Biomedical subjects
J Poole
Publications and source records attributed to J Poole.
Time for the Vatican to bend.
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CD10 antigen density in childhood common acute lymphoblastic leukaemia: comparisons of race and sex.
During the 25 month period from July 1989 until August 1991, 58 children with FAB defined acute lymphoblastic leukaemia (ALL) were referred for immunophenotypic analysis. Of these, 42 children with a common/pre-B phenotype (CD19/CD10-positive) were studied specifically to assess CD10 antigen density. A pattern of segregation was found between males and females and between black and white children. Black males, who are the worst prognostic group, had the lowest CD10 density, while white females, known to constitute the best prognostic group, had significantly higher CD10 antigen density than the other groups. Black females and white males occupied intermediate positions with respect to CD10 antigen density. A two way analysis of variance showed that although sex had contributed significantly to this variation (p = 0.0038), the contribution of race was marginal (p = 0.0530). It is hypothesized that low CD10 antigen density patterns in males and in Blacks could be causally related to poor prognosis.
The Miltenberger subsystem: is it obsolescent?
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Autoimmune hemolytic anemia associated with anti-Sc1.
A case of autoimmune hemolytic anemia (AIHA) in a young child is described. The hemolysis was resistant to steroid therapy but responded to splenectomy and intravenous immunoglobulin. The autoantibody was shown to be anti-Sc1 by both serologic and immunoblotting techniques. This seems to be the first report of an autoanti-Sc1 detected by immunoblotting and the first example of AIHA in a child caused by autoanti-Sc1.
Failure to find an association of blood group P1 with thyroid-associated ophthalmopathy.
OBJECTIVE: Genetic factors have been proposed to account for the development of ophthalmopathy in a proportion of patients with Graves' disease. The aim of this study was to confirm the previously reported association between blood group P1 and thyroid-associated ophthalmopathy. DESIGN: A prospective study of sequential Caucasian patients. PATIENTS: We studied 169 patients with Graves' disease, 84 of whom had grade 3, 4 or 6 ophthalmopathy and 85 had no eye signs. MEASUREMENTS: Blood group P1 was measured by a standard serological technique. RESULTS: The frequency of the P1 blood group was 74.1% in the patients without eye signs and 77.4% in those with ophthalmopathy (chi 2 = 0.25, P > 0.1). By Woolf's method there was no significant difference in the test for heterogeneity of estimates between the present and the previously reported series of Graves' patients. Combining the results (n = 279), the pooled relative risk for ophthalmopathy with blood group P1 did not differ significantly from 1.0 (chi 2 = 2.33, P > 0.1). CONCLUSIONS: The presence of blood group P1 in patients with Graves' disease does not appear to be associated with an increased risk of developing thyroid-associated ophthalmopathy.
TSEN: a novel MNS-related blood group antigen.
We report an antibody (anti-TSEN) that recognizes an antigen (TSEN) at the unique amino acid sequence that results from the junction of GPA58 to GPB27 if the GPB carries the S antigen. Red cells from several unrelated donors that possess this specific GP(A-B) hybrid molecule were agglutinated by anti-TSEN. Since a synthetic peptide with the amino acid sequence at this junction (Pro-Glu-Glu-Glu-Thr-Gly-Glu-Met-Gly-Gln-Leu-Val-His-Arg) specifically inhibited anti-TSEN, it must detect an antigen within this novel amino acid sequence. The TSEN antigen has been provisionally assigned the MNS blood group system number 002.033 on behalf of the ISBT Working Party on Terminology for Red Cell Surface Antigens.
MINY: a novel MNS-related blood group antigen.
We report an antibody (anti-MINY) that recognises a novel low-incidence MNS-related blood group antigen. Anti-MINY agglutinates all Hil-positive red cells tested (Mi.III, Mi.V, Mi.VI, GP.Kipp, GP.Mor and AG) and Hil-negative TSEN-positive red cells (Mi.IV, JR, JL, Oca. and Rag.). All MINY-positive red cells possess glycophorin A-B hybrid molecules. The MINY antigen occurs at the unique amino acid sequence which results from the junction of glycophorin A58 to glycophorin B27 regardless of whether the glycophorin B gene encodes methionine or threonine at amino acid residue 29 of normal glycophorin B. The MINY antigen has been provisionally assigned the MNS blood group system number 002.034 on behalf of the ISBT Working Party on Terminology for Red Cell Surface Antigens.
Legal and professional issues in critical care obstetrics.
The practice of critical care obstetrics is a challenging specialty that presents unique problems and issues in providing perinatal care. With the emergence of critical care obstetrics comes increased accountability and expanded responsibilities. This article addresses the legal and professional issues related to critical care obstetrics.
Pulmonary embolism.
A major cause of maternal morbidity and mortality during pregnancy and the puerperium is thromboembolic disease. Pregnancy is a hypercoagulative state that predisposes the gravida to thrombus formation. Once a thrombus forms in the venous system of the lower extremities, it can travel to the pulmonary arterial bed, which can lead to hypoxemia or death. Maternal mortality associated with pulmonary embolism (PE) is approximately 14%. Most gravidas who have PE during or after pregnancy have no history of thromboembolic disease at the time of insult.
Biochemical studies on red blood cells from a patient with the Inab phenotype (decay-accelerating factor deficiency).
A 38-year-old Russian woman (KZ) has been identified as the fourth proposita with the Inab blood group phenotype. Like the first two propositi, she has a chronic intestinal disorder and, as shown for the third proposita, her Inab phenotype is demonstrably inherited. KZ's serum contained anti-IFC, which reacted with a red blood cell (RBC) membrane component with an Mr of 70,000, which is decay accelerating factor (DAF). Her RBCs lacked all Cromer-related blood group antigens and DAF. Her RBCs were no more susceptible than normal control RBCs to lysis in acid lysis or in rabbit or human antibody-initiated complement lysis tests. Northern blots of total RNA isolated from KZ's Epstein-Barr virus-transformed lymphoblasts showed a marked reduction of DAF mRNA when compared with normal. Polymerase chain reaction (PCR) amplification of cDNA confirmed this reduced level of DAF mRNA. Sequencing of the PCR product showed a 44-nucleotide deletion in the mRNA close to the short consensus repeats IIIa/IIIb intron/exon boundary. This deletion results in a change in the reading frame that places a termination codon six amino acids after the deletion. The putative translation product would lack a glycosyl phosphatidyl-inositol linkage site and, therefore, would not be membrane-bound in the RBC.
P-31 spectroscopy study of response of superficial human tumors to therapy.
Studies were performed to characterize phosphorus-31 magnetic resonance (MR) spectra obtained from 10 superficial human tumors outside the brain and to determine whether P-31 MR spectroscopy could allow detection of a response to therapy before a change in tumor size was measured. The ratio of phosphomonoester to adenosine triphosphate peak intensities (PME/ATP) was unusually large in all tumors studied. The average PME/ATP in lymphomas (1.8 +/- 0.5) was greater than in nonlymphoma cancers (1.1 +/- 0.15). The average PME/ATP for all tumors studied (1.4 +/- 0.5) was much greater than that of underlying skeletal muscle (0.23 +/- .09). Eight of the tumors were studied before and after therapy. Responders were distinguished from nonresponders on the basis of changes in tumor size. PME/ATP decreased during therapy in three lymphomas that responded to therapy. In an adenocarcinoma and Ewing sarcoma that did not respond to therapy, PME/ATP increased. PME/ATP remained constant in two squamous cell carcinomas that responded to therapy and decreased in one squamous cell carcinoma that decreased in size by 40% but was classified as a nonresponder. Changes in PME/ATP did not always parallel changes in tumor size during therapy. In two patients, a decrease in PME/ATP preceded a decrease in tumor size. In four patients, PME/ATP increased transiently during periods when tumor size remained constant.
Statement: occupational therapy services management of persons with cognitive impairments.
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A low-incidence red cell antigen JAL associated with two unusual Rh gene complexes.
A multilaboratory investigation during several years has identified a low incidence antigen JAL on the red cells of 7 propositi. JAL appears to be associated with two unusual Rh complexes, one of which produces a depressed C antigen and the other a depressed c antigen. Family studies strongly suggest that the JAL antigen is encoded by the RH locus. Anti-JAL has been implicated in haemolytic disease of the newborn and is thus considered to be a clinically significant antibody.
The red cell antigen JAL in the Swiss population: family studies showing that JAL is an Rh antigen (RH48).
The JAL antigen was found to have an overall frequency of 0.004% in the Swiss population and 0.06% in French-speaking Swiss. Family studies of 5 JAL+ individuals have shown that the JAL antigen is not part of the ABO, MNSs, Fy, Jk and Co blood group systems, or the Se system, nor is it X- or Y-linked. JAL is encoded by the RH locus or by a very closely linked locus. The number RH48 (4.48) has been assigned for JAL by the International Society of Blood Transfusion Working Party on Terminology for Red Cell Surface Antigens.
Serological and immunochemical specificity of a human autoanti-Gerbich-like antibody.
An 85-year-old male with cardiac failure secondary to anaemia had an apparent anti-Ge2 (Ge = Gerbich) in his serum which did not agglutinate his own red cells even though they were Ge-positive in tests with alloanti-Ge. The direct antiglobulin test was negative; however, an antibody with apparent anti-Ge2 specificity was eluted from his red cells. The patient's autoantibody was shown in immunoblotting experiments to react with an antigenic determinant on beta-sialoglycoprotein. This case illustrates that an autoanti-Ge can masquerade as an alloantibody, thereby complicating antibody identification, and implies that the immunochemical specificity of autoanti-Ge2 is different from that of alloanti-Ge2.
Combined inheritance of epithelial and erythrocyte receptors for Haemophilus influenzae.
Haemophilus influenzae type b expressing fimbriae showed no adherence to buccal epithelial cells and no agglutination of erythrocytes from three AnWj-negative siblings in one family. Hemagglutination of erythrocytes from 13 AnWj-positive members of the same family and from 24 controls was normal, and H. influenzae adhered well to buccal epithelial cells from them. These data indicate that the expression of epithelial and erythrocyte receptors for H. influenzae is inherited concomitantly. Combined with previous data (L. van Alphen, J. Poole, L. Geelen, and H. Zanen, Infect. Immun. 55:2355-2358, 1987), the results show that the receptor molecules on the surfaces of the epithelial cell and the erythrocyte are different but that the binding sites for the fimbriae of H. influenzae are similar.
An application of immunoblotting in the classification of the Miltenberger series of blood group antigens.
A simple scheme is described for the classification of Miltenberger cell classes I to VI, which is consistent with the serologic definition of the determinants. The scheme is based on the reaction patterns obtained by immunoblotting the normal and abnormal sialoglycoproteins (SGPs) found in these cells with several murine monoclonal antibodies that recognize different epitopes on alpha-SGP (Glycophorin A). The abnormal alpha found in MiI and MiII cells is easily identified with these antibodies, as is the abnormal alpha-delta SGP found in MiV cells. Certain alpha-SGP antibodies recognize epitopes on the abnormal SGPs found in MiIII, MiIV, and MiVI cells, although the mode of inheritance of these abnormal SGPs suggests that they are related to delta-SGP (Glycophorin B). Antibody R18 reacts with the abnormal SGP of MiIII cells but not that of MiIV or MiVI cells, whereas antibody BRIC 119 reacts with MiIII, MiIV, and MiVI cells. None of the abnormal components in these three cell classes react with antibody R10 or with an antibody (BRIC 163) that recognizes an epitope on the cytoplasmic portion of alpha-SGP. The immunostaining of membranes from persons heterozygous for the MiVII and MiVIII classes revealed patterns identical to those of normal red cell membranes. However, antibody R18 did not react with any of the SGP components of homozygous MiVII cells.