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T Alarcon

Publications and source records attributed to T Alarcon.

5 recordsLinked to original sources
PubMed2006

Modelling aspects of cancer dynamics: a review.

Cancer is a complex disease in which a variety of factors interact over a wide range of spatial and temporal scales with huge datasets relating to the different scales available. However, these data do not always reveal the mechanisms underpinning the observed phenomena. In this paper, we explain why mathematics is a powerful tool for interpreting such data by presenting case studies that illustrate the types of insight that realistic theoretical models of solid tumour growth may yield. These range from discriminating between competing hypotheses for the formation of collagenous capsules associated with benign tumours to predicting the most likely stimulus for protease production in early breast cancer. We will also illustrate the benefits that may result when experimentalists and theoreticians collaborate by considering a novel anti-cancer therapy.

Animals↗
PubMed2002

Comparison of the E test and agar dilution method for antimicrobial suceptibility testing of Helicobacter pylori.

A multicentre study was carried out in order to validate the E test in comparison with the reference agar dilution method for testing the susceptibility of Helicobacter pylori to amoxicillin, clarithromycin, and metronidazole. Ten clinical isolates and one control collection isolate ( Helicobacter pylori ATCC 43504) were tested blindly at four centres according to a uniform methodology. The E test showed excellent intra- and inter-laboratory correlations with the agar dilution method for amoxicillin and clarithromycin (>98% agreement within 2 log(2) dilution steps). For metronidazole, however, the E test revealed significantly higher minimum inhibitory concentration values (>2 log(2)) against 5 of the 10 Helicobacter pylori strains tested. Overall, neither method was found reliable for testing the susceptibility of Helicobacter pylori to metronidazole, since both tended to lack reproducibility.

Amoxicillin↗
PubMed2000

Sequential inactivation of rdxA (HP0954) and frxA (HP0642) nitroreductase genes causes moderate and high-level metronidazole resistance in Helicobacter pylori.

Helicobacter pylori is a human-pathogenic bacterial species that is subdivided geographically, with different genotypes predominating in different parts of the world. Here we test and extend an earlier conclusion that metronidazole (Mtz) resistance is due to mutation in rdxA (HP0954), which encodes a nitroreductase that converts Mtz from prodrug to bactericidal agent. We found that (i) rdxA genes PCR amplified from 50 representative Mtz(r) strains from previously unstudied populations in Asia, South Africa, Europe, and the Americas could, in each case, transform Mtz(s) H. pylori to Mtz(r); (ii) Mtz(r) mutant derivatives of a cultured Mtz(s) strain resulted from mutation in rdxA; and (iii) transformation of Mtz(s) strains with rdxA-null alleles usually resulted in moderate level Mtz resistance (16 microg/ml). However, resistance to higher Mtz levels was common among clinical isolates, a result that implicates at least one additional gene. Expression in Escherichia coli of frxA (HP0642; flavin oxidoreductase), an rdxA paralog, made this normally resistant species Mtz(s), and frxA inactivation enhanced Mtz resistance in rdxA-deficient cells but had little effect on the Mtz susceptibility of rdxA(+) cells. Strains carrying frxA-null and rdxA-null alleles could mutate to even higher resistance, a result implicating one or more additional genes in residual Mtz susceptibility and hyperresistance. We conclude that most Mtz resistance in H. pylori depends on rdxA inactivation, that mutations in frxA can enhance resistance, and that genes that confer Mtz resistance without rdxA inactivation are rare or nonexistent in H. pylori populations.

Amino Acid Substitution↗
PubMed1997

Evolution of resistance to metronidazole and clarithromycin in Helicobacter pylori clinical isolates from Spain.

The aim of this study was to determine the frequency of resistance to amoxycillin, tetracycline, metronidazole and clarithromycin in 282 Helicobacter pylori clinical isolates from Spain and to evaluate the evolution of resistance over the five years of this study. The overall percentage of resistance was 19.9% for metronidazole and 3.5% for clarithromycin. Resistance to metronidazole rose from 9% in 1991 to 21.6% in 1995, although 33.3% resistance was found in 1993. Clarithromycin resistance was not detected in 1991 or 1992 and the rate was 4%, 3.4% and 4.4% in 1993, 1994 and 1995, respectively. No amoxycillin or tetracycline resistance was found.

Adolescent↗