Abstract Introduction Many factors influence age of presentation with and survival following ST-segment myocardial infarction (STEMI). These include age, mode of, and time-delay to emergency treatment, diabetes and smoking. We sought to assess whether overall social deprivation status is associated with age of presentation and mortality following STEMI patients treated with primary PCI. Methods All patients treated emergently for STEMI in a large Northern Irish tertiary hospital from 2013 – 2017 were reviewed. Social deprivation is determined as a composite score relating to income, crime etc, and assigned to small geographical regions by the Northern Ireland Statistics and Research Agency. Deprivation score was assigned to patients based on their postcode. The database was ranked by social deprivation score and divided in to quintiles. The most (Grp 1) and least (Grp 5) deprived quintiles were compared. Mortality was determined from a national electronic health record. Results 1,192 patients were included in the analysis. Mean follow up was 52.5 months (SD 15.6), minimum follow up was 35.6 months. There was no difference in gender: 70.1% male in Grp 1 vs 75.2% male in Grp 5 (p=0.68); no difference in ECG to balloon time: mean 89.9mins (95% CI 84.9–94.9) Grp 1 vs 90.5mins (95% CI 86.2–94.9) Grp 5 (p=0.86). The more deprived group was younger: mean age 60.6 (95% CI 59.5–61.6) vs 65.2 (95% CI 64.2–66.3) (p<0.000). Crude survival measured by Log-rank test was the same between the groups (p=0.52). Following Cox-regression adjustment for age, survival was longer in the least deprived group (p=0.042). Conclusion Social deprivation is associated with both a younger age of presentation with, and a higher mortality following STEMI. This is important variable is often overlooked in medical literature and should be further studied. Funding Acknowledgement Type of funding sources: None.
Previous studies of the human TCR-delta gene identified a single commonly used V delta segment, denoted V delta 1. To better understand the extent of the human TCR-delta V gene repertoire, TCR-delta transcripts and gene rearrangements were examined in a new panel of cloned human TCR-gamma/delta lymphocytes. Through this analysis we identified and determined the structures of two new V delta segments, denoted V delta 2 and V delta 3. These V delta segments are different from previously characterized V alpha segments, supporting the notion that the human V delta and V alpha repertoires are distinct. Examination of V gamma gene segment usage in these cells reveals that the V delta 2 gene segment is used in conjunction with the V gamma 2 gene segment. Blot hybridization indicates that the V delta 2 gene segment lies between V delta 1 and D delta-J delta-C delta, and within 100 kb of the latter. Analysis of genomic clones indicates that the V delta 3 gene segment lies in an inverted orientation, approximately 2 kb 3' of C delta. This implies that rearrangement of V delta 3 to D delta-J delta-C delta occurs by inversion. Together with previous mapping studies, these results indicate that human V delta segments are dispersed, rather than clustered, within the TCR-alpha/delta locus. The analysis of rearrangements in polyclonal thymocyte DNA suggests that there may be a limited number of additional V delta gene segments yet to be characterized.
Two clusters of overlapping cosmid clones comprising about 100 kilobases (kb) at the human T-cell antigen-receptor alpha/delta locus were isolated from a genomic library. The structure of the germ-line V delta 1 variable gene segment was determined. V delta 1 is located 8.5 kb downstream of the V alpha 13.1 gene segment, and both V segments are arranged in the same transcriptional orientation. The V alpha 17.1 segment is located between V delta 1 and the D delta, J delta, C delta region (containing the diversity, joining, and constant gene segments). Thus, V delta and V alpha segments are interspersed along the chromosome. The germ-line organization of the D delta 2, J delta 1, and J delta 2 segments was determined. Linkage of C delta to the J alpha region was established by identification of J alpha segments within 20 kb downstream of C delta. The organization of the locus was also analyzed by field-inversion gel electrophoresis. The unrearranged V delta 1 and D delta, J delta, C delta regions are quite distant from each other, apparently separated by a minimum of 175-180 kb.
The T-cell receptor (TCR) gamma gene product occurs in association with T3 (CD3) polypeptides on the surface of human T lymphocytes. TCR gamma lymphocytes express arrays of T3 polypeptides distinct from those typically observed on TCR alpha beta lymphocytes. This report demonstrates that identical T3 gamma, delta, and epsilon polypeptides are synthesized by TCR gamma lymphocytes and TCR alpha beta lymphocytes. However, the processing of T3 delta oligosaccharides is distinct in the two cell types. This observation may suggest distinct quaternary structures of these receptor complexes. Despite these structural differences, the T3 molecule on TCR gamma lymphocytes is functional. It is associated with and comodulates with TCR gamma and it serves as a substrate for protein kinase C-mediated phosphorylation. Anti-T3 monoclonal antibodies induce a rapid increase in cytoplasmic free calcium, indicating that the receptor complex is involved in signal transduction and triggering of TCR gamma lymphocytes.