Preoperative psychological evaluation and intervention in prospective amputees.
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Biomedical subjects
Publications and source records attributed to R Herron.
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Forced antipsychotic medication procedures are generally perceived to be clinically necessary options, albelt violations of individuals' bodies and autonomy. Previous studies have explored forcibly medicated patients' attitudes concerning these procedures, but as patients were interviewed while still in the hospital, this may have affected their responses. We interviewed consecutively forcibly medicated English-speaking acute-care inpatients after their discharge to the community. The interviews were conducted by telephone by a clinician not involved with their treatment. Of 65 such patients, 7 had already been rehospitalized, 3 could not recall the procedure, and 25 others refused the interview or were not locatable. Of the 30 who were successfully interviewed, only 47 percent had received any forced injections; the remainder had accepted oral medication under duress. Recollecting their experiences, 57 percent professed fear of side effects, 17 percent feared "addiction," and 17 percent objected to others' controlling them. Forty percent recalled feeling angry, 33 percent helpless, 23 percent fearful, 13 percent embarrassed, but 23 percent were relieved. Surprisingly, 60 percent retrospectively agreed with having been coerced, 53 percent stating they were more likely to take medication voluntarily in the future. Other forcibly medicated patients had poorer outcomes, such as rapid readmission or discharge to a state hospital: those patients may have harbored more negative feelings. However, a substantial fraction of the patients who were reached in the community appeared to support having received medication forcibly as inpatients.
OBJECTIVE: To survey transfusion medicine practices in 1990, to determine the distribution of defects in the transfusion process, to examine the relationship between defects and complications, and to recommend improvements in the transfusion process. DESIGN: A mail survey that divided the transfusion process into 24 risk-prone steps and gathered defect rates on each step, along with incidence data for eight known complications of transfusions and other demographic information. SETTINGS: Hospitals, independent laboratories, and blood centers that provide transfusion medicine services. OTHER PARTICIPANTS: Respondents were 1365 participants in the College of American Pathologists 1991 Blood Bank Quality Assurance Survey. RESULTS: While processing 6.2 million units of blood and blood products, respondents reported detecting over 88,000 defects: 41% in the preanalytic phase of testing, 55% in the postanalytic phase, and only 4% in the analytic phase, the phase to which most monitoring efforts were devoted. A median of eight steps were actively monitored by survey participants overall, whereas 96 facilities sought defects in all 24 steps. CONCLUSIONS: Analysis of the data showed several monitoring steps provide similar information. Although monitoring of the transfusion process could not be linked with prevention of the complications studied, active surveillance does focus attention on defect-prone steps and allows testing of strategies to improve the transfusion process. We describe how defect detection systems may be improved.
A patient without evident immune deficiency who received a transfusion of blood from a second-degree family member developed fatal transfusion-associated graft-versus-host disease (TA-GVHD). The donor was homozygous for an HLA haplotype for which the recipient was heterozygous (one-way HLA match). All 39 reported cases of TA-GVHD in immunocompetent patients were reviewed to ascertain the predisposing factors and to define the indications for irradiating blood for this population. HLA typing was described in 15 cases; in 13, including seven related and six unrelated donors, a one-way HLA match was present. Thirty-one (79%) of the 39 cases were reported from Japan (and 196 other cases are cited in the Japanese literature), but a one-way HLA match among unrelated donors at HLA-A, -B, -DR loci is only approximately two to four times more likely in Japanese persons than in whites. Fresh blood (< 96 hours old) was used in 29 (94%) of the 31 cases reported from Japan and in 33 (87%) of 38 cases overall (in one case, the age of the blood used was not reported). Thus, factors that appear to predispose to TA-GVHD in immunocompetent patients are a one-way HLA match, fresh blood, and, possibly, Japanese ancestry. Irradiating cellular blood components from all blood relatives of transfusion recipients will not completely eliminate the risk of TA-GVHD.
Immunoblotting with human anti-Sc1 and anti-Sc2 locates the Sc1 and Sc2 antigens to an erythrocyte membrane glycoprotein of apparent Mr 60,000. The antigens are destroyed by pronase, and require intact disulphide bonds for expression. A proportion of the molecules carrying the Sc1 and Sc2 antigens are associated with red cell cytoskeleton preparations. Treatment of intact cells with an Endo F preparation resulted in the loss of the Sc2 antigen but not the Sc1 antigen, suggesting that the Sc2 antigen is dependent on the presence of one or more complex N-glycans for its expression.
When the membrane components of Xg(a+) erythrocytes were separated by electrophoresis and immunoblotted with an anti-Xga of human origin, two diffuse bands of approximate Mr 22,000-25,000 and 26,500-29,000 were stained. These reactive components were not evident in membranes from proteinase-treated Xg(a+) erythrocytes. Neuraminidase treatment of erythrocytes before immunoblotting resulted in one diffuse Xga-reactive band, the leading edge of which had a slightly increased mobility corresponding to a decrease in Mr of approx. 1500. These results suggest that the membrane components that carry Xga are sialoglycoproteins. A genetic relationship exists between Xga and the antigen recognized by the monoclonal antibody 12E7. An immunochemical comparison of the structures that carry the Xga and 12E7 antigens demonstrated that they differ in Mr and in the way in which they are modified by neuraminidase. This is in accord with evidence that Xga and 12E7 are the products of two separate structural loci.
Ghosts were prepared from erythrocytes positive for the rare blood group antigen Pta. Immunoblotting of the solubilised ghosts with anti-Pta located the antigen on a band with an Mr of 31,600, about 1,100 higher than that of sialoglycoprotein gamma. Binding to the same band was also observed when cytoskeleton preparations from Pt(a+) erythrocytes were immunoblotted with the antibody. Haemagglutination and immunoblotting experiments were consistent in demonstrating that the Pta antigen is not inactivated by treatment of intact erythrocytes with neuraminidase or trypsin but is destroyed by treatment with alpha-chymotrypsin, papain or pronase. The data indicate that the Pta antigen is carried on a 'new' erythrocyte membrane protein.
A platelet suspension immunofluorescence test (PIFT) was compared with an enzyme-linked immunosorbent assay (ELISA) for measurement of platelet-associated IgG (PAIgG) in 108 patients with thrombocytopenia. The ELISA appeared to have greater sensitivity than the PIFT in detecting PAIgG in patients with idiopathic thrombocytopenic purpura, and in other groups of patients studied, and in many cases results were discrepant between the two assays. Possible explanations are given for the low sensitivity of the PIFT, and for the discrepant results.
A red cell IgM autoantibody with anti-e specificity was identified in the serum of a rhesus-negative (rr) patient presenting with haemolytic anaemia and a negative direct antiglobulin test. The autoantibody strongly agglutinated normal allogeneic rhesus-negative (rr) red cells in saline at 37 degrees C but had only weak activity for autologous red cells. Incubation of the patient's serum with subpopulations of normal allogeneic red cells obtained by density fractionation, demonstrated that the strong agglutinating activity of the autoantibody was for red cells with density greater than 1.090 g/ml. Young red cell subpopulations of lower density gave weak reactions and low titration scores equivalent to those obtained with autologous red cells during the haemolytic episode. The patient's red cells during remission however, when the patient's haemoglobin level had returned to normal, were strongly agglutinated by serum samples taken during the haemolytic episode; as was the case with normal allogeneic red cells, the strong activity was for patient red cells with density greater than 1.090 g/ml, red cell populations of lower density giving low titration scores. The findings in this case indicate that the patient's red cells which had survived haemolysis during the haemolytic episode were young red cells (density less than 1.090 g/ml), the weak sensitization of these cells being insufficient to cause their destruction by macrophages. Furthermore, these findings, together with observations that IgG autoantibodies may also bind less strongly to young red cells [Gray et al., Br. J. Haemat., 55: 335-345, 1983; Branch et al., Blood 63: 177-180, 1984].(ABSTRACT TRUNCATED AT 250 WORDS)
A mononuclear phagocyte assay has been used to measure the in vitro interaction of normal donor monocytes with the red cells from subjects with a positive direct antiglobulin test (DAT). The relationship between the in vivo haemolytic rate in these subjects and the results obtained in the assay, expressed as the number of red cells associated with 100 monocytes (ARC value), has been examined. From the results of assays in which normal donor monocytes were incubated with normal (DAT negative) donor red cells it was calculated that ARC values of greater than 2 could be considered significantly elevated. Assays performed on 24 patients with a positive DAT and warm autoimmune haemolytic anaemia resulted in a mean ARC value of 42 (range 1-212). Assay results for two of the patients in this group, however, were not significantly elevated from normal. The red cells from three patients with a negative DAT who were suspected of having autoimmune haemolytic anaemia showed no association with normal donor monocytes in the assay. The mean ARC value obtained for 14 non-haemolysing subjects with a positive DAT was 7 (range 1-47). Assay results for only 10 of the 14 subjects in this non-haemolysing group fell within the normal range. The correlation of assay results and in vivo haemolysis was strengthened when the assays were performed with autologous monocytes. A possible explanation for the unexpectedly low ARC values obtained in some cases of autoimmune haemolytic anaemia is discussed.
A 55-year-old man received a cadaver kidney from a donor whose serum contained red cell antibodies with anti-c specificity. Atypical antibodies were shown to be absent from the recipient's red cells and serum at the time of transplant. Blood was not transfused during surgery. Two weeks after the transplant, the recipient developed a positive direct antiglobulin test due to antibodies with anti-c specificity. Immune haemolysis was diagnosed in the patient 3 weeks after transplant. The possible mechanisms involved in antibody formation in the recipient are discussed.
The serum of an 85-year-old Caucasian male with no history of blood transfusion contained an IgG3 antibody with anti-LWab specificity. The antibody failed to react with dithiothreitol-treated red cells, and there was a marked reduction in titre of the antibody with pronase-treated cells, findings consistent with an antibody having this specificity. High association values were obtained in a mononuclear phagocyte assay when LW-positive red cells, sensitised in vitro with the patient's serum antibody, were incubated with peripheral blood monocytes from the patient. In vivo red cell survival studies demonstrated that 99mTc-labelled rhesus-negative (rr), LW-positive red cells had 53% survival at 1 h. The IgG subclass of the antibody, mononuclear phagocyte assay results and in vivo survival studies predicted a significant reduction in the posttransfusion survival of therapeutic volumes of rhesus-negative (rr), LW-positive red cells.
We describe a new analytical approach--"capsule chemistry"--for high-speed, selective analysis of a wide variety of analytes. Sequential micro-aliquots of sample and reagents are encapsulated within an inert fluorocarbon liquid. The resulting "test capsule" is introduced into a single analytical flow path, composed of a solid fluorocarbon, Teflon, where the sample is incubated, mixed, reacted, and measured as a moving series of individual tests. These randomly selective assays are processed at a rate of 720 per hour. The unique physical interaction between the liquid and solid fluorocarbon carrier materials effectively prevents detectable "carryover" of aqueous constituents between the successive test capsules. Reactions are monitored through the walls of the Teflon analytical channel at nine in-line detector stations for colorimetric and nephelometric measurements.
An H-deficient blood is described which, unlike other H-deficient, Bombay and para-Bombay bloods, has normal H transferase levels. In previous examples of Bombay and para-Bombay phenotypes the absence of H transferase has explained the lack of H substrate and therefore the weak A and B antigens which are characteristic of these phenotypes. This explanation obviously does not hold in the case described here and it is proposed that the biochemical block must be further back, either in the enzymes synthesising the oligosaccharide chains or in those making the GDP-fucose substrate for the H and the Le gene-specified fucosyltransferases. Inhibition of the synthesis of Leb substance, as well as H substance, although the saliva of the propositus contains the Le gene-specified transferase, supports this proposition.
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An acquired B antigen, present on the red blood cells of a healthy male blood donor, was investigated. An anti-B typing serum which initially detected the weak antigen on the donor cells contained a separable antibody that was specific for cells with the acquired B antigen and did not react with normal group B cells. A similar, specific, immune antibody was produced in a rabbit by the injection of red blood cells with an acquired B antigen.
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