Homogeneous ethylene-polymerization catalysts based on alkyl cations of the rare-earth metals: are dicationic mono(alkyl) complexes the active species?
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Biomedical subjects
Publications and source records attributed to Jun Okuda.
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Styrene is polymerized isospecifically by group 4 metal complexes that contain a C2-symmetrically coordinated 1,4-dithiabutane-linked bis(phenolato) ligand activated by methylaluminoxane.
In order to investigate why the thermostable direct hemolysin (TDH) and the TDH-related hemolysin (TRH) of Vibrio parahaemolyticus are produced at low levels from urease-positive strains, the effect of the functional urease gene cluster of V. parahaemolyticus on the expression of the tdh and trh genes was examined. Transcriptional lacZ fusions with the tdh1, tdh2, trh1 and trh2 genes representing variants of the tdh and trh genes were integrated into the chromosome of an Escherichia coli strain and a urease-negative V. parahaemolyticus strain. The plasmid-borne urease gene cluster introduced and expressed in these constructs did not affect expression of any of the fusion genes. The amount of TDH produced from a Kanagawa phenomenon-positive V. parahaemolyticus did not change by introduction of the urease gene cluster either. It was concluded therefore that the urease gene cluster is not involved in the regulation of tdh and trh expression.
Although pre-interventional thrombolysis has recently been shown to restore early patency and preserve left ventricular function in patients with acute myocardial infarction, the significance of Thrombolysis in Myocardial Infarction (TIMI) grade flow early after thrombolysis remains unclear. Patients were classified into 3 groups according to TIMI grade flow 45 min after thrombolysis; 38 patients with TIMI grade 0 or 1 flow (group T0) and 46 with TIMI grade 2 flow (group T2) additionally received immediate percutaneous coronary intervention (PCI) and 50 patients with TIMI grade 3 flow (group T3) were treated conservatively after thrombolysis. Although the door-to-balloon times did not differ in groups T0 and T2, group T2 had lower peak creatine kinase, a higher rate of complete (>/=70%) ST resolution and better regional wall motion at discharge as compared with group T0, similar to group T3 (group T2, group T3 vs group T0; 2,857+/-1,756, 2,314+/-1,948 vs 3,779 +/-2,214 mU/ml; 57, 72 vs 34%; -1.5+/-1.6, -1.2+/-1.6 vs -2.2+/-1.6; all p<0.01, respectively). These results suggest TIMI grade 2 flow at 45 min after thrombolysis followed by immediate PCI, as well as TIMI grade 3 flow, is associated with greater myocardial salvage than TIMI grade 0 or 1 flow.
In patients with recanalized acute myocardial infarction (AMI), the relation between the timing of preinfarction angina (PA) and microvascular reperfusion remains unclear. A total of 186 patients (114 with anterior and 72 with inferior AMI) who had total occlusion and TIMI 3 recanalization < or = 6 hours from the onset of AMI were divided into 4 groups according to the time interval between the last episode of PA and the onset of AMI: < or = 2 hours (group A, n = 52); 2 to 48 hours (group B, n = 43), > or = 48 hours (group C, n = 33), and no PA (group D, n = 58). The angiographic myocardial blush grade, a marker of microvascular reperfusion, was retrospectively assessed immediately after recanalization. There were no differences in baseline characteristics, except for sex among the 4 groups. Myocardial blush grade 3 was more frequent (42% vs 21%, 9%, and 14%) and peak creatine kinase was lower (2659 vs 3455, 4422, and 4622 mU/mL) in group A than in groups B, C, and D (all P < 0.05). Multivariate analysis showed that PA occurring < or = 2 hours before AMI (OR 3.88, P < 0.05), a smaller summed ST-segment elevation before recanalization (OR 0.84, P < 0.01), earlier time to recanalization (OR 0.52, P < 0.05), and interior AMI (OR 4.87, P < 0.05) were independently associated with adequate microvascular reperfusion. We conclude that PA < or = 2 hours before the onset of AMI is independently associated with adequate microvascular reperfusion after recanalization in patients with AMI.
Reaction of rare earth metal-alkyl complexes [Ln(CH2SiMe3)3(THF)2](Ln = Y, Lu) with B(C6X5)3(X = H, F) in the presence of crown ethers gives crystallographically characterized ion pairs [Ln(CH2SiMe3)2(CE)(THF)n]+[B(CH2SiMe3)(C6X5)3]-(CE = [12]-crown-4, n = 1; CE = [15]-crown-5 and [18]-crown-6, n = 0).
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We have cloned the DNA gyrase and topoisomerase IV genes of Enterococcus faecalis to examine the actions of quinolones against E. faecalis genetically and enzymatically. We first generated levofloxacin-resistant mutants of E. faecalis by stepwise selection with increasing drug concentrations and analyzed the quinolone resistance-determining regions of gyrA and parC from the resistant mutants. Isogenic mutants with low-level resistance contained a mutation in gyrA, whereas those with higher levels of resistance had mutations in both gyrA and parC. These results suggested that gyrA is the primary target for levofloxacin in E. faecalis. We then purified the recombinant DNA gyrase and topoisomerase IV enzymes of E. faecalis and measured the in vitro inhibitory activities of quinolones against these enzymes. The 50% inhibitory concentrations (IC(50)s) of levofloxacin, ciprofloxacin, sparfloxacin, tosufloxacin, and gatifloxacin for DNA gyrase were found to be higher than those for topoisomerase IV. In conflict with the genetic data, these results indicated that topoisomerase IV would be the primary target for quinolones in E. faecalis. Among the quinolones tested, the IC(50) of sitafloxacin (DU-6859a), which shows the greatest potency against enterococci, for DNA gyrase was almost equal to that for topoisomerase IV; its IC(50)s were the lowest among those of all the quinolones tested. These results indicated that other factors can modulate the effect of target affinity to determine the bacterial killing pathway, but the highest inhibitory actions against both enzymes correlated with good antienterococcal activities.