Search PubMed⌕ Search

Biomedical subjects

J N Whitaker

Publications and source records attributed to J N Whitaker.

At least 199 records · Page 11Linked to original sources
PubMed1977

A comparison of immunochemical methods for the detection of antibodies to myelin encephalitogenic protein.

The antibody titer to myelin encephalitogenic protein in rabbits and rats has been comparatively studied by double antibody radioimmunoassay, quantitative microcomplement fixation, and radioimmunoelectrophoresis. In general, these immunochemical tests quantitatively paralleled one another but minor differences were sometimes present. The desirability of using a combination of these methods in assesing the antibody response to myelin encephalitogenic protein is emphasized.

Animals↗
PubMed1977

Immunocytochemical localization of the sodium, potassium activated ATPase in knifefish brain.

Results presented in this paper demonstrate the feasibility of using immunocytochemical methods to localize the (Na+ + K+)-ATPase, and its subunits, in the C.N.S. We have shown that in the Black Ghost knifefish, Sternarchus albifrons, the enzyme is located on the plasma membrane of the somata and dendrites of neurons and on the somata and cellular processes of glia. In myelinated axons the enzyme is restricted in localization to those portions of the axolemma not covered by the myelin sheath. The capacity of cell plasma membranes to restrict mobility of functionally important proteins should be considered in models of membrane structure in which lateral mobility of membrane components is considered a major characteristic.

Adenosine Triphosphatases↗
PubMed1977

Corticosteroid-responsive skeletal muscle disease associated with partial carnitine deficiency: studies of liver and metabolic alterations.

A patient with progressive skeletal muscle weakness had lipid-containing vacuoles in type I muscle fibers and partial carnitine deficiency of skeletal muscle. Results of certain liver function tests were abnormal, marked morphologic abnormalities of liver were detected, and a reduced cyclic adenosine 3',5'-monophosphate response to glucagon was present. After the oral administration of prednisone the patient exhibited gradual but striking clinical improvement, skeletal muscle fiber vacuoles could no longer be demonstrated, and the glucagon-provoked cyclic AMP response reverted to normal, but liver abnormalities persisted. At the same time utilization by skeletal muscle of long-chain fatty acids, pyruvate and beta-hydroxybutyrate was depressed. It is possible that the involvement of skeletal muscles was due to an inability of carnitine to attach to or to penetrate the sarcolemmal membrane. Some of the derangement, perhaps related to liver malfunction, was apparently corrected by the oral administration of prednisone although skeletal muscle metabolism remained impaired.

Biopsy↗
PubMed1977

Skeletal muscle pseudohypertrophy in primary amyloidosis.

Macroglossia and skeletal muscle enlargement with weakness appeared in a 38-year-old male who was shown to have amyloidosis and light chain multiple myeloma. Free lambda light chains were present in serum and urine. Skeletal muscle contained large amounts of amyloid and other amorphous material infiltrating blood vessel walls and connective tissue. Muscle fibers, particularly the type II variety, were diminished in size. Amyloid and similar amorphous material also were present in skin. This patient represents an unusual, but somewhat uniform, type of involvement of the neuromuscular apparatus in nonfamilial primary amyloidosis.

Adult↗
PubMed1977

Myelin encephalitogenic protein fragments in cerebrospinal fluid of persons with multiple sclerosis.

With a double-antibody radioimmunoassay performed on unconcentrated cerebrospinal fluid, eight of 14 patients in an acute phase of multiple sclerosis had levels of 3.4 to 15.4 ng per milliliter of the P1 fragment (residues 43-88) of myelin encephalitogenic protein. Encephalitogenic protein-P1 was found only in the acute phase and was present in six of seven persons in the first week of an exacerbation and absent in 29 multiple sclerosis patients who were stable or had a gradually progressive course. Six of 117 controls had detectable cerebrospinal fluid encephalitogenic protein-P1. Only in two of these, one with a recent cerebral infarction and one with diabetic nephropathy who was in coma, were the levels in the range encountered in patients in the acute phase of multiple sclerosis. Although not entirely specific for multiple sclerosis, the presence of material in the cerebrospinal fluid of multiple sclerosis patients cross-reacting with encephalitogenic protein-P1 appears to be a characteristic of acute exacerbations.

Adolescent↗
PubMed1976

Immunogenetic analysis and serum viral antibody titers in multiple sclerosis.

In order to investigate the possible relationships between multiple sclerosis (MS) and the factors of genetic predisposition and exposure to infectious agents, studies were undertaken in 59 male patients with MS to determine the histocompatibility antigen (HL-A) type and the serum antibody titer to rubeola hemagglutinin (HA), rubeola envelope antigen (V), rubeola nucleocapsid antigen (S), rubella, herpes simplex, cytomegalovirus, and parainfluenza 1. The incidence of HL-A7 was significantly higher, and HL-A12 incidence was significantly lower, in the MS group than in control groups. The geometric mean titers to rubeola HA and to the V and S antigens were lower in the HL-A7 positive control patients than in either the non-HL-A7 controls or the MS patients. There were no specific relationships of the rubeola titer to HL-A12. Antibody titers to the other viruses studied were not significantly different in MS patients as compared to controls, nor was there any relationship of HL-A7 or HL-A12 and serum titer to those viruses. This study provides further evidence of a genetic predisposition to MS, and of a relationship between rubeola and this disease. These findings suggests that the failure of MS to appear in individuals who might be genetically predisposed to this disorder may be related to their immune response to rubeola.

Adult↗
PubMed1976

The effects of glutaraldehyde treatment and horesradish peroxidase conjugation on the immunoreactivity of bovine myelin encephalitogenic protein.

The effects of the immunoreactivity of bovine myelin encephalitogenic protein (EP) of treatment with glutaraldehyde and conjugation with horeradish peroxidase (HRP) were investigated by complement fixation and immunohistochemistry. Both glutaraldehyde treatment and HRP conjugation of EP decreased but did not abolish the reactivity of EP with rabbit anti-EP. Conjugation of EP to HRP by the two-step method of Avrameas had less detrimental effects on the immunochemical reactivity of EP than did the one-step procecure. The use of EP-HRP conjugates to probe for antibodies to EP is an immunochemically sound system with the major limitation that the number of antibody-producing cells is likely to be underestimated due to the failure to detect cells producing low levels of antibody or antibodies directed toward determinants altered by the modification procedures.

Aldehydes↗
PubMed1975

Antigenic determinants of bovine myelin encephalitogenic protein recognized by rabbit antibody to myelin encephalitogenic protein.

The antigenic determinants of bovine myelin encephalitogenic protein were investigated by quantitative complement fixation and hapten inhibition using rabbit anti-monkey protein and anti-bovine protein and purified and characterized fragments of bovine protein. The two regions of bovine encephalitogenic protein containing determinants were sequences 1 to 43 and 90 to 170. One rabbit antiserum recognized a determinant(s) probably in residues 15 to 40 while for another rabbit antiserum the determinant of 1 to 43 resided in 1 to 20. The determinant(s) of residues 90 to 170 involved the region around the tryptophan at position 116. Fragment 44-89, which contains the major encephalitogenic determinant for the rabbit, was virtually devoid of any reactivity with the rabbit anti-encephalitogenic protein. It appears that portions of the protein other than the encephalitogenic site are responsible for stimulation of bone marrow-derived cells and antibody production. In demonstrating selected regions of the protein as sites for antigenic determinants, the present immunochemical studies also suggest that the protein might have a more folded conformational alignment than previously suspected.

Amino Acids↗
PubMed1975

The antigenicity of myelin encephalitogenic protein: production of antibodies to encephalitogenic protein with deoxyribonucleic acid--encephalitogenic protein complexes.

Rabbits immunized with monkey encephalitogenic protein (EP) complexed to deoxyribonucleic acid (DNA) formed complement-fixing antibodies that reacted well with EP from monkey, bovine, and human brain and the large EP of rat brain. Reactivity with the small EP of rat brain was much less. The antibodies, analyzed by the quantitative micro-complement fixation test, were of the 7S class, were produced in high titer, and failed to react with histone, lysozyme, or acidic liver extracts. Immunohistochemical studies revealed that the antibodies bound to central nervous system white matter from human, rat, guinea pig, and mouse as well as human peripheral nerve myelin. These findings demonstrate that the immunogenicity of EP is greatly enhanced by attachment to DNA and perhaps other negatively charged molecules. This method makes available anti-EP with which to investigate immunochemically the antigenic and conformational features of EP.

Animals↗