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Table 1 percentage of trovafloxacin and its metabolites in urine, feces, and extracts of pooled serum from healthy male volunteers n 4 ; after single oral administration of 200 mg of [14c]trovafloxacin metabolites in urine 0 72 hr ; and fecal extracts 0 120 hr ; are expressed as percentage of the dose excreted, and the metabolites in the serum extracts pooled at 1, 5, and 12 hr ; are expressed as the percentage of radioactivity!
Table 2 ; . In these 15 patients at the transition between Zones I and II, the A2A3 cycle was 24-278 msec longer than the A1A1 cycle. In one patient, Zone II responses were never elicited and this patient had a markedly prolonged Zone L.42.
Thermal cis-trans isomerization of in poly d - ; 3-hydroxybutyrate ; and its hydroxyvalerate copolymer as a probe for characterizing their aging
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UPDATE ON ISOLOGEN Dr Cussell has now had more than 30 patients having Isolagen treatment for facial lines, depressions and wrinkles and also for acne scars and post-surgical scars. Age range so far is from 38-75yrs. Everyone has noticed definite improvements so far, although most are still very early days. One 68 year old I saw last week, some 6 weeks after having her injections, had almost completely resolved her naso-labial creases. For someone who was relatively unhappy with her results last year following two 0.7 cc syringes of temporary filler into her naso-labial creases, she was delighted with her Isolagen results so far. Age does not seem a barrier for improvement with Isolagen. Young acne scaring looks like being a winner with Isolagen also, with amazing early improvement seen so far. This mirrors results discussed with Dr Peter Ashby in.
Suggesting that the oxidation of this cofactor might be the cause of impaired NOS function in nitrate tolerance. Our findings are compatible with the same mechanism in humans. Previous findings in animal models 8, 20 ; suggest that abnormal NOS function is responsible, at least in part, for the increase in endothelial superoxide anion production associated with GTN treatment, and our results seem to be compatible with this hypothesis. A number of reports documented that antioxidant therapy can modify the development of tolerance 22, 23 ; , but, in our experience, the acute administration of vitamin C did not reverse tolerance to GTN 24 ; . We not believe that this latter observation is inconsistent with the present findings. If the trigger for NOS dysfunction or nitrate tolerance is a free radicalmediated process, it is possible that antioxidant supplementation can prevent this effect but be unable to reverse it. Continuous versus intermittent GTN therapy. In this investigation, subjects underwent continuous transdermal GTN, and it is possible that the observed responses to intra-arterial infusions would have been different if an intermittent regimen had been employed. Nevertheless, continuous GTN therapy is used in a significant number of patients, particularly in the setting of unstable angina. Furthermore, since there is some documentation that intermittent regimens have been associated with changes in exercise tolerance and rebound ischemic events 25, 26 ; , it is possible that intermittent therapy might lead to NOS dysfunction and superoxide production, as recently confirmed by an ex vivo animal study 16 ; . Whether similar responses would be observed during therapy with other long-acting nitrates is not known. Clinical relevance of our findings. We believe these observations have direct clinical relevance. The fact that GTN therapy can cause profound endothelial dysfunction in otherwise normal individuals is surprising, given the traditional concept that NO donors might have beneficial effects in the setting of decreased NO bioavailability 27 ; . This finding confirms our previous observation that therapy with continuous GTN worsens endothelial dysfunction in the coronary arteries of patients with coronary artery disease 7 ; . An impaired endothelium-dependent production of NO is now considered per se a risk factor for cardiovascular disease. The demonstration that therapy with GTN causes abnormalities in NOS function in humans in vivo provides support for the hypothesis generated by animal experiments that nitrate-induced abnormalities in NOS function might play an important role in the development of nitrate tolerance. As such, it is an important observation since mechanisms to prevent this effect and modify the development of tolerance can now be explored and truvada.
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Reactive oxygen species of CSF phagocytes and hippocampal neuronal apoptosis in experimental Streptococcus pneumoniae meningitis. J. Infect. Dis. 181: 20952098. Braun, J. S., J. E. Sublett, D. Freyer, T. J. Mitchell, J. L. Cleveland, E. I. Tuomanen, and J. R. Weber. 2002. Pneumococcal pneumolysin and H2O2 mediate brain cell apoptosis during meningitis. J. Clin. Investig. 109: 1927. Byrne, W. R., S. L. Welkos, M. L. Pitt, K. J. Davis, R. P. Brueckner, J. W. Ezzell, G. O. Nelson, J. R. Vaccaro, L. C. Battersby, and A. M. Friedlander. 1998. Antibiotic treatment of experimental pneumonic plague in mice. Antimicrob. Agents Chemother. 42: 675681. Cottagnoud, P., F. Acosta, M. Cottagnoud, K. Neftel, and M. G. Tauber. 2000. Synergy between trovafloxacin and ceftriaxone against penicillin-resistant pneumococci in the rabbit meningitis model and in vitro. Antimicrob. Agents Chemother. 44: 21792181. Evans, M. E., and M. Pollack. 1993. Effect of antibiotic class and concentration on the release of lipopolysaccharide from Escherichia coli. J. Infect. Dis. 167: 13361343. Gerber, J., H. Eiffert, H. Fleischer, A. Wellmer, U. Munzel, and R. Nau. 2001. Reduced release of DNA from Streptococcus pneumoniae after treatment with rifampin in comparison to spontaneous growth and ceftriaxone treatment. Eur. J. Clin. Microbiol. Infect. Dis. 20: 490493. Hausler, K. G., M. Prinz, C. Nolte, J. R. Weber, R. R. Schumann, H. Kettenmann, and U. K. Hanisch. 2002. Interferon-gamma differentially modulates the release of cytokines and chemokines in lipopolysaccharideand pneumococcal cell wall-stimulated mouse microglia and macrophages. Eur. J. Neurosci. 16: 21132122. Heumann, D., C. Barras, A. Severin, M. P. Glauser, and A. Tomasz. 1994. Gram-positive cell walls stimulate synthesis of tumor necrosis factor alpha and interleukin-6 by human monocytes. Infect. Immun. 62: 27152721. Kartalija, M., Y. Kim, M. L. White, R. Nau, J. H. Tureen, and M. G. Tauber. 1995. Effect of a recombinant N-terminal fragment of bactericidal permeability-increasing protein rBPI23 ; on cerebrospinal fluid inflammation induced by endotoxin. J. Infect. Dis. 171: 948953. Kim, Y. S., S. Kennedy, and M. G. Tauber. 1995. Toxicity of Streptococcus pneumoniae in neurons, astrocytes, and microglia in vitro. J. Infect. Dis. 171: 13631368. Molyneux, E. M., A. L. Walsh, H. Forsyth, M. Tembo, J. Mwenechanya, K. Kayira, L. Bwanaisa, A. Njobvu, S. Rogerson, and G. Malenga. 2002. Dexamethasone treatment in childhood bacterial meningitis in Malawi: a randomised controlled trial. Lancet 360: 211218. Mustafa, M. M., O. Ramilo, J. Mertsola, R. C. Risser, B. Beutler, E. J. Hansen, and G. H. McCracken, Jr. 1989. Modulation of inflammation and cachectin activity in relation to treatment of experimental Haemophilus influenzae type b meningitis. J. Infect. Dis. 160: 818825. Nau, R., T. Schmidt, K. Kaye, J. L. Froula, and M. G. Tauber. 1995. Quinolone antibiotics in therapy of experimental pneumococcal meningitis in rabbits. Antimicrob. Agents Chemother. 39: 593597. Nau, R., G. Zysk, H. Schmidt, F. R. Fischer, A. Stringaris, K. Stuertz, and W. Bruck. 1997. Trovafloxacin delays the antibiotic-induced inflammatory response in experimental pneumococcal meningitis. J. Antimicrob. Chemother. 39: 781788. Nau, R., A. Wellmer, A. Soto, K. Koch, O. Schneider, H. Schmidt, J. Gerber, U. Michel, and W. Bruck. 1999. Rifampicin reduces early mortality in experimental Streptococcus pneumoniae meningitis. J. Infect. Dis. 179: 15571560. Nau, R., and W. Bruck. 2002. Neuronal injury in bacterial meningitis: mech anisms and implications for therapy. Trends Neurosci. 25: 3845. Nau, R., and H. Eiffert. 2002. Modulation of the release of proinflammatory bacterial compounds by antibacterials: potential impact on the course of inflammation and outcome in sepsis and meningitis. Clin. Microbiol. Rev. 15: 95110. Scheld, W. M., U. Koedel, B. Nathan, and H. W. Pfister. 2002. Pathophysiology of bacterial meningitis: mechanism s ; of neuronal injury. J. Infect. Dis. 186 Suppl. 2 ; : S225S233. Schneider, O., U. Michel, G. Zysk, O. Dubuis, and R. Nau. 1999. Clinical outcome in pneumococcal meningitis correlates with CSF lipoteichoic acid concentrations. Neurology 53: 15841587. Stringaris, A. K., J. Geisenhainer, F. Bergmann, C. Balshusemann, U. Lee, G. Zysk, T. J. Mitchell, B. U. Keller, U. Kuhnt, J. Gerber, A. Spreer, M. Bahr, U. Michel, and R. Nau. 2002. Neurotoxicity of pneumolysin, a major pneumococcal virulence factor, involves calcium influx and depends on activation of p38 mitogen activated protein kinase. Neurobiol. Dis. 11: 355368. Stuertz, K., H. Schmidt, H. Eiffert, P. Schwartz, M. Mader, and R. Nau. 1998. Differential release of lipoteichoic and teichoic acids from Streptococcus pneumoniae as a result of exposure to -lactam antibiotics, rifamycins, trovafloxacin, and quinupristin-dalfopristin. Antimicrob. Agents Chemother. 42: 277281. Stuertz, K., H. Schmidt, F. Trostdorf, H. Eiffert, M. Mader, and R. Nau. 1999. Lower lipoteichoic and teichoic acid CSF concentrations during treatment of pneumococcal meningitis with non-bacteriolytic antibiotics than with ceftriaxone. Scand. J. Infect. Dis. 31: 367370. Trautmann, M., R. Zick, T. Rukavina, A. S. Cross, and R. Marre. 1998.
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Table 4. Development of quinolone potency against Gram-positive bacteria MIC90 mg L ; Quinolone Nalidixic acid Cinoxacin Enoxacin Ciprofloxacin Ofloxacin Levofloxacin Temafloxacin Sparfloxacin Grepafloxacin Gatifloxacin Trovafloxacin Moxifloxacin Clinafloxacin Gemifloxacin Garenoxacin S. aureus methicillin sensitive ; 64 2 S. pneumoniae 64 Group A streptococci 64 Enterococcus spp. 64 8 Clostridium perfringens 64 ND 0.25 and tums
Applegate, E. A. and Grivetti, L. E. 1997 ; Search for the competitive edge: a history of dietary fads and supplements. Journal of Nutrition, 127, 869S873S. Australia New Zealand Food Authority 2000 ; Report of the Expert Group on the Safety Aspects of Dietary Caffeine. ANZFA, Canberra. Bandura, A. 1986 ; Social Foundations of Thought and Action: A Social Cognitive Theory. Prentice-Hall, Englewood Cliffs, NJ. Bernstein, G. A., Carroll, M. E., Crosby, R. D., Perwien, A. R., Go, F. S. and Benowitz, N. L. 1994 ; Caffeine effects on learning, performance and anxiety in normal school-age children. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 407415. Bowering, J. and Clancy, K. L. 1986 ; Nutritional status of children and teenagers in relation to vitamin and mineral use. Journal of the American Dietetic Association, 86, 10331038. Britten, N. 1995 ; Qualitative interviews in medical research. British Medical Journal, 311, 251253. Crockett, L. J. and Petersen, A. C. 1993 ; Adolescent development: health risks and opportunities for health promotion In Millstein, S. G., Petersen, A. C. and Nightingale
Norfloxacin, ciprofloxacin, enoxacin, trovafloxacin ; are synthetic compounds based on the chemical structure and tysabri.
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Comparing in vitro activities of antimicrobial agents against Streptococcus pneumoniae using per cent susceptible to recommended MIC breakpoints is not optimal. In this study, MICs of penicillin G, ampicillin sulbactam, ceftriaxone, cefuroxime, erythromycin, tetracycline, trimethoprim sulfamethoxazole, ciprofloxacin, levofloxacin, trovafloxacin and moxifloxacin were determined for 646 strains. Drug activities were compared using MIC frequency distribution curves, scattergrams and linear regression analyses of MICs log2 ; . MIC frequency distributions did not always correspond to recommended breakpoints for distinguishing susceptible, intermediate and resistant strains. Penicillin G, ampicillin sulbactam and ceftriaxone had similar activities and were each c. 11.5 dilution steps more active than cefuroxime. For all -lactam drug pairs, there was a high correlation of MICs with regression line slopes a ~ 1 ; and coefficients of determination R 2 0.900.97 ; . Although -lactam~ resistant strains were more likely to be resistant to erythromycin, tetracycline and or trimethoprim sulfamethoxazole than were -lactam-susceptible strains, MIC correlations were relatively poor R 2 0.140.46 ; , as they were when the non lactam drugs were compared with each other R 2 0.100.25 ; . Trovafloxacin and moxifloxacin were each c. 2.5 dilution steps more active than ciprofloxacin and levofloxacin. There was no correlation of quinolone MICs with MICs of any other drug class R 2 ; . Among the quinolones, however, there was a high correlation of MICs with a ~1 and R 2 0.810.92. With the quinolone drug pairs, lines of ~ best fit were second-order polynomial equations, consistent with a dissociation of low level resistance mechanisms. In summary, -lactam and quinolone MICs were predictable within drug classes and testing multiple derivatives within each class is probably not necessary. Although there was some relationship between -lactam, erythromycin, tetracycline and trimethoprim sulfamethoxazole MICs, predictability of MICs between drug classes was poor. There was no relationship between quinolone MICs and MICs of any of the other drugs tested.
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Compared to 0.8% direct treatment tumor bearing ; 24 hr blood level. * Compared to 0.8% direct treatment tumor bearing ; 48 hr blood level and ubiquinone.
Blumenthal RS: Statins: effective antiatherosclerotic therapy. Heart J 2000, 139 4 ; : 577-583. Gresser U, Gathof BS: Atorvastatin: gold standard for prophylaxis of myocardial ischemia and stroke comparison of the clinical benefit of statins on the basis of randomized controlled endpoint studies. Eur J Med Res 2004, 9 1 ; : 1-17. Krishnan LL, Petersen NJ, Snow AL, Cully JA, Schulz PE, Graham DP, Morgan RO, Braun U, Moffett ML, Yu HJ, et al.: Prevalence of dementia among Veterans Affairs medical care system users. Dement Geriatr Cogn Disord 2005, 20 4 ; : 245-253. Zhou Z, Rahme E, Pilote L: Are statins created equal? Evidence from randomized trials of pravastatin, simvastatin, and atorvastatin for cardiovascular disease prevention. Heart J 2006, 151 2 ; : 273-281. Davidson MH: Emerging therapeutic strategies for the management of dyslipidemia in patients with the metabolic syndrome. J Cardiol 2004, 93 11A ; : 3C-11C. Hunninghake DB, Ballantyne CM, Maccubbin DL, Shah AK, Gumbiner B, Mitchel YB: Comparative effects of simvastatin and atorvastatin in hypercholesterolemic patients with characteristics of metabolic syndrome. Clin Ther 2003, 25 6 ; : 1670-1686. Karalis DG, Ross AM, Vacari RM, Zarren H, Scott R: Comparison of efficacy and safety of atorvastatin and simvastatin in patients with dyslipidemia with and without coronary heart disease. J Cardiol 2002, 89 6 ; : 667-671. Vuletic S, Riekse RG, Marcovina SM, Peskind ER, Hazzard WR, Albers JJ: Statins of Different Brain Penetrability Differentially Affect CSF PLTP Activity. Dement Geriatr Cogn Disord 2006, 22 5 ; : 392-398. Saheki A, Terasaki T, Tamai I, Tsuji A: In vivo and in vitro bloodbrain barrier transport of 3-hydroxy-3-methylglutaryl coenzyme A HMG-CoA ; reductase inhibitors. Pharm Res 1994, 11 2 ; : 305-311. Hawkins BT, Davis TP: The blood-brain barrier neurovascular unit in health and disease. Pharmacol Rev 2005, 57 2 ; : 173-185. Sironi L, Gianazza E, Gelosa P, Guerrini U, Nobili E, Gianella A, Cremonesi B, Paoletti R, Tremoli E: Rosuvastatin, but not simvastatin, provides end-organ protection in stroke-prone rats by antiinflammatory effects. Arterioscler Thromb Vasc Biol 2005, 25 3 ; : 598-603. Kinlay S, Schwartz GG, Olsson AG, Rifai N, Leslie SJ, Sasiela WJ, Szarek M, Libby P, Ganz P: High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation 2003, 108 13 ; : 1560-1566. Flockhart DA, Tanus-Santos JE: Implications of cytochrome P450 interactions when prescribing medication for hypertension. Arch Intern Med 2002, 162 4 ; : 405-412. Bottorff MB: Statin safety and drug interactions: clinical implications. J Cardiol 2006, 97 8A ; : 27C-31C. Cesari M, Pessina AC: Combined antihypertensive and lipid-lowering treatment. Curr Hypertens Rep 2004, 6 4 ; : 300-306. Chan P, Huang TY, Tomlinson B, Lee C, Lee YS: Short-term safety and efficacy of low-dose simvastatin in elderly patients with hypertensive hypercholesterolemia and fasting hyperinsulinemia. J Clin Pharmacol 1997, 37 6 ; : 496-501. Scranton RE, Young M, Lawler E, Solomon D, Gagnon D, Gaziano JM: Statin use and fracture risk: study of a US veterans population. Arch Intern Med 2005, 165 17 ; : 2007-2012. Wang PS, Solomon DH, Mogun H, Avorn J: HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients. Jama 2000, 283 24 ; : 3211-3216. Marz W, Koenig W: HMG-CoA reductase inhibition: antiinflammatory effects beyond lipid lowering? J Cardiovasc Risk 2003, 10 3 ; : 169-179. Wolozin B, Mange J, Bryant R, Cordy J, Green R, McKee A: Cholesterol, Alzheimer's disease and Statins: Re-assessing the relationship between cholesterol, statins and Alzheimer's disease. Acta Neuropathol Scandanavia 2006, 185: 63-70.
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| Trovafloxacin overdoseStandardized susceptibility test procedures require the use of laboratory control microorganisms to control the technical aspects of the laboratory procedures. Standard trovafloxacin mesylate powder should provide the following MIC values: Microorganism Neisseria gonorrhoeaeb ATCC 49226 and ursinus.
And Chemotherapy , New Orleans , Louisiana, 1993. Abstract 1509, p. 395. American Society for Microbiology, Washington, DC. 24. Soejima, R. & Shimada, K. 1989 ; . Tosufloxacin tosylate. Drugs of the Future 14, 5368. 25. Ohta, M. & Koga, H. 1991 ; . Three-dimensional structure activity relationships and receptor mapping of N1-substituents of quinolone antibacterials. Journal of Medicinal Chemistry 34, 1319. 26. Ross, D. L. & Riley, C. M. 1990 ; . Aqueous solubilities of some variously substituted quinolone antimicrobials. International Journal of Pharmaceutics 63, 23750. 27. Brighty, K. E., Gootz, T. D., Girard, A., Shanker, R., Castaldi, M. J., Girard, D. et al. 1994 ; . Prodrugs of CP-99, 219 for intravenous administration; synthesis and evaluation resulting in identification of CP-116, 517. In Program and Abstracts of the Thirty-Fourth Interscience Conference on Antimicrobial Agents and Chemotherapy, Orlando, FL, 1994. Abstract F28, p. 55. American Society for Microbiology, Washington, DC. 28. Srgel, F. & Kinzig, M. 1993 ; . Pharmacokinetics of gyrase inhibitors. Part 1: basic chemistry and gastrointestinal disposition. American Journal of Medicine 94, Suppl. 3A, 44S55S. 29. Teng, R., Tensfeldt, T. G., Liston, T. E. & Foulds, G. 1996 ; . Determination of trovafloxacin, a new quinolone antibiotic, in biological samples by reversed-phase high-performance liquid chromatography. Journal of Chromatography B: Biomedical Applications 657, 539. 30. Gooding, B. B. & Jones, R. N. 1993 ; . In vitro antimicrobial activity of CP-99, 219, a novel azabicyclo-naphthyridone. Antimi crobial Agents and Chemotherapy 37, 34953. 31. Eliopoulos, G. M., Klimm, K., Eliopoulos, C. T., Ferraro, M. J. & Moellering, R. C. 1993 ; . In vitro activity of CP-99, 219, a new fluoroquinolone, against clinical isolates of Gram-positive bacteria. Antimicrobial Agents and Chemotherapy 37, 36670. 32. Gootz, T. D. & McGuirk, P. R. 1994 ; . New quinolones in development. Expert Opinion on Investigational Drugs 3, 93114. 33. Child, J., Andrews, J., Boswell, F., Brenwald, N. & Wise, R. 1995 ; . The in-vitro activity of CP-99, 219, a new naphthyridone antimicrobial agent: a comparison with fluoroquinolone agents. Journal of Antimicrobial Chemotherapy 35, 86976. 34. Mulazimoglu, L., Drenning, S. D. & Yu, V. L. 1995 ; . In vitro activity of two novel oxazolidinones U-100592 and U-100766 ; , a new fluoroquinolone CP-99, 219-27 ; and a streptogramin Synercid ; against S. aureus and S. epidermidis. In Program and Abstracts of the Thirty-Fifth Interscience Conference on Antimicro bial Agents and Chemotherapy, San Francisco, CA, 1995. Abstract F210, p. 149. American Society for Microbiology, Washington, DC. 35. Cunha, B. A., Hussain Qadri, S. M., Ueno, Y., Walters, E. A. & Domenico, P. 1997 ; . Antibacterial activity of trovafloxacin against Gram-positive and Gram-negative isolates. Journal of Antimicro bial Chemotherapy 39, Suppl. B, 2934. 36. Felmingham, D., Robbins, M. J., Ingley, K., Mathias, I., Bhogal, H., Leakey, A. et al. 1997 ; . In-vitro activity of trovafloxacin, a new fluoroquinolone, against recent clinical isolates. Journal of Antimicrobial Chemotherapy 39, Suppl. B, 4350. 37. Fuchs, P. C., Barry, A. L., Brown, S. D. & Sewell, D. L. 1996 ; . In vitro activity and selection of disk content for disk diffusion susceptibility tests with trovafloxacin. European Journal of Clinical Microbiology and Infectious Diseases 15, 67882. 38. Klugman, K. & Wasas, A. 1995 ; . In-vitro activity of the fluoroquinolone trovafloxacin against penicillin-sensitive and penicillinresistant Streptococcus pneumoniae. Journal of Antimicrobial Chemotherapy 36, 8734. 39. Sefton, A. M., Maskell, J. P., Minassian, M. & Williams, J. D. 1995 ; . Comparative in vitro activity of CP-99, 219, a new quinolone, against respiratory pathogens. In Abstracts of the Sev enth European Congress of Clinical Microbiology and Infectious Diseases, Vienna, Austria, 1995. Abstract 738, p. 143. European Society of Clinical Microbiology and Infectious Diseases. 40. Coque, T. M., Singh, K. V. & Murray, B. E. 1996 ; . Comparative in-vitro study of the new fluoroquinolone trovafloxacin CP99, 219 ; against Gram-positive cocci. Journal of Antimicrobial Chemotherapy 37, 10116. 41. Shonekan, D., Handwerger, S. & Mildvan, D. 1997 ; . Comparative in vitro activities of RP59500 quinupristin dalfopristin ; , CL 329, 998, CL 331, 002, trovafloxacin, clinafloxacin, teicoplanin and vancomycin against Gram-positive bacteria. Journal of Antimicro bial Chemotherapy, 39, 4059. 42. Kenny, G. E. & Cartwright, F. D. 1995 ; . Susceptibilities of Mycoplasma pneumoniae, Mycoplasma hominis and Ureaplasma urealyticum to a new quinolone: CP-99, 219. In Abstracts of the Thirty-Fifth Interscience Conference on Antimicrobial Agents and Chemotherapy, San Francisco, CA, 1995. Abstract F236, p. 154. American Society for Microbiology, Washington, DC. 43. Neu, H. C. & Chin, N. X. 1994 ; . In-vitro activity of the new fluoroquinolone CP-99, 219. Antimicrobial Agents and Chemo therapy 38, 261522. 44. Verbist, L. & Verhaegen, J. 1995 ; . In vitro activity of CP99, 219, a new fluoroquinolone. In Abstracts of the Seventh Euro pean Congress of Clinical Microbiology and Infectious Diseases, Vienna, Austria, 1995. Abstract 731, p. 141. European Society of Clinical Microbiology and Infectious Diseases. 45. Rolston, K. V. I., Ho, D. H., LeBlanc, B., Streeter, H. & Dvorak, T. 1997 ; . In-vitro activity of trovafloxacin against bacterial isolates from patients with cancer. Journal of Antimicrobial Chemotherapy 39, Suppl. B, 1522. 46. Knapp, J. S., Neal, S. W., Parekh, M. C. & Rice, R. J. 1995 ; . In vitro activity of a new fluoroquinolone, CP-99, 219, against strains of Neisseria gonorrhoeae. Antimicrobial Agents and Chemotherapy 39, 9879. 47. Spangler, S. K., Jacobs, M. R. & Appelbaum, P. C. 1994 ; . Activity of CP-99, 219 compared with those of ciprofloxacin, grepafloxacin, metronidazole, cefoxitin, piperacillin, and piperacillin tazobactam against 489 anaerobes. Antimicrobial Agents and Chemotherapy 38, 24716. 48. Gootz, T. D., Brighty, K. E., Anderson, M. R., Schmieder, B. J., Haskell, S. L., Sutcliffe, J. A. et al. 1994 ; . In vitro activity of CP99, 219, a novel 7- 3-azabicyclo[3.1.0]hexyl ; naphthyridone antimicrobial. Diagnostic Microbiology and Infectious Disease 19, 23543. 49. Morrissey, I. 1996 ; . Bactericidal activity of trovafloxacin CP99, 219 ; . Journal of Antimicrobial Chemotherapy 38, 10616. 50. Gootz, T. D., Zaniewski, R., Tankovic, J., Courvalin, P., Haskell, S., Schmieder, B. et al. 1996 ; . Activity of trovafloxacin CP99, 219 ; against ciprofloxacin-resistant mutants of Streptococcus pneumoniae. In Abstracts of the Ninety-Sixth General Meeting of the American Society for Microbiology, New Orleans, LA, 1996. Abstract A113. American Society for Microbiology, Washington, DC.
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The Upper Limit of Autoregulation of Cerebral Blood Flow -- On the Pathogenesis of Hypertensive Encephalopathy Editorial ; -- Lassen NA Department of Clinical Physiology, Bispebjerg Hospital, Copenhagen, Denmark ; , Agnoli A -- Scand J Clin Lab Invest 30: 113-116 Oct ; 1972 How high blood pressure damages tissue has been discussed for more than a century. Excessive arteriolar constriction spasm theory ; was emphasized by Byrom as he demonstrated that pial arterioles in hypertensive rats were segmentally narrowed and the corresponding cortex was pale. On the other hand Giese showed that colloidal carbon enters the smooth muscle cell layer during angiotensininduced hypertension always in the zones of dilatation and never in zones of constriction. More recently Haggendal and Johansson demonstrated in cats that during a sudden increase in mean arterial blood pressure patchy extravasation of serum albumin bound with Evans blue dye into brain occurred and that sagittal sinus venous pressure increased. A gradual increase in arterial blood pressure caused no leak of the dye. They suggest that the extravasation results from overdistention of the microcirculation in the brief time preceding autoregulatory vasoconstriction. In another experiment by Haggendal et al. autoregulation was shown to be effective over lesser degrees of hypertension in dogs during hypercapnia. Skinh j has reported a patient with brain tissue acidosis who despite blood pressures of less than 180 mm Hg developed a clinical picture of hypertensive encephalopathy; yet blood flow was found to be low, apparently reflecting brain edema and decreased function. Others have noted that hypertensive encephalopathy often becomes symptomatic at night when Pco, is elevated. Hypocapnia may be useful, and opiates should be avoided in such patients. Finally the editorialists suggest that in hypertensive encephalopathy the stretched arterioles act as membranes which allow passage of water but not plasma proteins and valcyte.
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RESULTS Single-incubation mutation frequencies. i ; MIC90. The baseline and postincubation MIC90s for the seven bacterial strains are shown in Table 1. With the exception of trovafloxacin versus MSSA, all the test organisms exhibited a 16- to 32-fold increase in the MIC90. ii ; Mutation frequencies. No statistically significant differences in the frequency of detection of resistant mutants to ciprofloxacin, levofloxacin, or trovafloxacin occurred after a single incubation of MRSA, E. coli, K. pneumoniae, or P. aeruginosa in a concentration of test drug that was four times the baseline MIC data not shown ; . Significant differences in the frequency of detection of resistant mutants of MSSA, E. cloacae, and S. marcescens are shown in Table 2. For MSSA, trovafloxacin showed a statistically significant greater frequency of resistant mutants than did levofloxacin. For E. cloacae, the highest frequency of resistant mutants occurred after incubation with ciprofloxacin; differences between ciprofloxacin, levofloxacin, and trovafloxacin were statistically significant. For S. marcescens a higher frequency of resistant mutants occurred for levofloxacin and trovafloxacin than for ciprofloxacin and trovafloxacin.
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