/b0: hadronic decay | Lambda/c(2593): intermediate state | Lambda/c(2625): intermediate state | Sigma/c(2455): intermediate state | mass spectrum: mass difference | experimental results | Lambda/b0 --> Lambda/c+ pi+ 2pi- | Lambda/b0 --> Lambda/c+ pi- | 1960 GeV-cms ,TEVATRON ,Measurement of branching fraction - Abstract
We report an analysis of the Λb0→Λc+π-π+π- decay in a data sample collected by the CDF II detector at the Fermilab Tevatron corresponding to 2.4 fb-1 of integrated luminosity. We reconstruct the currently largest samples of the decay modes Λb0→Λc(2595)+π- (with Λc(2595)+→Λc+π+π-), b0→Λc(2625)+π- (with Λc(2625)+→Λc+π+π-), Λb0→Σc(2455)++π-π- (with Σc(2455)++→Λc+π+), and Λb0→Σc (2455)0π+π- (with Σc(2455)0→Λc+π-) and measure the branching fractions relative to the Λb0→Λc+π- branching fraction. We measure the ratio B(Λb0→Λc +π-π+π-)/ B(Λb0→Λc+π-)=3.04±0.33(stat)-0.55+0.70(syst) which is used to derive B(Λb0→Λc+π-π+π-)=(26.8-11.2+11.9)×10-3.
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- 2012
35. Application of multiplex ligation-dependent probe analysis to define a small deletion encompassing PMP22 exons 4 and 5 in hereditary neuropathy with liability to pressure palsies
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Richard M. Barber, Victoria H Lindley, Fiona MacDonald, Ian Sutton, John B Winer, R Jane Bryon, and A Paul Mocroft
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Adult ,Genetic Markers ,Male ,DNA Mutational Analysis ,Gene Dosage ,Neural Conduction ,Molecular Probe Techniques ,Locus (genetics) ,Biology ,Polymerase Chain Reaction ,Exon ,Charcot-Marie-Tooth Disease ,Predictive Value of Tests ,Humans ,Paralysis ,Genetic Predisposition to Disease ,Multiplex ,Genetic Testing ,Peripheral Nerves ,Multiplex ligation-dependent probe amplification ,Diagnostic laboratory ,Gene ,Pmp22 gene ,Myelin Sheath ,Genetics (clinical) ,Genetics ,Polymorphism, Genetic ,Exons ,Middle Aged ,Molecular biology ,Pedigree ,Neurology ,Mutation ,Pediatrics, Perinatology and Child Health ,Female ,Neurology (clinical) ,Hereditary Sensory and Motor Neuropathy ,Ligation ,Gene Deletion ,Myelin Proteins ,Chromosomes, Human, Pair 17 - Abstract
Hereditary neuropathy with liability to pressure palsies arises as a result of defects at the chromosome 17p11.2-12 locus and in 84% of cases a 1.5 Mb deletion containing the PMP22 gene is detected by analysis that utilises polymorphic (CA)n repeat markers which flank this gene. We report the clinical and electrophysiological findings observed in a kindred with three members affected by HNPP due to a deletion containing exons 4 and 5 of the PMP22 gene. This small deletion cannot be detected using standard analysis with polymorphic (CA)n repeat markers and a definitive diagnosis was made by multiplex ligation-dependent probe analysis of PMP22 exons 1A-5. MLPA can be readily utilised as a routine diagnostic laboratory test to detect the common HNPP 1.5 Mb deletion, as well as the reciprocal 1.5 Mb insertion observed in CMT1A, but has the advantage over other diagnostic techniques of being able to define single exon deletions.
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- 2004
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36. Coexistent hereditary and inflammatory neuropathy
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Rosalind H.M. King, Anthony R Kenton, J. R. Muddle, Richard W. Orrell, John B Winer, Omar Malik, Mary B Davis, David J. Sharp, and Lionel Ginsberg
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Adult ,Male ,medicine.medical_specialty ,Pathology ,Adolescent ,Biopsy ,Prednisolone ,Neural Conduction ,Chronic inflammatory demyelinating polyneuropathy ,Guillain-Barre Syndrome ,Gastroenterology ,Asymptomatic ,Connexins ,Charcot-Marie-Tooth Disease ,Internal medicine ,medicine ,Humans ,Glucocorticoids ,Aged ,Nerve biopsy ,Guillain-Barre syndrome ,medicine.diagnostic_test ,business.industry ,Immunoglobulins, Intravenous ,Middle Aged ,medicine.disease ,Treatment Outcome ,Acute Disease ,Disease Progression ,Female ,Neurology (clinical) ,medicine.symptom ,business ,Hereditary motor and sensory neuropathy ,Polyneuropathy ,Chromosomes, Human, Pair 17 ,medicine.drug - Abstract
Classically, the course of Charcot-Marie-Tooth (CMT) disease is gradually progressive. We describe eight atypical patients who developed acute or subacute deterioration. Seven of these had genetically proven CMT disease type 1A (CMT1A) due to chromosome 17p11.2-12 duplication, and one had X-linked disease (CMTX) due to a mutation in the GJB1 gene. In this group there was sufficient clinical, electrophysiological and neuropathological information to indicate a diagnosis of a superimposed inflammatory polyneuropathy. The age range of the patients was 18-69 years, with a mean of 39 years. A family history of a similar neuropathic condition was present in only four patients. All eight had an acute or subacute deterioration following a long asymptomatic or stable period. Seven had neuropathic pain or prominent positive sensory symptoms. Nerve biopsy demonstrated excess lymphocytic infiltration in all eight patients. Five patients were treated with steroids and/or intravenous immunoglobulin, with variable positive response; three patients received no immunomodulatory treatment. Inflammatory neuropathy has previously been recognized in patients with hereditary neuropathy, with uncharacterized genetic defects and with CMT1B. We present detailed assessments of patients with CMT1A and CMTX, including nerve biopsy, and conclude that coexistent inflammatory neuropathy is not genotype-specific in hereditary motor and sensory neuropathy. Although this was not a formal epidemiological study, estimates of the prevalence of CMT disease and chronic inflammatory demyelinating polyneuropathy indicate that the association is more frequent than would be expected by chance. This has implications for understanding the pathogenesis of inflammatory neuropathies and raises important considerations in the management of patients with hereditary neuropathies. If a patient with CMT disease experiences an acute or subacute deterioration in clinical condition, treatment of a coexistent inflammatory neuropathy with steroids or immunoglobulin should be considered.
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- 2004
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37. Measurement of the cross section for prompt isolated diphoton production in pp̄ collisions at √s=1.96TeV
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T. Aaltonen, B. c. Álvarez, S. Amerio, D. Amidei, A. Anastassov, A. Annovi, J. b. Antos, G. Apollinari, J. Appel, A. Apresyan, T. Arisawa, A. Artikov, J. Asaadi, W. Ashmanskas, B. Auerbach, A. Aurisano, F. Azfar, W. Badgett, A. Barbaro Galtieri, V. Barnes, B. Barnett, P. a. Barria, P. b. Bartos, M. a. Bauce, G. Bauer, F. Bedeschi, D. Beecher, S. Behari, G. a. Bellettini, J. Bellinger, D. Benjamin, A. Beretvas, A. Bhatti, M. Binkley, D. a. Bisello, I. c. Bizjak, K. Bland, B. Blumenfeld, A. Bocci, A. Bodek, D. Bortoletto, J. Boudreau, A. Boveia, B. b. Brau, L. g. Brigliadori, A. b. Brisuda, C. Bromberg, E. Brucken, M. a. Bucciantonio, J. Budagov, H. Budd, S. Budd, K. Burkett, G. a. Busetto, P. Bussey, A. c. cu, C. Calancha, S. Camarda, M. Campanelli, M. Campbell, F. p. bo, A. Canepa, B. Carls, D. Carlsmith, R. Carosi, S. b. Carrillo, S. Carron, B. Casal, M. Casarsa, A. g. Castro, P. Catastini, D. Cauz, V. a. Cavaliere, M. Cavalli Sforza, A. b. Cerri, L. c. Cerrito, Y. Chen, M. Chertok, G. Chiarelli, G. Chlachidze, F. Chlebana, K. c. cp, D. Chokheli, J. Chou, W. Chung, Y. Chung, C. c. Ciobanu, M. a. Ciocci, A. Clark, G. a. Compostella, M. Convery, J. Conway, M. c. Corbo, M. Cordelli, C. Cox, D. Cox, F. a. Crescioli, C. C. Almenar, J. c. Cuevas, R. Culbertson, D. Dagenhart, N. c. cw, M. Datta, P. D. Barbaro, S. D. Cecco, G. D. Lorenzo, M. a. Dell'Orso, C. Deluca, L. Demortier, J. b. Deng, M. Deninno, F. Devoto, M. a. D'Errico, A. a. Di, B. D. Ruzza, J. Dittmann, M. D'Onofrio, S. a. Donati, P. Dong, T. Dorigo, K. Ebina, A. Elagin, A. Eppig, R. Erbacher, D. Errede, S. Errede, R. Eusebi, H. Fang, S. Farrington, M. Feindt, J. Fernandez, C. a. Ferrazza, R. Field, G. c. Flanagan, R. Forrest, M. Frank, M. Franklin, J. Freeman, Y. Funakoshi, I. Furic, M. Gallinaro, J. Galyardt, J. Garcia, A. Garfinkel, P. a. Garosi, H. Gerberich, E. Gerchtein, S. b. Giagu, V. Giakoumopoulou, P. Giannetti, K. Gibson, C. Ginsburg, N. Giokaris, P. Giromini, M. Giunta, G. Giurgiu, V. Glagolev, D. Glenzinski, M. Gold, D. Goldin, N. Goldschmidt, A. Golossanov, G. Gomez, G. Gomez Ceballos, M. Goncharov, O. González, I. Gorelov, A. Goshaw, K. Goulianos, A. Gresele, S. Grinstein, C. Grosso Pilcher, R. Group, J. G. Da, Z. Gunay Unalan, C. Haber, S. Hahn, E. Halkiadakis, A. Hamaguchi, J. Han, F. Happacher, K. Hara, D. Hare, M. Hare, R. Harr, K. Hatakeyama, C. Hays, M. Heck, J. Heinrich, M. Herndon, S. Hewamanage, D. Hidas, A. Hocker, W. b. Hopkins, D. Horn, S. Hou, R. Hughes, M. Hurwitz, U. Husemann, N. c. cu, M. Hussein, J. Huston, G. Introzzi, M. b. Iori, A. c. Ivanov, E. James, D. Jang, B. Jayatilaka, E. c. cp, M. Jha, S. Jindariani, W. Johnson, M. Jones, S. Jun, T. Junk, T. Kamon, P. Karchin, Y. b. Kato, W. Ketchum, J. Keung, V. Khotilovich, B. Kilminster, D. c. cp, H. c. cp, J. c. cp, M. Kim, S. c. cp, S. Kim, Y. Kim, N. Kimura, M. Kirby, S. Klimenko, K. Kondo, J. Konigsberg, A. Kotwal, M. Kreps, J. Kroll, D. Krop, N. c. Krumnack, M. Kruse, V. b. Krutelyov, T. Kuhr, M. Kurata, S. Kwang, A. Laasanen, S. Lami, S. Lammel, M. Lancaster, R. Lander, K. c. Lannon, A. Lath, G. b. Latino, I. Lazzizzera, T. Lecompte, E. Lee, H. Lee, S. c. Lee, S. a. Leo, S. Leone, J. Lewis, C. Lin, J. Linacre, M. Lindgren, E. Lipeles, A. Lister, D. Litvintsev, C. Liu, Q. Liu, T. Liu, S. Lockwitz, N. Lockyer, A. Loginov, D. a. Lucchesi, J. Lueck, P. Lujan, P. Lukens, G. Lungu, J. Lys, R. b. Lysak, R. Madrak, K. Maeshima, K. Makhoul, P. Maksimovic, S. Malik, G. b. Manca, A. Manousakis Katsikakis, F. Margaroli, C. Marino, M. Martínez, R. Martínez Ballarín, P. Mastrandrea, M. Mathis, M. Mattson, P. Mazzanti, K. McFarland, P. McIntyre, R. b. McNulty, A. Mehta, P. Mehtala, A. Menzione, C. Mesropian, T. Miao, D. Mietlicki, A. Mitra, H. Miyake, S. Moed, N. Moggi, M. c. Mondragon, C. c. cp, R. Moore, M. Morello, J. Morlock, P. M. Fernandez, A. Mukherjee, T. Muller, P. Murat, M. g. Mussini, J. c. Nachtman, Y. Nagai, J. Naganoma, I. Nakano, A. Napier, J. Nett, C. Neu, M. Neubauer, J. b. Nielsen, L. Nodulman, O. Norniella, E. Nurse, L. Oakes, S. Oh, Y. c. cp, I. Oksuzian, T. Okusawa, R. Orava, L. Ortolan, S. a. Pagan, C. Pagliarone, E. b. Palencia, V. Papadimitriou, A. Paramonov, J. Patrick, G. b. Pauletta, M. Paulini, C. Paus, D. Pellett, A. Penzo, T. Phillips, G. Piacentino, E. Pianori, J. Pilot, K. Pitts, C. Plager, L. Pondrom, K. Potamianos, O. Poukhov, A. Pranko, F. c. Prokoshin, F. b. Ptohos, E. Pueschel, G. a. Punzi, J. Pursley, A. Rahaman, V. Ramakrishnan, N. Ranjan, I. Redondo, P. Renton, M. Rescigno, F. g. Rimondi, L. a. Ristori, A. Robson, T. Rodrigo, T. Rodriguez, E. Rogers, S. Rolli, R. Roser, M. Rossi, F. Rubbo, F. a. Ruffini, A. Ruiz, J. Russ, V. Rusu, A. Safonov, W. Sakumoto, Y. Sakurai, L. Sartori, K. Sato, V. c. cw, A. c. Savoy Navarro, P. Schlabach, A. Schmidt, E. Schmidt, M. Schmidt, M. Schmitt, T. Schwarz, L. Scodellaro, A. a. Scribano, F. Scuri, A. Sedov, S. Seidel, Y. Seiya, A. Semenov, F. a. Sforza, A. Sfyrla, D. Sgalaberna, S. Shalhout, T. Shears, P. Shepard, M. c. Shimojima, S. Shiraishi, M. Shochet, I. Shreyber, A. Simonenko, P. c. cu, A. Sissakian, K. Sliwa, J. Smith, F. Snider, A. Soha, S. Somalwar, V. Sorin, P. Squillacioti, M. Stancari, M. Stanitzki, R. S. Denis, B. c. cu, O. c. cu, D. Stentz, J. Strologas, G. Strycker, Y. Sudo, A. Sukhanov, I. Suslov, K. Takemasa, Y. Takeuchi, J. Tang, M. Tecchio, P. Teng, J. b. Thom, J. Thome, G. Thompson, E. Thomson, P. Ttito Guzmán, S. Tkaczyk, D. Toback, S. b. Tokar, K. Tollefson, T. Tomura, D. Tonelli, S. Torre, D. Torretta, M. a. Trovato, Y. Tu, F. Ukegawa, A. Varganov, F. b. Vázquez, G. Velev, C. Vellidis, M. Vidal, I. Vila, R. Vilar, J. Vizán, M. Vogel, G. a. Volpi, P. Wagner, R. Wagner, T. Wakisaka, R. Wallny, S. Wang, D. Waters, M. Weinberger, W. Wester, B. Whitehouse, D. b. Whiteson, A. Wicklund, E. Wicklund, S. Wilbur, F. Wick, H. Williams, J. Wilson, P. Wilson, B. Winer, P. b. Wittich, S. Wolbers, H. Wolfe, T. Wright, X. Wu, Z. Wu, K. Yamamoto, J. Yamaoka, T. Yang, U. c. Yang, W. Yao, G. Yeh, K. c. Yi, J. Yoh, K. Yorita, T. b. Yoshida, G. Yu, I. c. cp, S. Yu, J. Yun, Y. Zeng, S. g. Zucchelli, DORIGO, MIRCO, SANTI, LORENZO GIANNI, TOTARO, PIERLUIGI, ZANETTI, ANNA MARIA, T., Aaltonen, B. c., Álvarez, S., Amerio, D., Amidei, A., Anastassov, A., Annovi, J. b., Anto, G., Apollinari, J., Appel, A., Apresyan, T., Arisawa, A., Artikov, J., Asaadi, W., Ashmanska, B., Auerbach, A., Aurisano, F., Azfar, W., Badgett, A., Barbaro Galtieri, V., Barne, B., Barnett, P. a., Barria, P. b., Barto, M. a., Bauce, G., Bauer, F., Bedeschi, D., Beecher, S., Behari, G. a., Bellettini, J., Bellinger, D., Benjamin, A., Beretva, A., Bhatti, M. b., Binkley, D. a., Bisello, I. c., Bizjak, K., Bland, B., Blumenfeld, A., Bocci, A., Bodek, D., Bortoletto, J., Boudreau, A., Boveia, B. b., Brau, L. g., Brigliadori, A. b., Brisuda, C., Bromberg, E., Brucken, M. a., Bucciantonio, J., Budagov, H., Budd, S., Budd, K., Burkett, G. a., Busetto, P., Bussey, A. c., Cw, C., Calancha, S., Camarda, M., Campanelli, M., Campbell, F. p., Canelli, A., Canepa, B., Carl, D., Carlsmith, R., Carosi, S. c., Carrillo, S., Carron, B., Casal, M., Casarsa, A. g., Castro, P., Catastini, D., Cauz, V. a., Cavaliere, M., Cavalli Sforza, A. b., Cerri, L. c., Cerrito, Y., Chen, M., Chertok, G., Chiarelli, G., Chlachidze, F., Chlebana, K. c., Cr, D., Chokheli, J., Chou, W., Chung, Y., Chung, C., Ciobanu, M. a., Ciocci, A., Clark, G. a., Compostella, M., Convery, J., Conway, M., Corbo, M., Cordelli, C., Cox, D., Cox, F. a., Crescioli, C. C., Almenar, J. c., Cueva, R., Culbertson, D., Dagenhart, N. c., D'Ascenzo, M., Datta, P. D., Barbaro, S. D., Cecco, G. D., Lorenzo, M. a., Dell'Orso, C., Deluca, L., Demortier, J. b., Deng, M., Deninno, F., Devoto, M. a., D'Errico, A. a., Di, B. D., Ruzza, J., Dittmann, M., D'Onofrio, S. a., Donati, P., Dong, Dorigo, Mirco, T., Dorigo, K., Ebina, A., Elagin, A., Eppig, R., Erbacher, D., Errede, S., Errede, N. c., Ershaidat, R., Eusebi, H., Fang, S., Farrington, M., Feindt, J., Fernandez, C. a., Ferrazza, R., Field, G. c., Flanagan, R., Forrest, M., Frank, M., Franklin, J., Freeman, Y., Funakoshi, I., Furic, M., Gallinaro, J., Galyardt, J., Garcia, A., Garfinkel, P. a., Garosi, H., Gerberich, E., Gerchtein, S. b., Giagu, V., Giakoumopoulou, P., Giannetti, K., Gibson, C., Ginsburg, N., Giokari, P., Giromini, M., Giunta, G., Giurgiu, V., Glagolev, D., Glenzinski, M., Gold, D., Goldin, N., Goldschmidt, A., Golossanov, G., Gomez, G., Gomez Ceballo, M., Goncharov, O., González, I., Gorelov, A., Goshaw, K., Gouliano, A., Gresele, S., Grinstein, C., Grosso Pilcher, R., Group, J. G., Da, Z., Gunay Unalan, C., Haber, S., Hahn, E., Halkiadaki, A., Hamaguchi, J., Han, F., Happacher, K., Hara, D., Hare, M., Hare, R., Harr, K., Hatakeyama, C., Hay, M., Heck, J., Heinrich, M., Herndon, S., Hewamanage, D., Hida, A., Hocker, W. b., Hopkin, D., Horn, S., Hou, R., Hughe, M., Hurwitz, U., Husemann, N. c., Cw, M., Hussein, J., Huston, G., Introzzi, M. b., Iori, A. c., Ivanov, E., Jame, D., Jang, B., Jayatilaka, E. c., Cr, M., Jha, S., Jindariani, W., Johnson, M., Jone, S., Jun, T., Junk, T., Kamon, P., Karchin, Y. c., Kato, W., Ketchum, J., Keung, V., Khotilovich, B., Kilminster, D. c., Cr, H. c., Cr, J. c., Cr, M., Kim, S. c., Cr, S., Kim, Y., Kim, N., Kimura, M., Kirby, S., Klimenko, K., Kondo, J., Konigsberg, A., Kotwal, M., Krep, J., Kroll, D., Krop, N. c., Krumnack, M., Kruse, V. b., Krutelyov, T., Kuhr, M., Kurata, S., Kwang, A., Laasanen, S., Lami, S., Lammel, M., Lancaster, R., Lander, K. c., Lannon, A., Lath, G. b., Latino, I., Lazzizzera, T., Lecompte, E., Lee, H., Lee, S. c., Lee, S. a., Leo, S., Leone, J., Lewi, C., Lin, J., Linacre, M., Lindgren, E., Lipele, A., Lister, D., Litvintsev, C., Liu, Q., Liu, T., Liu, S., Lockwitz, N., Lockyer, A., Loginov, D. a., Lucchesi, J., Lueck, P., Lujan, P., Luken, G., Lungu, J., Ly, R. b., Lysak, R., Madrak, K., Maeshima, K., Makhoul, P., Maksimovic, S., Malik, G. b., Manca, A., Manousakis Katsikaki, F., Margaroli, C., Marino, M., Martínez, R., Martínez Ballarín, P., Mastrandrea, M., Mathi, M., Mattson, P., Mazzanti, K., Mcfarland, P., Mcintyre, R. b., Mcnulty, A., Mehta, P., Mehtala, A., Menzione, C., Mesropian, T., Miao, D., Mietlicki, A., Mitra, H., Miyake, S., Moed, N., Moggi, M. c., Mondragon, C. c., Cr, R., Moore, M., Morello, J., Morlock, P. M., Fernandez, A., Mukherjee, T., Muller, P., Murat, M. g., Mussini, J. c., Nachtman, Y., Nagai, J., Naganoma, I., Nakano, A., Napier, J., Nett, C., Neu, M., Neubauer, J. b., Nielsen, L., Nodulman, O., Norniella, E., Nurse, L., Oake, S., Oh, Y. c., Cr, I., Oksuzian, T., Okusawa, R., Orava, L., Ortolan, S. a., Pagan, C., Pagliarone, E. b., Palencia, V., Papadimitriou, A., Paramonov, J., Patrick, G. b., Pauletta, M., Paulini, C., Pau, D., Pellett, A., Penzo, T., Phillip, G., Piacentino, E., Pianori, J., Pilot, K., Pitt, C., Plager, L., Pondrom, K., Potamiano, O. b., Poukhov, A., Pranko, F. c., Prokoshin, F. b., Ptoho, E., Pueschel, G. a., Punzi, J., Pursley, A., Rahaman, V., Ramakrishnan, N., Ranjan, I., Redondo, P., Renton, M., Rescigno, F. g., Rimondi, L. a., Ristori, A., Robson, T., Rodrigo, T., Rodriguez, E., Roger, S., Rolli, R., Roser, M., Rossi, F., Rubbo, F. a., Ruffini, A., Ruiz, J., Ru, V., Rusu, A., Safonov, W., Sakumoto, Y., Sakurai, Santi, LORENZO GIANNI, L., Sartori, K., Sato, V. c., Saveliev, A., Savoy Navarro, P., Schlabach, A., Schmidt, E., Schmidt, M. b., Schmidt, M., Schmitt, T., Schwarz, L., Scodellaro, A. a., Scribano, F., Scuri, A., Sedov, S., Seidel, Y., Seiya, A., Semenov, F. a., Sforza, A., Sfyrla, D., Sgalaberna, S., Shalhout, T., Shear, P., Shepard, M. c., Shimojima, S., Shiraishi, M., Shochet, I., Shreyber, A., Simonenko, P. c., Cw, A. b., Sissakian, K., Sliwa, J., Smith, F., Snider, A., Soha, S., Somalwar, V., Sorin, P., Squillacioti, M., Stancari, M., Stanitzki, R. S., Deni, B. c., Cw, O. c., Cw, D., Stentz, J., Strologa, G., Strycker, Y., Sudo, A., Sukhanov, I., Suslov, K., Takemasa, Y., Takeuchi, J., Tang, M., Tecchio, P., Teng, J. b., Thom, J., Thome, G., Thompson, E., Thomson, P., Ttito Guzmán, S., Tkaczyk, D., Toback, S. b., Tokar, K., Tollefson, T., Tomura, D., Tonelli, S., Torre, D., Torretta, Totaro, Pierluigi, M. a., Trovato, Y., Tu, F., Ukegawa, A., Varganov, F. c., Vázquez, G., Velev, C., Vellidi, M., Vidal, I., Vila, R., Vilar, J., Vizán, M., Vogel, G. a., Volpi, P., Wagner, R., Wagner, T., Wakisaka, R., Wallny, S., Wang, D., Water, M., Weinberger, W., Wester, B., Whitehouse, D. b., Whiteson, A., Wicklund, E., Wicklund, S., Wilbur, F., Wick, H., William, J., Wilson, P., Wilson, B., Winer, P. b., Wittich, S., Wolber, H., Wolfe, T., Wright, X., Wu, Z., Wu, K., Yamamoto, J., Yamaoka, T., Yang, U. c., Yang, W., Yao, G., Yeh, K. c., Yi, J., Yoh, K., Yorita, T. b., Yoshida, G., Yu, I. c., Cr, S., Yu, J., Yun, A., Zanetti, Y., Zeng, S. g., Zucchelli, M., Binkley, A. c., Cu, F. p., Bo, S. b., Carrillo, K. c., Cp, C. c., Ciobanu, M. c., Corbo, N. c., Cu, E. c., Cp, Y. b., Kato, D. c., Cp, H. c., Cp, J. c., Cp, S. c., Cp, C. c., Cp, Y. c., Cp, O., Poukhov, V. c., Cw, A. c., Savoy Navarro, M., Schmidt, P. c., Cu, A., Sissakian, B. c., Cu, O. c., Cu, F. b., Vázquez, I. c., Cp, and Zanetti, ANNA MARIA
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Photon radiation ,Integrated luminosity ,Photons ,Cross section ,Kinematic variables ,Fermilab Tevatron ,Parton showers ,photons ,High Energy Physics::Phenomenology ,photon ,Cross section, Fermilab Tevatron, Integrated luminosity, Isolated photons, Kinematic variables, Leading orders, Next-to-leading orders, Parton showers, Perturbative QCD, Photon radiation, Total energy ,Leading orders ,Physics and Astronomy (all) ,Tellurium compounds ,Forecasting, Photons ,Total energy ,Forecasting, Photon ,Perturbative QCD ,High Energy Physics::Experiment ,Isolated photons ,Next-to-leading orders ,Forecasting - Abstract
This article reports a measurement of the production cross section of prompt isolated photon pairs in proton-antiproton collisions at √s=1.96TeV using the CDF II detector at the Fermilab Tevatron collider. The data correspond to an integrated luminosity of 5.36fb -1. The cross section is presented as a function of kinematic variables sensitive to the reaction mechanisms. The results are compared with three perturbative QCD calculations: (1) a leading-order parton shower Monte Carlo, (2) a fixed next-to-leading-order calculation and (3) a next-to-leading-order/next-to-next-to-leading-log resummed calculation. The comparisons show that, within their known limitations, all calculations predict the main features of the data, but no calculation adequately describes all aspects of the data. © 2011 American Physical Society.
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- 2011
38. CLINICAL EVALUATION AND INVESTIGATION OF NEUROPATHY
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John B Winer and Hugh J. Willison
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medicine.medical_specialty ,Neuromuscular disease ,Sensory Receptor Cells ,Biopsy ,Disease ,Neurological disorder ,Guillain-Barre Syndrome ,Journal Article ,medicine ,Humans ,Peripheral Nerves ,Medical diagnosis ,Intensive care medicine ,Stroke ,Aged ,business.industry ,Peripheral Nervous System Diseases ,Polyradiculoneuropathy ,medicine.disease ,Surgery ,Psychiatry and Mental health ,Peripheral neuropathy ,Etiology ,Neurology (clinical) ,business ,Algorithms - Abstract
The assessment and investigation of a possible neuropathy is one of the most common clinical problems facing the general neurologist. Studies of the prevalence of neuropathy in the community are rare but suggest a figure of between 2–8%,1 making peripheral neuropathy at least as common as stroke. Despite this high prevalence of neuropathy, it is only a small proportion of patients with neuropathies who are referred for detailed evaluation, principally those individuals with disabling disease, or with none of the obvious risk factors such as diabetes or alcoholism. A logical approach to the assessment of such patients is essential and can be organised into a number of basic questions. The neurologist faced with a patient with a neuropathy has to deal with literally thousands of possible causes, many extremely uncommon, and these can only be simplified by defining the neuropathy by other features that lead to the select few of most likely diagnoses. This is in part a process of pattern recognition but can be helped by a stepwise approach. Several algorithms2 and review articles3 have been published to aid this process and a typical one has been constructed here (fig 1). Figure 1 Algorithm showing a stepwise approach to the assessment and investigation of a possible neuropathy. CIDP, chronic inflammatory demyelinating polyradiculoneuropathy; CMT, Charcot-Marie-Tooth; EMG, electromyography; GBS, Guillain-Barre syndrome; HNPP, hereditary neuropathy with liability to pressure palsies; NCS, nerve conduction studies. The approach adopted in this article is to present the evaluation as a list of commonly asked questions that, if correctly addressed and answered, are likely to yield diagnostically important information, and hence direct appropriate management. This is not intended as an exhaustive account of neuropathy but is a personal view, illustrative of a diagnostic process that is commonly adopted. This question can usually be answered easily, …
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- 2003
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39. Intravenous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy: a systematic review
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Marinus Vermeulen, John B Winer, Rob J. de Haan, and Ivo N. van Schaik
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medicine.medical_specialty ,Prednisolone ,Anti-Inflammatory Agents ,Controlled studies ,Placebo ,Oral prednisolone ,Internal medicine ,medicine ,Humans ,In patient ,Randomized Controlled Trials as Topic ,Plasma Exchange ,biology ,business.industry ,Immunoglobulins, Intravenous ,Polyradiculoneuropathy ,medicine.disease ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Relative risk ,Immunology ,biology.protein ,Neurology (clinical) ,Antibody ,business ,Algorithms ,medicine.drug - Abstract
Summary This review discusses the efficacy and safety in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) of intravenous immunoglobulin and compares this treatment with plasma exchange and prednisolone. We searched publications from 1985 onwards for randomised controlled studies examining the effects of intravenous immunoglobulin in patients with this immune-mediated neuromuscular disorder. Six trials, with 170 patients in total, were judged eligible. A significantly higher proportion of patients improved in disability within a month after the start of treatment with intravenous immunoglobulin than with placebo (relative risk 3·17 [95% CI 1·74 to 5·75]). During this period, intravenous immunoglobulin has similar efficacy to plasma exchange and oral prednisolone; therefore which of these treatments should be the first choice is currently uncertain. An algorithm on treatment approaches for CIDP is proposed.
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- 2002
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40. Guillain–Barré syndrome: Clinical variants and their pathogenesis
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John B. Winer
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Guillain-Barre syndrome ,business.industry ,Immunology ,Polyradiculoneuropathy ,Genetic Variation ,Guillain-Barre Syndrome ,medicine.disease ,nervous system diseases ,Pathogenesis ,Polyneuropathies ,Neurology ,immune system diseases ,hemic and lymphatic diseases ,medicine ,Animals ,Humans ,Immunology and Allergy ,Miller-Fisher syndrome ,Neurology (clinical) ,business - Abstract
Numerous clinical subtypes of Guillain-Barré syndrome have been described over the century since the original description of the syndrome. These variants of Guillain-Barré syndrome are discussed and their immunological pathogenesis reviewed.
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- 2011
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41. Having the vision to measure calcium
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John B Winer, Lucy H. A. Strens, Neil Gittoes, John Ayuk, and Rajarshi Mukhopadhyay
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medicine.medical_specialty ,Visual acuity ,medicine.diagnostic_test ,business.industry ,Parathyroid hormone ,Magnetic resonance imaging ,medicine.disease ,Optic neuropathy ,Neurology ,Erythrocyte sedimentation rate ,Ophthalmology ,medicine ,Hypocalcaemia ,Neurology (clinical) ,medicine.symptom ,business ,Neuroscience ,Calcification ,Primary Hypoparathyroidism - Abstract
A 49-year-old Caucasian woman presented to a primary care optician with a 4-week history of worsening vision. She also complained of intermittent generalised headaches, nausea and fatigue for 2 weeks prior to presentation. She was taking fluoxetine for mild depression, was a nonsmoker and drank alcohol occasionally. On initial assessment, the patient had perception of hand movements only in the right eye and left visual acuity was 6/12. Visual fields were impossible to assess in the right eye and she had a left eye altitudinal defect (Fig. 1a). The right optic disc was pale and the left was swollen (Fig. 1b). She was admitted urgently for a detailed assessment and cranial imaging. On subsequent clinical examination, there were no other systemic or neurological abnormalities found. Cranial magnetic resonance imaging (MRI) showed extensive signal abnormality within the basal ganglia, thalami and cerebellum bilaterally, consistent with calcium deposition (Fig. 1c). Subsequent CT scanning confirmed extensive calcification of the cerebellum and basal ganglia (Fig. 1d). Cerebrospinal fluid (CSF) opening pressure was 8.5 mmH20 (normal \ 20.0). CSF composition was normal, as was full blood count, international normalised ratio, C-reactive protein, urea and electrolytes, liver function tests and erythrocyte sedimentation rate. Serum corrected calcium was 1.07 mmol/l (normal 2.10–2.60), parathyroid hormone was 11.9 ng/l (normal 15–65), serum phosphate was 2.49 mmol/l (normal 0.8–1.4) and serum 25-hydroxyvitamin D concentration was normal. Parathyroid antibodies were negative. An electrocardiogram (ECG) revealed a prolonged QT interval (QTc 532 ms; upper limit of normal in females 460 ms). A diagnosis of severe (chronic) hypocalcaemia due to primary hypoparathyroidism with subsequent optic neuropathy was made. Calcitriol and elemental calcium supplements were initiated. Six weeks later, the patient’s serum calcium and ECG were normal. The visual acuity in her left eye had improved markedly to 6/6, although visual fields remained severely constricted bilaterally (Fig. 1e). R. Mukhopadhyay J. A. Ayuk N. J. L. Gittoes Department of Endocrinology, Queen Elizabeth Hospital, University Hospitals Birmingham, Edgbaston, Birmingham B15 2TH, UK
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- 2010
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42. Intravenous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy
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Rob J. de Haan, Ivo N. van Schaik, John B Winer, Filip Eftimov, and Marinus Vermeulen
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medicine.medical_specialty ,Plasma Exchange ,business.industry ,Prednisolone ,Immunoglobulins, Intravenous ,Cochrane Library ,Placebo ,Clinical trial ,Polyradiculoneuropathy, Chronic Inflammatory Demyelinating ,Methylprednisolone ,Adrenal Cortex Hormones ,hemic and lymphatic diseases ,Meta-analysis ,Relative risk ,Internal medicine ,Physical therapy ,medicine ,Number needed to treat ,Humans ,Pharmacology (medical) ,Adverse effect ,business ,Randomized Controlled Trials as Topic ,medicine.drug - Abstract
Background Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) causes progressive or relapsing weakness and numbness of the limbs, developing over at least two months. Uncontrolled studies suggest that intravenous immunoglobulin (IVIg) helps. This review was first published in 2002 and has since been updated, most recently in 2013. Objectives To review systematically the evidence from randomised controlled trials (RCTs) concerning the efficacy and safety of IVIg in CIDP. Search methods On 4 December 2012, we searched the Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL (2012, issue 11 in the Cochrane Library), MEDLINE and EMBASE to December 2012 and ISI from January 1985 to May 2008. We searched for ongoing trials through two metaRegistries (World Health Organization International Clinical Trials Registry Platform Search Portal and Current Controlled Trials). Selection criteria We selected RCTs testing any dose of IVIg versus placebo, plasma exchange or corticosteroids in definite or probable CIDP. Data collection and analysis Two authors reviewed literature searches to identify potentially relevant RCTs, scored their quality and extracted data independently. We contacted authors for additional information. Main results We considered eight RCTs, including 332 participants, to be eligible for inclusion in the review. These trials were homogeneous and the overall risk of bias low. Five studies, in a total of 235 participants compared IVIg against placebo. One trial with 20 participants compared IVIg with plasma exchange, one trial compared IVIg with prednisolone in 32 participants, and one trial, newly included at this update, compared IVIg with intravenous methylprednisolone in 46 participants. A significantly higher proportion of participants improved in disability within one month after IVIg treatment as compared with placebo (risk ratio (RR) 2.40, 95% confidence interval (CI) 1.72 to 3.36; number needed to treat for an additional beneficial outcome 3.03 (95% CI 2.33 to 4.55), high quality evidence). Whether all these improvements are equally clinically relevant cannot be deduced from this analysis because each trial used different disability scales and definitions of significant improvement. In three trials, including 84 participants, the disability score could be transformed to the modified Rankin score, on which improvement of one point after IVIg treatment compared to placebo was barely significant (RR 2.40, 95% CI 0.98 to 5.83) (moderate quality evidence). Only one placebo-controlled study included in this review had a long-term follow-up. The results of this study suggest that IVIg improves disability more than placebo over 24 and 48 weeks. The mean disability score revealed no significant difference between IVIg and plasma exchange at six weeks (moderate quality evidence). There was no significant difference in improvement in disability on prednisolone compared with IVIg after two or six weeks, or on methylprednisolone compared to IVIg after two weeks or six months (moderate quality evidence). There were no statistically significant differences in frequencies of side effects between the three types of treatment for which data were available (IVg versus placebo or steroids). (moderate or high quality evidence) Mild and transient adverse events were found in 49% of participants treated with IVIg, while serious adverse events were found in six per cent. Authors' conclusions The evidence from RCTs shows that IVIg improves disability for at least two to six weeks compared with placebo, with an NNTB of three. During this period it has similar efficacy to plasma exchange, oral prednisolone and intravenous methylprednisolone. In one large trial, the benefit of IVIg persisted for 24 and possibly 48 weeks. Further research is needed to compare the long-term benefits as well as side effects of IVIg with other treatments.
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- 2013
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43. Neuropathies
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John B Winer
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General Medicine - Published
- 2000
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44. The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes
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Matthew H. Liang, W. Neal Roberts, John B. Winer, Robin L. Brey, Bonnie I. Glanz, Susan D. Denburg, Joseph M. McCune, Elizabeth Waterhouse, Christopher M. Filley, John M. Esdaile, Daniel J. Wallace, Patricia M. Moore, Elaine M. Hay, Michael D. Lockshin, Robert A. Lew, David A. Isenberg, Elizabeth W. Karlson, Sterling G. West, Pontus Harten, Caroline Gordon, Judah A. Denburg, Robert G. Lahita, John G. Hanly, Wayne D. Cornblath, Peter H. Schur, Paul R. Fortin, Michelle Petri, John D. Fisk, Sang Cheol Bae, Shahram Khoshbin, Michael Corzillius, Grant L. Iverson, Elizabeth Kozora, Steven R. Levine, Malcolm P. Rogers, Jorge Sánchez-Guerrero, Martin Veilleux, Graciela S. Alarcón, and Karin V. Straaton
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medicine.medical_specialty ,Pathology ,business.industry ,Immunology ,Alternative medicine ,Lupus syndromes ,medicine.disease ,Dermatology ,Rheumatology ,Neuropsychiatric systemic lupus erythematosus ,Internal medicine ,medicine ,Immunology and Allergy ,Pharmacology (medical) ,Lupus vasculitis ,business ,Nomenclature - Published
- 1999
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- View/download PDF
45. The CDF II eXtremely Fast Tracker upgrade
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A. Abulencia, D. Errede, H. Gerberich, T. Junk, M. Kasten, S. Levine, R. Mokos, K. Pitts, E. Rogers, G. Veramendi, P. Azzurri, S. Donati, J.R. Dittmann, S. Hewamanage, N. Krumnack, J.S. Wilson, R. Erbacher, R. Forrest, A. Ivanov, A. Lister, A. Soha, I. Fedorko, N. Giokaris, A. Staveris-Polykalas, E. Cochran, J. Efron, J. Gartner, R. Hughes, M. Johnson, B. Kilmninster, K. Lannon, J. McKim, D. Olivito, B. Parks, J. Slaunwhite, B. Winer, G. Flanagan, T. Jones, S. Holm, R. Klein, E.E. Schmidt, L. Scott, T. Shaw, and P.J. Wilson
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Physics ,Nuclear and High Energy Physics ,Physics::Instrumentation and Detectors ,business.industry ,Track (disk drive) ,Instrumentation ,Computer Science::Computational Geometry ,Tracking (particle physics) ,Charged particle ,Nuclear physics ,Transverse plane ,Upgrade ,High Energy Physics::Experiment ,Aerospace engineering ,business - Abstract
The CDF II Extremely Fast Tracker is the trigger track processor which reconstructs charged particle tracks in the transverse plane of the CDF II central outer tracking chamber. The system is now being upgraded to perform a three dimensional track reconstruction. A review of the upgrade is presented here.
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- 2007
- Full Text
- View/download PDF
46. Serum kynurenine-to-tryptophan ratio increases with progressive disease in HIV-infected patients
- Author
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Jonathan D C Ross, Rachel Round, Mohsen Shahmanesh, Mia Huengsberg, John B. Winer, and Mark Gompels
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Adult ,Male ,AIDS Dementia Complex ,Clinical Biochemistry ,Asymptomatic ,Pathogenesis ,chemistry.chemical_compound ,HIV Seronegativity ,medicine ,Humans ,Prospective Studies ,Kynurenine ,Aged ,Retrospective Studies ,Acquired Immunodeficiency Syndrome ,biology ,Biochemistry (medical) ,Tryptophan ,Peripheral Nervous System Diseases ,Middle Aged ,biology.organism_classification ,medicine.disease ,Tryptophan Oxygenase ,CD4 Lymphocyte Count ,chemistry ,Lentivirus ,Immunology ,Female ,Viral disease ,medicine.symptom ,Progressive disease ,Quinolinic acid - Abstract
An alternative pathway of Trp metabolism involves the conversion of Trp to kynurenine by indoleamine-2,3-dioxygenase, which leads to synthesis of the neurotoxin, quinolinic acid. This study explores the relationship of indoleamine-2,3-dioxygenase activity with stages of HIV infection. Sera from 206 HIV-positive and 72 seronegative subjects were analyzed for Trp and kynurenine. The kynurenine-to-Trp (KT) ratio was calculated. The mean KT ratio of seronegative controls was 36.6 ± 10.9, and the median ratio was 34.9. The upper limit of the seronegative KT ratio, defined as mean + 2 SD, was 58.4. Patients with HIV infection showed a reciprocal relationship between the KT ratio, the CD4 count, and the stage of the disease. The median KT ratios for asymptomatic and AIDS patients were 50.5 and 117.0, respectively. This study shows that the serum Trp concentration is markedly decreased and that the kynurenine concentration is increased with immune stimulation in HIV infection. This may lead to changes in quinolinic acid and explain some of the pathogenesis of AIDS dementia.
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- 1998
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47. Thermosensory threshold: a sensitive test of HIV associated peripheral neuropathy?
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Jonathan D C Ross, Mia Huengsberg, Mohsen Shahmanesh, and John B. Winer
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medicine.medical_specialty ,business.industry ,Human immunodeficiency virus (HIV) ,medicine.disease ,medicine.disease_cause ,Gastroenterology ,Surgery ,Cellular and Molecular Neuroscience ,Peripheral neuropathy ,medicine.anatomical_structure ,Neurology ,Acquired immunodeficiency syndrome (AIDS) ,Forearm ,Virology ,Internal medicine ,Sensory threshold ,Sensation ,medicine ,Dementia ,Neurology (clinical) ,business ,Foot (unit) - Abstract
The purpose of the study was to assess the prevalence of thermosensory abnormalities in patients infected with HIV infection. Using a Thermo Sensory Analyser, we assessed thermosensory threshold for warm sensation (WS) and cold sensation (CS) of the forearm and foot in 40 controls and 75 HIV positive patients, including five patients with clinically evident peripheral neuropathy, three with AIDS-related dementia and 20 with AIDS. We found that thermosensory threshold is a reproducible test. The 95th centile for normal WS of the forearm was 1.4oC above and CS 0.9oC below the baseline temperature of 32oC, and for WS of the foot was 5.3oC and CS 4.4oC respectively. The median WS of the foot for controls was 1.4 (IQR 0.7-2.8) oC, for asymptomatic HIV positive patients was 1.9 (1.1-4.2) oC, for patients with AIDS was 3.5 (1.6-5.7) oC and for those with peripheral neuropathy was 5.4 (1.7-14.9) oC (P
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- 1998
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48. Metabolic and Nutritional Neuropathies
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John B. Winer, Edward Littleton, and Alex Barling
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- 2013
- Full Text
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49. A randomized controlled trial of recombinant interferon-beta 1a in Guillain-Barre syndrome
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Hugh J. Willison, Ian Sutton, Jane Pritchard, Bryan Lecky, I A Gray, John B Winer, Z R Idrissova, A. V. Swan, and Richard A. C. Hughes
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Male ,medicine.medical_specialty ,medicine.medical_treatment ,Pilot Projects ,Guillain-Barre Syndrome ,Placebo ,Gastroenterology ,law.invention ,Disability Evaluation ,Randomized controlled trial ,law ,Lymphopenia ,hemic and lymphatic diseases ,Internal medicine ,medicine ,Humans ,Beta (finance) ,Fatigue ,Recombinant interferon beta-1a ,Chemotherapy ,Dose-Response Relationship, Drug ,biology ,Guillain-Barre syndrome ,business.industry ,Interferon beta-1a ,Immunoglobulins, Intravenous ,Interferon-beta ,Middle Aged ,medicine.disease ,Recombinant Proteins ,Treatment Outcome ,Immunology ,biology.protein ,Cytokines ,Female ,Neurology (clinical) ,Antibody ,business ,medicine.drug - Abstract
The authors recruited 19 nonambulant patients with Guillain-Barré syndrome into a pilot, double-blind, randomized, placebo-controlled safety trial of interferon beta 1a (IFN[beta]-1a) (Rebif). Participants received IFN[beta]-1a or placebo subcutaneously three times weekly, 22 microg for the first week and then 44 microg for up to 24 weeks, in addition to IV immunoglobulin (IVIg). IFN[beta] did not have any unexpected interaction with IVIg and there was no significant difference in rate of improvement.
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- 2003
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50. Clinical and myopathological characteristics of desminopathy caused by a mutation in desmin tail domain
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Catherine McGorrian, Paul Maddison, Caroline Sewry, Hee Suk-U.-K. Lee, Aleksey Shatunov, Lev G. Goldfarb, John B Winer, Maxwell S. Damian, and Zagaa Odgerel
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Adult ,Male ,Intermediate Filaments ,Biology ,medicine.disease_cause ,Article ,Desmin ,Muscular Diseases ,medicine ,Myofibrillar myopathy ,Humans ,In patient ,Intermediate filament ,Aged ,Genetics ,Mutation ,Middle Aged ,Phenotype ,Skeletal myopathy ,Pedigree ,Neurology ,Domain (ring theory) ,Female ,Neurology (clinical) - Abstract
Background: Most of the previously described pathogenic mutations in desmin are located in highly conserved α-helical domains that play an important role in intermediate filament assembly. The role of the C-terminus non-α-helical ‘tail’ domain is much less investigated and until recently mutations in this domain have been implicated in only a few patients. The majority of reported desminopathy cases caused by the tail mutations were sporadic, creating a representation bias regarding the disease frequency and phenotypic characteristics. Methods: We performed detailed genotype-phenotype analysis of autosomal dominant desminopathy associated with tail domain mutations in a four-generation autosomal dominant family with 16 members affected by a progressive cardiac and/or skeletal myopathy caused by a c.1346A>C (p.Lys449Thr) mutation located in the tail domain of desmin. Results: Phenotypic features in patients with tail domain mutations are similar to those in patients with mutations localized in the 1B and 2B α-helical domains. Conclusion: We recommend that the tail domain is searched for mutations as intensely as desmin coil domains which until recently were considered to be more ‘functional’.
- Published
- 2012
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