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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 194 (2001), S. 0 
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: A strain of Corynebacterium pseudotuberculosis, designated Toxminus, that has been rationally attenuated by deletion of the phospholipase D gene, is being developed as a live vaccine vector for the delivery of veterinary vaccine antigens. In the present study a recombinant form of the basic protease gene of the ovine footrot causative bacterium, Dichelobacter nodosus, was introduced into the vector strain using the high copy number plasmid pEP2. This strain secreted the basic protease protein. Vaccination trials in sheep with the recombinant strain demonstrated that, although an IgG immune response was elicited, the animals were not protected from footrot following artificial challenge under pen conditions. Although the sheep were not protected there was evidence that the progression of the disease was slowed.
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Company
    Nature biotechnology 16 (1998), S. 190-195 
    ISSN: 1546-1696
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: [Auszug] Low-molecular-weight synthetic molecules that mimic the activity of native biological macromolecules have therapeutic potential, utility in large-scale production of biopharmaceuticals, and the capacity to act as probes to study molecular recognition events. We have developed a nonpeptidyl mimic ...
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    The protein journal 7 (1988), S. 157-164 
    ISSN: 1573-4943
    Keywords: Bacteroides nodosus ; amino acid sequence ; pilus ; pilin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Amino acid sequences of pilin from a strain of Bacteroides nodosus from serogroup B (234) and serogroup C (217) were determined. The amino-terminal N-methylphenlalanine residue of both proteins was followed by a hydrophobic sequence of 30 residues closely related to the N-terminal sequence of other pili having an amino-terminal residue of N-methylphenylalanine. These data lend support to the hypothesis that in pilins of this type, the amino-terminal sequence functions as a transport signal necessary for pilin to reach its external environment, as well as promoting intersubunit interactions for muintenance of the structural integrity of the pilus. Two hydrophilic hypervariable regions can be discerned across the pilin sequences, indicating possible locations of antigenic domains.
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  • 4
    ISSN: 1573-0662
    Keywords: δ3-carene ; chlorine atoms ; isoprene ; kinetics ; methacrolein and methyl vinyl ketone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Geosciences
    Notes: Abstract The rate coefficients for the reaction between atomic chlorine and a number of naturally occurring species have been measured at ambient temperature and atmospheric pressure using the relative rate technique. The values obtained were (4.0 ± 0.8) × 10-10, (2.1 ± 0.5) × 10-10, (3.2 ± 0.5) × 10-10, and (4.9 ± 0.5) × 10-10 cm3 molecule-1 s-1, for reactions with isoprene, methyl vinyl ketone, methacrolein and δ3-carene, respectively. The value obtained for isoprene compares favourably with previously reported values. No values have been reported to date for the rate constants of the other reactions.
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  • 5
    ISSN: 1573-0646
    Keywords: resistance ; active ; passive ; competitive ; noncompetitive ; dose-response curve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary With chemotherapy, the in vitro and clinical dose-response curve is steep in some situations, but is relatively flat in others, possibly due to the mechanism by which tumors are resistant to chemotherapy. For tumors with resistance due to factors that actively decrease chemotherapy efficacy (e.g., p-glycoprotein, glutathione, etc.), one would predict that high dose chemotherapy and therapy with some resistance modulating agents would increase therapeutic efficacy. Such “active” resistance would most likely generally arise from gene amplification or over expression, and would be characterized by a shoulder on the log response vs. dose curve, with eventual saturation of the protective mechanism. On the other hand, one would expect that high dose chemotherapy and most resistance modulating agents would be of little value for rumors with resistance due to defective apoptosis or due to a deficiency in or decreased drug affinity for a drug target, drug activating enzyme, drug active uptake system, or essential cofactor. Such “passive” resistance would most likely generally arise from gene down regulation, deletion, or mutation, and would probably be characterized by a relatively flat log response vs. dose curve, or by a curve in which a steep initial section is followed by a plateau, as target, etc., is saturated. (If response were plotted vs. log dose, then compared to the curve for a sensitive cell line, the curve for active resistance would be analogous to the pharmacodynamic curve seen with competitive antagonism [i.e., a sigmoid curve shifted to the right], and the curve for most types of passive resistance would be analogous to the pharmacodynamic curve seen with noncompetitive antagonism [i.e., a sigmoid curve with reduced maximal efficacy]. As such, one might also refer to active vs. passive resistance as competitive vs. noncompetitive resistance, respectively.) Many tumor types probably possess a combination of active and passive mechanisms of resistance. New in vivo strategies could be helpful in defining dose-response relationships, mechanisms of resistance, and targets for resistance modulation. Such in vivo studies would be conducted initially in animals, but might also be tested clinically if animal studies demonstrated them to be feasible and useful. These in vivo studies would be conducted by randomizing 5–25 subjects to one of 10–20 dose levels over a potentially useful therapeutic range. Nonlinear regression analysis would then be used to define the characteristics of a curve generated by plotting against dose the log percent tumor remaining after the first course of therapy. While this might offer insight into the nature of resistance mechanisms present initially, plotting further tumor shrinkage vs. dose-intensity vs. course number for each later treatment course (or plotting dose-intensity vs. time to tumor progression) might provide information on how tumors become increasingly resistant to drugs following treatment.
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  • 6
    ISSN: 1573-0646
    Keywords: chemotherapy ; carboplatin ; resistance modulators ; pentoxifylline ; metronidazole ; tamoxifen ; dipyridamole ; ketoconazole ; novobiocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Background: Chemotherapy resistance is probably multifactorial; hence, we assessed the feasibility of adding to carboplatin 6 concurrent resistance modulators in 53 patients with resistant cancers. Methods: Pentoxifylline and dipyridamole were added to carboplatin 400 mg/m2 in cohort 1, and metronidazole was also given in cohort 2. Mannitol and saline were administered in each cohort with the theoretical objective of improving carboplatin delivery to tumors by reducing blood viscosity. Because of excessive toxicity in cohort 2, cohort 3 received the same modulators as in cohort 2 but with a reduced dose of carboplatin (200 mg/m2). Subsequent patients had the following drugs added to those in the previous cohort: novobiocin (cohort 4), tamoxifen (cohort 5), ketoconazole (cohort 6). Cohort 7 patients received the 6 cohort 6 modulators along with carboplatin 300 mg/m2. Results: Thrombocytopenia was excessive in early cohorts with a carboplatin dose of 400 mg/m2, but was minimal at lower doses. Other toxicity was generally tolerable and reversible, particularly at carboplatin doses ≤ 300 mg/m2, although gastrointestinal and neurological toxicity tended to worsen as additional modulators were added. No major responses (but 4 minor responses) were seen in this patient population with heavily pretreated or primarily resistant cancers. Conclusions: Acceptable doses for phase II studies are carboplatin 300 mg/m2, 20% mannitol 250 ml plus normal saline 500 ml over 1 hr prior to carboplatin, pentoxifylline 700 mg/m2/day p.o. from 3 days before carboplatin to cessation of therapy, dipyridamole 100 mg/m2 p.o. q6h × 6 days starting 24 hr before carboplatin, metronidazole (750 mg/m2 p.o. 12 hr and immediately before, and 24 hr after carboplatin; 250 mg/m2 suppository p.r. 12 hr and immediately before, and 6 and 24 hr after carboplatin; and 500 mg/m2 i.v. right after carboplatin), novobiocin 600 mg/m2 p.o. q12h × 6 days starting 24 hr before carboplatin, and tamoxifen 100 mg/m2/day plus ketoconazole 700 mg/m2/day × 3 days starting the day before carboplatin, with oral dexamethasone and ondansetron as antimetics.
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  • 7
    ISSN: 1573-0646
    Keywords: breast cancer ; hormone therapy ; flutamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The National Cancer Institute of Canada (NCIC) Clinical Trials Group conducted a phase II study of the oral antiandrogen flutamide in 33 patients with metastatic breast cancer. Eight patients had received no prior systemic therapy for their metastatic disease and 13 had only one site of metastasis. Toxicity occurred in 18 of the 33 patients and was primarily gastrointestinal. It ranged in severity from mild to severe with 4 patients discontinuing treatment early because of nausea, vomiting, diarrhea or stomatitis. One response, of 8 weeks duration, was noted in 29 evaluable patients. We conclude that flutamide does not have meaningful anti-tumour activity in breast cancer and plan no further trials of the drug in this disease.
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  • 8
    ISSN: 1573-0646
    Keywords: menogarilm ; phase I ; oral chemotherapy ; weekly chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Forty-seven patients with solid tumors were treated on a phase I study of menogaril administered by mouth once per week. Nausea and vomiting were excessive at weekly doses of 350 and 450 mg/m2/week but were tolerable and controlled reasonably well by antiemetics at lower doses. There appeared to be a relatively shallow dose-vs-granulocytopenia curve above a menogaril dose of 180 mg/m2/week. No patient receiving chronic dexamethasone for cerebral edema developed granulocytopenia, even at menogaril doses of 350–450 mg/m2/week. Two patients developed neutropenic infection. No patient developed thrombocytopenia. Mild arrhythmias were seen in 3 patients. Two patients suffered possible myocardial infarcts that may not have been related to treatment. Asymptomatic blood pressure fluctuations were common and were probably not related to treatment. Diarrhea was dose-related but was generally not severe. Alopecia and stomatitis occurred occasionally. Minor responses were seen in two patients with gliomas, and three of five evaluable prostate cancer patients experienced marked pain relief. The dose recommended for phase II studies is 250–300 mg/m2/week with antiemetic pretreatment. This schedule appears to allow an oral menogaril doseintensity that is approximately double that attainable with other oral schedules that have been studied.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Investigational new drugs 9 (1991), S. 343-344 
    ISSN: 1573-0646
    Keywords: lonidamine ; prostate cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Investigational new drugs 4 (1986), S. 387-394 
    ISSN: 1573-0646
    Keywords: tiazofurin ; pharmacology ; phase I
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract A pharmacokinetic study of tiazofurin was carried out in 13 patients treated in a phase I clinical trial of the drug and in 7 patients undergoing surgical resection of brain tumor (in conjunction with studies on penetration of drug into central nervous system tumors). Tiazofurin was found to be rapidly eliminated from the plasma and red blood cell fraction of both groups of patients with kinetics consistent with a two-compartment model of elimination. Operative conditions did not significantly change the pharmacokinetics of tiazofurin in CNS patients. Pharmacokinetics were linear over the dose range 500–2700 mg/m2. The data suggest that there is only a small degree of tissue binding of drug and that the drug is not concentrated by tissues. Uptake into RBC was rapid and elimination from RBC was essentially parallel to drug elimination from plasma. There was no evidence that RBC sequestration of drug contributes to toxicity. Much of the drug was excreted unchanged in the urine, but there was little correlation between creatinine clearance and plasma pharmacokinetics of tiazofurin, suggesting that renal tubular secretion may be a more important method of elimination than is glomerular filtration. Patients with high AUC values and low plasma clearance values were particularly prone to develop toxicity.
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