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Biomedical subjects

N Abramson

Publications and source records attributed to N Abramson.

67 records · Page 4Linked to original sources
PubMed1970

The interaction between human monocytes and red cells. Binding characteristics.

Red cells coated with IgG globulin were bound firmly to human mononuclear cells and formed rosettes. Rosette formation occurred when red cells were coated with IgG attached either immunologically (anti-D, anti-penicillin, or Donath-Landsteiner antibodies) or nonimmunologically with chromic chloride; no attachment was observed with cells coated with albumin. Rosette formation was blocked by pretreatment of white cells with sulfhydryl-binding reagents. Metabolic inhibitors did not prevent red cell adherence. White cells of other primates demonstrated a high degree of species specificity. Ultrastructural studies showed that the predominant leukocytes involved in rosette formation were monocytes, but some cells with characteristics of lymphocytes also formed rosettes. Considerable interdigitation of cell surfaces occurred at attachment sites and bound red cells appeared deformed. Thus, these studies confirm the presence of specific surface receptors for IgG on human monocytes and suggest that such receptors may provide a mechanism by which large numbers of red cells are eventually destroyed.

Antigen-Antibody Reactions↗
PubMed1970

The interaction between human monocytes and red cells. Specificity for IgG subclasses and IgG fragments.

Studies were carried out in order to characterize the specificity of IgG sub-classes and IgG fragments for rosette formation using red cells and human mononuclear cells. Rosette formation of red cells coated with anti-D was inhibited by free IgG(1) and IgG(3); less inhibition occurred with IgG(2) and IgG(4). Red cells specifically coated with IgG(1) and IgG(3) by chromic chloride were bound to monocytes. Rosette inhibition of anti-D-coated red cells occurred with free Fc fragment of IgG globulin, and only partly with F(ab')(2). Inhibitory capacity of Fc fragments of IgG and gamma(1) heavy chain from heavy chain disease was reversed by the cleavage of disulfide bonds. No inhibition was noted with Fab, or with pepsin components II, III, or IV. These studies indicated that the mononuclear receptor was specific for IgG(1) and IgG(3). The peptide portion of IgG globulin which attached to the mononuclear cell appeared to reside in the N-terminal portion of the Fc fragment and also appeared to require the integrity of the inter-heavy chain disulfide bond. A specific receptor for C3 was not confirmed.

Binding Sites↗
PubMed1970

Studies in vivo and in vitro on an abnormality in the metabolism of C3 in a patient with increased susceptibility to infection.

In a patient with increased susceptibility to infection, lowered serum C3 concentration, and continuously circulating C3b, it was shown that purified (125)I-labeled C3 was converted to labeled C3b shortly after intravenous administration. The fractional catabolic rate of C3 was approximately five times normal at 10% of the plasma pool per hr. The synthesis rate and pool distribution of C3 were normal. Despite this evidence of C3 instability in vivo, no accelerated inactivation of C3 was found in vitro. Similarly, no free proteolytic activity could be detected in the patient's serum, and serum concentrations of known protease inhibitors were normal.Complement-mediated functions, which were markedly deficient in the patient's serum, could be restored partially or completely by the addition of a 5-6S heat-labile beta pseudoglobulin from normal serum. The C3 proinactivator, which has these physicochemical characteristics, was also shown to be either absent or nonfunctional in the patient's serum. An unidentified 6S beta pseudoglobulin to which a monospecific antiserum was available was not detectable in the patient's serum. This last protein appeared not to be a complement component, nor was it the C3 inactivator or proinactivator. Finally, the substance or substances necessary for the conversion of C3b to C3c were missing from the patient's serum. The administration of 500 ml of normal plasma to the patient corrected all of his abnormalities partially or completely for as long as 17 days. The changes in C3 were dramatic; serum concentration rose from 8 to 70 mg/100 ml, and C3b could no longer be detected. A second metabolic study during this normalization period showed a decrease in fractional catabolic rate toward normal. The patient's histamine excretion was constantly elevated but increased further after a warm shower and after receiving normal plasma; at both times he had urticaria. These observations were consistent with the endogenous production of C3a and the resulting histamine release from mast cells. The inactivating mechanism for C3a was apparently intact in the patient's serum. The difference in the electrophoretic mobilities of C3b and C3c was shown as well as the electrophoretic heterogeneity of C3c. Suggestive evidence was also presented that the form of C3 with an activated combining site for red cells, previously postulated by others, is a transient C3 conversion product with an electrophoretic mobility slower than that of C3 on agarose electrophoresis.

Adult↗
PubMedDate not supplied

Case report: intestinal bypass and severe coagulopathy.

A 29-year-old woman, two years post-ileojejunal bypass, developed a serious coagulopathy. Studies utilizing heparin, epsilon-aminocaproic acid, and plasma, in vivo, indicated that the coagulation abnormalities were multiple in origin. Correction of most of the abnormalities permitted revision of bypass which led rapidly to total permanent correction of the coagulopathy.

Adult↗
PubMedDate not supplied

Glucocorticoid treatment does not improve neurological recovery following cardiac arrest. Brain Resuscitation Clinical Trial I Study Group.

Glucocorticoids are commonly given to patients with global brain ischemia, although their efficacy has not been proved. The database of the Brain Resuscitation Clinical Trial I, a multi-institutional study designed to evaluate the effect of thiopental sodium therapy on neurological outcome following brain ischemia, was used for a retrospective review of the effects of glucocorticoid treatment on neurological outcome after global brain ischemia. This study included 262 initially comatose cardiac arrest survivors who made no purposeful response to pain after restoration of spontaneous circulation. The standard treatment protocol left glucocorticoid therapy to the discretion of the hospital investigators. This resulted in four patient groups that received either no, low, medium, or high doses of glucocorticoids in the first 8 hours after arrest. Neurological outcome was scored using a modification of the Glasgow Cerebral Performance Category Scale. None of the steroid regimens statistically improved mean group survival rate or neurological recovery rate over that observed in the group that did not receive steroids. The routine clinical practice of administrating glucocorticoids after global brain ischemia may be associated with serious complications and is not justified.

Aged↗