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Drugs Exp. Clin. Res. 18: 299302. 3. Dalhoff, A., U. Petersen, and R. Endermann. 1996. In vitro activity of BAY 12-8039, a new 8-methoxyquinolone. Chemotherapy 42: 410425. 4. Derendorf, H. 1989. Pharmacokinetic evaluation of beta-lactam antibiotics. J. Antimicrob. Chemother. 24: 407413. 5. Eichler, H. G., and M. Muller. 1998. Drug distribution--the forgotten relative of clinical pharmacokinetics. Clin. Pharmacokinet. 34: 9599. 6. Elmquist, W. F., and R. J. Sawchuk. 1997. Application of microdialysis in pharmacokinetic studies. Pharm. Res. 14: 267288. 7. Goldstein, E. J., D. M. Citron, M. Hudspeth, S. H. Gerardo, and C. V. Merriam. 1997. In vitro activity of Bay 12-8039, a new 8-methoxyquinolone, compared to the activities of 11 other oral antimicrobial agents against 390 aerobic and anaerobic bacteria isolated from human and animal bite wound skin and soft tissue infections in humans. Antimicrob. Agents Chemother. 41: 15521557. 8. Hyatt, J. M., P. S. McKinnon, G. S. Zimmer, and J. J. Schentag. 1995. The importance of pharmacokinetic pharmacodynamic surrogate markers to outcome. Clin. Pharmacokinet. 28: 143160. 9. Klugman, K. P., and T. Capper. 1997. Concentration-dependent killing of antibiotic-resistant pneumococci by the methoxyquinolone moxifloxacin. J. Antimicrob. Chemother. 40: 797802. 10. Kunin, C. M., W. A. Craig, M. Kornguth, and R. Monson. 1973. Influence of binding on the pharmacologic activity of antibiotics. Ann. N.Y. Acad. Sci. 226: 214224. 11. Lonnroth, P., P. A. Jansson, and U. Smith. 1987. A microdialysis method al lowing characterization of interstitial water space in humans. Am. J. Physiol. 16: E228E231. 12. Merrikin, D. J., J. Briant, and G. N. Rolison. 1983. Effect of protein binding on antibiotic activity in vivo. J. Antimicrob. Chemother. 11: 233238. 13. Moller, J. G., H. Sta, R. Heinig, and G. Blaschke. 1998. Capillary electro phoresis with laser induced fluorescence: a routine method to determine moxifloxacin in human body fluids in very small sample volumes. J. Chromatogr. 716: 325334. 14. Muller, M., O. Haag, T. Burgdorff, A. Georgopoulos, W. Weninger, B. Jansen, G. Stanek, H. Pehamberger, E. Agneter, and H. G. Eichler. 1996. Characterization of peripheral compartment kinetics of antibiotics by in vivo microdialysis in humans. Antimicrob. Agents Chemother. 40: 27032709. 15. Muller, M., M. Brunner, R. Schmid, E. M. Putz, A. Schmiedberger, I. Wallner, and H. G. Eichler. 1998. Comparison of three different experimental methods for the assessment of peripheral compartment pharmacokinetics in humans. Life Sci. 62: PL227PL234. 16. Ryan, D. M. 1993. Pharmacokinetics of antibiotics in natural and experimental superficial compartments in animals and humans. J. Antimicrob. Chemother. 31 Suppl. D ; : 116. 17. Stahle, L., P. Arner, and U. Ungerstedt. 1991. Drug distribution studies with microdialysis. III: Extracellular concentration of caffeine in adipose tissue in man. Life Sci. 49: 18531858. 18. Stass, H., and A. Dalhoff. 1997. Determination of BAY 12-8039, a new 8-methoxyquinolone, in human body fluids by high-performance liquid chromatography with fluorescence detection using on-column focusing. J. Chromatogr. B 702: 163174. 19. Stass, H., A. Dalhoff, D. Kubitza, and U. Schuhly. 1998. Pharmacokinetics, safety, and tolerability of ascending single doses of moxifloxacin, a new 8-methoxy quinolone, administered to healthy subjects. Antimicrob. Agents Chemother. 42: 20602065. 20. Visalli, M. A., M. R. Jacobs, and P. C. Appelbaum. 1997. Antipneumococcal activity of BAY 12-8039, a new quinolone, compared with activities of three other quinolones and four oral beta-lactams. Antimicrob. Agents Chemother. 41: 27862789. 21. Woodcock, J. M., J. M. Andrews, F. J. Boswell, N. P. Brenwald, and R. Wise. 1997. In vitro activity of BAY 12-8039, a new fluoroquinolone. Antimicrob. Agents Chemother. 41: 101106.
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FIG. 4. Blood serum concentration-time curves after a single intravenous dose of M-DCMG A ; and moxifloxacin B ; . The results of four independent experiments are presented means standard deviations.
DANA DABIRI, University of Washington , GAMAL KHALIL, JAMES CALLIS, YOUNAN XIA, MARTIN GOUTERMAN, BRENDEN CARLSON, University of Washington -- We have recently synthesized pressure sensitive microbeads PSBeads ; consisting of a platinum octaethylporphryin luminophore in a polystyrene matrix, and a novel osmium-based luminophore in a silicon dioxide matrix. Since these PSBeads are to provide simultaneous measurements of pressure and velocity in turbulent and or high speed flows, their response times must be sufficiently fast. A shock tube was constructed to provide a test facility where the response time of the microspheres could be reliably measured. Initial studies showed response times are on the order of 20 s when exposed to shock strengths of 1.07 M P 10-12 kPa ; . We further use this facility to obtain preliminary simultaneous pressure and velocity measurements before and after a shock wave.
Can still compensate for the urinary or colonic salt losses Hummler E, unpublished data ; . Because circadian changes in sodium handling in the distal nephron can be monitored by variations in amiloride-sensitive rectal PD PDamil ; 33 ; , we measured in vivo the rectal PDamil in these transgenic rescue mice. We found that the lowered ENaC-mediated sodium transport reflects the diminished ENaC activity in the kidney.
1. Alvirez-Freites, E. J., J. A. Carter, and M. H. Cynamon. 2002. In vitro and in vivo activities of gatifloxacin against Mycobacterium tuberculosis. Antimicrob. Agents Chemother. 46: 10221025. 2. Cambau, E., W. Sougakoff, M. Besson, C. Truffot-Pernot, J. Grosset, and V. Jarlier. 1994. Selection of a gyrA mutant of Mycobacterium tuberculosis resistant to fluoroquinolones during treatment with ofloxacin. J. Infect. Dis. 170: 479483. 3. Crofton, J., P. Chaulet, and D. Maher. 1997. Guidelines for the management of drug-resistant tuberculosis. Report WHO TB 96.210. World Health Organization, Geneva, Switzerland. 4. Espinal, M. A., A. Laszlo, L. Simonsen, F. Boulahbal, S. J. Kim, A. Reniero, S. Hoffner, H. L. Rieder, N. Binkin, C. Dye, R. Williams, and M. C. Raviglione. 2001. Global trends in resistance to antituberculosis drugs. N. Engl. J. Med. 344: 12941303. 5. Grosset, J., and B. Ji. 1998. Experimental chemotherapy of mycobacterial diseases, p. 5197. In P. R. Gandharam and P. A. Jenkins ed. ; , Mycobacteria, vol. II. Chemotherapy. Chapman & Hall, New York, N.Y. 6. Guillemin, I., V. Jarlier, and E. Cambau. 1998. Correlation between quinolone susceptibility patterns and sequences in the A and B subunits of DNA gyrase in mycobacteria. Antimicrob. Agents Chemother. 42: 20842088. 7. Hu, Y., A. R. M. Coates, and D. A. Mitchison. 2003. Sterilizing activities of fluoroquinolones against rifampin-tolerant populations of Mycobacterium tuberculosis. Antimicrob. Agents Chemother. 47: 653657. 8. Ji, B., N. Lounis, C. Truffot-Pernot, and J. Grosset. 1995. In vitro and in vivo activities of levofloxacin against Mycobacterium tuberculosis. Antimicrob. Agents Chemother. 39: 13411344. 9. Ji, B., N. Lounis, C. Maslo, C. Truffot-Pernot, P. Bonnafous, and J. Grosset. 1998. In vitro and in vivo activities of moxifloxacin and clinafloxacin against Mycobacterium tuberculosis. Antimicrob. Agents Chemother. 42: 20662069. 10. Lecoeur, H. F., C. Truffot-Pernot, and J. H. Grosset. 1989. Experimental.
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Double-strand oligonucleotide containing an HIF-1 consensus binding site 40 ng ; was labeled with Klenow Enzyme Boehringer ; for 30 minutes at 37C with the use of 25 Ci -32P]dATP. Nuclear extracts19 were incubated on ice with probe alone HIF-1 ; , with double-strand competitor oligonucleotides HIF-1 or mutated HIF-1, 100-fold nuclear excess ; , with an affinity-purified antiarylic hydro and mrv.
Cecilia Carnrot, the author of this thesis, received her graduate education at the Dept. of Molecular Biosciences, Div. of Veterinary Medical Biochemistry, SLU, Uppsala. Her undergraduate degree is from LiU, Linkping.
7-OMEN B16 + ADR Table 1 Drug uptake and survival of exponentially growing and plateau-phase CHO cells exposed to 7-OMEN The exponentially growing and plateau-phase cells consisted of 7 x 106 and 4 x 107 cells, respectively, per T75 flask in 50 ml medium. The plateau-phase cells were allowed to grow for 36 hr past the time when cells became confluent. Survival was determined by cloning. Exponentially growing and plateau-phase cells had cloning efficiencies of about 70 to 87%. 7cellsfig 106 OMEN cells0.53 fig ml ; 1.0 growing survival0.35 of 0a cellsfig 106 cells0.27 survival67.7 of 4.6 3.6 and multivitamin.
Moxifloxacin compared with a number of antibiotics regarded as standard therapy Baseline health status established to allow measuring the return to baseline A double-blind study including novel parameters such as quality of life Concomitant medication taken into account e.g. corticosteroids Long-term follow-up, including utilisation of healthcare resources.
Objective: To investigate intraocular penetration of moxifloxacin hydrochloride after oral administration. Methods: Prospective study of 15 patients scheduled for and murine.
TCM has been widely used as combined therapies in treating HCC in China. The novelty and innovation of the research consist in researching the mechanism of treatment of FJD to the hepatocellular carcinoma with mole-biological method. Mechanisms of FJD healing HCC may partially be explained by enhancing the expression of PTEN in liver.
Catherine Airth Acting Director Office of Canada's Drug Strategy Health Canada 3502D MacDonald Building 123 Slater Street Ottawa, ON K1A 0K9 Tel.: 613 ; 957-8337 Fax: 613 ; 952-0601 cathy airth hcsc.gc and muse
Two of the patients had stable anticoagulation regimens and then experienced persistent elevations in their inrs shortly after therapy with moxifloxacin was started.
The hospital executive is a 52-year-old president and CEO of a community hospital in Pennsylvania, about one hour from the author's offices. This individual noted onset of severe lumbar pain while lifting a heavy object. Evaluation at his hospital showed herniated disk posteriorly at L3-4. He underwent nine months of physical therapy with some slight improvement in his pain but no improvement in his disability. The patient was subsequently evaluated at our institution, and DRS with IDD Therapy administered. Despite the 20 treatments that were advised, the patient felt well enough after 11 treatments that he did not wish further therapy. Upon discharge--after six weeks of IDD Therapy consisting of only 11 of the 20 recommended treatments--he had much improved range of motion, decreased pain, and improved abilities to perform activities of daily living and activities at work. An MRI performed at the same time showed substantial improve and mycostatin.
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Janet K. Allen and John B. Whitfield 1346 Use ofImmobilized Enzymes for Glucose Analysis in a Small Laboratory Dorothy F. Wease, Yvonne J. Anderson, and Donald M. Ducharme 1347 HB5Ag, AntI-HBs, Antl-HBc, and AntI-HAV in Joyce Compton, Dean Bonderman, Gary Proksch, and John Griep 1349 Free Thyroxine Assay and Thyroxine Index Compared Lawrence M. Demers 1350 Analysis for Urea in Urine with the Beckman BUN Analyzer 2 Mark D. S. Shepherd and Callum G. Fraser 1350 A Correction to the Fluorescencelmmunoassay Review Irwin Wieder.
To assess whether a new antimicrobial drug is likely to be of value in the therapy and or prophylaxis of bacterial GI infections, it is important to determine the tissue concentrations of the agent, since drug concentrations in plasma do not reliably predict clinical efficacy.5 The objective of the present study, therefore, was to determine the tissue concentrations of moxifloxacin in tissues of the alimentary tract and to compare these concentrations with the serum concentrations in order to evaluate whether this new quinolone accumulates in GI-tract tissues. The highest tissue concentrations of moxifloxacin were found in the mucosa of the stomach 10.9 5.1 mg kg these were up to 9.7 times higher than the serum concentrations, indicating accumulation of the drug in these tissues. The lowest mucosal tissue concentrations were observed in the small bowel 5.4 0.5 mg kg ; , which nonetheless exceeded the MIC90 for most anaerobic bacteria 2 mg L ; .6 Serum concentrations of moxifloxacin determined 17 h after the first drug administration were within the range of those found by Stass & Kubitza, 7 whereas moxifloxacin serum concentrations measured 5 h after the second administration were somewhat lower than expected, most likely due to serum dilution effects, i.e. iv fluid application and blood loss during surgery and mysoline.
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A 400 mg single dose study was conducted in 18 young males and females. The comparison of moxifloxacin pharmacokinetics in this study 9 young females and 9 young males ; showed no differences in AUC or Cmax due to gender. Dosage adjustments based on gender are not necessary. Race Steady-state moxifloxacin pharmacokinetics in male Japanese subjects were similar to those determined in Caucasians, with a mean Cmax of 4.1 g mL, an AUC24 of 47 gh mL, and an elimination half-life of 14 hours, following 400 mg p.o. daily. Renal Insufficiency The pharmacokinetic parameters of moxifloxacin are not significantly altered in mild, moderate, severe, or end-stage renal disease. No dosage adjustment is necessary in patients with renal impairment, including those patients requiring hemodialysis HD ; or continuous ambulatory peritoneal dialysis CAPD ; . In a single oral dose study of 24 patients with varying degrees of renal function from normal to severely impaired, the mean peak concentrations Cmax ; of moxifloxacin were reduced by 21% and 28% in the patients with moderate CLCR 30 and 60 mL min ; and severe CLCR 30 mL min ; renal impairment, respectively. The mean systemic exposure AUC ; in these patients was increased by 13%. In the moderate and severe renally impaired patients, the mean AUC for the sulfate conjugate M1 ; increased by 1.7-fold ranging up to 2.8-fold ; and mean AUC and Cmax for the glucuronide conjugate M2 ; increased by 2.8-fold ranging up to 4.8-fold ; and 1.4-fold ranging up to 2.5-fold ; , respectively. The pharmacokinetics of single dose and multiple dose moxifloxacin were studied in patients with CLCR 20 mL min on either hemodialysis or continuous ambulatory peritoneal dialysis 8 HD, 8 CAPD ; . Following a single 400 mg oral dose, the AUC of moxifloxacin in these HD and CAPD patients did not vary significantly from the AUC generally found in healthy volunteers. Cmax values of moxifloxacin were reduced by about 45% and 33% in HD and CAPD patients, respectively, compared to healthy, historical controls. The exposure AUC ; to the sulfate conjugate M1 ; increased by 1.4- to 1.5-fold in these patients. The mean AUC of the glucuronide conjugate M2 ; increased by a factor of 7.5, whereas the mean Cmax values of the glucuronide conjugate M2 ; increased by a factor of 2.5 to 3, compared to healthy subjects. The sulfate and the glucuronide conjugates of moxifloxacin are not microbiologically active, and the clinical implication of increased exposure to these metabolites in patients with renal disease including those undergoing HD and CAPD has not been studied. Oral administration of 400 mg QD moxifloxacin for 7 days to patients on HD or CAPD produced mean systemic exposure AUCss ; to moxifloxacin similar to that generally seen in healthy volunteers. Steady-state Cmax values were about 22% lower in HD patients but were comparable between CAPD patients and healthy volunteers. Both HD and CAPD removed only small amounts of moxifloxacin from the body approximately 9% by HD, and 3% by CAPD ; . HD and CAPD also removed about 4% and 2% of the glucuronide metabolite M2 ; , respectively. Hepatic Insufficiency In 400 mg single oral dose studies in 6 patients with mild Child Pugh Class A ; , and 10 patients with moderate Child Pugh Class B ; , hepatic insufficiency, moxifloxacin mean systemic exposure AUC ; was 78% and 102%, respectively, of 18 healthy controls and mean peak concentration Cmax ; was 79% and 84% of controls. The mean AUC of the sulfate conjugate of moxifloxacin M1 ; increased by 3.9-fold ranging up to 5.9-fold ; and 5.7-fold ranging up to 8.0-fold ; in the mild and moderate groups, respectively. The mean Cmax of M1 increased by approximately 3-fold in both groups ranging up to 4.7- and 3.9-fold ; . The mean AUC of the glucuronide conjugate of moxifloxacin M2 ; increased by 1.5-fold ranging up to 2.5-fold ; in both groups. The mean Cmax of M2 increased by 1.6- and 1.3-fold ranging up to 2.7- and 2.1-fold ; , respectively. The clinical significance of increased exposure to the sulfate and glucuronide conjugates has not been studied. No dosage adjustment is recommended for mild or moderate hepatic insufficiency Child Pugh Classes A and B ; . The pharmacokinetics of moxifloxacin in severe hepatic insufficiency Child Pugh Class C ; have not been studied. See DOSAGE AND ADMINISTRATION. ; Photosensitivity Potential A study of the skin response to ultraviolet UVA and UVB ; and visible radiation conducted in 32 healthy volunteers 8 per group ; demonstrated that moxifloxacin does not show phototoxicity in comparison to placebo. The minimum erythematous dose MED ; was measured before and after treatment with moxifloxacin 200 mg or 400 mg once daily ; , lomefloxacin 400 mg once daily ; , or placebo. In this study, the MED measured for both doses of moxifloxacin were not significantly different from placebo, while lomefloxacin significantly lowered the MED. See PRECAUTIONS, Information for Patients and nadolol.
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Morphine and other opioids cause histamine release, and this is said to contribute to asthma or urticaria in allergic patients. 133, 230, 231 ; There is no published information on the incidence of this phenomenon and, in our experience, it is very rare. However, it is not uncommon for patients to claim that they are `allergic' to morphine. This usually means that they have had a bad experience with the drug but, on investigation, what they describe are its common sideeffects. There is no doubt that most patients experience some adverse effects when they first start regular morphine treatment. Most commonly this is sedation, nausea, and, less often, vomiting. All patients must be warned about this and appropriate measures must be taken, as described above. If patients are not warned and experience unpleasant adverse effects they will be discouraged from continuing with the drug, and if they do not understand what is going on they may assume they that are `allergic' to it.
Regardless of the mechanisms involved, our may be important in the treatment of copd with lb who also have excessive mucous that needs to be cleared by cough and nafcillin.
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