Troponin T elevation and prognosis after multivessel compared with single-vessel elective percutaneous coronary intervention

Background. Although techniques for percutaneous coronary intervention (PCI) have improved, patients with PCI of more vessels may still have an increased risk. We performed a prospective observational study evaluating the differences between multivessel and single-vessel procedures according to postprocedural troponin T (TnT) elevation and events during follow-up. Methods. The study included 713 patients without elevated TnT (<0.05 ng/ml) before PCI. Primary endpoint was the combined endpoint of death, myocardial infarction, stroke, repeat coronary angiography and readmission for anginal symptoms during the mean follow-up of 10.9 months. Results. TnT after PCI was elevated in 150 patients (21%) and was significantly associated with an increased incidence of the primary endpoint (RR 1.55, 95% CI 1.01 to 2.38). PCI of more than one vessel was performed in 146 patients (20%). These patients more often had increased TnT levels after the procedure (31.5 vs. 18.3%, p=0.001) and an increased incidence of the primary endpoint during follow-up (28 vs. 19%, p=0.01). After multivariable analysis, multivessel PCI was a statistically significant predictor of postprocedural TnT increase (OR 1.90, 95% CI 1.17 to 3.06). Multivessel PCI was also associated with an increased risk of the primary endpoint (OR 1.73, 95% CI 1.18 to 2.52), but after adjusting for multivessel disease this association was not statistically significant (OR 1.42, 95% CI 0.92 to 2.19). Conclusion. Elective PCI of more vessels in one session is, in comparison with single-vessel PCI, more often associated with postprocedural troponin T rise and a (nonsignificantly) higher incidence of cardiac events during follow-up. Whether staged PCI is associated with less morbidity has to be assessed. (Neth Heart J 2007;15:178-83.)     

Structure and function of the enhancer 3'' to the human A gamma globin gene.

An enhancer is located immediately 3' to the A gamma globin gene. We have used DNase I footprinting to map the sites of interaction of nuclear proteins with the DNA sequences of this enhancer. Eight footprints were discovered, distributed over 600 base pairs of DNA. Three of these contain a consensus binding site for the erythroid specific factor GATA-I. Each of these GATA-1 sites had an enhancer activity when inserted into a reporter plasmid and tested in human erythroleukemia cells. Other footprints within the enhancer contained consensus binding sequences for the ubiquitous, positive regulatory proteins AP2 and CBP-1. An Sp1-like recognition sequence was also identified. Synthetic oligonucleotides encompassing two of the footprints generated a slowly migrating complex in gel mobility shift assays. The same complex forms on a fragment of the human gamma globin gene promoter extending from -260 to -200. The DNaseI footprint of this protein complex with the enhancer overlapped a sequence, AGGAGGA, found within the binding site for a protein that interacts with the chicken beta globin promoter and enhancer, termed the stage selector element. We propose that this complex of proteins may be involved in the human gamma globin promoter-enhancer interaction.     

Trifolitoxin Production Increases Nodulation Competitiveness of Rhizobium etli CE3 under Agricultural Conditions

A major barrier to the use of nitrogen-fixing inoculum strains for the enhancement of legume productivity is the inability of commercially available strains to compete with indigenous rhizobia for nodule formation. Despite extensive research on nodulation competitiveness, there are no examples of field efficacy studies of strains that have been genetically improved for nodulation competitiveness. We have shown previously that production of the peptide antibiotic trifolitoxin (TFX) by Rhizobium etli results in significantly increased nodule occupancy values in nonsterile soil in growth chamber experiments (E. A. Robleto, A. J. Scupham, and E. W. Triplett, Mol. Plant-Microbe Interact. 10:228–233, 1997). To determine whether TFX production by Rhizobium etli increases nodulation competitiveness in field-grown plants, seeds of Phaseolus vulgaris were inoculated with mixtures of Rhizobium etli strains at different ratios. The three nearly isogenic inoculum strains used included TFX-producing and non-TFX-producing strains, as well as a TFX-sensitive reference strain. Data was obtained over 2 years for nodule occupancy and over 3 years for assessment of the effect of the TFX production phenotype on grain yield. In comparable mixtures in which the test strain accounted for between 5 and 50% of the inoculum, the TFX-producing strain exhibited at least 20% greater nodule occupancy than the non-TFX-producing strain in both years. The TFX production phenotype had no effect on grain yield over 3 years; the average yields reached 2,400 kg/ha. These results show that addition of the TFX production phenotype significantly increases nodule occupancy under field conditions without adverse effects on grain yield. As we used common inoculation methods in this work, there are no practical barriers to the commercial adoption of the TFX system for agriculture.     

Impact of scoring error and reproducibility RAPD data on RAPD based estimates of genetic distance

RAPD band reproducibility and scoring error were evaluated for RAPDs generated by 50 RAPD primers among ten snap bean (Phaseolus vulgaris L.) genotypes. Genetic distances based on different sets of RAPD bands were compared to evaluate the impact of scoring error, reproducibility, and differences in relative amplification strength on the reproducibility of RAPD based genetic distance estimates. The measured RAPD data scoring error was 2%. Reproducibility, expressed as the percentage of RAPD bands scored that are also scored in replicate data, was 76%. The results indicate that the probability of a scored RAPD band being scored in replicate data is strongly dependent on the uniformity of amplification conditions between experiments, as well as the relative amplification strength of the RAPD band. Significant improvement in the reproducibility of scored bands and some reduction in scoring error was achieved by reducing differences in reaction conditions between replicates. Observed primer variability for the reproducibility of scored RAPDs may also facilitate the selection of primers, resulting in dramatic improvements in the reproducibility of RAPD data used in germplasm studies. Variance of genetic distances across replicates due to sampling error was found to be more than six times greater than that due to scoring error for a set of 192 RAPD bands. Genetic distance matrices computed from the RAPD bands scored in replicated data and RAPD bands that failed to be scored in replicated data were not significantly different. Differences in the ethidium bromide staining intensity of RAPD bands were not associated with significant differences in resulting genetic distance matrices. The assumption of sampling error as the only source of error was sufficient to account for the observed variation in genetic distance estimates across independent sets of RAPD bands.     

Causes of the eelgrass wasting disease: Van der Werff's changing theories

The 1930's wasting disease among the North Atlantic population of eelgrass,Zostera marina, is still an ecological and historical enigma, despite several attractive theories. Van der Werff investigated the die-back of eelgrass in the thirties in the Dutch Wadden Sea, and he considered the micro-organismLabyrinthula as the possible cause of the disease. In 1980, Grevelingen lagoon, harbouring an extensive population ofZostera marina, experienced a major decline of the area covered by the submerged macrophyte. Speculations about the cause of this dramatic decline induced us to think that the wasting disease had struck again. Van der Werff investigated the Grevelingen population and found bothLabyrinthula and a Chaetophoracean endophytic alga to be presumably responsible for the decline. During the quest for the ultimate cause of the wasting disease the question remains whether both micro-organisms are the cause of the disease or simply an effect of decomposition processes triggered by other factors.     

Localization of the human alpha-globin structural gene to chromosome 16 in somatic cell hybrids by molecular hybridization assay

We have used 16 human × mouse somatic cell hybrids containing a variable number of human chromosomes to demonstrate that the human α-globin gene is on chromosome 16. Globin gene sequences were detected by annealing purified human α-globin complementary DNA to DNA extracted from hybrid cells. Human and mouse chromosomes were distinguished by Hoechst fluorescent centromeric banding, and the individual human chromosomes were identified in the same spreads by Giemsa trypsin banding. Isozyme markers for 17 different human chromosomes were also tested in the 16 clones which have been characterized. The absence of chromosomal translocation in all hybrid clones strongly positive for the α-globin gene was established by differential staining of mouse and human chromosomes with Giemsa 11 staining. The presence of human chromosomes in hybrid cell clones which were devoid of human α-globin genes served to exclude all human chromosomes except 6, 9, 14 and 16. Among the clones negative for human α-globin sequences, one contained chromosome 2 (JFA 14a 5), three contained chromosome 4 (AHA 16E, AHA 3D and WAV R4D) and two contained chromosome 5 (AHA 16E and JFA14a 13 5) in >10% of metaphase spreads. These data excluded human chromosomes 2, 4 and 5 which had been suggested by other investigators to contain human globin genes. Only chromosome 16 was present in each one of the three hybrid cell clones found to be strongly positive for the human α-globin gene. Two clones (WAIV A and WAV) positive for the human α-globin gene and chromosome 16 were counter-selected in medium which kills cells retaining chromosome 16. In each case, the resulting hybrid populations lacked both human chromosome 16 and the α-globin gene. These studies establish the localization of the human α-globin gene to chromosome 16 and represent the first assignment of a nonexpressed unique gene by direct detection of its DNA sequences in somatic cell hybrids.