Regarding clinical factors, nicotine pack years, serum creatinine

Regarding clinical factors, nicotine pack years, serum creatinine and AAA expansion rate were found to be much higher for male patients.

Conclusion: These findings may help to explain higher risks for AAA growth in males and the ruptures of smaller-sized AAAs in females. (C) 2013 European Society for Vascular Surgery. Published by Elsevier

Ltd. All rights reserved.”
“Background: With a US Food and Drug Administration-labeled indication to treat attention-deficit/hyperactivity disorder (ADHD), the nonstimulant guanfacine has become the preferred alpha(2)-agonist for ADHD treatment. However, significant interindividual variability has been observed in response to guanfacine. Consequently, hypotheses SB202190 inhibitor of a contributing interaction with the ubiquitously expressed drug transporter, P-glycoprotein (P-gp), have arisen. We performed an in vitro study to determine if guanfacine is indeed a substrate of click here P-gp.

Methods: Intracellular

accumulation of guanfacine was compared between P-gp expressing LLC-PK1/MDR1 cells and P-gp-negative LLC-PK1 cells to evaluate the potential interaction between P-gp and guanfacine. Cellular retention of guanfacine was analyzed using a high-performance liquid chromatographic-ultraviolet method. Rhodamine6G, a known P-gp substrate, was included in the study as a positive control.

Results: At guanfacine concentrations of 50 mu M and 5 mu M, intracellular accumulation of guanfacine in LLC-PK1/MDR1 cells was, 35.9% +/- 4.8% and 49.0% +/- 28.3% respectively, of that in LLC-PK1 cells. In comparison, the concentration of rhodamine6G, the positive P-gp substrate, in LLC-PK1/MDR1 cells was only 5% of that in LLC-PK1 cells.

Conclusion: AZD7762 The results of the intracellular accumulation study suggest that guanfacine is, at best, a weak P-gp substrate. Therefore, it is unlikely that P-gp, or any genetic variants thereof, are a determining factor in the interindividual

variability of response observed with guanfacine therapy.”
“Objective: To document the treatment of all patients with infected aortic grafts at Christchurch Hospital between 1999 and 2010, focussing on the mortality and morbidity of those treated without graft explantation.

Methods: Cases of infected aortic grafts were reviewed. Cases required a compatible clinical syndrome, CT imaging and tissue/blood culture results.

Results: Eighteen patients were identified. Organisms isolated at diagnosis from blood or graft site were Staphylococcus aureus 6 (M RSA 1), beta haemolytic streptococci 2, enteric organisms 9. There was no isolate from 2. One case had graft explantation and brief antimicrobial therapy. Seventeen patients had the graft retained. Of these, 14 received intravenous antimicrobial therapy for 6 weeks and 14 lifelong oral therapy. None died during their initial admission or within 30 days.

Comments are closed.