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J Poole

Publications and source records attributed to J Poole.

At least 37 records · Page 2Linked to original sources
PubMed1999

Glycophorin A mutation Ala65 --> Pro gives rise to a novel pair of MNS alleles ENEP (MNS39) and HAG (MNS41) and altered Wrb expression: direct evidence for GPA/band 3 interaction necessary for normal Wrb expression.

We report here a novel Glycophorin A (GPA) mutation Ala65 --> Pro which gives rise to a low-incidence antigen HAG, lack of a high-incidence antigen ENEP and aberrant expression of the high-incidence Wrb antigen. Anti-ENEP was identified in the serum of a transfused male patient (E.H.) who was homozygous for a GPA Ala65 --> Pro mutation and possessed a novel low-incidence antigen which we have called HAG. An unrelated HAG-positive individual, heterozygous for the Ala65 --> Pro mutation, has also been identified. Anti-HAG was present in several multispecific antisera to low-incidence antigens and in one monospecific serum. Normal expression of the Wrb antigen depends on the presence of amino acid Glu658 of band 3 and on the presence of GPA. However, a specific epitope on GPA has not previously been implicated. DNA sequence analysis of band 3 from patient E.H. was normal in the region of Wra/Wrb polymorphism with homozygous presence of Glu658 and therefore the abnormal Wrb expression results from the Ala65 --> Pro mutation in GPA. The ENEP and HAG antigens have been assigned the MNS blood group system numbers 002.039 and 002.041, respectively, by the ISBT Working Party on Terminology for Red Cell Surface Antigens.

Alanine↗
PubMed1999

A chemiluminescence test for predicting the outcome of transfusing incompatible blood.

A chemiluminescent test (CLT) which measures the metabolic response of human monocytes to sensitized red cells was developed to distinguish antibodies capable of causing the increased destruction of transfused incompatible red cells from antibodies which are clinically benign. Thirty sera containing IgG antibodies to high-frequency antigens were tested; 27 of these sera were also tested using the monocyte monolayer assay (MMA). The clinical significance of antibodies in 14 of the sera was known: three (anti-Ata (two), -JMH) caused accelerated clearance of 51Cr-labelled cells, five (anti-'MiIII', -Yta, three unidentified) caused haemolytic transfusion reactions and six (anti-Yta, -Ge, -JMH, -Xga, -Kna (two)) did not appear to affect red cell survival. Overall, results from the MMA and CLT showed good agreement; seven sera were negative in both assays, 18 sera were positive in both assays and two sera were positive in the MMA but negative in the CLT. There was no clear relationship between the activity of different antibodies and the level of sensitization as determined by flow cytometry. Antibody activity could be either increased or decreased by incubation of sensitized red cells with fresh serum. MMA results were in concordance with the clinical significance of antibodies where known in eight of 10 cases. CLT results were in concordance with clinical significance in 12 of 14 cases. Both assays gave false-positive results with serum from a patient with anti-Kna who had received red cell transfusions without adverse effect. This appeared to be due to the ability of anti-Kna to cross-link complement receptor 1 (CR1) on red cells to CR1 on monocytes; negative results were obtained using autologous monocytes.

Blood Group Antigens↗
PubMed1998

The Fy(x) phenotype is associated with a missense mutation in the Fy(b) allele predicting Arg89Cys in the Duffy glycoprotein.

The molecular basis of the three major alleles (Fy(a)/Fy(b)/Fy) of the Duffy (FY) blood group system has recently been established but the Fy(x) phenotype associated with weak expression of the Fy(b) and other FY antigens is poorly understood. In the Fy(x) genes of five unrelated British and Swedish donors with the Fy(a+b+weak) phenotype we found two missense mutations predicting amino acid changes Arg89Cys and Ala100Thr in the FY glycoprotein. The same mutations were found in two Fy(a-b+weak) samples from individuals of Swedish and Algerian origin. Their red blood cells showed a marked decrease in Fy(b), Fy3 and Fy6 expression measured by routine serology and flow cytometry. The rare FY genotypes Fy(x)Fy(x) and Fy(x)Fy were confirmed by family studies and DNA sequencing. Screening by allele-specific primer PCR (ASP-PCR) for these mutations among 100 Caucasian and 100 Black random blood donors indicated allele frequencies of 2.5% and 0% respectively. Ala100Thr alone was present in 33% of the Caucasians (but none of the Blacks) with no weakening of FY expression. A novel allele at the FY locus associated with the Fy(x) phenotype was studied. Mistyping of this weak Fy(b) antigen in clinical transfusion medicine may lead to delayed haemolytic transfusion reactions in immunized patients. A potential role for genomic typing is proposed.

Alleles↗
PubMed1997

The Rhnull phenotype in an English individual: haematological, serological and immunological studies.

We have characterized the first case of Rhnull phenotype to be identified in England. The red cells were serologically negative for C, c, Cw, D, E, e, f, hr B, Rh17, Lw a, Lw ab and Duclos, while the patient's serum contained anti-Rh29, which was subsequently boosted by transfusion. The Rh phenotype of the patient's son (R1r) confirmed that this was a regulator type of Rhnull in the patient. Follow up studies confirmed the presence of a mild chronic anaemia with stomatocytes and spherocytes; electron microscopy revealed the presence of cells with deep central indentations. Osmotic fragility was increased to a level intermediate between normal and hereditary spherocytic controls. The presence of ongoing haemolysis was indicated by a mild reticulocytosis and splenomegaly. The potent anti-Rh29 has made the provision of compatible blood difficult and autologous units have been frozen. The case illustrates the rare phenomenon of the Rhnull phenotype which not only causes problems for the transfusionist but should also be recognized as a cause of haemolytic anaemia secondary to a membrane defect. Blood film and Rh phenotyping are useful preliminary investigations in suspected cases.

Aged↗
PubMed1997

Analysis of Knops blood group antigens on CR1 (CD35) by the MAIEA test and by immunoblotting.

Kna, McCa, Sla and Yka are red cell antigens of relatively high frequency, located on complement receptor 1 (CR1, CD35). Antibodies to these Knops system antigens are not uncommon. They are not haemolytic and do not reduce the survival of transfused incompatible red cells, but they are a nuisance in transfusion laboratories as they can cause an incompatible crossmatch and must be identified before they can be dismissed as clinically insignificant. Human red cell alloantibodies can be shown to be Knops system antibodies by the monoclonal-antibody-specific immobilization of erythrocyte antigens (MAIEA) test, using murine monoclonal anti-CR1. In addition to confirming that Kna, McCa, Sla and Yka are located on CR1, the MAIEA test was used to confirm that Csa is not on CR1. Red cells of the Helgeson phenotype, the null phenotype of the Knops system by conventional serological methods, have levels of Kna, McCa, Sla and Yka intermediate between those of alpha-chymotrypsin-treated cells (which lack Knops system antigens) and those of positive control cells. Level of expression of Knops system antigens is very variable and intensity of staining of immunoblots probed with monoclonal anti-CR1 correlated with strength of Knops system antigens, as determined by the MAIEA test. In individuals heterozygous for alleles producing different allotypes, separate bands representing each allotype on an immunoblot showed identical intensity of staining, suggesting that the quantity of CR1 on red cells is controlled, at least in part, by a locus independent of CR1. An analysis of CR1 on red cells of individuals who have made Knops system antibodies suggested that the Knops system antigens and the antibodies that detect them are complex and heterogeneous.

Antibodies↗
PubMed1997

Co-presence of a point mutation and a deletion of exon 3 in the glycophorin C gene and concomitant production of a Gerbich-related antibody.

BACKGROUND: Antigens of the human blood group system Gerbich (Ge) are located on sialoglycoproteins glycophorin C (GPC) and glycophorin D (GPD). CASE REPORT: The Ge+ proposita (RW) produced an alloanti-Ge after receiving 2 units of red cells (RBCs) during surgery. Further studies were carried out to characterize the antibody specificity, RBC GPC and/or GPD (GPC/GPD), and the glycophorin C gene (GYPC) from RW and her compatible siblings. RW's serum contained an alloanti-Ge that did not react with RBCs from RW or four of her siblings or with RBCs with Ge-negative phenotypes. An eluate of RW's antibody reacted weakly with GPC in Western blotting. RW's RBCs were positive with 20 alloanti-Ge2, 1 autoanti-Ge2, 4 alloanti-Ge3, and 1 alloanti-Ge4. Titrations revealed weak expression of these antigens on her RBCs and those of her compatible siblings as compared with controls. In contrast, titrations of mouse and rat monoclonal antibodies specific for GPC/GPD showed no differences. Western blotting of RBC membranes using GPC/GPD specific monoclonal antibodies showed a broad diffuse band corresponding to GPC.Ge in addition to GPC and GPD. Blotting of membranes from trypsin-treated RBCs from these individuals revealed an increase of 1500 in M(r) of membrane-bound tryptic fragment over that in the membranes from typsin-treated RBCs from persons with normal GPC/GPD. In RT-PCR, two products were obtained for RW and her compatible siblings: one had a complete deletion of exon 3 and the other had a base change (A-->T) in nucleotide 173 in exon 3 (confirmed by genomic DNA sequencing of exon 3). This point mutation has resulted in the loss of restriction enzyme Tth111 I-sensitive site in the mutant GYPC. CONCLUSION: The specificity of antibody in RW's serum was serologically anti-Ge2. Two genetic events occurred in exon 3 in GYPC of RW and her compatible siblings. The exon 3 deletion confirmed a Ge:-2,-3,4 haplotype. The abnormal tryptic fragment obtained was due to the (A173-->T) base change in exon 3 that resulted in Asp58-->Val in the deduced amino acid sequence at the membrane boundary.

Animals↗
PubMed1997

Three new members of the mouse prolactin/growth hormone family are homologous to proteins expressed in the rat.

A search of a mouse expressed sequence tag database for novel messenger RNAs (mRNAs) in the PRL/GH family has identified three clones that are homologous to the rat PRL-like protein A (PLP-A), PRL-like protein B (PLP-B), and decidual/trophoblast PRL-related protein (d/tPRP). Full-length complementary DNA clones for each of these three mouse mRNAs have been sequenced. Mouse PLP-A is predicted to be synthesized as a precursor of 227 residues and secreted as a glycoprotein of 196 amino acids; the secreted protein shares 78% identity with rat PLP-A. The open reading frame for mouse PLP-B encodes a protein of 230 residues; the putative mature glycoprotein of 201 amino acids is 66% identical to rat PLP-B. The third mouse complementary DNA clone encodes a precursor protein of 240 residues and a secreted glycoprotein of 211 amino acids with 64% identity to rat d/tPRP. All three mouse mRNAs are expressed specifically in the placenta or decidua. The highest levels of the PLP-A mRNA are detected on day 12, at which time expression is localized to a subset of trophoblast giant cells, especially those cells that line maternal blood sinuses. PLP-B mRNA levels are high on day 10 in decidual cells and on day 12 in spongiotrophoblasts. The mRNA similar to rat d/tPRP is present at high levels even earlier in gestation (day 8) and is localized to the decidual layer. The identification of PRL-related mRNAs in common between the mouse and rat indicates that the encoded hormones are evolutionarily conserved and, therefore, likely to play important roles in reproductive physiology.

Amino Acid Sequence↗
PubMed1997

Two novel members of the prolactin/growth hormone family are expressed in the mouse placenta.

Two novel members of the mouse PRL/GH family have been identified through a search of an expressed sequence tag database. The encoded proteins do not appear to be homologs of other known members of this hormone family. One of these proteins, designated PRL-like protein E (PLP-E), is predicted to be synthesized as a precursor of 265 amino acids, modified by N-linked glycosylation, and secreted as a mature glycoprotein of 236 residues. The second clone encodes a protein of 253 residues with consensus sites for N-linked glycosylation; the secreted form of the protein, designated PRL-like protein F (PLP-F), is predicted to be 223 amino acids in length. Both of these messenger RNAs are expressed specifically in the placenta, with peak levels of PLP-E on days 10-12 and of PLP-F on days 14-16. Expression of PLP-E is restricted to the trophoblast giant cells, whereas PLP-F is synthesized only in the spongiotrophoblasts. The genes for both of these proteins map to a 700-kilobase region of mouse chromosome 13 that includes other members of the PRL/GH family.

Amino Acid Sequence↗
PubMed1996

Management of acute myocardial infarction in Auckland.

AIM: To analyse the utilisation of therapies in coronary care units for patients with acute myocardial infarction. METHODS: An evaluation form was completed prospectively by a designated nurse in each coronary care unit of the four Auckland hospitals in 1993. RESULTS: One thousand and eighty one patients who were admitted with definite or probable acute myocardial infarction had a coronary care unit stay of 63.4 (SD 49.3) hours, and hospital stay of 7.3 (5.1) days. The mortality for definite myocardial infarction was 13.7% (< 70 years 7.1%). Coronary angiography was performed on 10% of patients during their hospital admission, and 4.9% underwent revascularisation. Thrombolytic therapy was administered to 52% (495/948) of patients with definite infarction and 4% had contraindications. Patients aged > or = 70 years (47% vs 55% p = 0.02) or diabetics (46% vs 56%, p = 0.04) were less likely to receive thrombolysis. The utilisation of aspirin and oral beta-blockers was 86% and 40%, respectively, in patients with definite infarction and both were used less frequently in patients > or = 70 years. Intravenous beta-blockers were administered to < 1% of patients. Angiotensin converting enzyme (ACE) inhibitors were prescribed in 21%, intravenous or long acting nitrates in 41% and calcium antagonists in 14%; the latter two therapies were used more frequently in patients > or = 70 years. There was no evidence of gender or ethnic bias for either investigation or treatment. CONCLUSION: On the basis of results of recent clinical trials, there may be under utilisation of some treatments for acute myocardial infarction including aspirin, thrombolytic therapy, beta-blockers and ACE inhibitors, while calcium antagonists may be over used.

Adrenergic beta-Antagonists↗
PubMed1996

Maternal behavior in male rats: effects of medial preoptic area lesions and presence of maternal aggression.

Male rats exhibit maternal behavior prepuberally and in adulthood, but the neural mechanisms and the ability of males to respond to hormones that stimulate maternal aggression (following arousal of maternal behavior) in females have not been studies. In Experiment 1, males were exposed to pups to stimulate maternal behavior (sensitization) after either radiofrequency lesions of the MPOA or sham lesions with nonactivated electrodes that penetrated the MPOA. Nonsurgical males served as a CONTROL group. The LESION male group showed severe deficits in all components of maternal behavior compared to the latter two groups that showed no behavioral deficits. Females in the LESION group and those given SHAM 1 lesions (produced by electrodes without current introduced into the MPOA) also showed severe deficits in maternal behavior compared to SHAM 2 females (electrode lowered to above the MPOA without current) and nonsurgical CONTROL females. In Experiment 2, prolonged estradiol (E2), progesterone (P) treatment followed by an injection of either 20 micrograms or 100 micrograms/ kg estradiol benzoate (EB) or oil in castrated males was effective in stimulating short-latency maternal behavior, mainly in the 100 micrograms/kg EB group. Males of this group also showed a high level of maternal aggression that was inversely correlated with their latencies for maternal behavior. All groups showed maternal aggression when maternal behavior was established. The results indicate the MPOA mediates maternal behavior in males as it does in females; maternal aggression in males accompanies the stimulation of maternal behavior and may be stimulated by the same hormones.

Aggression↗
PubMed1996

Haemolytic disease of the newborn due to anti-G.

Mrs P. presented at 13 weeks of gestation with apparent anti-C+D. At week 34, with antibody levels of 168 IU/ml, a D-negative (r'r) baby was delivered with a strongly positive DAT and an Hb of 3.0 g/dl. Anti-G in maternal serum was isolated by adsorption and elution from R2R2 cells and shown, using flow-cytometric and chemiluminescence assays, to sensitize r'r cells at levels of cell-bound IgG consistent with fetal haemolysis. In an analysis of 28 sera from alloimmunized women with over 5 IU/ml anti-C+D, 2 sera were shown to contain levels of anti-G consistent with moderate or severe haemolytic disease of the newborn (HDN). Thus HDN due to anti-G may not be rare. An analysis of 187,037 blood donors in the south-west of England showed the r' gene frequency to be 0.005897 suggesting that approximately 2.9% of matings of rr women with D-negative fathers can produce an r'r baby. These findings highlight the need for the continuous non-invasive monitoring of D-negative fetuses of women with apparent anti-C+D.

Antibodies, Anti-Idiotypic↗
PubMed1996

Does the Nursing Care Plan help in the management of psychiatric risk?

The Nursing Care Plan (NCP) is routinely used to direct the nursing care of psychiatric in-patients, but the impact of NCPs on patient care and clinical outcome is not firmly established. NCPs from 246 patients, chosen at random from admissions to acute psychiatric wards, were analysed. The NCPs were scored for quality and also specifically for the presence of recorded risk assessment and appropriate level of nursing supervision. NCPs were evaluated in relation to psychiatric risk factors present prior to admission, and in relation to risk behaviour during hospitalization. Quality of NCP records was generally poor, with scores in all areas assessed being approximately half of the possible maximum. Patients with a perceived high risk of suicide prior to admission had significantly better NCP quality than other patients, but about a third of these high risk patients had no recorded risk assessment or supervision level in the nursing notes. Patients who had actually self-harmed within 4 weeks prior to admission were more likely to have a recorded risk assessment but did not score more highly than the rest of the patient population on any other measures of NCP quality. Patients who had made suicidal threats prior to admission but who were not deemed to be of high suicide risk before admission had significantly lower quality NCPs and were less likely to have a record of supervision level than the rest of the patients. The highest rate of supervision records occurred in patients who had shown dangerous behaviour prior to admission. Outcome in terms of two risk behaviours during admission (self-harm and violence) was not related to whether or not risk assessment and supervision levels had been recorded. Patients admitted compulsorily to hospital were more likely to have a supervision level recorded but were also more likely to abscond. It is concluded that issues of psychiatric risk were not adequately addressed in this sample of NCPs. Furthermore, the data raise serious questions about the usefulness of the NCP in helping to predict and prevent risky behaviour amongst psychiatric in-patients.

Acute Disease↗
PubMed1996

A high-involvement health care model.

Integrating a traditional approach into a high-involvement culture can result in successful redesign. Examples of successful redesign efforts as well as those that failed are discussed.

Decision Making, Organizational↗
PubMed1995

Evidence that the Gya, Hy and Joa antigens belong to the Dombrock blood group system.

Ten red cell samples lacking the high incidence Gya antigen were found to have the previously undescribed Do(a-b-) phenotype. Fifteen Hy- red cell samples were Do(a-b+) with weak expression of Dob and 6 Jo(a-) red cell samples were Do(a+) with weak expression of Doa. Five of the 6 Jo(a-) samples had extremely weak expression of Dob. The sixth Jo(a-) was Do(b-). Immune precipitates were prepared from radio-iodinated antigen-positive red cells with anti-Gya, -Hy, -Doa and Dob. Immunoblotting of these immune precipitates with affinity-purified anti-Gya and anti-Dob under non-reducing conditions revealed similar broadly migrating bands of M(r) 48,700-59,750, suggesting that the Doa and Dob antigens are carried on the same glycoprotein as Gya and Hy. The phenotypically associated high incidence Joa antigen has previously been shown to reside on the Gya/Hy glycoprotein. Enzyme-treated and chemically modified red cells tested with anti-Doa, -Dob, -Gya, -Hy and -Joa gave the same pattern of reactivity. We propose that Gya, Hy and Joa become part of the Dombrock blood group system and that, henceforth, the Gya/Hy-active glycoprotein be renamed the Dombrock-active glycoprotein. The Gy(a)-Hy- Jo(a-) phenotype constitutes the 'null' phenotype within the Dombrock system.

Blood Group Antigens↗