Negative direct antiglobulin test in autoimmune hemolytic anemia.
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Biomedical subjects
Publications and source records attributed to J Blank.
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Autologous marrow recovery without engraftment of donor marrow was observed after bone marrow transplantation (BMT) for two patients with acute lymphoblastic leukemia. Each had received marrow from a haploidentical mixed lymphocyte culture (MLC) reactive donor after pretransplant conditioning with total body irradiation and high-dose cyclophosphamide. To minimize graft-vs-host disease, the marrow was depleted of T cells in vitro by treatment with a monoclonal anti-T-cell antibody and complement. Two weeks after each transplant, reactive lymphocytes were noted transiently in the blood of each patient. Analysis of karyotype, HLA type, and in vitro MLC responsiveness proved the lymphocytes to be of host, not donor, origin. MLC studies showed rapid proliferative responses specifically to stimulating cells from the BMT donor, indicating in vivo sensitization to donor antigens. Return of hematopoietic function was markedly delayed, but it eventually normalized after several months, without evidence of chimerism. These studies confirm that some immune and hematopoietic stem cells of host origin survive the high-dose chemoradiotherapy used as transplant conditioning. Because these immune cells are specifically reactive to donor alloantigens, more potent suppression of host immunity may be needed to prevent nonengraftment of T-cell-depleted, HLA-mismatched bone marrow.
Leukemic relapses and graft versus host disease (GvHD) remain major complications following allogeneic bone marrow transplantation for leukemia. We present clinical and laboratory details for an eight-year-old boy who received a T-cell-depleted HLA-mismatched marrow transplant as therapy for acute lymphoblastic leukemia (ALL) in second remission. Engraftment with donor marrow was prompt and without any acute GvHD. Nevertheless, the patient's original ALL recurred and proved fatal. The patient remained a chimera with persistent donor lymphocytes present at the time of posttransplant relapse and subsequent to treatment with unsuccessful reinduction chemotherapy. In vitro immune studies showed that these leukemic cells could be recognized and destroyed by the donor's lymphocytes. The relapse itself suggests, however, that the donor's lymphocytes did not effectively destroy the patient's histoincompatible ALL cells in vivo following establishment of the chimeric state. Potential mechanisms are presented to account for this presumed "escape" from the postulated "graft versus leukemia" effect.
The B antigen activity was severely diminished in a patient's RBCs at the preleukemic stage prior to chemo- or radiotherapy. The amount of H sites of the patient's RBC membranes was found to be comparable to that of O RBC membranes. The activity of alpha (1----2) fucosyltransferase (H enzyme) was not severely decreased in the patient's plasma and bone marrow. However, the activity of alpha (1----3) galactosyltransferase (B enzyme), which converts H substance to B substance, was drastically reduced in the patient's bone marrow. Thus, the diminished B antigen in the patient's RBCs was caused mainly by the blockage of conversion of the H substance to B substance. It is suggested that the viral oncogene linked to the ABO locus at q34 of chromosome No. 9 would occasionally suppress the expression of blood group A and B enzymes and A and B antigens.
Increasingly, transfusions of component blood products are used in the setting of the neonatal intensive care unit. There is a need to analyze the indications and potential complications of this therapy critically. We review here the problems primarily unique to the neonatal population and suggest an approach to the transfusion requirements of this group. Specifically, we discuss the rationale, indications and complications of red cell, granulocyte, and platelet transfusions in these patients. Discussion of exchange transfusion and the particular blood banking requirements of these patients will be reviewed in subsequent articles.
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RESIDUAL GENTAMICIN ON A MILLIPORE MEMBRANE WAS INACTIVATED BY MODIFICATION WITH TWO DIFFERENT ENZYMES: gentamicin adenylyltransferase and 3-N-acetyltransferase. Both modifications allowed the growth of susceptible strains of Escherichia coli and Bacillus subtilis.
Six children who developed acute myelomonocytic leukemia presented with a preleukemic syndrome. The incidence of preleukemic presentation of AMML was 17% of children with acute nonlymphocytic leukemia, or 2.9% of all children with acute leukemia at this institution, incidences similar to those in adults. During the preleukemic phase, which lasted from three to 35 months, all children had anemia, all had infectious complications, and three of six had hemorrhagic tendencies. Three received steroids before the diagnosis of AMML, and all had some objective response. Two patients died before receiving therapy for AMML. Four children who received AMML therapy with combinations including cytosine arabinoside and an anthracycline achieved complete remission. Ultimately, all patients died. Clues to diagnosis of preleukemia include unexplained cytopenias, either absolute or functional, peripheral blasts, progressive megaloblastosis with an elevated B12 value, dyserythropoiesis, abnormalities of nuclear segmentation, nonrandom chromosomal alterations, and reduced marrow colony to cluster ratio in vitro. Until there is a highly effective therapy for ANLL, precisely when to treat the child with preleukemia remains uncertain. However, treatment should be started before infectious complications or hemorrhagic tendencies become life-threatening.
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Investigations on the load capacity of an ultrasonic weld in transverse fractures, oblique fractures, and multiple fragment fractures by means of homologous bone fragments and Fimomed were taken up in vitro on 84 human femur diaphyses. It was possible to demonstrate the essential influence of the form of the fracture on the stability of the weld. The mechanical density was the highest in transverse fractures, small in oblique fractures, and the smallest in multiple fragment fractures. Conclusions were drawn up for the clinical use.
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Four enzymes involved in ribonucleoside and deoxyribonucleoside catabolism (deoxyribose-5-P aldolase, thymidine phosphorylase, phosphodeoxyribomutase, and purine nucleoside phosphorylase) are coded for by four closely linked structural genes on the Salmonella chromosome. The genetic order of these genes is (deoC-deoA-deoB-deoD)-serB-thr. Studies on polarity mutants and induction patterns indicate that the deoB and deoD genes may constitute a single operon and that the deoC and deoA genes may constitute a second closely linked operon.
A patient who developed anti-Cob in response to transfusion was studied. The antibody was a warm-reactive, high-titered, IgG alloantibody that did not fix complement, and reacted strongly in the antiglobulin phase. During a period of transfusion the patient developed a positive direct immunoglobulin test with anti-Cob recoverable in the eluate. Reactions were stronger with enzyme-treated red cells. Survival studies with 51Chromium-labeled red cells showed: 1) normal survival of Co(b-) red cells, and 2) accelerated destruction of Co(b+) red cells; initially, cells were destroyed with a one-half disappearance time of 4 days, but after about 4 days, the rate of destruction increased. This study, together with reported suspected transfusion reactions attributed to anti-Cob, suggest that anti-Cob should be considered a clinically significant antibody.
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