Biomedical subjects
Publications and source records attributed to M E Reid.
A red blood cell sample typed as Gy(a-) on direct testing did not absorb or elute anti-Gya, but unexpectedly absorbed and eluted anti-Hy. Three other Gy(a-) red blood cell samples from unrelated individuals failed to absorb and elute anti-Hy.
Explore the source record for details and available documents.
The serum from a 47-year-old man who had not been transfused previously was tested with reagent red cells selected from different commercial manufacturers to confirm the presence of an alloanti -N. Agglutination of homozygous N-positive red cells at 22 degrees C ranged from score 3 to 12. This variable reactivity was found to be due to pH, and the optimal reactivity was in test media below pH 7.
Explore the source record for details and available documents.
Six examples of IgG anti-Cra were absorbed onto group O, Cr(a+) red cells and subsequently eluted by five elution methods. Five of the anti-Cra antibodies were eluted only by the digitonin-acid method. The sixth example was recovered by all elution methods; however, the digitonin-acid and Lui freeze-thaw methods recovered more antibody activity than did the dichloromethane, ether, or 56 degrees C heat methods. This is the first report of multiple examples of antibodies with the same specificity demonstrated preferentially by a single elution technique.
Explore the source record for details and available documents.
BACKGROUND: The Gerbich-related Lsa blood group antigen (Ge6) resides on the higher-molecular-weight forms of glycophorin C (GPC) and glycophorin D (GPD). Southern blot analysis has previously revealed an additional GPC exon 3 insert in the genomic DNA from an Ls(a+) individual. STUDY DESIGN AND METHODS: To confirm the duplication of exon 3 in the GPC mRNA, total RNA prepared from the Epstein-Barr virus-transformed lymphocytes of an Ls(a+) individual was used in the synthesis of first-strand cDNA. The first-strand cDNA served as a template for the amplification of GPC-related DNA by polymerase chain reaction. After subcloning, the polymerase chain reaction cDNA was sequenced with a kit. Hemagglutination inhibition of anti-Lsa sera with synthetic peptides was performed to identify the location of Lsa on the GPC.Lsa protein. RESULTS: Sequencing the GPC.Lsa cDNA showed an insert of 84 nucleotides, which corresponds to the entire sequence of exon 3 in the GPC gene (GYPC). Since the exon 3-duplicated exon 3 boundary of GYPC.Lsa encodes a novel amino acid sequence on GPC.Lsa and GPD.Lsa, synthetic peptides consisting of the amino acids flanking this junction were used to determine the amino acid sequence that is essential for expression of Lsa. The peptide DIVVIA/EPDPG was noninhibitory, while peptides with the sequence TPTIMDIVVIA/EPDPG or SPSVLDIVVIA/EPDPG inhibited anti-Lsa reactivity. CONCLUSION: Lsa is located within the sequence of amino acids encoded by the nucleotides at the exon 3-duplicated exon 3 boundary, and the conformation of this peptide sequence is important for recognition of Lsa by human anti-Lsa.
BACKGROUND: The Kell blood group system is complex, containing at least 21 antigens. Some antigens are organized in five allelic sets; other, mostly high-incidence antigens, may be independently expressed. In this study, the molecular basis of five high-incidence antigens in the Kell system are described. STUDY DESIGN AND METHODS: Genomic DNA sequences from K:-12 (KEL:-12), K:-18 (KEL:-18), K:-19 (KEL:-19), K:-22 (KEL:-22), and TOU-(KEL:-26) persons were sequenced and compared to those from persons with a common Kell phenotype. RESULTS: The various Kell phenotypes are due to point mutations that encode amino acid substitutions. In KEL:-18, two mutations in the same codon were noted. In the various phenotypes, the following KEL mutations were noted: in KEL:-12: A1763G, His548Arg; in KEL:-18: C508T and G509A, Arg130Trp and Arg130Gln; in KEL:-19: G1595A, Arg492Gln; in KEL:-22: C1085T, Ala322Val; and in TOU-:G1337A, Arg406Gln. A son of one of the two people with the TOU-phenotype was heterozygous, and he also had the G1337A mutation. CONCLUSION: The high-incidence antigens of the Kell blood group system are characterized by point mutations leading to amino acid substitutions. The KEL:-18 phenotype could be due to either of two point mutations in the same codon replacing arginine with tryptophan or glutamine. TOU was confirmed as a Kell system antigen, and the inheritance of the mutation was demonstrated.
BACKGROUND: In a Moroccan family, the partial D phenotype DBT is defined by an RHD-CE-D gene in which exons 5 to 7 of RHD were replaced by those of RHCE. In this study, the molecular basis and inheritance of DBT in a Japanese family are described. STUDY DESIGN AND METHODS: A Japanese proposita exhibiting the DBT phenotype was analyzed by serologic methods and molecular techniques. The RH transcripts of the proposita were sequenced and compared with those of normal donors. The inheritance and structure of the RH genes in the family were determined by Southern blot analysis and exon-specific polymerase chain reaction. RESULTS: The proposita typed weak D and C+c+E+e+Rh:32. Family data indicated a cotransmission of Rh32 with DBT and a linkage of C and e with DBT. Southern blot testing of the proposita's genomic DNA indicated a partial and a total absence of RHD on the respective homologous chromosomes. Sequencing of her cDNA showed expression of Ce, cE, and RHD-CE-D transcripts but not D. The RHD-CE-D hybrid was characterized by a conversion of five RHD exons into RHCE exons (exons 5-9). The 5' and 3' breakpoints in the fusion gene were localized to the intron 4/exon 5 region and intron 9. CONCLUSION: The new RHD-CE-D gene defines a separate genetic origin of DBT in the Japanese family. The proximal sequence encoded by RHD exon 4 and RHCE exon 5, together with the distal RHCE sequence, may involve the cotransmission of Rh32 and DBT which behave as codominant and recessive characters, respectively.
It is unclear whether smoking is a risk factor for epithelial ovarian cancer, although some studies have suggested that it may be associated with an increased risk of mucinous tumors. This study investigated the effect of smoking and environmental tobacco smoke (ETS) on ovarian cancer risk among 434 women with primary epithelial ovarian, peritoneal, or fallopian cancers and 868 age- and region-matched hospital controls with nonneoplastic conditions. All participants completed a comprehensive epidemiologic questionnaire. Results indicate that decreased risk of ovarian cancer was associated with being a nonsmoker exposed to ETS (adjusted odds ratio [aOR] 0.68, 95% confidence interval [CI] 0.46-0.99), a former smoker (aOR 0.76, 95% CI 0.53-1.10), or a current smoker (aOR 0.53, 95% CI 0.32-0.88). A similar protective effect was noted for smokers with moderate or high exposure based on smoking intensity, duration, and cumulative exposure, as well as for never smokers exposed to ETS. Results did not differ substantially by histologic subtype. Although prevailing theories of ovarian cancer etiology implicate incessant ovulation, characteristics of the study population suggest that anovulation was not the protective mechanism in this study. Immunosuppression by nicotine or upregulation of enzymes that metabolize carcinogens may be responsible for the effects observed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The objective of this cross-sectional study was to determine whether plasma selenium concentration predicts the prevalence of adenomatous polyps of the colon and rectum. The source population for the study was 101 patients undergoing sequential colonoscopies at the Veterans Affairs Medical Center, Tucson, AZ. The study population was then limited to the 48 patients (all male) undergoing their initial colonoscopy who did not have a diagnosis of colorectal cancer. For each of these patients, a prediagnostic fasting plasma selenium concentration was determined. The data from this study suggest that fasting plasma selenium concentrations may be an important risk factor for colorectal adenomas. Patients with fasting plasma selenium concentrations below the median (< 128 mcg/liter) were significantly more likely to have one or more adenomatous polyps (prevalence odds ratio 4.2) and more adenomatous polyps (3.5 times) per patient. There was also a suggestion of a more proximal distribution of adenomatous polyps in the patients with a lower level of selenium. These associations were not confounded by age or smoking. The results of this study are consistent with the experimental animal studies, geographic mortality studies, and prospective cohort studies of selenium and colorectal cancer.