6 results on '"Strand C"'
Search Results
2. An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies.
- Author
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de Silva R, Lashley T, Strand C, Shiarli AM, Shi J, Tian J, Bailey KL, Davies P, Bigio EH, Arima K, Iseki E, Murayama S, Kretzschmar H, Neumann M, Lippa C, Halliday G, MacKenzie J, Ravid R, Dickson D, Wszolek Z, Iwatsubo T, Pickering-Brown SM, Holton J, Lees A, Revesz T, and Mann DM
- Subjects
- Adult, Aged, Brain metabolism, Dementia genetics, Female, Humans, Immunohistochemistry, Male, Middle Aged, Mutation, Nerve Tissue Proteins genetics, Protein Isoforms metabolism, Antibodies, Monoclonal, Brain pathology, Dementia metabolism, Dementia pathology, tau Proteins metabolism
- Abstract
The pathological distinctions between the various clinical and pathological manifestations of frontotemporal lobar degeneration (FTLD) remain unclear. Using monoclonal antibodies specific for 3- and 4-repeat isoforms of the microtubule associated protein, tau (3R- and 4R-tau), we have performed an immunohistochemical study of the tau pathology present in 14 cases of sporadic forms of FTLD, 12 cases with Pick bodies and two cases without and in 27 cases of familial FTLD associated with 12 different mutations in the tau gene (MAPT), five cases with Pick bodies and 22 cases without. In all 12 cases of sporadic FTLD where Pick bodies were present, these contained only 3R-tau isoforms. Clinically, ten of these cases had frontotemporal dementia and two had progressive apraxia. Only 3R-tau isoforms were present in Pick bodies in those patients with familial FTLD associated with L266V, Q336R, E342V, K369I or G389R MAPT mutations. Patients with familial FTLD associated with exon 10 N279K, N296H or +16 splice site mutations showed tau pathology characterised by neuronal neurofibrillary tangles (NFT) and glial cell tangles that contained only 4R-tau isoforms, as did the NFT in P301L MAPT mutation. With the R406W mutation, NFT contained both 3R- and 4R-tau isoforms. We also observed two patients with sporadic FTLD, but without Pick bodies, in whom the tau pathology comprised only of 4R-tau isoforms. We have therefore shown by immunohistochemistry that different specific tau isoform compositions underlie the various kinds of tau pathology present in sporadic and familial FTLD. The use of such tau isoform specific antibodies may refine pathological criteria underpinning FTLD.
- Published
- 2006
- Full Text
- View/download PDF
3. Use of combination of leflunomide with biological agents in treatment of rheumatoid arthritis.
- Author
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Kalden JR, Antoni C, Alvaro-Gracia JM, Combe B, Emery P, Kremer JM, Strand CV, Van Riel P, and Smolen JS
- Subjects
- Drug Therapy, Combination, Humans, Leflunomide, Antibodies, Monoclonal therapeutic use, Arthritis, Rheumatoid drug therapy, Immunologic Factors therapeutic use, Immunosuppressive Agents therapeutic use, Isoxazoles therapeutic use
- Abstract
An Expert Panel Meeting was held in May 2004 to assess experience with combination therapy with leflunomide and biological agents in the treatment of rheumatoid arthritis (RA), to identify both optimal use of such combinations and precautions for use. Eleven published prospective or retrospective studies were reviewed, principally evaluating combination of leflunomide with infliximab, as well as patient registry data. Available data suggest that combination therapies are more efficacious than monotherapies, reflecting the complementarity of mechanisms of action. Information on side effects remains contradictory, and tolerability of these combinations may vary between different patient groups. In some studies, tolerability is equivalent to that seen with monotherapy; in others a high rate of adverse events has led to frequent treatment discontinuation. Dermatological reactions may be a specific side effect of these combination therapies. Combination therapy is considered justified for treatment of patients diagnosed early who are at risk for rapid progression and for patients who fail to respond to monotherapy. The majority of participants favored adding biological agents to a previously established leflunomide monotherapy rather than starting both treatments simultaneously. On the other hand, combination therapy should be considered with caution in patients with a history of treatment failure, with hepatic comorbidity, or with other autoimmune disease, and in immunocompromised patients. When considering initiation of combination therapy, it is important to provide full information to the patient on the potential benefits and risks of such treatment and to integrate patients as far as possible into the decision-making process.
- Published
- 2005
4. Lefunomide in combination therapy.
- Author
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Kalden JR, Smolen JS, Emery P, van Riel PL, Dougados M, Strand CV, and Breedveld FC
- Subjects
- Antibodies, Monoclonal adverse effects, Arthritis, Rheumatoid diagnosis, Dose-Response Relationship, Drug, Drug Administration Schedule, Drug Therapy, Combination, Female, Humans, Infliximab, Isoxazoles adverse effects, Leflunomide, Male, Randomized Controlled Trials as Topic, Risk Factors, Sulfasalazine adverse effects, Treatment Outcome, Antibodies, Monoclonal administration & dosage, Antirheumatic Agents administration & dosage, Arthritis, Rheumatoid drug therapy, Isoxazoles administration & dosage, Sulfasalazine administration & dosage
- Abstract
In most studies of disease modifying antirheumatic drug therapy, in combination with either leflunomide or biological agents, patients are given an additional agent after they have failed treatment with methotrexate (MTX). This review of clinical studies shows that leflunomide is clinically efficacious and well tolerated when added to either sulfasalazine or MTX, as both an initial and ongoing treatment for rheumatoid arthritis (RA). Experience in combining leflunomide with biological agents is limited to a small number of open-label studies with infliximab. According to the opinion obtained at an International Expert Panel Meeting held in Paris in May 2003, leflunomide can be used in combination therapy: 61% of the Expert Panel would use leflunomide with MTX, 71% with sulfasalazine, 43% with infliximab, 33% with adalimumab, 19% with etanercept, and 38% with anakinra. The Expert Panel stated that the combination of leflunomide and infliximab warrants a prospective, randomized, controlled trial in patients with incomplete clinical responses to leflunomide monotherapy, provided leflunomide is started first, without a loading dose, and infliximab is added after good tolerability to leflunomide has been established. The Expert Panel concluded that combination therapy with leflunomide has a place in the treatment of RA. Caution is advised, however, when using combination treatments and, therefore, the patient's safety should be carefully monitored.
- Published
- 2004
5. Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies.
- Author
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de Silva R, Lashley T, Gibb G, Hanger D, Hope A, Reid A, Bandopadhyay R, Utton M, Strand C, Jowett T, Khan N, Anderton B, Wood N, Holton J, Revesz T, and Lees A
- Subjects
- Animals, Blotting, Western, Brain metabolism, Brain ultrastructure, Cell Line, Humans, Immunohistochemistry, Inclusion Bodies metabolism, Inclusion Bodies pathology, Inclusion Bodies ultrastructure, Microscopy, Immunoelectron, Microtubules chemistry, Neuroblastoma chemistry, Neuroblastoma genetics, Neurofibrillary Tangles chemistry, Neurons metabolism, Neurons pathology, Protein Isoforms biosynthesis, Protein Isoforms chemistry, Protein Isoforms genetics, Protein Isoforms immunology, Rats, Recombinant Proteins, Tauopathies genetics, Tauopathies metabolism, Tauopathies pathology, tau Proteins biosynthesis, tau Proteins genetics, Antibodies, Monoclonal, Antibody Specificity, Brain pathology, Tauopathies immunology, tau Proteins analysis, tau Proteins immunology
- Abstract
Pathological inclusions containing fibrillar aggregates of hyperphosphorylated tau protein are a characteristic feature in the tauopathies, which include Alzheimer's disease, frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), progressive supranuclear palsy, corticobasal degeneration and Pick's disease. Tau isoform composition and cellular and regional distribution as well as morphology of these inclusions vary in each disorder. Recently, several pathological missense and exon 10 splice-donor site mutations of the tau gene were identified in FTDP-17. Exon 10 codes for the second of four microtubule-binding repeat domains. The splice-site mutations result in increased inclusion of exon 10 which causes a relative increase in tau isoforms containing four microtubule-binding repeat domains over those containing three repeat domains. This could be a central aetiological mechanism in FTDP-17 and, perhaps, other related tauopathies. We have investigated changes in the ratio and distribution of three-repeat and four-repeat tau in the different tauopathies as a basis of the phenotypic range of these disorders and the selective vulnerability of different subsets of neurones. In this study, we have developed two monoclonal antibodies, RD3 and RD4 that effectively distinguish these closely related tau isoforms. These new isoform-specific antibodies are useful tools for analysing tau isoform expression and distribution as well as pathological changes in the human brain.
- Published
- 2003
- Full Text
- View/download PDF
6. Lymphocyte subsets in Sjogren's syndrome: a quantitative analysis using monoclonal antibodies and the fluorescence-activated cell sorter.
- Author
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Bakhshi A, Miyasaka N, Kavathas P, Daniels TE, Strand CV, Herzenberg LA, and Talal N
- Subjects
- Adult, Aged, Animals, Cell Separation, Concanavalin A pharmacology, Female, Goats, HLA-DR Antigens, Histocompatibility Antigens Class II immunology, Humans, Lymphocyte Activation, Lymphocytes immunology, Male, Middle Aged, Phytohemagglutinins pharmacology, Pokeweed Mitogens pharmacology, T-Lymphocytes classification, T-Lymphocytes immunology, Antibodies, Monoclonal immunology, Flow Cytometry, Lymphocytes classification, Sjogren's Syndrome immunology
- Abstract
Lymphocyte subsets in the peripheral blood of 18 patients with Sjogren's syndrome (SS) were studied using monoclonal antibodies and the fluorescence-activated cell sorter (FACS). The percentage of T cells was decreased when compared to normal controls. In primary SS, there was a proportional decrease in both suppressor/cytotoxic (anti-Leu-2a reactive) and helper/inducer (anti-Leu-3a reactive) T cells with an unchanged helper/suppressor ratio (1.8 vs. 1.7 for normals). In SS with an associated connective tissue disorder, there was a significant decrease only in the suppressor/cytotoxic subset. There was increase in B cells and null cells in primary SS compared to controls. Quantitative immunofluorescence allowed the calculation of determinant density per cell. Cells expressing low antigen density Leu-2a were increased in 8 patients (4 with primary SS and 4 with SS with an associated disorder). Thus, in addition to quantitative changes in lymphocyte subsets, we found changes in Leu-2a expression suggesting abnormal differentiation of the suppressor/cytotoxic subset. These changes may contribute to the immunoregulatory disturbance in Sjogren's syndrome.
- Published
- 1983
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