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Biomedical subjects

N Greenspan

Publications and source records attributed to N Greenspan.

7 recordsLinked to original sources
PubMed2000

Cardiopulmonary rehabilitation in a patient with Noonan syndrome.

Noonan syndrome, an autosomal dominant disease occurring with an incidence of 1 in 1,000 to 1 in 2,500 live births, is characterized by its particular cardiovascular abnormalities, including pulmonic valve stenosis, pulmonary artery stenosis, and, more rarely, septal defects and coarctation of the aorta. The case of a 20-year-old man admitted for inpatient cardiopulmonary rehabilitation after pulmonic valve repair, left pulmonary artery angioplasty, and pectus excavatum repair is presented. His endurance was markedly decreased, thus limiting his ability to perform activities of daily living and reducing his exercise tolerance. With participation in a comprehensive cardiopulmonary rehabilitation program, he experienced marked improvement with independence in his activities of daily living and an increase in his metabolic equivalent levels from to 2.8 to 5.4. After inpatient rehabilitation, he underwent left pulmonary stent placement before being discharged home. Subsequent outpatient cardiopulmonary rehabilitation has continued to improve significantly his overall exercise tolerance. Given that Noonan syndrome is viewed as the most common syndrome associated with congenital heart disease after Down syndrome, physiatrists must be familiar with its presentation, its associated abnormalities, and the treatment approach to optimize the patient's cardiopulmonary, musculoskeletal, and psychological status.

Adult↗
PubMed1997

Exploring the basis of peptide-carbohydrate crossreactivity: evidence for discrimination by peptides between closely related anti-carbohydrate antibodies.

To investigate the molecular basis of antigenic mimicry by peptides, we studied a panel of closely related mAbs directed against the cell-wall polysaccharide of group A Streptococcus. These antibodies have restricted V-gene usage, indicating a shared mechanism of binding to a single epitope. Epitope mapping studies using synthetic fragments of the cell-wall polysaccharide supported this conclusion. All of the mAbs isolated crossreactive peptides from a panel of phage-displayed libraries, and competition studies indicated that many of the peptides bind at or near the carbohydrate binding site. Surprisingly, the peptides isolated by each mAb fell into distinct consensus-sequence groups that discriminated between the mAbs, and in general, the peptides bound only to the mAbs used for their isolation. Similar results were obtained with polyclonal antibodies directed against synthetic oligosaccharide fragments of the streptococcal cell-wall polysaccharide. Thus, the peptides appear to be specific for their isolating antibodies and are not recognized by the same mechanism as their carbohydrate counterparts.

Amino Acid Sequence↗
PubMed1995

Class I MHC alpha 3 domain can function as an independent structural unit to bind CD8 alpha.

Functional interactions between CD8-dependent cytotoxic T cells and their targets require physical contact between CD8 and a non-polymorphic determinant on the alpha 3 domain of the class I MHC molecule. We developed a cell-free assay to directly monitor this molecular interaction, specifically excluding the participation of other cellular proteins and lipids. This assay employed a soluble CD8 derivative and a plate-bound HLA-A2.1 derivative, alpha 3/MalE, in which the alpha 3 domain has been expressed independently of its neighboring polypeptide domains on the native class I MHC molecule and beta 2-microglobulin (beta 2-m). These proteins were produced using eukaryotic and prokaryotic expression systems, respectively. Our data demonstrated specific, saturable binding between soluble CD8 alpha (sCD8 alpha) and alpha 3/MalE, and the Kd of this interaction was determined to be 4.5 x 10(-7) M. Monoclonal antibodies (mAb) directed against either CD8 or the alpha 3 domain of class I MHC inhibited binding; mAb directed against other sites on class I MHC and beta 2-m did not. Our data suggest that the interaction between CD8 alpha and the alpha 3 domain of class I MHC does not require the participation of neighboring class I sequences or beta 2-m.

Base Sequence↗
PubMed1982

Modification of cytotoxic T-cell response patterns by administration of hemagglutinin-specific monoclonal antibodies to mice infected with influenza A viruses.

Mice injected with any influenza A virus develop a range of virus-immune cytotoxic T lymphocytes, some of which tend to be more lytic for cells expressing the virus used for priming (subtype-specific) while others are cross-reactive for targets infected with all influenza A viruses. Treatment with large doses of either of two monoclonal antibodies (which bind to the influenza virus hemagglutinin molecule) at 3-48 h after exposure to virus tends to selectively block the generation of the more subtype-specific cytotoxic T lymphocyte subset, although the magnitude of cross-reactive effector function may also be diminished. Inhibition that is less obviously selective is also seen for a third monoclonal antibody. A reasonable explanation for these findings is that there is afferent blockage at the level of T-cell recognition of the influenza virus hemagglutinin molecule expressed on stimulator cells. The inhibitory effect of the monoclonal antibody is apparently steric. Priming with parental strain virus followed by exposure to monoclonal antibody induces a population of cytotoxic T lymphocytes which manifest decreased cytotoxic activity for target cells infected with either the parental strain virus or with a variant virus to which the monoclonal antibody does not bind. A more practical consideration is that the administration of large doses of specific immunoglobulin may interfere with the development of cell-mediated immune mechanisms. This should be considered when developing possible therapeutic protocols using monoclonal antibodies.

Animals↗
PubMed1982

Capacity of influenza virus-monoclonal antibody mixtures to stimulate memory and cytotoxic T lymphocyte populations.

The magnitude of the cytotoxic T lymphocyte response in both immunologically naive mice and in mice primed with a serologically non-cross-reactive influenza A virus was greatly diminished if the virus used for challenge was first incubated with excess hemagglutinin-specific monoclonal antibody. However, the level of T cell stimulation was, when compared with virus stocks that are simply diluted, greater than would be expected from the infectivity titer remaining after exposure to the monoclonal antibody. Also, mice given mixtures of virus and monoclonal antibody were primed for a secondary cytotoxic T lymphocyte response, the frequency of memory T cells being approximately fourfold lower than that found for animals injected with virus alone. The possibility that such virus-antibody mixtures might be of value for immunization is worth further investigation.

Animals↗