Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0424790 (rigors)
 822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

T10B9.1A-31 is an immunoglobulin Mk (lgMk), CD3b class, murine monoclonal antibody. It is not itself mitogenic, but it partially blocks mitogenesis produced by concanavilin-A, phytohemagglutinin, and a soluble antigen cocktail and is lytic for human peripheral blood T lymphocytes (PB-T) in the presence of fresh autologous human complement and rabbit complement. It reacts with a monomorphic epitope found on all mature PB-Ts that modulates in vitro and in vivo with the CD3/T-cell antigen receptor (TCR) complex, but unlike OKT3, which reacts with CD3 proteins, T10B9.1A-31 reacts with an epitope of the TCR alpha/beta heterodimer. Immunoprecipitation of HPB-ALL with T10B9.1A-31 or OKT3 revealed that T10B9.1A-31 does not react with the 20-to 26-kd polypeptides that compose CD3, and T10B9.1A-31 failed to bind to the PEER cell, which is CD3 gamma/delta positive, TCR alpha/beta negative. Phase 1 clinical trials demonstrated that T10B9.1A-31 caused a rapid decrease in PB-Ts and no toxic effects other than fever, chills, rigors, and transient hypotension. These side effects were absent in methylprednisolone (MP)-pretreated patients. Phase II studies revealed that T10B9.1A-31 reversed steroid refractory acute rejection in three of five renal allografts treated with cyclosporine (CyA) and prednisone (P) maintenance immunosuppression, reversed steroid and polyclonal antisera refractory rejection in three cardiac allograft recipients receiving CyA/P, and attenuated acute rejection in three of three renal patients receiving baseline azathioprine/prednisone (AZA/P) when used as primary therapy. Rerejection was not seen when patients received CyA baseline immunosuppression but was seen in patients maintained on AZA/P OKT3 was efficacious in treating rejection following T10B9.1A-31 therapy. Side effects of T10B9.1A-31 appears to reverse acute rejection crisis effectively in renal and cardiac transplantation with a low incidence of rerejection in CyA-maintained patients and with fewer, milder side effects. Sequential therapy with OKT3 is possible because OKT3 and T10B9.1A-31 are of different isotypes and idiotypes.
 ...
PMID:T10B9.1A-31 anti-T-cell monoclonal antibody: preclinical studies and clinical treatment of solid organ allograft rejection. 247 65

IN NORMAL ANIMALS (DOGS, CATS AND RABBITS) WHICH WERE KILLED BY EXSANGUINATION, THE BEGINNING OF RIGOR IN PRACTICALLY ALL CASES WAS SEPARATED FROM RESPIRATORY DEATH BY TWO WELL CHARACTERIZED PERIODS: (1) a period of pulsation during which each ventricle still exhibited some spontaneous contractions, and (2) a period of relaxation during which the ventricles, while showing neither spontaneous contractions nor rigor, are more relaxed than in normal diastole, and during which the ventricles gradually lose their irritability. (The cardiac rigor or tonic contraction which was observed by recent investigators to set in immediately after death is an artificial phenomenon produced by filling the heart with saline and connecting it with a manometer.) In the right ventricle both periods are longer than in the left ventricle, i. e., rigor sets in later. Moreover the development of rigor from onset to maximum is also longer in the right ventricle than in the left, although here the difference is less striking. The stopping of spontaneous beating, the disappearance of irritability, and the development of rigor, manifest in both ventricles a topographical progress from the base toward the apex, i. e., the stoppage of beating, the disappearance of irritability and the setting in of rigor occur first at the uppermost part of the ventricle and last at the lowest point of the ventricle. It often occurred that rigor was already present in the basal part of a ventricle while the apex was still beating. It is probable also that the loss of vital activity and irritability and the development of rigor progress topographically from the endocardial to the epicardial surfaces. Prolonged etherization retards the onset, but hastens the development of rigor; atropinization hastens both onset and development. Repeated prolonged stoppages of the heart caused by antemortem (and postmortem) stimulations of the pneumogastric nerves hasten the onset as well as the development of rigor of the heart. All three periods are affected by the inhibitory influence of the stimulation, the period of relaxation, however, seems to be the one which is shortened most. The most probable interpretation of this phenomenon is the assumption that it is caused by an asphyxiation of the cardiac tissues. The stimulations of the pneumogastric nerves seem to hasten also the onset of the general rigor-probably this, too, is the result of some premature asphyxiation of the skeletal muscles.
 ...
PMID:THE POSTMORTEM RIGOR OF THE MAMMALIAN HEART AND THE INFLUENCE OF AN ANTEMORTEM STIMULATION OF THE PNEUMOGASTRIC NERVES UPON ITS DEVELOPMENT. 1986 50