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Moxifloxacin is to be used only by the patient for whom it is prescribed. Schacher S and Wu F. Synapse formation in the absence of cell bodies requires protein synthesis. J Neurosci 22: 18311839, 2002. Sherff CM and Carew TJ. Coincident induction of long-term facilitation in Aplysia: cooperativity between cell bodies and remote synapses. Science 285: 19111914, 1999. Smit AB, Syed NI, Schaap D, van Minnen J, Klumperman J, Kits KS, Lodder H, van der Schors RC, van Elk R, Sorgedrager B, Brejc K, Sixma TK, and Geraerts WP. A glia-derived acetylcholine-binding protein that modulates synaptic transmission. Nature 411: 261268, 2001. Syed NI, Bulloch AG, and Lukowiak K. In vitro reconstruction of the respiratory central pattern generator of the mollusk Lymnaea. Science 250: 282285, 1990. Syed NI and Winlow W. Respiratory behaviour in the pond snail Lymnaea stagnalis. II. Neural elements of the central pattern generator CPG ; . J Comp Physiol A 169: 557568, 1991. Syed NI, Zaidi H, and Lovell P. In vitro reconstruction of neuronal networks: a simple model system approach. In: Modern Techniques in Neuroscience Research, edited by U Windhurst and H Johansson. Berlin: Springer, 1999, p. 361377. Trudeau LE and Castellucci VF. Postsynaptic modifications in long-term facilitation in Aplysia: upregulation of excitatory amino acid receptors. J Neurosci 15: 12751284, 1995. van Minnen J, Bergman JJ, van Kesteren ER, Smit AB, Geraerts WP, Lukowiak K, Hasan SU, and Syed NI. De novo protein synthesis in isolated axons of identified neurons. Neuroscience 80: 17, 1997. van Minnen J, Meems R, Munno D, Geraerts WP, and Syed NI. Specific synapse formation between presynaptic somata and the isolated axons from postsynaptic Lymnaea neurons. Soc Neurosci Abstr 261, 2000. van Minnen J and Syed NI. Local protein synthesis in invertebrate axons: from dogma to dilemma. Results Prob Cell Differ 34: 175196, 2001. Wong RG, Hadley RD, Kater SB, and Hauser GC. Neurite outgrowth in molluscan organ and cell cultures: the role of conditioning factor s ; . J Neurosci 1: 1008 1021, Woodin MA, Munno DW, and Syed NI. Trophic factor-induced excitatory synaptogenesis involves postsynaptic modulation of nicotinic acetylcholine receptors. J Neurosci 22: 505514, 2002.
Plemented with 1% wt vol ; sterile-filtered glucose TSBgluc1% ; with shaking at 130 rpm. All experiments were performed at 37C in ambient air. Antimicrobial agents. Cefazolin, tetracycline, vancomycin, trimethoprim, and sulfamethoxazole Sigma-Aldrich, St. Louis, MO ; , daptomycin Cubist Pharmaceuticals, Lexington, MA ; , linezolid Pharmacia & Upjohn, Kalamazoo, MI ; , moxifloxacin Bayer Pharmaceuticals, West Haven, CT ; , quinupristin-dalfopristin King Pharmaceuticals, Bristol, TN ; , and rifampin Bedford Labs, Bedford, OH ; powders were prepared for use in susceptibility assays and microtiter plate biofilm assays as described in the Clinical and Laboratory Standards Institute CLSI ; susceptibility testing guidelines 34 ; . Trimethoprim and sulfamethoxazole were prepared separately and mixed immediately before use. -Lactamase screening. Cefinase disks BD BBL ; were used to screen isolates for -lactamase production. mecA PCR. DNA prepared by alkaline wash 15 ; was tested for the presence of mecA by PCR as previously described 27 ; . Planktonic antimicrobial susceptibility testing. MIC and MBC assays against the 10 antimicrobial agents listed in Table 2 were performed in cation-adjusted Mueller-Hinton broth CAMHB ; according to CLSI guidelines for broth microdilution susceptibility testing 33, 34 ; . S. aureus ATCC 29213 and Enterococcus faecalis ATCC 29212 were used as quality control strains for MICs and MBCs. Biofilm antimicrobial susceptibility testing. Biofilm bactericidal concentrations BBCs ; were determined by using an adaptation of a previously published biofilm susceptibility testing method 32 ; . Briefly, isolates grown for 22 h in TSBgluc1% were adjusted to a turbidity of 1.0 McFarland corresponding to ca.

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FIG. 4. Effect of moxifloxacin on the viability of S. aureus ATCC 25923 ingested by THP-1 cells. Antibacterial effect of moxifloxacin was expressed as the mean number of viable bacteria obtained in three determinations. This was normalized for the control growth curve to allow comparison between antibiotic concentrations. Symbols: s, control; , 0.2 mg liter; , 0.5 mg liter; , 1 mg liter; E, 2 mg liter; OE, 4 mg liter; 8 mg liter.

Programs and the geography served is essential in study planning and data interpretation. hance quality. There was unanimous lish a clinical agreement that the SOTM national should estabresearch subcommittee to oversee and direct national transport research netimportant clinical quesstudies. In interactive Also, severity of illness measures should to be furmade if such scoring modalities enther defined and a determination. Also in other countries Maruyama et al., 1979; Ripa et al., 2001; Seppala et al., 1993 ; . Although tetracycline has not been recommended for the therapy of GAS diseases, selective pressure from the intensive use of tetracycline to treat a variety of human and veterinary infections may have contributed to the emergence of this resistance among GAS isolates around the world. Genetic diversity Both phenotypic and genotypic methods have been used in the epidemiological surveillance of GAS. M serotyping is a well-established typing system with at least 80 recognized types, but its discriminatory power is considered to be poor because different genotypes may share the same M type Nguyen et al., 1997; Single & Martin, 1992 ; . Genomic typing methods have rarely been used to characterize the epidemiology of GAS. Among these methods, PFGE of chromosomal DNA has been used with success Bert et al., 1997; Nguyen et al., 1997 ; , as it is able to distinguish between isolates within the same M serotype Jasir et al., 2000; Nguyen et al., 1997 ; . Although it is complex, PFGE is established as the most sensitive and specific system for bacterial typing. Until the present study, there have been no Brazilian data on the genetic diversity of isolates of S. pyogenes obtained from asymptomatic carriage or clinical infection in human populations. Thus, using this approach, we established the extensive genetic diversity among the GAS population studied. Considerable genetic diversity was previously reported in a study involving an urban area of low endemicity Paris ; , where 18 unrelated clones, without a dominant type, were found in a group of 25 patients Nguyen et al., 1997 ; . In contrast, two genetically unrelated, dominant clones were isolated from 35 of 52 patients 67 % ; living in a semiclosed area, the Ile de la Reunion in France, where streptococcal infections were hyperendemic Nguyen et al., 1997 ; . Clonality was also demonstrated in a population of 500 GAS clinical isolates from Belgium. Although 136 unrelated PFGE types were identified, two PFGE types predominated among and mrv.

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PK PD established data, macrolides will not provide coverage for H. influenzae, which is a major pathogen in the disease. High-dose amoxicillin clavulanate or `respiratory' fluoroquinolones levofloxacin, gatifloxacin, and moxifloxacin ; are recommended for severe AECB, and these are appropriate agents according to PK PD breakpoints. CAP guidelines include macrolides throughout the treatment recommendations, while, as noted above, PK PD data show that these agents are not effective against H. influenzae or macrolide-resistant pneumococci. PK PD breakpoints show high efficacy for amoxicillin clavulanate, ceftriaxone, and respiratory fluoroquinolones against the three primary respiratory pathogens.35 Macrolides should be prescribed with a suitable -lactam agent for treatment of CAP in patients requiring hospitalization.40 Fluoroquinolone will provide coverage for the atypical pathogens in addition to the common respiratory pathogens.41 The therapeutic outcomes model TOM ; proposed by Poole uses a mathematical model to predict and calculate bacteriologic and clinical efficacy.42 TOM identifies the major variables needed for accurate estimates of outcomes.When used in rhinosinusitis, the variables are: likelihood of spontaneous resolution of a nonbacterial infection; likelihood of spontaneous resolution of a bacterial.
Figure. Distribution of MICs of ciprofloxacin ; and moxifloxacin ; for 462 referred pneumococci a ; and 807 invasive pneumococci from the surveillance programme b and multivitamin!

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Parable to that of moxifloxacin. DW-224a inhibited 90% of the E. coli, K. pneumoniae, Klebsiella oxytoca, Enterobacter cloacae, Enterobacter aerogenes, and Morganella morganii isolates at concentrations of 1, 0.25, and 0.5 g ml, respectively. Against Acinetobacter baumannii MIC90, 4 g ml ; , Acinetobacter calcoaceticus MIC90, 0.008 g ml ; , and Stenotrophomonas maltophilia MIC90, 1 g ml ; , DW-224a showed an activity comparable to the other compounds. DW-224a was highly active against H. influenzae MIC90, 0.008 g ml ; and M. catarrhalis MIC90, 0.03 g ml ; . Against N. gonorrhoeae, DW224a MIC90, 1 g ml ; was eightfold more active than ciprofloxacin. The activity of DW-224a against Pseudomonas aeruginosa MIC90, 64 g ml ; was inferior to those of ciprofloxacin and gemifloxacin, but it was comparable to that of moxifloxacin. The protective efficacy of DW-224a against systemic infections in mice was compared with those of ciprofloxacin, moxifloxacin, and gemifloxacin Table 2 ; . DW-224a exhibited the most potent protective effects against systemic infections caused by gram-positive bacteria. Against infection caused by S. aureus giorgio, the ED50s of DW-224a, ciprofloxacin, moxifloxacin, and gemifloxacin were 1.11, 16.52, 1.78, and 1.37 mg kg of body weight, respectively. Especially against quinolone-resistant S. aureus P197 an MRSA ; , DW-224a ED50, 15.52 mg kg ; was more effective than ciprofloxacin ED50, 40 mg kg ; , moxifloxacin ED50, 35.35 mg kg ; , and gemifloxacin ED50, 26.58 mg kg ; . DW-224a was also the most effective drug against infections caused by streptococci, including S. pneumoniae and S. pyogenes strains, for which the ED50s were 0.53 and 2.65 mg kg, respectively. But, DW-224a was shown to be less effective than the test compounds against infections caused by gram-negative organisms. Against E. coli 851E, DW-224a ED50, 6.08 mg kg ; was less active than ciprofloxacin ED50, 0.78 mg kg ; , moxifloxacin ED50, 2.17 mg kg ; , and gemifloxacin ED50, 1.16 mg kg ; . Against K. pneumoniae P427, the ED50s of DW-224a, ciprofloxacin, moxifloxacin, and gemifloxacin were 9.77, 0.70, 2.64, and 5.36 mg kg, respectively. DW-224a ED50, 4.83 mg kg ; was less active than ciprofloxacin ED50, 1.41 mg kg ; and gemifloxacin ED50, 3.41 mg kg ; against M. morganii 1375E but more active than moxifloxacin ED50, 5.28 mg kg ; . In general, the ED50s of DW-224a were well correlated with in vitro MICs. DW-224a demonstrated potent in vitro and in vivo antibacterial activities against both gram-positive and gram-negative bacteria. The overall antibacterial activities of DW-224a against gram-positive pathogens, such as MRSA, methicillinresistant coagulase-negative staphylococci, S. pneumoniae, S. pyogenes, and E. faecalis, were more potent than those of the reference compounds, such as ciprofloxacin, moxifloxacin, and gemifloxacin. DW-224a especially showed increased potency against S. pneumoniae, which is the bacterial strain most frequently isolated from patients with community-acquired pneumonia and continues to be a significant cause of mortality. However, DW-224a was slightly less active than other fluoro and murine.

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Table 1. Correlation between the Severity of Azotemia and Cholesterol Ester Accumulation BUN, mg dL Day 7 36 46 Day 14 33 44 Free cholesterol nmol mol Pi ; 300 299 338 r 0.98 250 273 r 0.93 Cholesterol ester nmol mol Pi ; 15.4 19.4 21.8 r 0.99 4.9 10.8 r 0.90.
A number of older agents are being reviewed as we search for adequate, appropriate antimicrobial options: Clindamycin has been successfully used to treat CA-MRSA disease, 11 but resistance to this drug has been reported as high as 15% in some regions.12 Inducible clindamycin resistance is also a concern. An interesting aspect to clindamycin therapy is the ability of the antibiotic to inhibit the PVL expression. Trimethoprim-sulphamethoxazole TMP-SMX ; is frequently the most active agent from an in-vitro aspect. Recent clinical trials are lacking, but a study of bacteremic S aureus skin infections among IV drug users showed an 85% success rate compared to 98% for vancomycin, a parenteral-only agent. Tetracycline or related agents such as minocycline have been successfully used to treat MRSA infections, although few well-designed studies exist. Fluoroquinolones--have variable activity against CA-MRSA. Experience from hospital-associated MRSA in the 1990s showed a rapid emergence of resistance to fluoroquinolones. Whether the CA variants will maintain the 4050% susceptibility remains to be observed.13 Of the agents tested in-vitro against MRSA, moxifloxacin and gemifloxacin were the most active and muse. Goldyne Savad Institute of Gene Therapy, Department of Bone Marrow Transplantation, Hadassah University Hospital, Jerusalem, Israel; Weizmann Institute of Science, Rehovot, Israel; Bone Marrow Transplantation Department, Chaim Sheba Medical Center, Tel-Hashomer, Israel; Department of Medicine, Children's Hospital and Harvard Medical School, Boston, MA 02115; Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; #Cyclotron Radiochemistry Unit, Department of Medicinal Biophysics and Nuclear Medicine, Hadassah University Hospital, Jerusalem, Israel; and * Laboratories of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Received for publication August 1, 2005. Accepted for publication January 23, 2006. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. This work was supported by the Israel Cancer Association through a donation from David Brown in memory of Melvin M. Brown. This study was supported by the Horowitz Foundation, the Israeli Ministry of Sciencethe Knowledge Center for Gene Therapy, the Blum Foundation, and the Grinspoon Foundation.
Proportion of those receiving thrice-weekly moxifloxacin were male; otherwise, the study arms were well balanced for baseline characteristics. Of the 277 patients in the efficacy analysis, 274 99% ; had sputum specimens obtained at the 2-mo time point. There was no significant interaction between the two interventions evaluated moxifloxacin vs. ethambutol, treatment 5 d wk vs. 3 d wk, p 0.27 ; , so the analysis proceeded using the factorial design. Two-month cultures were negative in 99 71% ; of 139 patients treated with moxifloxacin versus 98 71% ; of 138 patients treated with ethambutol p 0.97; Table 3 ; . Two-month culture status was also similar among patients who received therapy 5 d wk versus 3 d wk 100 [74%] of 136 vs. 97 [69%] of 141 patients, p 0.39 ; . We performed two post hoc analyses of the effect of treatment assignment see online supplement for additional and mycostatin.

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Like other fluoroquinolones, moxifloxacin pronounced moks-i-floks-a-sin ; works by interfering with the replication, transcription and repair of bacterial DNA.1 It is active in vitro against respiratory pathogens such as meticillin * sensitive Staphylococcus aureus, Streptococcus pneumoniae, Moraxella catarrhalis, Haemophilus influenzae, Klebsiella pneumoniae, Chlamydia pneumoniae and Mycoplasma pneumoniae.2 Moxifloxacin is more active in vitro against S. pneumoniae and Streptococcus pyogenes than other fluoroquinolones available in the UK.2 The drug is not active against Pseudomonas aeruginosa or meticillinresistant Staphylococcus aureus. The emergence of strains of S. pneumoniae resistant to fluoroquinolones including moxifloxacin has been reported in England3 and Asia.4.
Tibilities of equine isolates of Clostridium difficile and molecular characterization of metronidazole-resistant strains. Clinical Infectious Diseases 25, S2667. 7. Pelez, T., Alonso, R., Prez, C., Alcal, L., Cuevas, O. & Bouza, E. 2002 ; . In vitro activity of linezolid against Clostridium difficile. Antimicrobial Agents and Chemotherapy 46, 16178. 8. Ackermann, G., Tang, Y. T., Kueper, R., Heisig, P., Rodloff, A. C., Silva, J., Jr et al. 2001 ; . Resistance to moxifloxacin in toxigenic Clostridium difficile isolates is associated with mutations in the gyrA gene. Antimicrobial Agents and Chemotherapy 4, 234853. 9. Wilcox, M. H., Fawley, W., Freeman, J. & Brayson, J. 2000 ; . In vitro activity of new generation fluoroquinolones against genotypically distinct and indistinguishable Clostridium difficile isolates. Journal of Antimicrobial Chemotherapy 46, 5515. 10. Arthur, M., Brisson-Nol, A. & Courvalin, P. 1987 ; . Origin and evolution of genes specifying resistance to macrolide, lincosamide and streptogramin antibiotics: data and hypotheses. Journal of Antimicrobial Chemotherapy 20, 783802. 11. Sutcliffe, J., Tait-Kamradt, A. & Wondrack, L. 1996 ; . Streptococcus pneumoniae and Streptococcus pyogenes resistant to macrolides but sensitive to clindamycin: a common resistance pattern mediated by an efflux system. Antimicrobial Agents and Chemotherapy 40, 181724. 12. Weisblum, B. 1995 ; . Erythromycin resistance by ribosome modification. Antimicrobial Agents and Chemotherapy 39, 57785. 13. Wst, J. & Hardegger, U. 1983 ; . Transferable resistance to clindamycin, erythromycin, and tetracycline in Clostridium difficile. Antimicrobial Agents and Chemotherapy 2, 7846. 14. Farrow, K. A., Lyras, D. & Rodd, J. I. 2001 ; . Genomic analysis of the erythromycin resistance element Tn5398 from Clostridium difficile. Microbiology 147, 271728. 15. Mullany, P., Wilks, M. & Tabaqchali, S. 1995 ; . Transfer of B MLS ; resistance in and mysoline. Table 3 Summary of base case and sensitivity analyses results for the cost-effectiveness model * Parameter modified Parameter value Incremental cost MLY MoH Base case Time horizon Discount rate NA 6 years 0.00 0.03 ' 25% Probability of CDMS 25% Indirect costs ' 25% Mono indirect costs 0% 50% Dose of oral prednisone 1 mg day for 14 days 110 116 098 243 685 828 NA NA NA 692 SOC 789 335 382 776 567 241 709 869 828 798 and moxifloxacin.

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Susceptibility testing was performed using serial twofold broth microdilution as described previously Brown et al., 1992; NCCLS, 2000; Wallace et al., 1986 ; . Microdilution plates were prepared inhouse using Middlebrook 7H9 broth Difco ; supplemented with 5 % oleic acid albumin dextrose enrichment. A range of seven or eight concentrations was tested for each antimicrobial. Stock concentrations of the following antimicrobial agents were prepared from manufacturers' powders: rifampicin, ethambutol, isoniazid, amikacin and sulfamethoxazole Sigma ; , ciprofloxacin and moxifloxacin Bayer ; , rifabutin and linezolid Pharmacia ; , streptomycin ICN ; , clarithro mycin Abbott ; and levofloxacin Jansen-Othro ; . The 13 Quebec isolates and strain 00-250T from the case history were tested at a final inoculum of 103104 c.f.u. ml21. Microdilution plates were sealed in plastic bags and incubated at 37 uC until macroscopic growth was sufficient for interpretation 714 days ; . MICs were defined as the lowest concentration of drug to inhibit visible growth, with the exception of sulfamethoxazole, for which the MIC is determined at 80 % inhibition of growth compared with the growth control well. Quality control was performed using M. avium ATCC 700898, Mycobacterium marinum ATCC 927T Wallace et al., 1986 ; and M. avium NJ-9141 Heifets et al., 1993 ; . Staphylococcus aureus ATCC 29213 was used as a quality-control strain in cation-supplemented MuellerHinton broth when MIC ranges for mycobacteria were not available and nadolol.

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By fluoroquinolones. Antimicrobial Agents and Chemotherapy 44, 316973. 9. Blank, M., George, J., Fishman, P., Levy, Y., Toder, V., Savion, S. et al. 1998 ; . Ciprofloxacin immunomodulation of experimental antiphospholipid syndrome associated with elevation of interleukin-3 and granulocyte-macrophage colony-stimulating factor expression. Arthritis and Rheumatism 41, 22432. 10. Shalit, I., Kletter, Y., Halperin, D., Waldman, D., Vasserman, E., Nagler, A. et al. 2001 ; . Immunomodulatory effects of moxifloxacin in comparison to ciprofloxacin and G-CSF in a murine model of cyclophosphamide-induced leukopenia. European Journal of Haematology 66, 28796. 11. Casey, L. C. 1997 ; . Antibiotics: more than just `bug' killers. Critical Care Medicine 25, 12701. 12. Reisbeck, K., Forsgren, A., Henriksson, A. & Bredberg, A. 1998 ; . Ciprofloxacin induces an immunomodulatory stress response in human T lymphocytes. Antimicrobial Agents and Chemotherapy 42, 192330. 13. Riesbeck, K., Sigvardsson, M., Leanderson, T. & Forsgren, A. 1994 ; . Superinduction of cytokine gene transcription by ciprofloxacin. Journal of Immunology 153, 34352. 14. Riesbeck, K. & Forsgren, A. 1990 ; . Selective enhancement of synthesis of interleukin-2 in lymphocytes in the presence of ciprofloxacin. European Journal of Clinical Microbiology and Infectious Diseases 9, 409. 15. Bailly, S., Fay, M., Ferrua, B. & Gougerot-Pocidalo, M. A. 1991 ; . Ciprofloxacin treatment in vivo increases the ex vivo capacity of lipopolysaccharide-stimulated human monocytes to produce IL-1, IL-6 and tumor necrosis factor-alpha. Clinical Experimental Immunology 85, 3314. 16. Galley, H. F., Nelson S. J., Dubbels A. M. & Webster N. R. 1997 ; . Effect of ciprofloxacin on the accumulation of interleukin-6, interleukin-8, and nitrite from a human endothelial cell model of sepsis. Critical Care Medicine 25, 13925. 17. Gallay, P., Heumann, D., Le Roy, D., Barras, C. & Glauser, M. P. 1994 ; . Mode of action of anti-lipopolysaccharide-binding protein antibodies for prevention of endotoxemic shock in mice. Proceedings of the National Academy of Sciences, USA 91, 79226. 18. Richards, C. D. & Gauldie, J. 1995 ; . Role of cytokines in acutephase response. In Human Cytokines: Their Role in Disease and Therapy Agarwal, B. B. & Puri, R. K., Eds ; , pp. 25369. Blackwell Science, Cambridge, MA, USA. 19. Parrillo, J. E., Parker, M. M., Natanson, C., Suffredini, A. F., Danner, R. L., Cunnion, R. E. et al. 1991 ; . Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction and therapy. Annals of Internal Medicine 113, 22732. 20. Trinchieri, G. 1995 ; . Interleukin-12: a proinflammatory cytokine with immunoregulatory functions that bridge innate resistance and antigen-specific adaptive immunity. Annual Review of Immunology 13, 25176. 21. Schluter, G. 1989 ; . Ciprofloxacin: toxicologic evaluation of additional safety data. American Journal of Medicine 87, S379. 22. Kashida, Y. & Kato, M. 1997 ; . Characterization of fluoroquinolone-induced achilles tendon toxicity in rats: comparison of toxicities of 10 fluoroquinolones and effects of anti-inflammatory compounds. Antimicrobial Agents and Chemotherapy 41, 238993.

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LITERATURE CITED 1. Okey, R., M. M. Lyman, A. G. Harris, B. Einset and W. Hain 1959 Dietary fat and cholesterol metabolism: Effects of unsaturation of dietary fats on liver and serum lipids. Metabolism, 8: 241. 2. Kinsell, L. W., J. Partridge, L. Boling, S. Margen and G. Michaels 1952 Dietary modifications of serum cholesterol and phos pholipid levels. J. Clin. Endocrinol., 12: 909. 3. Beveridge, J. M. R., W. F. Connell, G. A. Mayer, J. B. Firstbrook and M. S. DeWolfe 1955 The effects of certain vegetable and animal fats on the plasma lipids of humans. J. Nutrition, 56: 311. 4. Boyd, E. M. 1942 Species variation in nor mal plasma lipids estimated by oxidative micromethods. J. Biol. Chem., 143: 131. 5. Fillios, L. C., S. B. Andrus, G. V. Mann and F. J. Stare 1956 Experimental production of gross atherosclerosis in the rat. J. Exp. Med., 104: 539. 6. Folch, J., I. Ascoli, M. Lees, J. A. Meath and F. N. LeBaron 1951 Preparation of lipide extracts from brain tissue. J. Biol. Chem., 192: 833. 7. Abell, L. L., B. B. Levy, B. B. Brodie and F. E. Kendall 1952 A simplified method for the estimation of total cholesterol in serum and demonstration of its specificity. J. Biol. Chem., 195: 357 and nafcillin. INTRODUCTION The mainstay of current therapy for disease caused by the Mycobacterium avium complex hereafter referred to as MAC ; are macrolide agents 2, 4, 12, ; , while ethambutol and rifabutin are also used as part of a macrolide containing regimen 15, 21 ; . Moxifloxacin and ketolides, including telithromycin, have been shown in experimental animal systems to be active and mrv.

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