IgM monoclonal antibody against terminal moiety of GM2, GalNAc-GD1a and GalNAc-GM1b from a pure motor chronic demyelinating polyneuropathy patient: effects on neurotransmitter release

2001 ◽  
Vol 119 (1) ◽  
pp. 114-123 ◽  
Author(s):  
N. Ortiz ◽  
R. Rosa ◽  
E. Gallardo ◽  
I. Illa ◽  
J. Tomas ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Neurotransmitter Release ◽  
Demyelinating Polyneuropathy ◽  
Pure Motor

Remission of Demyelinating Polyneuropathy With Immunoadsorption, Low Dose Corticosteroids and Anti-CD20 Monoclonal Antibody

2008 ◽  
Vol 12 (3) ◽  
pp. 205-208 ◽  
Author(s):  
Jürgen Rech ◽  
Axel J Hueber ◽  
Stefan Kallert ◽  
Jan Leipe ◽  
Jochen R Kalden ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Low Dose ◽  
Demyelinating Polyneuropathy ◽  
Anti Cd20

scholarly journals Treatment of Chronic Inflammatory Demyelinating Polyneuropathy: From Molecular Bases to Practical Considerations

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Paolo Ripellino ◽  
Thomas Fleetwood ◽  
Roberto Cantello ◽  
Cristoforo Comi
Keyword(s):  
Immune Responses ◽  
Chronic Inflammatory Demyelinating Polyneuropathy ◽  
Demyelinating Polyneuropathy ◽  
Variable Degree ◽  
Disease Evolution ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Inflammatory Demyelinating Polyneuropathy ◽  
Molecular Bases ◽  
Pure Motor

Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disease of the peripheral nervous system, in which both cellular and humoral immune responses are involved. The disease is clinically heterogeneous with some patients displaying pure motor form and others also showing a variable degree of sensory dysfunction; disease evolution may also differ from patient to patient, since monophasic, progressive, and relapsing forms are reported. Underlying such clinical variability there is probably a broad spectrum of molecular dysfunctions that are and will be the target of therapeutic strategies. In this review we first explore the biological bases of current treatments and subsequently we focus on the practical management that must also take into account pharmacoeconomic issues.

Pure motor chronic inflammatory demyelinating polyneuropathy

2001 ◽  
Vol 248 (9) ◽  
pp. 772-777 ◽  
Author(s):  
Mario Sabatelli ◽  
F. Madia ◽  
T. Mignogna ◽  
G. Lippi ◽  
L. Quaranta ◽  
...  
Keyword(s):  
Chronic Inflammatory Demyelinating Polyneuropathy ◽  
Demyelinating Polyneuropathy ◽  
Inflammatory Demyelinating Polyneuropathy ◽  
Pure Motor

P214 Pure motor chronic inflammatory demyelinating polyneuropathy

2008 ◽  
Vol 119 ◽  
pp. S125
Author(s):  
Semai Bek ◽  
Güray Koç ◽  
Erdal Eroğlu ◽  
Ümit Hidir Ulaş ◽  
Zeki Odabaşi
Keyword(s):  
Chronic Inflammatory Demyelinating Polyneuropathy ◽  
Demyelinating Polyneuropathy ◽  
Inflammatory Demyelinating Polyneuropathy ◽  
Pure Motor

A web-like network of type vi collagen in human skin is revealed by immuno-electron microscopy

1988 ◽  
Vol 46 ◽  
pp. 382-383
Author(s):  
Douglas R. Keene ◽  
Robert W. Glanville ◽  
Eva Engvall
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Human Skin ◽  
Basement Membranes ◽  
Primary Antibody ◽  
Fat Cells ◽  
Secondary Antibody ◽  
Type Vi Collagen ◽  
Dermal Matrix ◽  
Immuno Electron Microscopy

A mouse monoclonal antibody (5C6) prepared against human type VI collagen (1) has been used in this study to immunolocalize type VI collagen in human skin. The enbloc method used involves exposing whole tissue pieces to primary antibody and 5 nm gold conjugated secondary antibody before fixation, and has been described in detail elsewhere (2).Biopsies were taken from individuals ranging in age from neonate to 65 years old. By immuno-electron microscopy, type VI collagen is found to be distributed as a fine branching network closely associated with (but not attached to) banded collagen fibrils containing types I and III collagen (Fig. 1). It appears to enwrap fibers, to weave between individual fibrils within a fiber, and to span the distance separating fibers, creating a “web-like network” which entraps fibers within deep papillary and reticular dermal layers (Fig. 2). Relative to that in the dermal matrix, the concentration of type VI collagen is higher around endothelial basement membranes limiting the outer boundaries of nerves, capillaries, and fat cells (Fig. 3).

High-voltage electron microscopy of subretinal scar formation

1992 ◽  
Vol 50 (1) ◽  
pp. 486-487
Author(s):  
G.E. Korte ◽  
M. Marko ◽  
G. Hageman
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Retinal Pigment Epithelium ◽  
Glial Cells ◽  
High Voltage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Sodium Iodate ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron

Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).

Identification of the pulmonary syndrome hantavirus by direct and colloidal gold immune Electron Microscopy

1994 ◽  
Vol 52 ◽  
pp. 274-275
Author(s):  
C. D. Humphrey ◽  
C.S. Goldsmith ◽  
L. Elliott ◽  
S.R. Zaki
Keyword(s):  
Electron Microscopy ◽  
United States ◽  
Monoclonal Antibody ◽  
Colloidal Gold ◽  
Phosphotungstic Acid ◽  
Uranyl Acetate ◽  
Hantavirus Pulmonary Syndrome ◽  
Deer Mice ◽  
Immune Electron Microscopy ◽  
Negative Stain

An outbreak of unexplained acute pulmonary syndrome with high fatality was recognized in the spring of 1993 in the southwestern United States. The cause of the illness was quickly identified serologically and genetically as a hantavirus and the disease was named hantavirus pulmonary syndrome (HPS). Recently, the virus was isolated from deer mice which had been trapped near the homes of HPS patients, and cultivated in Vero E6 cells. We identified the cultivated virus by negative-stain direct and colloidal gold immune electron microscopy (EM).Virus was extracted, clarified, and concentrated from unfixed and 0.25% glutaraldehyde fixed supernatant fluids of infected Vero E6 cells by a procedure described previously. Concentrated virus suspensions tested by direct EM were applied to glow-discharge treated formvar-carbon filmed grids, blotted, and stained with 0.5% uranyl acetate (UA) or with 2% phosphotungstic acid (PTA) pH 6.5. Virus suspensions for immune colloidal gold identification were adsorbed similarly to filmed grids but incubated for 1 hr on drops of 1:50 diluted monoclonal antibody to Prospect Hill virus nucleoprotein or with 1:50 diluted sera from HPS virus infected deer mice.

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